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Did you mean raf and cell transformation, Neoplastic (1,036 results)?
Oncogenic and sorafenib-sensitive ARAF mutations in lung adenocarcinoma.
Imielinski M, Greulich H, Kaplan B, Araujo L, Amann J, Horn L, Schiller J, Villalona-Calero MA, Meyerson M, Carbone DP. Imielinski M, et al. J Clin Invest. 2014 Apr;124(4):1582-6. doi: 10.1172/JCI72763. Epub 2014 Feb 24. J Clin Invest. 2014. PMID: 24569458 Free PMC article.
The ARAF mutations were shown to transform immortalized human airway epithelial cells in a sorafenib-sensitive manner. These results suggest that mutant ARAF is an oncogenic driver in lung adenocarcinoma and an indicator of sorafenib response....
The ARAF mutations were shown to transform immortalized human airway epithelial cells in a sorafenib-sensitive manner. These results …
A-Raf: A new star of the family of raf kinases.
An S, Yang Y, Ward R, Liu Y, Guo XX, Xu TR. An S, et al. Crit Rev Biochem Mol Biol. 2015;50(6):520-31. doi: 10.3109/10409238.2015.1102858. Epub 2015 Oct 27. Crit Rev Biochem Mol Biol. 2015. PMID: 26508523 Review.
The Ras-Raf-MEK-MAPK (mitogen-activated protein kinase)-signaling pathway plays a key role in the regulation of many cellular functions, including cell proliferation, differentiation and transformation, by transmitting signals from membrane receptors to various cyto …
The Ras-Raf-MEK-MAPK (mitogen-activated protein kinase)-signaling pathway plays a key role in the regulation of many cellular functions, inc …
TC21 causes transformation by Raf-independent signaling pathways.
Graham SM, Vojtek AB, Huff SY, Cox AD, Clark GJ, Cooper JA, Der CJ. Graham SM, et al. Mol Cell Biol. 1996 Nov;16(11):6132-40. doi: 10.1128/MCB.16.11.6132. Mol Cell Biol. 1996. PMID: 8887643 Free PMC article.
Therefore, like Ras, TC21 may activate signaling pathways that control normal cell growth and differentiation. To address this possibility, we determined if regulators and effectors of Ras are also important for controlling TC21 activity. ...Thus, Raf kinases are effectors …
Therefore, like Ras, TC21 may activate signaling pathways that control normal cell growth and differentiation. To address this possib …
B-Raf deficiency impairs tumor initiation and progression in a murine breast cancer model.
Köhler M, Ehrenfeld S, Halbach S, Lauinger M, Burk U, Reischmann N, Cheng S, Spohr C, Uhl FM, Köhler N, Ringwald K, Braun S, Peters C, Zeiser R, Reinheckel T, Brummer T. Köhler M, et al. Oncogene. 2019 Feb;38(8):1324-1339. doi: 10.1038/s41388-018-0663-8. Epub 2019 Jan 18. Oncogene. 2019. PMID: 30659267
Aberrant RTK signaling is mimicked by the polyoma middle T antigen (PyMT), which activates various oncogenic signaling pathways, incl. the RAS/ERK axis, in a similar manner as RTKs in human breast cancer. Mammary epithelial cell directed expression of PyMT in mice by the M …
Aberrant RTK signaling is mimicked by the polyoma middle T antigen (PyMT), which activates various oncogenic signaling pathways, incl. the R …
ERK signalling and oncogene transformation are not impaired in cells lacking A-Raf.
Mercer K, Chiloeches A, Hüser M, Kiernan M, Marais R, Pritchard C. Mercer K, et al. Oncogene. 2002 Jan 17;21(3):347-55. doi: 10.1038/sj.onc.1205101. Oncogene. 2002. PMID: 11821947
To investigate the specific role of A-Raf in this process we generated A-Raf deficient mouse embryonic fibroblasts (MEFs) and embryonic stem (ES) cells by gene targeting and characterized their ability to undergo proliferation, differentiation, apoptosis, ERK activation, and t …
To investigate the specific role of A-Raf in this process we generated A-Raf deficient mouse embryonic fibroblasts (MEFs) and embryonic stem …
Stabilization of C-RAF:KSR1 complex by DiRas3 reduces availability of C-RAF for dimerization with B-RAF.
