Official Symbol: BRAFprovided by HGNC
Official Full Name: v-raf murine sarcoma viral oncogene homolog B1provided by HGNC
Primary Source: HGNC:1097
See related: Ensembl:ENSG00000157764; HPRD:01264; MIM:164757
Gene type: protein coding
RefSeq status: REVIEWED
Organism: Homo sapiens
Lineage: Eukaryota; Metazoa; Chordata; Craniata; Vertebrata; Euteleostomi; Mammalia; Eutheria; Euarchontoglires; Primates; Haplorrhini; Catarrhini; Hominidae; Homo
Also known as: BRAF1; RAFB1; B-RAF1; FLJ95109; MGC126806; MGC138284; BRAF
Summary: This gene encodes a protein belonging to the raf/mil family of serine/threonine protein kinases. This protein plays a role in regulating the MAP kinase/ERKs signaling pathway, which affects cell division, differentiation, and secretion. Mutations in this gene are associated with cardiofaciocutaneous syndrome, a disease characterized by heart defects, mental retardation and a distinctive facial appearance. Mutations in this gene have also been associated with various cancers, including non-Hodgkin lymphoma, colorectal cancer, malignant melanoma, thyroid carcinoma, non-small cell lung carcinoma, and adenocarcinoma of lung. A pseudogene, which is located on chromosome X, has been identified for this gene. [provided by RefSeq]

[Top][Help]Genomic regions, transcripts, and products

(minus strand) Go to reference sequence details Try our new Sequence Viewer

[Top][Help]Genomic context

chromosome: 7; Location: 7q34See BRAF in MapViewer

[Top][Help]Bibliography

GeneRIFs: Gene References Into Function What's a GeneRIF?

