Disease relevance of FOS

• CONCLUSIONS: We conclude that independent expression of RAS, JUN, and FOS occurred significantly more often in large tubulovillous adenomas and adenocarcinomas while p53 expression occurred primarily in adenocarcinomas [1].
• EXPERIMENTAL DESIGN: We examined the expression of two nuclear oncoproteins, JUN and FOS (Abbreviations used in this paper are lower case letters for oncogenes and upper case letters for oncoproteins), that have not been previously associated with development of colorectal cancer [1].
• Immunohistochemical detection of RAS, JUN, FOS, and p53 oncoprotein expression in human colorectal adenomas and carcinomas [1].
• Drastically increased expression of MYC and FOS protooncogenes during in vitro differentiation of chronic lymphocytic leukemia cells [2].
• Helicobacter pylori infection activates FOS and stress-response genes and alters expression of genes in gastric cancer-specific loci [3].

Psychiatry related information on FOS

• Genetic analysis of the cellular oncogene fos in patients with chromosome 14 encoded Alzheimer's disease [4].
• While auditory perception is critical for both sexes, the responses of the immediate early genes (IEGs) ZENK and FOS differ in auditory brain areas of d30 males and females [5].

High impact information on FOS

• These results raise the possibility that FOS and JUN participate in the regulation of MYC [6].
• A FOS protein is present in a complex that binds a negative regulator of MYC [6].
• Recovered populations were verified to be both viable and unstressed by evaluation of the transcriptional expression of two genes, HSPA6 and FOS, known indicators of cellular stress [7].
• In vitro inhibition of FOS using small interfering RNA and 3-hydroxy-3-methyl-glutaryl CoA reductase inhibitor simvastatin (statin) affected monocyte activation and suggested an important role in pathogenesis [8].
• The Finkel-Biskis-Jinkins osteosarcoma (FOS) gene was significantly increased in patients, and the highest levels of FOS associated with patients who had previously undergone coronary revascularization [8].

Chemical compound and disease context of FOS

• Lack of adverse toxicity seen with CMI at this dosage is consistent with a similar lack of significant toxicity exhibited by other dietary carbohydrates (sorbitol, sucrose, glucose), oligofructoses (inulin/FOS) and carboxylated cellulose in repeated-dose rat studies at approximately the same dosage [9].
• 2-keto-3-deoxy-D-glycero-D-galactonononic acid; KDO, 2-keto-3-deoxyoctulosonic acid; FOS, fructooligosaccharides; GF5, GF6, and GF7, oligofructans: Hib, Haemophilus influenzae type b; FAB, fast atom bombardment; ESI, electrospray ionization; MALDI-TOF, matrix assisted laser desorption ionization-time of flight [10].

Biological context of FOS

• Perturbations in the expression levels of the proto-oncogenes FOS, JUN and MYC after exposure to sham and RF fields were assessed by real-time RT-PCR [11].
• Consequently, a short-term reduction in gene expression in microgravity may have a more dramatic effect over the long term, since both the JUN and FOS protein families are required for normal cell cycle progression [12].
• 3. The c-fos gene (FOS), localised to 14q24.3-q31, is a candidate for the AD gene since it may be involved in the transcription regulation of the amyloid precursor protein gene (APP) [4].
• The 4 exons of FOS were sequenced in one pathologically confirmed AD patient in each family [4].
• The RFLP is detected in BstNI digested DNA and is located near the 3' end of FOS [4].

Anatomical context of FOS

• Multivariate analysis independently demonstrated a significant prognostic value for lymph node involvement, VEGF and FOS [13].
• Although the efficiency of AdA- FOS in therapy would need to be further analyzed with other cisplatin-resistant and mdr cell lines, these results suggest that AP-1 is a therapeutic molecular target and that inhibition of AP-1 DNA binding may be of clinical value in treating chemotherapeutic resistance [14].
• Since proto-oncogenes play a central role in the regulation of cellular growth and differentiation, localization of MYC, FOS, and JUN proteins has been studied in the testis of the lizard, Podarcis s. sicula, during the annual reproductive cycle by immunocytochemistry using antisera against c-myc, c-fos, and c-jun products [15].
• The pAT 133 gene is immediately induced, with FOS-like kinetics, in human T cells and in fibroblasts [16].
• Intrinsic to this maturation is the induction of a class of immediate early genes in the monocyte that includes the transcription factors JUN and FOS [17].

Associations of FOS with chemical compounds

• In freshly isolated cells, both FOS and FOSB mRNAs increase dramatically in response to the protein synthesis inhibitor cycloheximide [18].
• The exchange of either leucine 1, 3, or 5 of the leucine repeat of FOS B to a proline dramatically inhibits its association with JUN proteins [19].
• 1,25-Dihydroxy vitamin D3 and 12-O-tetradecanoyl phorbol-13-acetate synergistically induce monocytic cell differentiation: FOS and RB expression [20].
• Unique patterns of FOS, phospho-CREB and BrdU immunoreactivity in the female rat brain following chronic stress and citalopram treatment [21].
• 8-Cl-cAMP increased the level of cAMP-response element (CRE) binding protein in addition to inducing FOS mRNA, whose promoter contains CRE [22].

Physical interactions of FOS

• Thus, JUN and FOS bind to the AP-1 site in the promoters of cellular genes and activate their transcription, resulting in maturation of the monocyte into a macrophage [17].

Regulatory relationships of FOS

• In this resistance profile, FOS was up-regulated and NM23 down-regulated [23].
• These results demonstrate that any major alteration in the alpha-helical structure of the 'leucine zipper' completely inhibits the interaction of FOS B with any of the three JUN proteins [19].
• Here it is reported that in animal cap explants of the amphibian Pleurodeles waltl, noggin can induce upregulation of a FOS-related protein in a calcium-dependent manner [24].

Other interactions of FOS

• Differential sensitivity of FOS and JUN family members to calpains [25].
• FRA-1, a member of the FOS family of transcription factors, is overexpressed in a variety of human tumors, and contributes to tumor progression [26].
• These differences in expression of FOS and FOSB suggest different roles and regulation [18].
• Induction of cyclin gene expression by serum is reduced concomitantly with the decline in FOS induction in aging HDFs, suggesting a possible relationship to the decrease in the proliferative response to mitogens during cellular senescence [27].
• The oncogene FOS was the most overexpressed gene (from eight- to 14-fold), followed by tumor-necrosis-factor-receptor 1 (TNFRSF1A) [28].

Analytical, diagnostic and therapeutic context of FOS

• The FOS oncogene could play an important role in bone development because SV40 is able to induce FOS in cell culture [29].
• In GH3B6 cells stimulated with TRH or KCl, enhanced FOS protein levels were detected by immunofluorescence and localized in the nucleus with confocal microscopy [30].
• Multiparameter flow cytometry was used to simultaneously measure nuclear DNA content, RB protein, and MYC or FOS protein per cell [31].
• Comparative gene mapping in mammals suggests that the bovine immunoglobulin heavy chain genes, IGHG4 and IGHM might be syntenic with the FOS oncogene [32].
• In situ hybridization using cDNAs complementary to specific regions of the mRNAs encoding four members of the FOS transcription factor gene family reveals modest levels of hybridization over superficial lamina of the nucleus caudalis of the spinal tract of the trigeminal in sections taken from unstimulated brains [33].

References