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1. |
HNRNPR enhanced transcription from the c-fos promoter. |
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2. |
Data suggest that c-fos may play a role in the molecular mechanisms of estrogen action on the induction, promotion or progression of endometriosis. |
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3. |
Report FOS proliferating network construction in early colorectal cancer (CRC) based on integrative significant function cluster and inferring analysis. |
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4. |
study found surface parameters for Fra-1 are similar in general to those of c-Fos and c-Jun; differences were found in the interactions of the three proteins with phospholipids |
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5. |
the role of calmodulin in PACAP-induced FOS gene expression |
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6. |
AP-1 proteins (jun/fos) are differentially expressed in ovarian tumors of differing malignant potential. No correlation with the proliferative and invasive potential of ovarian cancer cell lines could be found. |
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7. |
Data suggest that the single nucleotide variants of the TGACTCA motif modulate energetics and orientation of binding of the Jun-Fos heterodimer and that such behavior may be a critical determinant of differential regulation of specific genes. |
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8. |
Promoter analysis showed that PRIP acted through serum-responsive factor to regulate FOS gene expression. |
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9. |
Trolox prevents osteoclast formation and bone loss by inhibiting both RANKL induction in osteoblasts and c-Fos expression in osteoclast precursors. |
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10. |
These results indicate that the rat model shows symptoms similar to those in patients with orofacial cancer, for example, induction of feeding disorder and neuropathic pain. |
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11. |
c-Fos is a requisite and specific component for inducible NOS2 expression |
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12. |
LPS-induced c-fos and c-jun expressions are mediated by two different signaling pathways: one through phosphoinositide-phospholipase C, and the second through activation of protein kinase A (PKA). |
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13. |
c-Fos overexpression increases the proliferation of human hepatocytes by stabilizing nuclear Cyclin D1. |
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14. |
confirmed the downregulation of the FOS-JUNB pathway at transcriptional and protein level |
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15. |
Observational study of gene-disease association and gene-environment interaction. (HuGE Navigator) |
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16. |
The SAF-1.c-Fos.c-Jun ternary complex efficiently promotes transcription from both SAF-1 and AP-1 sites of human MMP-1 promoter. |
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17. |
the enhanced ability of tumor-derived LMP1 to induce and stabilize the c-Fos oncogene can be localized to two amino acids in the C terminus of LMP1 |
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18. |
bexarotene increased the occupancy of the identified enhancer element in IGFBP-6 gene by RXRalpha, RARbeta, cJun, cFos, and p300 |
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19. |
both SF1 and LRH1 can transcriptionally cooperate with the AP-1 family members c-JUN and c-FOS, known to be associated with enhanced proliferation of endometrial carcinoma cells, to further enhance activation of the STAR, HSD3B2, and CYP19A1 PII promoters |
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20. |
Activator protein-1 and smad proteins synergistically regulate human follicle-stimulating hormone beta-promoter activity. |
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21. |
Overexpression experiments implicate AP-1 family member Fra-1 in regulation of matrix metalloproteinase-1 expression in myeloid cells during inflammation. |
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22. |
Peptidylarginine deiminase Intergenic Enhancer is a strong enhancer of the PADI3 promoter in Ca2+-differentiated epidermal keratinocytes, and requires bound |
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23. |
The thermodynamics of heterodimerization of leucine zippers of Jun and Fos was characterized. |
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24. |
Expression of c-fos in the human endometrium may be regulated by 17beta-E(2), and c-fos may be involved in development of endometriosis by promoting MMP-9 gene expression and subsequently the invasive potential of endometrial explants. |
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25. |
Fast regulation of AP-1 activity through interaction of lamin A/C, ERK1/2, and c-Fos at the nuclear envelope. |
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26. |
loss of c-Fos expression is associated with tumour progression in ovarian carcinoma and that c-Fos may be a prognostic factor |
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27. |
identify c-JUN and c-FOS as important regulators of human replication origin selection |
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28. |
FOS-related genes, which have been implicated in early hypoxia as well as the development of breast cancers, were differentially expressed before and after surgery. |
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29. |
Thrombin also stimulated the expression of c-fos in GFs within 1 hour of exposure. The stimulation of c-fos mRNA expression by thrombin can be attenuated by D-Phe-Pro-ArgCH(2)Cl, a serine-proteinase inhibitor. |
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30. |
Results describe the effects of estradiol on cyclin D1, PS2, and c-fos gene expression by measuring levels of RNA polymerase II on DNA templates, levels of nascent transcripts associated with RNA polymerase II, and levels of RNAs. |
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31. |
FRA2 and AP1 have roles in development of pulmonary fibrosis |
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32. |
GPR30-mediated inhibition of urothelial cell proliferation is the result of decreased cyclin D1 by down-regulation of activation protein-1 signaling. |
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33. |
an unexpected function for c-Fos as a direct regulator of Tcrb recombination, rather than its usual function as a transcription regulator. |