	1.	Mutations in BRAF protein is associated with Colorectal Carcinoma.
	2.	simultaneous depletion of both MITF and BRAF(V600E) significantly inhibited melanoma growth even for the melanoma cell lines resistant to MITF depletion
	3.	BRAF mutations represent an alternative molecular pathway in the early tumorigenesis of a subset of KIT/PDGFRA wild-type GISTs and are per se not associated with a high risk of malignancy.
	4.	Reverse transcription polymerase chain reaction-based sequencing revealed a fusion product between KIAA1549 and BRAF in pediatric low-grade astrocytomas
	5.	Results suggest that the mutations of EGFR, KRAS, BRAF between primary tumors and corresponding lymph node metastases should be considered whenever mutations are used for the selection of patients for EGFR-directed tyrosine kinase inhibitor therapy.
	6.	data confirm that KRAS and BRAF mutations do occur in the same cell and that BRAF V600E mutation is associated with CIMP+ status.
	7.	BRAF V600E mutation analysis can significantly improve FNAB diagnostic accuracy.
	8.	Sorafenib inhibits NSCLC cell growth by targeting B-RAF in cells with wild-type KRAS and C-RAF in those with mutant KRAS.
	9.	strong inter-relation between DR4 AND DR5 overexpression and presence of oncogenic KRAS/ BRAF mutations in colon cancer.
	10.	Observational study of gene-disease association and DATA ERROR. (HuGE Navigator)
	11.	Expression levels of fibronectin, vimentin and CITED1 were positively correlated with those of BRAFV600E, suggesting pathophysiological links between activated BRAF and overexpression of these genes.
	12.	study concludes that a BRAF mutation is a negative prognostic marker in patients with metastatic colorectal cancer
	13.	Assessing KRAS and BRAF mutations might help optimising the selection of the candidate metastatic colorectal cancer patients to receive anti-EGFR moAbs.
	14.	BRAF(V600E)'alone' does not represent a marker for poor outcome
	15.	Mutations in BRAF were found 10% patients in the low-grade carcinoma group, however, they were not found in the high-grade carcinoma group. KRAS and BRAF mutations were mutually exclusive, and both mutations were observed in 40%.
	16.	MLH1-hypermethylated tumors harbor fewer APC and KRAS mutations and more BRAF mutations, suggesting that they develop distinctly from an MGMT methylator pathway.
	17.	BRAF V600E mutation is not the target gene for abnormal DNA mismatch repair in patients with sporadic endometrial cancer.
	18.	Pilocytic astrocytomas had BRAF fusions in 70% of cases but not IDH1 or IDH2 mutations. Diffuse astrocytomas had IDH1 mutations in 76% of cases but not IDH2 mutations or BRAF fusions. Analysis of BRAF and IDH1 separates pilocytic from diffuse astrocytoma.
	19.	BRAF mutations may not play an important role in the oncogenesis or therapy of prostate adenocarcinoma
	20.	The RAS/RAF/MEK/ERK signaling pathway has emerged as a major player in the induction and maintenance of melanoma, particularly the protein kinase BRAF, mutated in approximately 44% of melanoma cases. Review.
	21.	BRAF (P=0.01) mutations predicted reduced progress free survival in response to cetuximab salvage therapy in patients with metastatic colorectal cancer .
	22.	Investigated BRAF mutations in 30 bladder tumors. Detected two tumor specimens bearing two different mutations, both of which were found in exon 15. One sample showed the T1799A (V600E) and the other the G1798T (V600L) mutation.
	23.	There is a higher frequency of the BRAF(V600E) mutation in papillary thyroid carcinomas than in normal thyroid tissue.
	24.	BRAF V600E mutation was significantly found in papillary thyroid carcinoma.
	25.	mismatch repair deficiency is not a crucial event for BRAF mutation in melanocytic tumors
	26.	B-RAF mutation was found to be significantly higher in papillary carcinomas when compared to follicular variant of papillary thyroid carcinomas (55.6% vs 14.3%, P = 0.05).
	27.	BRAF(V600E) is associated some of the aggressive clinicopathological features of papillary thyroid carcinoma including younger age at diagnosis, larger tumor size, and classic histological type, as well as also extrathyroidal invasion.
	28.	BRAF and RET/PTC dual mutations are associated with recurrent papillary thyroid carcinoma
	29.	Targeting NRAS alone or both BRAF and CRAF in combination or both BRAF and PIK3CA together showed delay in tumor growth.
	30.	BRAF mutated tumors occurred with a much greater frequency in proximal colon tumors than in either distal colon or rectal tumors
	31.	Findings provide evidence for a wide phenotypic diversity associated with mutations affecting BRAF, and occurrence of a clinical continuum associated with these molecular lesions.
	32.	The murine model of mutant BRAF-induced melanoma formation provides an important tool for identifying further genetic alterations that cooperates with BRAF and that may be useful in enhancing susceptibility to BRAF-targeted therapeutics in melanoma.
	33.	In BRAF mutated colorectal carcinoma cells quercetin, luteolin and ursolic acid decreased Akt phosphorylation
	34.	BRAFT1799A mutation or RET/PTC rearrangement, mainly corresponding to follicular variants, maintain a thyroid differentiation expression level close to that of normal tissue.
	35.	Mutation in BRAF is associated with adrenocortical carcinomas.
	36.	If BRAF is mutated in the primary thyroid neoplasm, it is likely that the metastases will harbor the defect.
	37.	Report efficient molecular screening of Lynch syndrome by specific 3' promoter methylation of the MLH1 or BRAF mutation in colorectal cancer with high-frequency microsatellite instability.
	38.	Sessile serrated adenomas are encountered commonly in routine endoscopy practice and the histological diagnosis correlates strongly with the presence of BRAF mutation.
	39.	a subpopulation of melanocytes possesses the ability to survive BRAF(V600E)-induced senescence
	40.	NRAS and BRAF mutations increase from the radial to the vertical growth phase in cutaneous melanoma
	41.	Targets of phosphorylation by B-Raf signaling are investigated in melanoma.
	42.	oncogenic BRAF(V600E) induces the uncoupling of LKB1-AMPKalpha complexes providing at the same time a possible mechanism in cell proliferation that engages cell growth and cell division in response to mitogenic stimuli
	43.	(novel) mutation in the activation kinase domain of the BRAF (A598V), this mutation led to the up-regulation of the BRAF kinase activity and its downstream signaling factors.
	44.	Mutation in BRAF is associated with ERK1/2 activation and MEK1/2 inhibitor therapy in colorectal cancer.
	45.	Both BRAF and RKIP expression levels exhibit a decrease from normal skin tissue and actinic keratosis, going to squamous cell carcinoma.
	46.	Mutations are absent or rare in the kinase domain of B-RAF in Japanese head and neck squamous cell carcinoma.
	47.	GDC-0879-mediated efficacy was associated strictly with BRAF(V600E) status, MEK inhibition also attenuated proliferation and tumor growth of cell lines expressing wild-type BRAF.
	48.	REVIEW summarizes the literature on NRAS and BRAF activating mutations in melanoma tumors with respect to available data on histogenetic classification as well as body site and presumed UV-exposure.
	49.	The genes whose expression is associated with BRAF mutations are not simply restricted to the MAPK/ERK signaling but also converge to enhanced immune responsiveness, cell motility and melanosomes processing involved in the adaptative UV response
	50.	The T1799A BRAF mutation does not appear to play a role in the tumorigenesis of the cribriform-morular variant of papillary carcinoma.
	51.	Observational study of gene-disease association and genetic testing. (HuGE Navigator)
	52.	a correlation between a gene mutation--BRAF V600E--and cisplatin resistance in nonseminomatous germ cell tumors.
	53.	Our data provide evidence that PIK3CA and BRAF contribute to the tumorigenesis of IPMN/IPMC, but at a lower frequency than KRAS.
	54.	ERK activation was induced by PKD2 overexpression via B-Raf signaling, providing a possible molecular mechanism of cystogenesis
	55.	the presence of the braf protein mutation increases prohibitin promoter activity and therefore potentially mediates effects of this mutation on the behavior of BRAF protein
	56.	BRAF(V600E) mutation is assocciated with aggressive papillary thyroid microcarcinoma.
	57.	K-ras, EGFR, and BRAF mutations are disproportionately seen in adenocarcinomas of lung with a dominant micropapillary growth pattern compared with conventional adenocarcinoma in our institutional experience.
	58.	BRAF* melanomas appear to be associated with a specific profile of DNA copy number aberrations that is distinct from those found in NRAS* and BRAF/NRAS(wt/wt) tumors.
	59.	BRAF(V600E) mutation may play some roles in local carcinoma development, there is no evidence that BRAF(V600E) mutation significantly reflects the aggressive characteristics and poor prognosis of patients with papillary carcinoma in Japan.
	60.	BRAF V600E appeared to be the most commonly mutated gene in both the melanocytic aggregate (seven of 18, 39%) and the melanoma (four of 18, 22%)
	61.	G12D mutation may be more likely selected in a BRAF mutated context
	62.	Distinct BRAF (V600E) and KRAS mutations in high microsatellite instability sporadic colorectal cancer in African Americans.
	63.	In Korean patients with papillary thyroid carcinoma, the BRAFV600E mutation is associated with a lower frequency of background Hashimoto thyroiditis and a high frequency of lymph node metastasis.
	64.	Clinical trial of gene-disease association, gene-environment interaction, and pharmacogenomic / toxicogenomic. (HuGE Navigator)
	65.	influence of B-RAF-specific RNA interference on the proliferation and apoptosis of gastric cancer BGC823 cell line
	66.	study identified a group of melanomas with low-activity BRAF mutations (G469E- and D594G) that are reliant upon CRAF-mediated survival activity
	67.	study concludes a single endogenous BRAF(V600E) allele is sufficient to repress BIM & prevent death from growth factor withdrawal; colorectal cancer cells with V600E mutations are addicted to the ERK1/2 pathway for repression of BIM
