Disease relevance of Genes, fos

• During cardiocyte hypertrophy evoked by endothelin-1, Phenylephrine, or PMA, the steady state level of BNP mRNA increased as rapidly as the "immediate-early" induction of the c-fos gene expression, and reached a maximal level within 1 h [1].
• Well differentiated hepatoma cells (Fao) possess both the long and short forms of the leptin receptor and respond to leptin with a stimulation of c-fos gene expression [2].
• Previous studies showed that T antigen could activate simple promoters containing the TATA elements from the hsp70 and c-fos gene promoters but failed to significantly activate similar promoters containing the TATA elements from the promoters of the SV40 early and adenovirus E2a genes [3].
• Retinoic acid suppresses polyoma virus transformation by inhibiting transcription of the c-fos proto-oncogene [4].
• Previous studies have reported that the c-fos gene via formation of activator protein-1 (AP-1) transcription factor contributes to adaptive responses to continuous hypoxia [5].

Psychiatry related information on Genes, fos

• The c-FOS gene product, a putative transacting transcriptional regulator of the amyloid precursor protein (APP) gene, is a candidate locus for the familial Alzheimer's disease (FAD) mutation on chromosome 14 (FAD14) [6].
• Upon activation of opiate receptors by morphine, the c-fos gene is activated and Fos protein may act as a signal transducer uniquely involved in the mechanism of opiate addiction at the level of gene regulation [7].

High impact information on Genes, fos

• Through its SH2 domain, p91 directly interacts with the EGF receptor in a ligand-dependent manner. p91 is a necessary component of an EGF-induced DNA-binding factor that recognizes a previously identified regulatory element, SIE (c-sis-inducible element), in the c-fos gene promoter [8].
• Transcription factor p91 interacts with the epidermal growth factor receptor and mediates activation of the c-fos gene promoter [8].
• We report here that transport of the protein product of the c-fos proto-oncogene from the cytoplasm, where it is synthesized, into the nucleus, where it operates as part of the AP-1 transcription complex, is not spontaneous but depends on the continuous stimulation of cells by serum factors [9].
• The functional association between DNA topoisomerase I and gene activity has been analyzed using the tightly regulated c-fos proto-oncogene, which undergoes rapid transitions between active and inactive states of transcription [10].
• There is a dramatic increase in the FSE2 binding complex when Fos levels are induced with serum, benzodiazepine, and nerve growth factor or are expressed from a v-fos gene [11].

Chemical compound and disease context of Genes, fos

• This activation of c-fos gene expression may be an important mechanism in the angiotensin-induced smooth muscle hypertrophy [12].
• These results suggest that expression of the c-fos gene can influence cisplatin sensitivity, and that c-fos antisense oligonucleotide based therapy may be effective at killing parental and cisplatin-resistant ovarian carcinoma cells, either alone or in combination with cisplatin [13].
• Estrogen regulation of c-fos gene expression through phosphatidylinositol-3-kinase-dependent activation of serum response factor in MCF-7 breast cancer cells [14].
• Regulation of c-fos gene expression by lipopolysaccharide and cycloheximide in C6 rat glioma cells [15].
• Also, induction of promoter activity of beta-MHC and c-fos genes analyzed by chloramphenicol acetyl transferase assay confirmed the induction of cardiac hypertrophy upon direct injection of the full-length cDNA of the 182-kDa protein [16].

Biological context of Genes, fos

• Serum response factor (SRF) is a mammalian transcription factor that binds to the serum response element in the enhancer of the c-fos proto-oncogene and thus may mediate serum-induction of c-fos transcription [17].
• DNA topoisomerase II cleaves at specific sites in the 5' flanking region of c-fos proto-oncogenes in vitro [18].
• However, in contrast to that of the c-fos gene, the regulation of insulin-like growth factor I gene expression by GH is not mediated by means of the activation of protein kinase C, and, in line with this, prostaglandin F2 alpha and 4 beta-phorbol-12,13-didecanoate were ineffective [19].
• Thus, the region between -225 and -113 in IFN-beta 2, which contains DNA motifs similar to the regulatory elements in the human c-fos gene, appears to contain the major cis-acting regulatory elements responsible for the activation of the IFN-beta 2 promoter by several different cytokines, viruses, and second messenger agonists [20].
• However, the Ca2+/cAMP response element of the c-fos gene was not sufficient to confer Ang II responsiveness to the c-fos promoter, and inhibitors of protein kinase A had no effects on Ang II-induced c-fos expression [21].