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34. |
Results suggest that ganoderic acids-A and -H mediate their biological effects through the inhibition of AP-1 and NF-kappaB, resulting in the down-regulation of expression of Cdk4 and the suppression of secretion of uPA, respectively. |
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35. |
Binding of Fos-Jun bZIP domains to both tetradecanoylphorbol acetate (TRE) and CRE response elements is under enthalpic control and accompanied by entropic penalty at physiological temperatures. |
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36. |
These data demonstrate the role of Cx43 in the proliferation and migration of human saphenous vein smooth muscle cells and angiotensin II-induced Cx43 expression via mitogen-activated protein kinases (MAPK)-AP-1 signaling pathway. |
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37. |
vFLIP suppresses the AP-1 pathway, which is essential for KSHV lytic replication, by activating the NF-kappaB pathway. |
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38. |
These results demonstrated that D-alpha-tocopherol may be able to prevent the IL-8 upregulation and the increase in AP-1 activation induced by UVA irradiation through down-modulating cellular oxidative stress. |
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39. |
These results suggest that promotion of endothelial migration and proliferation by Ang-1 is mediated, in part, through the production of IL-8, which acts in an autocrine fashion to suppress apoptosis and facilitate cell proliferation and migration. |
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40. |
The present data indicate that bovine dialyzable leukocyte extract can block the AP-1 DNA-binding activity and expression of several transcriptions factors in breast cancer cells. |
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41. |
A loss of c-fos expression is correlated with a more advanced stage, lymph node metastasis, lymphatic invasion and shorter survival in gastric carcinoma. |
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42. |
AP-1 plays an essential role in the growth of at least some of NSCLC cells. |
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43. |
The physical interaction of AP-1 with p22(phox) gene promoter facilitates NADPHox regulation. |
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44. |
Coordinated down- and up-regulation of the various AP-1 subunits in the course of epidermal wound healing is important for its undisturbed progress, putatively by influencing inflammation and cell-cell communication. |
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45. |
Ras/MAPK cascade acts as the upstream signaling for AP-1 activation and IL-8 expression in toxin A-stimulated intestinal epithelial cells. |
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46. |
Observational study of gene-disease association. (HuGE Navigator) |
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47. |
c-Fos may undergo cell cycle dependent phosphorylation, in which some kinases including Aurora-A play a role in catalyzing the post translational modification of c-Fos. |
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48. |
VEGF, p-IkappaB-alpha, NF-kappaB, c-FOS, p-c-JUN, EGF-R and COX-2 were expressed in stromal myofibroblasts surrounding colon adenocarcinomas in the majority of cases. |
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49. |
Dimerization with the Jun proteins inhibits c-Fos nuclear exit. |
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50. |
In the paraventricular nucleus anandamide and N-arachidonoyl-serotonin increased significantly c-Fos expression. In the arcuate nucleus only OMDM-1 increased c-Fos expression. |
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51. |
Amino acid residues required for physical and cooperative transcriptional interaction of STAT3 and AP-1 proteins c-Jun and c-Fos. |
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52. |
During mitosis, HSF2 is bound to the HSE promoter elements of other heat shock genes, including hsp90 and hsp27, and the proto-oncogene c-fos. The presence of HSF2 is important for expression of these genes. |
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53. |
c-fos expression in the medial geniculate body triggered by cortical activation is elicited via a direct corticothalamic pathway, not by the pathway through the thalamic reticular nucleus. |
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54. |
These data indicate that the aberrant expression of PTEN contributes to the activation of the PI3kinase/Akt pathway and its transcription factor mediators in glioma. |
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55. |
Phosphorylation of the carboxy-terminal transactivation domain of c-FGOS by extracellular signal-related kinase mediates the transcriptional activation of AP-1 and cellular neoplastic transformation by PDGF. |
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56. |
SDF-1/CXCL12 enhanced cell survival in synergy with other cytokines involves activation of CREB and induction of Mcl-1 and c-Fos |
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57. |
Up-regulation of c-Fos in the lymphocytes of rheumatoid arthritis patients. |
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58. |
VEGF and PlGF induced expression of both full-length FosB mRNA and an alternatively spliced variant. |
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59. |
In psoriatic epidermis, c-Jun expression was prominent in both hyperproliferating basal and suprabasal keratinocytes, whereas c-Fos expression was unchanged. |
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60. |
Effects of fluid shear stress on expression of proto-oncogenes c-fos and c-myc in cultured human umbilical vein endothelial cells. |
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61. |
p53 and c-fos are significantly overexpressed in thyroid cancer patients, indicating their role in the genetic mechanisms leading to thyroid tumorigenesis |
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62. |
loss of Net and constitutive c-fos expression appear to be a key event in the transformation of cervical cancer cells. |
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63. |
c-fos and AP-1 are regulated by JNK and p38 MAPK |
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64. |
c-Fos/c-Jun AP-1 dimer activity is downregulated by SUMO-1, SUMO-2, and SUMO-3 |
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65. |
Vasoactive intestinal peptide induces FOS expression in a prostatic neoplasm cell line. |
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66. |