	68.	Genetic extinction of BRAF(V600E) in established prostate tumors did not lead to tumor regression, indicating that while sufficient to initiate development of invasive prostate adenocarcinoma, BRAF(V600E) is not required for its maintenance.
	69.	N-RAS(Q61K) and B-RAF(V600E) contribute to melanoma's resistance to apoptosis in part by downregulating Bim expression
	70.	BRAF pseudogene activation may play a role in thyroid tumor development.
	71.	hyperactivation of the MAPK pathway following activation of an inducible form of oncogenic C-Raf induces a senescence-like proliferation arrest in B-Raf mutant melanoma cells
	72.	Hereditary pancreatitis patients with PRSS1 mutations also had mutations in BRAF and KRAS2.
	73.	BRAF mutation is associated with the CpG island methylator phenotype in colorectal cancer from young patients
	74.	The frequencies of LOHs of 17q21, 17p13, 10q23, and 22q13 were higher in tumors with lymph node metastasis, suggesting that these LOHs may be important in increased lymph node metastasis.
	75.	CIMP-high appears to be an independent predictor of a low colon cancer-specific mortality, while BRAF mutation is associated with a high colon cancer-specific mortality.
	76.	Observational study and meta-analysis of gene-disease association. (HuGE Navigator)
	77.	Examined associations between BRAF mutations, morphology, and apoptosis in early colorectal cancer.
	78.	Wild-type BRAF is required for response to panitumumab or cetuximab in metastatic colorectal cancer.
	79.	BRAF-V600E mutation is uncommon in endocrine tumors other than thyroid papillary carcinomas
	80.	8% of sporadic colorectal tumors in this study harbor mutation in the BRAF gene.
	81.	ovarian cancer patients with KRAS or BRAF mutations may benefit from CI-1040 treatment
	82.	Identification and functional characterization of a novel T599I-VKSR(600-603)del BRAF mutation in a patient with follicular variant papillary thyroid carcinoma.
	83.	study shows high expression of p16(INK4a) or the absence of activated B-RAF correlates with in vivo response of melanoma to cytotoxic drugs
	84.	presence of the BRAF (V600E) mutation,the incidence of microsatellite instability high colorectal cancer in populations based study.
	85.	These data suggest that regulation of BIM expression by BRAF-->MEK-->ERK signaling is one mechanism by which oncogenic BRAF(V600E) can influence the aberrant physiology of melanoma cells.
	86.	MLH1 methylation and BRAF mutations are associated with microsatellite unstable colon tumors
	87.	V600E BRAF mutation is associated with imatinib-resistant gastrointestinal stromal tumors
	88.	The BRAF(V600E) mutation was demonstrated to be a poor prognostic factor independent from other clinicopathological features.
	89.	the T1799A BRAF mutation is present in a proportion of posterior uveal melanomas but within these tumours the distribution of the mutation is heterogeneous.
	90.	rearrangement, which was not observed in a series of 244 higher-grade astrocytomas, results in an in-frame fusion gene incorporating the kinase domain of the BRAF oncogene
	91.	With at least 3 markers methylated, new CIMP-positive colorectal cancers were closely associated with proximal tumor location, low frequency of KRAS mutation, and high frequency of BRAF mutation.
	92.	BRAF mutation occurs independently of CpG island methylator phenotype and MSI in all types of serrated polyps and may serve as a marker of serrated pathway of colorectal carcinogenesis
	93.	These data implicates a mitotic role for B-Raf in regulating spindle formation and the spindle checkpoint in human somatic cells.
	94.	BRAF, KRAS and PIK3CA mutations occur prior to malignant transformation demonstrating that these oncogenic alterations are primary genetic events in colorectal carcinogenesis
	95.	People of southern European origin had lower risk of colorectal cancers with CIMP and BRAF mutation than people of Anglo-Celtic origin, which may in part be due to genetic factors that are less common in people of southern European origin.
	96.	Shorter overall survival in primary melanoma was associated with the presence of ulceration and BRAF exon 15 mutations, as well as the absence of nuclear activation of Akt and of cytoplasmic activation of ERK.
	97.	study revealed a significant correlation of BRAFV600E mutation with a lower expression of both sodium iodide symporter and thyroperoxidase in papillary thyroid cancer
	98.	This study confirms that the known MC1R-melanoma risk association is confined to subjects whose melanomas harbor BRAF mutations.
	99.	Follicular histotypes of oncocytic thyroid carcinomas do not carry BRAF mutations
	100.	focal gains at chromosome 7q34 and increased BRAF-MEK-ERK signaling are common findings in sporadic pilocytic astrocytomas
	101.	Rac1b and B-Raf(V600E) functionally cooperate to sustain colorectal cell viability and suggest they constitute an alternative survival pathway to oncogenic K-Ras
	102.	KRAS and BRAF mutations can impair response to anti-EGFR therapy for colorectal neoplasms
	103.	lung adenocarcinoma of mixed type with a high incidence of papillary and lepidic growth may be worthwhile investigating for BRAF-V600E mutation as more genetically oriented drug therapies emerge.
	104.	BRAF regulates melanoma proliferation through the lineage specific factor MITF
	105.	CST6, CXCL14, DHRS3, and SPP1 are regulated by BRAF signaling and may play a role in papillary thyroid carcinoma pathogenesis
	106.	oncogenic BRAF inhibition can have a different effect on cell fate depending on the cellular type
	107.	aberrant methylation of the hMLH1 gene may play a role in BRAF mutation-promoted thyroid tumorigenesis
	108.	a significant relationship in overall survival in colon cancer patients with defective DNA mismatch repair and the presence of a specific mutation in BRAF (V600E)
	109.	Mitogen-activated protein kinase (MAPK) activity is subject to regulation even in BRAF/NRAS mutant melanoma cells and that high MAPK pathway signaling may be important only in distinct subsets of tumor cells.
	110.	Presence of BRAF V600E in very early stages of papillary thyroid carcinoma.
	111.	in melanocytic lesions, BRAF(V600E) mutation can affect a subset of the cells and is associated with the type and quantity of sun exposure
	112.	study describes the biochemical characterization of novel BRAF and MEK germline mutations in cardio-facio-cutaneous syndrome
	113.	co-overexpression of KIT/CDK4 is a potential mechanism of oncogenic transformation in some BRAF/NRAS wild-type melanomas
	114.	BRAF and MEK1/2 mutations may be more common than anticipated in ovarian cancer which could have important implications for treatment of patients with this disease and suggests potential new therapeutic avenues
	115.	BRAF mutation testing of papillary thyroid carcinoma might improve the diagnosis, prognostic stratification and treatment of these tumors.
	116.	Compared to melanomas without BRAF mutations, melanomas with BRAF mutations showed statistically significantly higher degrees of intraepidermal scatter of melanocytes, and a higher proportion of melanocytes arranged in nests.
	117.	Observational study of gene-disease association, gene-environment interaction, and pharmacogenomic / toxicogenomic. (HuGE Navigator)
	118.	is commonly activated by somatic point mutation, it may provide possible diagnostic and therapeutic targets in human malignant tumors.
	119.	RKIP could play an important role in the down-regulation of wild-type BRAF, serving thus as an endogenous inhibitor of the MAPK pathway in nasal polyps and their adjacent turbinate mucosa.
	120.	BRAF mutation is associated with disease stabilization in melanoma
	121.	Detecting BRAF mutation by pyrosequencing is more sensitive, faster, and less expensive than direct DNA sequencing.
	122.	Thyroid cancers with BRAF mutation are preferentially sensitive to MEK inhibitors.
	123.	CpG island methylator phenotype in colorectal neoplasms may result from activating mutations in either BRAF or KRAS.
	124.	Results implicate aberrant activation of the MAPK pathway due to gene duplication or mutation of BRAF as a molecular mechanism of pathogenesis in low-grade astrocytomas and suggest inhibition of the MAPK pathway as a potential treatment.
	125.	Mutant B-RAF mediates resistance to anoikis via Bad and Bim.
	126.	BRAF mutations in colorectal cancer microsatellite-stable cases are associated with high levels of chromosomal instability that are likely responsible for the adverse outcomes in these cases
	127.	Akt3 and mutant V600E B-Raf cooperate to promote early melanoma development.
	128.	frequency of the occurrence of BRAF mutation and/or RET/PTC in H4-PTEN positive tumors was extremely high (75%) in papillary thyroid carcinoma
	129.	B-Raf(V600E) signaling deregulates the mitotic spindle checkpoint through stabilizing Mps1 levels in melanoma cells.
	130.	Aberrant BRAF and INK4A functionally interact to promote growth and survival of melanoma cells.
	131.	BRAF-V600E mutation is associated with familial non-medullary thyroid carcinoma
	132.	BRAF(V600E) mutation is asscoiated with papillary thyroid cancer
	133.	BRAF T1799A mutation is associated with aggressive pathological outcomes of papillary thyroid cancer
	134.	Important signalling role in T cell development.
	135.	BRAF mutation is not associated with cutaneous melanoma
	136.	MSI is rare in UC-related neoplasia as well as non-neoplastic lesions, and does not contribute to the development of dysplasia.
	137.	K-RAS and BRAF mutations are a frequent genetic event in our samples of sporadic papillary and medullary thyroid carcinoma.
	138.	Observational study of gene-disease association and gene-gene interaction. (HuGE Navigator)
	139.	A worse clinical outcome was found for CIMP-high, microsatellite stable colorectal cancer with KRAS/BRAF mutation but not for those lacking KRAS/BRAF mutation.
	140.	BRAF mutation represents a novel indicator of the progression and aggressiveness of papillary thyroid cancer (Review)