Baljuls A, Dobrzyński M, Rauch J, Rauch N, Kolch W. Baljuls A, et al. Cell Signal. 2016 Oct;28(10):1451-62. doi: 10.1016/j.cellsig.2016.06.019. Epub 2016 Jun 29. Cell Signal. 2016. PMID: 27368419
This mechanism, which is shared between A-RAF and C-RAF, may be involved in the regulation of Ras12V-induced cell transformation by DiRas3....
This mechanism, which is shared between A-RAF and C-RAF, may be involved in the regulation of Ras12V-induced cell transformation …
Integrated genomic analysis identifies recurrent mutations and evolution patterns driving the initiation and progression of follicular lymphoma.
Okosun J, Bödör C, Wang J, Araf S, Yang CY, Pan C, Boller S, Cittaro D, Bozek M, Iqbal S, Matthews J, Wrench D, Marzec J, Tawana K, Popov N, O'Riain C, O'Shea D, Carlotti E, Davies A, Lawrie CH, Matolcsy A, Calaminici M, Norton A, Byers RJ, Mein C, Stupka E, Lister TA, Lenz G, Montoto S, Gribben JG, Fan Y, Grosschedl R, Chelala C, Fitzgibbon J. Okosun J, et al. Nat Genet. 2014 Feb;46(2):176-181. doi: 10.1038/ng.2856. Epub 2013 Dec 22. Nat Genet. 2014. PMID: 24362818 Free PMC article.
Follicular lymphoma is an incurable malignancy, with transformation to an aggressive subtype representing a critical event during disease progression. ...We identified recurrent mutations in linker histone, JAK-STAT signaling, NF-kappaB signaling and B cell developm …
Follicular lymphoma is an incurable malignancy, with transformation to an aggressive subtype representing a critical event during dis …
IGHV sequencing reveals acquired N-glycosylation sites as a clonal and stable event during follicular lymphoma evolution.
Odabashian M, Carlotti E, Araf S, Okosun J, Spada F, Gribben JG, Forconi F, Stevenson FK, Calaminici M, Krysov S. Odabashian M, et al. Blood. 2020 Mar 12;135(11):834-844. doi: 10.1182/blood.2019002279. Blood. 2020. PMID: 31932843 Free PMC article.
SHM introduces DNA sequences encoding N-glycosylation sites asparagine-X-serine/threonine (N-gly sites) within the V-region that are rarely found in normal B-cell counterparts. Unique attached oligomannoses activate B-cell receptor signaling pathways after engagemen …
SHM introduces DNA sequences encoding N-glycosylation sites asparagine-X-serine/threonine (N-gly sites) within the V-region that are rarely …
Splicing factor hnRNP A2 activates the Ras-MAPK-ERK pathway by controlling A-Raf splicing in hepatocellular carcinoma development.
Shilo A, Ben Hur V, Denichenko P, Stein I, Pikarsky E, Rauch J, Kolch W, Zender L, Karni R. Shilo A, et al. RNA. 2014 Apr;20(4):505-15. doi: 10.1261/rna.042259.113. Epub 2014 Feb 26. RNA. 2014. PMID: 24572810 Free PMC article.
Overexpression of hnRNP A1 or hnRNP A2, but not the splicing isoform hnRNP B1, induced tumor formation of immortalized liver progenitor cells, while knockdown of these proteins inhibited anchorage-independent growth and tumor growth of human liver cancer cell lines. In add …
Overexpression of hnRNP A1 or hnRNP A2, but not the splicing isoform hnRNP B1, induced tumor formation of immortalized liver progenitor cell …
Transformation of immortalized colorectal crypt cells by microcystin involving constitutive activation of Akt and MAPK cascade.
Zhu Y, Zhong X, Zheng S, Ge Z, Du Q, Zhang S. Zhu Y, et al. Carcinogenesis. 2005 Jul;26(7):1207-14. doi: 10.1093/carcin/bgi069. Epub 2005 Mar 17. Carcinogenesis. 2005. PMID: 15774489
It has been shown by epidemiological and animal studies that microcystin is an important exogenous factor involved in the carcinogenesis of colorectal cancer (CRC). However, details of the mechanism remain unclear. Transformation of colorectal cells is an important initial …
It has been shown by epidemiological and animal studies that microcystin is an important exogenous factor involved in the carcinogenesis of …
22 results