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Validated All-in-One™ qPCR Primer for FOS(NM_005252.3) Search again
Product ID:
HQP054675
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
AP-1, C-FOS, p55
Gene Description:
Fos proto-oncogene, AP-1 transcription factor subunit
Target Gene Accession:
NM_005252.3(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Validated result:
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| A | B |
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Each All-in-One™ qPCR Primer is experimentally validated to yield a single dissociation curve peak and to generate a single amplification of the correct size for the targeted gene. A cDNA Pool, containing reverse transcript products of 8 different human tissue total RNA(Liver, Testis,Muscle,Thyroid,Brain,Spleen,Stomach,Small Intestine)),was used as the qPCR validation template. qPCR was performed using 0.2 µM primer with 2XAll-in-One™ qPCR Mix (Catalog#: QP001,QP002,QP004,QP005). Reactions were incubated for 10min. at 95°C, followed by 40 cycles of 95°C for 10 sec.; 60°C, 20 sec. and 72°C, 15sec. using Bio-Rad iQ5™ Instrument. At the end of the last cycle, temperature was increased from 72 to 95°C to produce a melting curve. Panel A: Validated Result for Amplification Curve; Panel B: Validated Result for Melting Curve. |
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Summary
The Fos gene family consists of 4 members: FOS, FOSB, FOSL1, and FOSL2. These genes encode leucine zipper proteins that can dimerize with proteins of the JUN family, thereby forming the transcription factor complex AP-1. As such, the FOS proteins have been implicated as regulators of cell proliferation, differentiation, and transformation. In some cases, expression of the FOS gene has also been associated with apoptotic cell death.
Gene References into function
- Crystal structure of a ternary SAP-1/SRF/c-fos SRE DNA complex
- 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
- Analysis of heterophilic and homophilic interactions of cadherins using the c-Jun/c-Fos dimerization domains
- Retinoic acid receptors inhibit AP1 activation by regulating extracellular signal-regulated kinase and CBP recruitment to an AP1-responsive promotor (transcription factor AP1)
- Effects of fluid shear stress on expression of proto-oncogenes c-fos and c-myc in cultured human umbilical vein endothelial cells.
- candidate genes that may be involved in the origination of ameloblastoma and several genes previously unidentified in relation to human tooth development.
- Review. AP1 plays a crucial role during human papillomavirus (HPV) early gene expression, in particular of the expression of E6 and E7 oncoproteins.
- results suggest that Hic-5 participates in the transcriptional regulation of c-fos as a scaffold in transcriptional complexes
- 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
- Tumor promoter arsenite stimulates histone H3 phosphoacetylation of this and c-jun proto-oncogene chromatin in diploid fibroblasts.
- Expression of c-fos was induced by TPA and Saikosaponin a during 30 min to 6 h of treatment.
- independent and cooperative activation of chromosomal c-fos promoter by STAT3
- p53 and c-fos are significantly overexpressed in thyroid cancer patients, indicating their role in the genetic mechanisms leading to thyroid tumorigenesis
- 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
- Up-regulation of c-Fos in the lymphocytes of rheumatoid arthritis patients.
- a physical interaction between c-Fos and STAT-1 participates in NOS2 gene transcriptional activation in lung epithelium
- 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.
- c-fos and AP-1 are regulated by JNK and p38 MAPK
- c-Fos proto-oncoprotein is degraded by the proteasome independently of its own ubiquitinylation
- 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.
- VEGF and PlGF induced expression of both full-length FosB mRNA and an alternatively spliced variant.
- 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.
- FOS is the primary target of up-regulation in Helicobacter pylori infections in human gastric cancer cells.
- AP-1 and JNK have roles in reactive oxygen species activation in tobacco-induced mucin production in lung cells
- c-jun, junD, junB, and c-fos and Notch2 are expressed in splenic marginal zone lymphoma
- loss of Net and constitutive c-fos expression appear to be a key event in the transformation of cervical cancer cells.
- SDF-1/CXCL12 enhanced cell survival in synergy with other cytokines involves activation of CREB and induction of Mcl-1 and c-Fos
- In psoriatic epidermis, c-Jun expression was prominent in both hyperproliferating basal and suprabasal keratinocytes, whereas c-Fos expression was unchanged.
- p38alpha and -beta mediate UV-induced, AP-1-mediated, c-Fos phosphorylation
- 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
- Vasoactive intestinal peptide induces FOS expression in a prostatic neoplasm cell line.
- In hepatoma-associated anorexia-cachexia c-Fos was induced in several brain areas of thes forebrain.
- 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.
- 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
- c-Fos/c-Jun AP-1 dimer activity is downregulated by SUMO-1, SUMO-2, and SUMO-3
- 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
- INI1/hSNF5/BAF47 could be recruited to the region of c-fos promoter to reduce histone acetylation
- 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.
- 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.
- 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.
- Sustained ERK5 activity and the E3 ligase UBR1 regulate the stability and subcellular localization of c-Fos.
- phosphorylation of tyrosine residues 10 and 30 of c-Fos regulate the rate of synthesis of phospholipids by regulating c-Fos/endoplasmic reticulum association.
- 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.
- 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
- 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.
- 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.
- 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.
- 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.
- Amino acid residues required for physical and cooperative transcriptional interaction of STAT3 and AP-1 proteins c-Jun and c-Fos.
- Ras/MAPK cascade acts as the upstream signaling for AP-1 activation and IL-8 expression in toxin A-stimulated intestinal epithelial cells.
- Dimerization with the Jun proteins inhibits c-Fos nuclear exit.
- 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.
- 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.
- 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.
- 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.
- A loss of c-fos expression is correlated with a more advanced stage, lymph node metastasis, lymphatic invasion and shorter survival in gastric carcinoma.
- 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.
- 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.
- AP-1 plays an essential role in the growth of at least some of NSCLC cells.
- vFLIP suppresses the AP-1 pathway, which is essential for KSHV lytic replication, by activating the NF-kappaB pathway.
- The physical interaction of AP-1 with p22(phox) gene promoter facilitates NADPHox regulation.
- 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.
- 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.
- 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.
- 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.
- GPR30-mediated inhibition of urothelial cell proliferation is the result of decreased cyclin D1 by down-regulation of activation protein-1 signaling.
- an unexpected function for c-Fos as a direct regulator of Tcrb recombination, rather than its usual function as a transcription regulator.
- 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.
- FRA2 and AP1 have roles in development of pulmonary fibrosis
- 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.
- Activator protein-1 and smad proteins synergistically regulate human follicle-stimulating hormone beta-promoter activity.
- The thermodynamics of heterodimerization of leucine zippers of Jun and Fos was characterized.
- Overexpression experiments implicate AP-1 family member Fra-1 in regulation of matrix metalloproteinase-1 expression in myeloid cells during inflammation.
- 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.
- identify c-JUN and c-FOS as important regulators of human replication origin selection
- loss of c-Fos expression is associated with tumour progression in ovarian carcinoma and that c-Fos may be a prognostic factor
- Peptidylarginine deiminase Intergenic Enhancer is a strong enhancer of the PADI3 promoter in Ca2+-differentiated epidermal keratinocytes, and requires bound
- bexarotene increased the occupancy of the identified enhancer element in IGFBP-6 gene by RXRalpha, RARbeta, cJun, cFos, and p300
- 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
- Fast regulation of AP-1 activity through interaction of lamin A/C, ERK1/2, and c-Fos at the nuclear envelope.
- 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 promoter
- 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.