	141.	BRAF provides proliferation and survival signals in MSI colorectal carcinoma cells displaying BRAF(V600E) but not KRAS mutations.
	142.	Observational study of genotype prevalence, gene-disease association, and genetic testing. (HuGE Navigator)
	143.	Meta-analysis of gene-disease association. (HuGE Navigator)
	144.	Observational study of genetic testing. (HuGE Navigator)
	145.	Observational study of gene-disease association and gene-environment interaction. (HuGE Navigator)
	146.	Observational study of gene-environment interaction and pharmacogenomic / toxicogenomic. (HuGE Navigator)
	147.	Observational study of genotype prevalence. (HuGE Navigator)
	148.	Observational study of gene-disease association. (HuGE Navigator)
	149.	Observational study of genotype prevalence and gene-disease association. (HuGE Navigator)
	150.	BRAF interacts with PLCepsilon1 in nephrotic syndrome type 3. Both proteins are coexpressed and colocalize in developing and mature glomerular podocytes.
	151.	A genome-wide RNA-interference screening to identify genes required for an activated BRAF oncogene to block proliferation of fibroblasts and melanocytes revealed that a IGFBP7, has a central role in BRAF-mediated senescence and apoptosis.
	152.	Detection of BRAF improves the diagnosis in fine-needle biopsy with cytological findings suspicious for papillary thyroid carcinoma.
	153.	the results of HRAS, BRAF and MAP2K1/2 mutation screening in a large cohort of patients with CS and CFC
	154.	Because of the very sensitive pyrophosphorolysis-activated polymerization (PAP)technology, B-RAF mutations were found in cell lines and primary uveal melanomas.
	155.	mutation of N-RAS or B-RAF, signature genetic lesions present in most MMs, potently induced the expression of cell-surface CD200, a repressor of DC function.
	156.	MEK inhibition is cytostatic in papillary thyroid cancer and anaplastic thyroid cancer cells bearing a BRAF mutation
	157.	BRAF gene plays a "gatekeeper" role but does not act as a predisposition gene in the development of low-grade ovarian serous carcinomas
	158.	effects of a MEK inhibitor, CI-1040, on thyroid cancer cells, some of which, particularly cell proliferation and tumor growth, seemed to be BRAF mutation or RAS mutation selective
	159.	BRAF(V600E) mutation detected on fine-needle aspiration biopsy specimens, more than RET/PTC rearrangements, is highly specific for papillary thyroid carcinoma.
	160.	5 unreported mutations (T241P, Q262R, G464R, E501V, N581K) were found in cardio-facio-cutaneous syndrome. A hotspot in exon 6 at Q257 was found.
	161.	diffuse expression of wild-type and/or mutant B-Raf may be involved in the tumorigenic process
	162.	There was no coexistence of BRAF (V600E) mutation in papillary thyroid carcinoma.
	163.	The BRAF mutation is common in melanomas, but variation in rates across melanoma subtypes points to a complex interplay between BRAF activation and other factors (eg, sun exposure).
	164.	BRAF V600E mutation is associated with high-risk papillary thyroid carcinoma
	165.	no BRAF mutations identified in 65 screened JMML patients; this gene is unlikely to play a role in the pathogenesis of JMML.
	166.	BRAF mutation is associated as early as the hyperplastic polyp stage followed by microsatellite instability at the carcinoma stage
	167.	BRAF V600E mutation is primarily present in conventional papillary thyroid cancer; it is associated with an aggressive tumor phenotype and higher risk of recurrent and persistent disease in patients with conventional papillary thyroid cancer
	168.	In this small study, the T1799A BRAF mutation was identified in almost half of the iris melanoma tissues samples examined. This finding suggests that there may be genetic as well as clinical differences between iris and posterior uveal melanomas.
	169.	BRAFV600E mutations were found in 41.2% of the papillary thyroid carcinomas
	170.	These results suggest that papillary thyroid carcinomas with BRAF (V600E) mutation are more aggressive than those with wildtype BRAF.
	171.	B-RAF has been identified as the most mutated gene in invasive cells and therefore an attractive therapeutic target in melanoma.
	172.	PPARbeta/delta has a role in growth of RAF-induced lung adenomas
	173.	data showed differences in gene expression between nevi with and without the V600E BRAF mutation. Moreover, nevi with mutations showed over-expression of genes involved in melanocytic senescence and cell cycle inhibition
	174.	We conclude that screening for BRAF 15 exon mutation is an efficient tool in the diagnostic strategy for HNPCC
	175.	c-kit expression is not alternative to BRAF and/or KRAS activation.
	176.	KLF6 and p53 mutations are involved in the development of nonpolypoid colorectal carcinoma, whereas K-ras and B-raf mutations are not
	177.	Normally, BRAF alone is responsible for signaling to MEK. However, when RAS is mutated in melanoma, melanocytes switch their signaling from BRAF to CRAF.
	178.	data indicate that both early-life UV exposure and nevus propensity contribute to occurrence of BRAF+ melanoma, whereas nevus propensity and later-life sun exposure influence the occurrence of NRAS+ melanoma
	179.	The heterogeneous distribution of BRAF mutations suggests that discrete tumor foci in multifocal PTC may occur as independent tumors.
	180.	In contrast to C-RAF that requires farnesylated H-Ras, cytosolic B-RAF associates effectively and with significantly higher affinity with both farnesylated and nonfarnesylated H-Ras.
	181.	T1790A BRAF mutation (L597Q) in childhood acute lymphoblastic leukemia is a functional oncogene
	182.	prevalence of BRAF mutation and RET/PTC were determined in diffuse sclerosing variant of papillary thyroid carcinoma; none of the cases showed a BRAF mutation
	183.	RNA interference and pharmacologic approaches were used to assess the role of B-Raf activation in the growth of human melanomas and additionally determined if a similar role for mutant B-Raf is seen for colorectal carcinoma cell lines.
	184.	BRAF V600E mutation in papillary carcinoma of the thyroid may facilitate tumor cell growth and progression once seeded in the lymph nodes.
	185.	Develompment of malignant strumo ovarii with papillary thyroid carcinoma features is associated with BRAF mutations.
	186.	RASSF1A methylation was observed in a high frequency in endometrioid endometrial carcinoma whereas K-ras and B-raf mutations were observed in a low frequency
	187.	among 23 melanomas located at body sites with chronic UV exposure, only a single tumour harboured the B-raf V599E mutation which was a significantly lower frequency in comparison to melanomas from sun-protected body sites
	188.	frequency of the BRAF mutation and the associations between BRAF mutation and clinicopathologic parameters in papillary thyroid carcinoma were evaluated by meta-analysis
	189.	Molecular diagnosis and careful observations should be considered in children with Cardio-facio-cutaneous syndrome because they have germline mutations in BRAF and might develop malignancy.
	190.	BRAF V600E mutation in PTCs is associated with reduced expression of key genes involved in iodine metabolism
	191.	These data suggest that MITF is an anti-proliferation factor that is down-regulated by B-RAF signaling and that this is a crucial event for the progression of melanomas that harbor oncogenic B-RAF.
	192.	Mutations of BRAF are associated with extensive hMLH1 promoter methylation in sporadic colorectal carcinomas
	193.	BRAF(V600E) mutation is identified in a subset of cutaneous metastases from papillary thyroid carcinomas
	194.	BRAF mutations are restricted to papillary carcinomas and poorly differentiated and anaplastic carcinomas arising from papillary carcinomas
	195.	3 cell lines derived from human choroidal melanoma express B-Raf containing the V599E mutation and showed a 10-fold increase in endogenous B-RafV599E kinase activity and a constitutive activation of the MEK/ERK pathway that is independent of Ras
	196.	High prevalence of BRAF mutations in thyroid cancer is genetic evidence for constitutive activation of the RET/PTC-RAS-BRAF signaling pathway in papillary thyroid carcinoma.
	197.	BRAF V600E mutation was occasionally observed in anaplastic carcinomas with papillary carcinoma.
	198.	Our findings of a high frequency of BRAF mutations at codon 599 in benign melanocytic lesions of the skin indicate that this mutation is not sufficient by itself for malignant transformation.
	199.	B-RAF (V600E) was confirmed to be associated with the papillary growth pattern, but not with poorer differentiated papillary thyroid carcinoma variants.
	200.	Copy gain of PDGFB occurs in a subset of tumors showing no evidence of mutated BRAF or rearranged ret, suggesting that copy gain of PDGFB may underlie the increased expression of platelet-derived growth factor described recently in the literature.
	201.	The aim of this study was to identify the effect that BRAF oncogene has on post-transcriptional regulation in papillary thyroid carcinoma by using microRNA analysis.
	202.	gene is mutated in skin melanoma, but not in uveal melanomas
	203.	BRAF mutations are as uncommon as KRAS mutations in prostate adenocarcinoma
	204.	BRAF mutation is associated with thyroid carcinogenesis
	205.	Both BRAF and FBXW7 mutations functionally activate kinase effectors important in pancreatic cancer and extend potential options for therapeutic targeting of kinases in treatment of phenotypically distinct pancreatic adenocarcinoma subsets.
	206.	Missense mutation is marker of colonic but not gastric cancer.
	207.	BRAF T1976A mutation is present at high frequency in benign naevi such as Spitz and Reed.
	208.	These studies identify isoprenylcysteine carboxyl methyltransferase as a potential target for reducing the growth of K-Ras- and B-Raf-induced malignancies.
	209.	results demonstrate that the mutational status of BRAF and KRAS is distinctly different among histologic types of ovarian serous carcinoma, occurring most frequently in invasive micropapillary serous carcinomas and its precursors, serous borderline tumors