Anatomical context of Genes, fos

• The data suggest that the c-myc and c-fos proto-oncogenes play an important role in mediating the multiple effects of IL-3 on hemopoietic progenitor cells [22].
• In contrast, NE did not increase cytosolic Ca2+ in quiescent myocytes, and pretreatment with BAPTA-AM did not inhibit the NE-stimulated increase in c-fos gene expression [23].
• Slight expressions of the c-jun gene were observed in unstimulated cardiac myocytes, and Ang II increased expressions of the c-jun gene as well as the c-fos gene [24].
• Multiple members of the jun and fos gene families were frequently expressed at the mRNA level in vitro, with detectable functional activity (as defined by AP-1-specific DNA binding and/or transactivation of an AP-1-driven reporter construct) present in all 10 NSCLC cell lines examined [25].
• Previous experiments have shown that noxious stimulation increases expression of the c-fos proto-oncogene in subpopulations of spinal cord neurons. c-fos expression was assessed by immunostaining for Fos, the nuclear phosphoprotein product of the c-fos gene [26].

Associations of Genes, fos with chemical compounds

• We postulate that c-fos antisense RNA blocks expression of the endogenous c-fos gene by accelerating the degradation of c-fos mRNA and that cycloheximide treatment interferes with this degradation [27].
• Expression of genes for retinoic acid receptors (RARs) and activator protein-1 (encoded by the c-Jun and c-Fos genes) in lung tissue specimens was examined by western blotting [28].
• Ferrets given a beta-carotene supplement and exposed to tobacco smoke had threefold to fourfold elevated expression of the c-Jun and c-Fos genes [28].
• Activation of AP-1 by PDTC was dependent on protein synthesis and involved transcriptional induction of c-jun and c-fos genes [29].
• The exogenous fos gene was rapidly induced to maximal levels within 1-2 hr of estrogen addition [30].

Gene context of Genes, fos

• Although JAK1 is phosphorylated in response to EGF, it is not required for STAT activation or for induction of the c-fos gene [31].
• Induction of c-fos gene expression and DNA synthesis were also abolished by the inhibition of EGF-R function [32].
• Furthermore, we demonstrate that BMP2 inhibits PDGF-induced transcription of c-fos gene, a natural target of Elk-1 that normally forms a ternary complex that activates the serum response element of the c-fos gene [33].
• While Epo is known to activate c-fos gene expression, the mechanism of AP-1 activation is unknown [34].
• These data argue for a combined regulation of cpcA that includes a translational regulation like that of yeast GCN4 as well as a transcriptional regulation like that of the mammalian jun and fos genes [35].

Analytical, diagnostic and therapeutic context of Genes, fos

• Nuclear extracts from LPS- and zymosan-treated cells showed strong AP-1 activity by gel-shift analysis, and supershift analysis showed the AP-1 complexes contained specific members of both the jun and fos gene families [36].
• Functional dissection of p56lck, a protein tyrosine kinase which mediates interleukin-2-induced activation of the c-fos gene [37].
• Further analysis of RNA extracted from regressing ventral prostate glands at sequential 12-h intervals after castration showed that the c-fos gene was induced at 36 h, earlier than c-myc, alpha-tubulin, and hsp 70.(ABSTRACT TRUNCATED AT 250 WORDS)[38]
• In situ hybridization histochemistry showed that i.c.v. administration of AM2 (0.2, 1, and 2 nmol/rat) caused marked induction of the expression of the c-fos gene in the PVN and the SON [39].
• The number of superficial (laminae I-II) and deep (laminae III-VI) spinal dorsal horn cells expressing the c-fos proto-oncogene 2 h after subcutaneous injection of formalin was reduced by 34% and 50%, respectively, in animals with an ipsilateral DRt lesion as compared to non-lesioned rats [40].

References