studies suggest that the cooperative interaction of the estrogen receptor with Fos and Jun proteins helps confer estrogen responsiveness to the endogenous progesterone receptor gene |
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67. |
results suggest that Hic-5 participates in the transcriptional regulation of c-fos as a scaffold in transcriptional complexes |
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68. |
FOS is the primary target of up-regulation in Helicobacter pylori infections in human gastric cancer cells. |
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69. |
AP-1 and JNK have roles in reactive oxygen species activation in tobacco-induced mucin production in lung cells |
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70. |
TBP affects the NF1 and c-fos promoters in a manner reciprocal to that of TLF, stimulating the c-fos promoter and inhibiting NF1 transcription |
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71. |
Results showed that certain regulation involved in c-myc, c-fos, and c-jun was present in the apoptosis, and the c-Myc dependent-on and Jun N-terminal kinase (JNK) pathway also play roles. |
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72. |
The increase in c-Fos-immunoreactive neurons induced by butyric acid was reproduced with hydrochloric acid at the same pH but not with sodium butyrate. |
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73. |
data demonstratre that c-Fos physically and functionally interacts with JCV major early regulatory protein large T-Ag and that this interaction modulates JCV transcription and replication in glial cells |
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74. |
expression of Egr-1, c-fos and cyclin D1 varies in esophageal precancerous lesions and cancer tissues, suggesting an involvement of these genes in the development of esophageal carcinoma. |
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75. |
independent and cooperative activation of chromosomal c-fos promoter by STAT3 |
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76. |
c-Fos produced in D1 receptor-expressing neurons integrates mechanisms to facilitate both the acquisition and extinction of cocaine-induced persistent changes in brains of Drd-1-Cre transgenic mice. |
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77. |
Tumor promoter arsenite stimulates histone H3 phosphoacetylation of this and c-jun proto-oncogene chromatin in diploid fibroblasts. |
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78. |
a physical interaction between c-Fos and STAT-1 participates in NOS2 gene transcriptional activation in lung epithelium |
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79. |
candidate genes that may be involved in the origination of ameloblastoma and several genes previously unidentified in relation to human tooth development. |
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80. |
p38alpha and -beta mediate UV-induced, AP-1-mediated, c-Fos phosphorylation |
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81. |
Crystal structure of a ternary SAP-1/SRF/c-fos SRE DNA complex |
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82. |
Analysis of heterophilic and homophilic interactions of cadherins using the c-Jun/c-Fos dimerization domains |
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83. |
In hepatoma-associated anorexia-cachexia c-Fos was induced in several brain areas of thes forebrain. |
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84. |
Sustained ERK5 activity and the E3 ligase UBR1 regulate the stability and subcellular localization of c-Fos. |
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85. |
c-jun, junD, junB, and c-fos and Notch2 are expressed in splenic marginal zone lymphoma |
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86. |
c-Fos binding at the TGFbeta1 promoter proximal AP-1 site in human colon carcinoma cells is required for TGFbeta1 production by the tumor cells. |
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87. |
RET(Y791F) and RET(S891A) induce STAT3 Ser(727) phosphorylation via a canonical Ras/ERK1/2 pathway and integration of the Ras/ERK1/2/ELK-1 and STAT3 pathways was required for up-regulation of the c-fos promoter by FMTC-RET |
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88. |
Review. AP1 plays a crucial role during human papillomavirus (HPV) early gene expression, in particular of the expression of E6 and E7 oncoproteins. |
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89. |
The positive c-fos immunoreactivity observed in sudden infant death syndrome suggests that the neurons of the dorsal motor vagal nucleus involved in the regulation of breathing are able to yield an intense, immediate ventilatory response to hypoxia. |
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90. |
INI1/hSNF5/BAF47 could be recruited to the region of c-fos promoter to reduce histone acetylation |
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91. |
Expression of c-fos was induced by TPA and Saikosaponin a during 30 min to 6 h of treatment. |
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92. |
c-Fos proto-oncoprotein is degraded by the proteasome independently of its own ubiquitinylation |
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93. |
phosphorylation of tyrosine residues 10 and 30 of c-Fos regulate the rate of synthesis of phospholipids by regulating c-Fos/endoplasmic reticulum association. |
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94. |
Bombesin antagonists inhibit growth of MDA-MB-435 estrogen-independent breast cancers and decrease the expression of the ErbB-2/HER-2 oncoprotein and c-jun and c-fos oncogenes |
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95. |
activity of the AP-1 components c-Jun, ATF2, and c-Fos is altered in renal cystic tissue of patients with autosomal dominant polycystic kidney disease |
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96. |
PGE2 increases the expression and secretion of VEGF in HCC cells by activating the transcription factor c-fos, promotes the angiogenesis of hepatocellular carcinoma and plays an important role in the pathogenesis of liver cancer. |
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97. |
c-Fos represents a novel target for the isomerizing activity of Pin1, which has a role in the mechanism by which c-Jun and c-Fos cooperate to regulate AP-1-dependent gene transcription |
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98. |
Retinoic acid receptors inhibit AP1 activation by regulating extracellular signal-regulated kinase and CBP recruitment to an AP1-responsive promotor (transcription factor AP1) |