	210.	The finding of tandem mutations in thin melanomas makes it more likely that they arise as a simultaneous rather than sequential event.
	211.	determination of mutation specific gene expression profiles in papillary thyroid carcinoma
	212.	BRAF mutation does not seem to be sufficient to produce MAPK activation in melanocytic nevi.
	213.	Uceal melanomas arise independent of oncogenic BRAF and NRAS mutations.
	214.	activation of this gene may be one of the early events in the pathogenesis of some melanomas.
	215.	Mutations of BRAF or KRAS oncogenes are early events in the serrated polyp neoplasia pathway. CpG island methylation plays a role in serrated polyp progression to colorectal carcinoma.
	216.	B-raf V599E and V599K oncogenic mutations are likely to affect melanocyte-specific pathways controlling proliferation and differentiation
	217.	Mutations are not detectable in plasma cell leukemia and multiple myeloma.
	218.	findings show that MC1R variants are strongly associated with BRAF mutations in non-chronic sun-induced damage melanomas; in this subtype, risk for melanoma associated with MC1R is due to increase in risk of developing melanomas with BRAF mutations
	219.	Expression of p27Kip1 in melanoma is regulated by B-RAF at the mRNA level and via B-RAF control of Cks1/Skp2-mediated proteolysis.
	220.	BRAF(V599E) mutation is seven times higher in lesions with structural changes and 13 times higher in growing lesions as compared with lesions without changes
	221.	Single-cell clones with efficient knockdown of (V 600 E)B-RAF could be propagated in the presence of basic fibroblast growth factor but underwent apoptosis or senescence-like growth arrest upon withdrawal of this growth factor
	222.	mutational analysis of KRAS, BRAF, and MAP2K1/2 in 56 patients with CFC syndrome; comparison of the genotype-phenotype correlation of CFC with that of Costello syndrome suggest a significant clinical overlap but not genotype overlap.
	223.	BRAF is occasionally mutated in NHL, and BRAF mutation may contribute to tumor development in some NHLs
	224.	sustained BRAF(V600E) expression in human melanocytes induces cell cycle arrest, which is accompanied by the induction of both p16(INK4a) and senescence-associated acidic beta-galactosidase (SA-beta-Gal) activity, a commonly used senescence marker
	225.	BRAF mutation in melanoma is most likely to occur prior to the development of metastatic disease
	226.	Activating BRAF mutation is associated with papillary thyroid carcinoma
	227.	B-raf is involved in adhesion-independent ERK1/2 signaling in melanocytes
	228.	Mutations in BRAF gene is associated with malignant melanomas
	229.	in contrast to cutaneous melanoma, BRAF does not appear to be involved in the pathogenesis of uveal melanoma
	230.	B-Raf kinase activity regulation by tuberin and Rheb is mammalian target of rapamycin (mTOR)-independent
	231.	mutated in childhood acute lymphoblastic leukemia.
	232.	a novel Ras-independent ERK1/2 activation system in which p110gamma/Raf-1/MEK1/2 and PKA/B-Raf/MEK1/2 cooperate to activate ERK1/2.
	233.	AKAP9-BRAF fusion was preferentially found in radiation-induced papillary carcinomas developing after a short latency, whereas BRAF point mutations were absent in this group
	234.	activating BRAF mutations may be an important event in the development of papillary thyroid cancer
	235.	BRAF mutations were seen in stomach neoplasms.
	236.	In patients with papillary thyroid cancer, BRAF mutation is associated with poorer clinicopathological outcomes and independently predicts recurrence.
	237.	copy number gain may represent another mechanism of BRAF activation in thyroid tumors
	238.	B-Raf has a role in extracellular signal-regulated kinase (ERK) signaling in T cells and prevents antigen-presenting cell-induced anergy
	239.	13 germline BRAF variants, 4 of which were silent mutations in coding regions & 9 nucleotide substitutions in introns, were found in melanoma patients and melanoma family, but none appeared statistically likely to be a melanoma susceptibility gene.
	240.	Although BRAF and NRAS mutations are likely to be important for the initiation and maintenance of some melanomas, other factors might be more significant for proliferation and prognosis in subgroups of aggressive melanoma
	241.	Merlin and MLK3 can interact in situ and merlin can disrupt the interactions between B-Raf and Raf-1 or those between MLK3 and either B-Raf or Raf-1.
	242.	A subset of Spitz nevi, some with atypical histologic features, possess BRAF mutations. The BRAF mutational status does not separate all Spitz nevi from spitzoid melanomas and non-Spitz types of melanocytic proliferations, contrary to previous reports.
	243.	CpG island methylator phenotype-positive colorectal tumors represent a distinct subset, encompassing almost all cases of tumors with BRAF mutation
	244.	phosphorylation on both S365 and S429 participate in the differential regulation of B-Raf isoforms through distinct mechanisms
	245.	BRAF mutation remained a significant prognostic factor for lymph node metastasis (odds ratio = 10.8, 95% confidence interval, 3.5-34.0, P < 0.0001).
	246.	Absence of association between BRAF mutation and activation of MAPK pathway in papillary thyroid carcinoma suggests the presence of mechanisms that downregulate MAPK activation.
	247.	finding of a strong association between BRAF mutations and serrated histology in hyperplastic aberrant crypt foci supports the idea that these lesions are an early, sentinel, or a potentially initiating step on the serrated pathway to colorectal carcinoma
	248.	The BRAF(V599E) mutation appears to be an alternative event to RET/PTC rearrangement rather than to RAS mutations, which are rare in PTC. BRAF(V599E) may represent an alternative pathway to oncogenic MAPK activation in PTCs without RET/PTC activation.
	249.	mutation of BRAF gene could be a potentially useful marker of prognosis of patients with advanced thyroid cancers
	250.	NRAS and BRAF mutations arise early during melanoma pathogenesis and are preserved throughout tumor progression
	251.	BRAF mutations, which are present in a variety of other human cancers, do not seem to be involved in gastric cancer development
	252.	Radiation-induced tumors have a low prevalence of BRAF point mutations and high prevalence of RET/PTC rearrangements
	253.	Our data indicate that BRAF gene mutations are rare to absent events in uveal melanoma of humans.
	254.	The lack or low prevalence of BRAF mutation in other thyroid neoplasms is consistent with the notion that other previously defined genetic alterations on the same signaling pathway are sufficient to cause tumorigenesis in most thyroid neoplasms.
	255.	we found 19 cases (38%) to harbor somatic B-raf exon 15 mutations.
	256.	autoinhibition was negatively regulated by acidic substitutions at phosphorylation sites within the activation loop
	257.	The oncogenic B-raf mutations V599E and V599K, as early events in melanocyte transformation, persist throughout metastasis with important prognostic implications.
	258.	As the BRAF oncogene is frequently found to be mutated in human cutaneous melanomas, it may constitute a risk factor for melanoma formation within CMN and DMN.
	259.	Mutation and elevated expression of BRAF is associated with the development of testicular germ cell tumors
	260.	aberrant B-Raf activity in angiomyolipomas leads to abnormal cellular differentiation and migration [review]
	261.	BRAF V600E is associated with a high risk of recurrence and less differentiated papillary thyroid carcinoma due to the impairment of Na+/I- targeting to the membrane
	262.	BRAF mutation is associated with melanoma and melanocytic nevi.
	263.	Rheb has a central role in the regulation of the Ras/B-Raf/C-Raf/MEK signaling network
	264.	findings show that RASSF1A hypermethylation and KRAS mutations and BRAF mutations are inversely correlated and play an important role in the development of cervical adenocarcinomas
	265.	low rate of RAS-RAF mutations (2/22, 9.1%) observed in Spitz melanocytic nevi suggests that these lesions harbor as yet undetected activating mutations in other components of the RAS-RAF-MEK-ERK-MAPK pathway
	266.	The V599E BRAF mutation appears to be a somatic mutation associated with melanoma development and/or progression in a proportion of affected individuals.
	267.	BRAF mutation may be acquired during development of metastasis but is not a significant factor for primary melanoma development and disease outcome.
	268.	New enriched PCR-RFLP assay for detecting mutations of BRAF codon 599 mutation in pleural mesotheliomas.
	269.	BRAF mutations are frequently present in sporadic colorectal cancer with methylated hMLH1
	270.	Data provide evidence that B-Raf is a positive regulator of T cell receptor-mediated sustained ERK activation, which is required for NFAT activation and the full production of IL-2.
	271.	The data of this study suggest that activating mutations of B-RAF are not a frequent event in gliomas; nevertheless, when present they are associated with high-grade malignant lesions.
	272.	Data show that the the RET receptor (RET/PTC), Ras and BRAF function along a linear oncogenic signaling cascade in which RET/PTC induces RAS-dependent BRAF activation and RAS- and BRAF-dependent ERK activation.
	273.	selective reduction in catalytic activity and expression of B-Raf but not Raf-1 suggest that B-Raf may be playing an important role in altered ERK signaling in brain of suicide subjects, and thus in the pathophysiology of suicide
	274.	KSHV-infected cell lines expressed higher levels of B-Raf and VEGF-A; B-Raf-induced VEGF-A expression was demonstrated to be sufficient to enhance tubule formation in endothelial cells
	275.	B-Raf and ERK are activated by cyclic AMP after calcium restriction
	276.	REVIEW: our understanding of B-RAF as an oncogene and of its role in cancer
	277.	In this study, this BRAF mutation was demonstrated in some conjunctival melanoma tissue samples, suggesting that some conjunctival melanomas may share biological features in common with cutaneous melanoma.
	278.	BRAF mutations proved to be absent in tumors from hereditary nonpolyposis colorectal cancer syndrome (HNPCC) families with germline mutations in the MMR genes MLH1 and MSH2.
	279.	Anaplastic thyroid carcinomas which are derived from papillary carcinomas are due to BRAF and p53 mutations
	280.	The increasing frequency of BRAF mutations as a function of age could help account for the well documented but poorly understood observation that age is a relevant prognostic indicator for patients with papillary thyroid carcinoma.
	281.	Mutations of the BRAF gene are partly involved in the malignant transformation of the endometrium.
	282.	V599E BRAF mutation was uncommon in Japanese lung cancer.
	283.	wild-type B-Raf-mediated ERK1/2 activation plays a major role in proliferation and transformation of uveal melanocytes; Raf-1 is not involved in this activation
	284.	Braf mutations in thyroid tumorigenesis.
	285.	data support a model in which mutational activation of BRAF in human melanomas contributes to constitutive induction of NF-kappaB activity and to increased survival of melanoma cells
	286.	The role for BRAF activation in thyroid cancer development and establishing the potential therapeutic efficacy of BRAF-targeted agents in patients with thyroid cancerwill be reviewed.
	287.	characterization of the T1799-1801del and A1799-1816ins BRAF mutations in papillary thyroid cancer; the two new mutations resulted in constitutive activation of the BRAF kinase and caused NIH3T3 cell transformation
	288.	BRAF mutations in colorectal cancers occur only in tumours that do not carry mutations in a RAS gene known as KRAS, and BRAF mutation is linked to the proficiency of these tumours in repairing mismatched bases in DNA
	289.	cAMP activates ERK and increases proliferation of autosomal dominant polycystic kindey epithelial cells through the sequential phosphorylation of PKA, B-Raf and MAPK in a pathway separate from the classical receptor tyrosine kinase cascade
	290.	BRAF mutations are associated with proximal colon tumors with mismatch repair deficiency and MLH1 hypermethylation.
	291.	RAS or BRAF mutations are detected in about 32% of all Barrett's adenocarcinomas; the disruption of the Raf/MEK/ERK (MAPK) kinase pathway is a frequent but also early event in the development of Barrett's adenocarcinoma
	292.	BRAF mutations are rather rare in solitary cold adenomas and adenomatous nodules and do not explain the molecular etiology of ras mutation-negative cold thyroid nodules.
	293.	mutated in papillary thyroid cancer.
	294.	High frequency of BRAF mutations in nevi
	295.	These results suggest that the BRAF mutation is unlikely to be involved in gastric carcinogenesis.
	296.	Mutations within the BRAF gene are useful markers for the differential diagnosis between Spitz nevus and malignant melanoma.
	297.	These results suggest that BRAF mutations do not have a role in tumorigenesis of neuroendocrine gastroenteropancreatic tumors.
	298.	Mutations in the BRAF protooncogene (V599E)may be an alternative pathway of tumorigenesis of familial colorectal cancer.
	299.	The results showed that conjunctival nevi, similar to skin nevi, have a high frequency of oncogenic BRAF mutations.
	300.	Data suggest that B-RAF activates C-RAF through a mechanism involving 14-3-3 mediated heterooligomerization and C-RAF transphosphorylation.
	301.	The estimated proportion of attributable risk of melanoma due to variants in BRAF is 1.6%, but the burden of disease associated with this variant is greater than that associated with the major melanoma locus (CDKN2A) which has a risk of 0.2%.
	302.	Melanoma cells require either B-RAF or phosphoinositide-3 kinase activation for protection from anoikis.
	303.	a BRAFT1799A mutation may have a role in poor differentiation of thyroid carcinoma
	304.	Thus, we propose that the hitherto unidentified function of the B-Raf amino-terminal region is to mediate calcium-dependent activation of B-Raf and the following MEK activation, which may occur in the absence of Ras activation.
	305.	BRAF mutation was frequent in hyperplastic polyps (67%) and sessile serrated adenomas (81%).
	306.	BRAF mutations are associated with colorectal cancers
	307.	BRAFV600E activates not only MAPK but also NF-kappaB signaling pathway in human thyroid cancer cells, leading to an acquisition of apoptotic resistance and promotion of invasion.
	308.	data provide evidence that oncogenic properties of BRAF contribute to the tumorigenesis of intraductal papillary mucinous neoplasm/carcinoma (IPMN/IPMC), but at a lower frequency than KRAS
	309.	there is a subgroup of colorectal carcinomas which develop via the microsatellite instability pathway that carry an alteration of the BRAF gene
	310.	Overexpression of B-Raf mRNA and protein may be a feature of nonfunctioning pituitary adenomas, highlighting overactivity of the Ras-B-Raf-MAP kinase pathway in these tumors.
	311.	data suggest that BRAF mutations might be present less frequently than KRAS mutations in Greek patients with colorectal carcinomas
	312.	Data suggest that BRAF T1796A activating mutation is not common in primary uveal melanoma.
	313.	Mutations were found in exon 15 in colorectal adenocarcinoma.
	314.	BRAF(V599E) is more common genetic alteration found to date in adult sporadic papillary thyroid carcinomas (PTCs). It is unique for this thyroid cancer histotype, and it might drive the development of PTCs of classic papillary subtype.
	315.	Data suggest that Rit is involved in a novel pathway of neuronal development and regeneration by coupling specific trophic factor signals to sustained activation of the B-Raf/ERK and p38 MAP kinase cascades.
	316.	B-raf mutations surrounding Thr439 found in human cancers are unlikely to contribute to increased oncogenic properties of B-raf
	317.	Role of BRAF mutation in facilitating metastasis and progression of papillary thyroid cancer in lymph nodes.
	318.	V600E B-Raf requires the Hsp90 chaperone for stability and is degraded in response to Hsp90 inhibitors.
	319.	The authors have developed and run a high-throughput screen to find inhibitors of V600E BRAF using an enzyme cascade assay in which oncogenic BRAF activates MEK1, which in turn activates ERK2, which then phosphorylates the transcription factor ELK1.
	320.	mutations in the BRAF gene and to some extent in the N-ras gene represent early somatic events that occur in melanocytic nevi
	321.	possible cooperation between BRAF activation and PTEN loss in melanoma development.
	322.	Data suggest that SPRY2, an inhibitor of ERK signaling, may be bypassed in melanoma cells either by down-regulation of its expression in WT BRAF cells, or by the presence of the BRAF mutation.
	323.	The most frequent B-RAF gene alterations are not involved in prostate carcinogenesis
	324.	mucosal melanomas of the head and neck do not frequently harbor an activating mutation of BRAF
	325.	somatic missense mutations in 66% of malignant melanomas and at lower frequency in a wide range of human cancers
	326.	ovarian serous cystadenomas do not contain mutations in either BRAF or KRAS genes
	327.	BRAF mutations are associated with conjunctival neoplasms
	328.	We found mutations in p53, K-ras, and BRAF genes in 35%, 30%, and 4% of tumors, respectively, and observed a minimal or no co-presence of these gene alterations.
	329.	BRAF mutation occurs later in thyroid tumor progression and is restricted mainly to papillary thyroid carcinoma and anaplastic thyroid carcinoma
	330.	findings demonstrate that heterogeneous de novo missense mutations in three genes within the mitogen-activated protein kinase pathway, BRAF, MEK1 and MEK2 cause cardio-facio-cutaneous syndrome
	331.	Cardio-facio-cutaneous (CFC) syndrome involves dysregulation of the RAS-RAF-ERK pathway.
	332.	gain-of-function BRAF signaling is strongly associated with in vivo tumorigenicity
	333.	NRAS and BRAF activating mutations can coexist in the same melanoma, but are mutually exclusive at the single-cell level
	334.	Aberrant methylation and hence silencing of TIMP3, SLC5A8, DAPK and RARbeta2, in association with BRAF mutation, may be an important step in PTC tumorigenesis and progression.
	335.	BRAF, K-ras and BAT26 are expressed in colorectal polyps and stool
	336.	Previously identified associations between smoking and colon cancer, whether microsatellite unstable or stable, appear to be explained by the association of smoking with BRAF mutation.
	337.	BRAF(T1799A) mutation is associated with a lower rate of tumor proliferation.
	338.	B-RAF mutations are a rare event in pituitary tumorigenesis.
	339.	analysis of a BRAF mutation-associated gene expression signature in melanoma
	340.	BRAF has a role in in squamous cell carcinoma of the head and neck through uncommon mutations
	341.	None of the cases of gastric cancer showed braf mutations
	342.	Mucinous ovarian cancers without a KRAS mutation have not sustained alternative activation of this signaling pathway through mutation of the BRAF oncogene.
	343.	activating mutations of PDGFR-alpha, c-kit and B-RAF are absent in gliosarcomas
	344.	UV light is not necessarily required for the acquisition of the BRAF(V600E) mutation, and non-mutagenic effects of UV light to melanocytes may be more important in the nevogenesis
	345.	Single nucleotide polymorphism found exclusively in papillary thyroid carcinoma.
	346.	Concomitant KRAS and BRAF mutations increased along progression of MSS colorectal cancer, suggesting that activation of both genes is likely to harbour a synergistic effect
	347.	Extracellular signal-regulated kinase-3 (ERK3/MAPK6) is highly expressed in response to BRAF signaling.
	348.	Association with preexisting nevi and pronounced infiltration of lymphocytes was significantly higher in BRAF mutated melanoma tumours
	349.	BRAF-V600E mutations are mainly involved in colorectal cancer families characterized by an increased risk of other common malignancies
	350.	BRAFV600E represents a detectable marker in the plasma/serum from melanoma patients for monitoring but not diagnostic purposes
	351.	BRAF, K-ras and BAT26 are expressed in colorectal polyps and stool [BAT26]
	352.	MEK1 interacts with B-Raf.

Submit: New GeneRIF Correction

[Top][Help]Interactions

Description ..........
Product	Interactant	Other Gene	Complex	Source	Pubs

NP_004324.1	AKT1	AKT1		HPRD	PubMed

NP_004324.1	H-Ras	HRAS		HPRD	PubMed

NP_004324.1	MEK1	MAP2K1		HPRD	PubMed

NP_004324.1	MAP2K2	MAP2K2		HPRD	PubMed

NP_004324.1	MRAS	MRAS		HPRD	PubMed

NP_004324.1	NP_002871.1	RAF1		HPRD	PubMed

NP_004324.1	14-3-3 Beta	YWHAB		HPRD	PubMed

NP_004324.1	14-3-3 Eta	YWHAH		HPRD	PubMed

NP_004324.1	14-3-3 theta	YWHAQ		HPRD	PubMed

NP_004324.1	14-3-3 zeta	YWHAZ		HPRD	PubMed

NP_004324.1	RAP1			HPRD	PubMed
MEK1 interacts with B-Raf.
NP_004324.2	NP_002746.1	MAP2K1		BIND	PubMed
B-RAF interacts with OIP5.
NP_004324.2	NP_009211.1	OIP5		BIND	PubMed
B-RAF interacts with C-RAF. This interaction was modelled on a demonstrated interaction between human B-RAF and monkey C-RAF .
NP_004324.2	NP_002871.1	RAF1		BIND	PubMed
B-RAF interacts with TIMM50.
NP_004324.2	NP_001001563.1	TIMM50		BIND	PubMed
B-RAF interacts with 14-3-3-beta.
NP_004324.2	NP_003395.1	YWHAB		BIND	PubMed
BRAF (B-Raf) interacts with an unspecified isoform of YWHAB (14-3-3-beta).
NP_004324.2		YWHAB		BIND	PubMed
Affinity Capture-Western; Biochemical Activity
BioGRID:107141	BioGRID:106710	AKT1		BioGRID	PubMed
Reconstituted Complex; Two-hybrid
BioGRID:107141	BioGRID:109501	HRAS		BioGRID	PubMed
Phenotypic Enhancement
BioGRID:107141	BioGRID:111581	MAPK3		BioGRID	PubMed
Affinity Capture-Western
BioGRID:107141	BioGRID:116486	MRAS		BioGRID	PubMed
Affinity Capture-Western
BioGRID:107141	BioGRID:111831	RAF1		BioGRID	PubMed
Reconstituted Complex
BioGRID:107141	BioGRID:111841	RAP1A		BioGRID	PubMed
Reconstituted Complex
BioGRID:107141	BioGRID:111844	RAP1GAP		BioGRID	PubMed
Affinity Capture-MS
BioGRID:107141	BioGRID:109072	SFN		BioGRID	PubMed
Affinity Capture-MS; Affinity Capture-Western
BioGRID:107141	BioGRID:113361	YWHAB		BioGRID	PubMed
Affinity Capture-MS
BioGRID:107141	BioGRID:113364	YWHAG		BioGRID	PubMed
Affinity Capture-MS
BioGRID:107141	BioGRID:116168	YWHAQ		BioGRID	PubMed
Affinity Capture-MS
BioGRID:107141	BioGRID:113366	YWHAZ		BioGRID	PubMed

[Top][Help]General gene information

Markers

SHGC-35884(e-PCR): Links: UniSTS:18946

GDB:1317924(e-PCR): Links: UniSTS:24602

GDB:1318226(e-PCR): Links: UniSTS:20310

GDB:1318374(e-PCR): Links: UniSTS:27484

STS-T28237(e-PCR): Links: UniSTS:26491

D7S2227(e-PCR): Links: UniSTS:65428

D7S1672(e-PCR): Links: UniSTS:62114

RH122643(e-PCR): Links: UniSTS:135088

Braf(e-PCR), detects polymorphism: Links: UniSTS:259512

WI-17864(e-PCR): Links: UniSTS:55019

Phenotypes

Adenocarcinoma of lung, somatic: MIM: 211980
Cardiofaciocutaneous syndrome: MIM: 115150
Colorectal cancer, somatic: MIM: 164757
Melanoma, melignant, somatic: MIM: 164757
Nonsmall cell lung cancer, somatic: MIM: 164757

Genotypes

See BRAF SNP Genotype Report

See BRAF SNP Geneview Report

Related pseudogene(s)

1 foundReview record(s) in Gene

Homology

Homologs of the BRAF gene The BRAF gene is conserved in chimpanzee, dog, cow, mouse, rat, chicken, zebrafish, fruit fly, mosquito, and C.elegans.

Map Viewer (Mouse, Rat)

Pathways

KEGG pathway: Acute myeloid leukemia: 05221
KEGG pathway: Bladder cancer: 05219
KEGG pathway: Chemokine signaling pathway: 04062
KEGG pathway: Chronic myeloid leukemia: 05220
KEGG pathway: Colorectal cancer: 05210
KEGG pathway: Endometrial cancer: 05213
KEGG pathway: ErbB signaling pathway: 04012
KEGG pathway: Focal adhesion: 04510
KEGG pathway: Glioma: 05214
KEGG pathway: Insulin signaling pathway: 04910
KEGG pathway: Long-term depression: 04730
KEGG pathway: Long-term potentiation: 04720
KEGG pathway: MAPK signaling pathway: 04010
KEGG pathway: Melanoma: 05218
KEGG pathway: Natural killer cell mediated cytotoxicity: 04650
KEGG pathway: Neurotrophin signaling pathway: 04722
KEGG pathway: Non-small cell lung cancer: 05223
KEGG pathway: Pancreatic cancer: 05212
KEGG pathway: Pathways in cancer: 05200
KEGG pathway: Progesterone-mediated oocyte maturation: 04914
KEGG pathway: Prostate cancer: 05215
KEGG pathway: Regulation of actin cytoskeleton: 04810
KEGG pathway: Renal cell carcinoma: 05211
KEGG pathway: Thyroid cancer: 05216
KEGG pathway: Vascular smooth muscle contraction: 04270
KEGG pathway: mTOR signaling pathway: 04150
Reactome Event:Signalling by NGF: REACT_11061

Gene Ontology Provided by GOA

Function	Evidence
ATP binding	IEA
MAP kinase kinase kinase activity	IEA
metal ion binding	IEA
mitogen-activated protein kinase kinase binding	IEA
nucleotide binding	IEA
protein binding	IPI	PubMed
protein heterodimerization activity	IEA
protein serine/threonine kinase activity	IEA
receptor signaling protein activity	IEA
transferase activity	IEA
zinc ion binding	IEA

Process	Evidence
MAPKKK cascade	IEA
anti-apoptosis	TAS	PubMed
organ morphogenesis	TAS	PubMed
protein amino acid phosphorylation	TAS	PubMed
protein heterooligomerization	IEA
small GTPase mediated signal transduction	EXP	PubMed

Component	Evidence
cytoplasm	IDA	PubMed
cytoplasm	IEA
nucleus	IDA	PubMed
plasma membrane	IEA

[Top][Help]General protein information

Preferred Names: B-Raf

Names: B-Raf; 94 kDa B-raf protein; murine sarcoma viral (v-raf) oncogene homolog B1; B-Raf proto-oncogene serine/threonine-protein kinase (p94)

NP_004324.2: EC 2.7.11.1

[Top][Help]NCBI Reference Sequences (RefSeq)

RefSeqs maintained independently of Annotated Genomes

These reference sequences exist independently of genome builds. Explain

Genomic

NG_007873.1 RefSeqGene

Range

5000..195752

Download

GenBank FASTA Sequence Viewer (Graphics)

mRNA and Protein(s)

NM_004333.4 → NP_004324.2 B-Raf

Source sequence(s)

AA252358,AW971583,BC101757,DB454480,M95712

Consensus CDS

CCDS5863.1

UniProtKB/TrEMBL

A4D1T4

UniProtKB/Swiss-Prot

P15056

Conserved Domains (4) summary

cd00029
Location:235 – 280
Blast Score: 158

C1; Protein kinase C conserved region 1 (C1) . Cysteine-rich zinc binding domain. Some members of this domain family bind phorbol esters and diacylglycerol, some are reported to bind RasGTP. May occur in tandem arrangement. Diacylglycerol (DAG) is a second...

cd01816
Location:156 – 227
Blast Score: 299

Raf_RBD; CR2 and CR3. CR1 has two Ras binding domains (RBD and CRD), CR2 is a serine/threonine rich domain and CR3 is the catalytic kinase domain. The RBD of Raf is structurally similar to ubiquitin with little of no sequence similarity.The Raf signalling...

pfam00069
Location:457 – 713
Blast Score: 642

Pkinase; Protein kinase domain

cd00192
Location:462 – 715
Blast Score: 546

PTKc; Catalytic Domain of Protein Tyrosine Kinases

RefSeqs of Annotated Genomes: Build 37.1

The following sections contain reference sequences that belong to a specific genome build. Explain

Genome Reference Consortium Human Build 37 (GRCh37), Primary_Assembly

Genomic

NC_000007.13

Range

140433811..140624563, complement

Download

GenBank FASTA Sequence Viewer (Graphics)
NT_007914.15

Range

1029434..1220186, complement

Download

GenBank FASTA Sequence Viewer (Graphics)

Alternate assembly (Celera)

Genomic

AC_000050.1

Range

135155866..135346613, complement

Download

GenBank FASTA Sequence Viewer (Graphics)
NW_923640.1

Range

37914617..38105364, complement

Download

GenBank FASTA Sequence Viewer (Graphics)

Alternate assembly (HuRef)

Genomic

AC_000139.1

Range

134729458..134920528, complement

Download

GenBank FASTA Sequence Viewer (Graphics)
NW_001839073.1

Range

1029911..1220981, complement

Download

GenBank FASTA Sequence Viewer (Graphics)

Alternate assembly (CRA_TCAGchr7v2)

Genomic

AC_000068.1

Range

139771988..139962885, complement

Download

GenBank FASTA Sequence Viewer (Graphics)
NT_079596.2

Range

39807556..39998453, complement

Download

GenBank FASTA Sequence Viewer (Graphics)

[Top][Help]Related Sequences

Nucleotide		Protein
genomic	AC006006.2	AAS00359.1
genomic	AC006344.2	AAD43193.1
genomic	AC006347.2	AAD15551.1
genomic	AC079339.5	None
genomic	CH236950.1	EAL24023.1
genomic	CH471070.1	EAW83964.1
		EAW83965.1
genomic	X65187.1	CAA46301.1
mRNA	AA252358.1	None
mRNA	AA834931.1	None
mRNA	AI203435.1	None
mRNA	AK054801.1	None
mRNA	AK314346.1	None
mRNA	AW971583.1	None
mRNA	BC038966.1	None
mRNA	BC101757.1	AAI01758.1
mRNA	BC112079.1	AAI12080.1
mRNA	BM263585.1	None
mRNA	DB454480.1	None
mRNA	DN996440.1	None
mRNA	M21001.1	AAA96495.1
mRNA	M95712.2	AAA35609.2