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Validated All-in-One™ qPCR Primer for JUN(NM_002228.3) Search again
Product ID:
HQP009853
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
AP-1, AP1, c-Jun, cJUN, p39
Gene Description:
Jun proto-oncogene, AP-1 transcription factor subunit
Target Gene Accession:
NM_002228.3(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
This gene is the putative transforming gene of avian sarcoma virus 17. It encodes a protein which is highly similar to the viral protein, and which interacts directly with specific target DNA sequences to regulate gene expression. This gene is intronless and is mapped to 1p32-p31, a chromosomal region involved in both translocations and deletions in human malignancies.
Gene References into function
- c-Jun regulates vascular smooth muscle cell growth and neointima formation after arterial injury
- 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
- An alternative model of H ferritin promoter transactivation by c-Jun (H ferritin, also called isoferritin)
- Analysis of heterophilic and homophilic interactions of cadherins using the c-Jun/c-Fos dimerization domains
- Functional role of ERK1/2 activation in phorbol ester-induced promoter activation of human 12(S)-lipoxygenase gene.
- Activation of human monoamine oxidase B gene expression by a protein kinase C MAPK signal transduction pathway involves c-Jun and Egr-1.
- c-Jun associates with the oncoprotein Ski and suppresses Smad2 transcriptional activity
- Retinoic acid receptors inhibit AP1 activation by regulating extracellular signal-regulated kinase and CBP recruitment to an AP1-responsive promotor (transcription factor AP1)
- Kip1 inhibits Jab1 mediated c-Jun dependent transcription
- Aberrantly expressed c-Jun and JunB are a hallmark of Hodgkin lymphoma cells, stimulate proliferation and synergize with NF-kappa B.
- Review.AP1 plays a crucial role during human papillomavirus (HPV) early gene expression, in particular of the expression of E6 and E7 oncoproteins.
- Epstein-Barr virus latent membrane protein 2A may exploit MAPK kinases and affect both the phosphorylation and stability of c-Jun protein
- structurally distinct modes of recognition of the KIX domain of CBP by CREB and this protein
- results suggest strongly that human amylin induces apoptosis in pancreatic islet beta-cells through stimulation of expression and activation of c-Jun
- 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 c-fos and this proto-oncogene chromatin in diploid fibroblasts.
- Phosphorylation of c-jun was induced by TPA only. On the other hand, expression of proto-oncogene c-jun was induced by TPA and Saikosaponin a during 30 min to 6 h of treatment.
- conclude that Ras regulates TNF-alpha-induced chemokine expression by activating the AP-1 pathway and enhancing transcriptional function of NF-kappaB, whereas MEKK1 activates both the AP-1 and NF-kappaB pathways
- AP-1 (c-Jun & FosB) binds to a site in the 5' untranslated region of the CD95L gene. Transdominant negative Jun mutants reduce CD95L promoter activity. FosB dimerized with c-Jun has an important role in TCR/CD3-mediated activation-induced cell death.
- Critical role of the transcription factor AP-1 for the constitutive and interferon-induced expression of IFI 16.
- data demonstratre that c-Jun 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
- c-Jun has an important functional role in the induction of cell cycle arrest and proliferation arrest of myeloid leukemia cells because of the ligation of the cell surface adhesion receptor CD44 by anti-CD44 antibody.
- The expression of c-Jun protein and c-jun mRNA is significantly increased in the cerebellar vermis of patients with schizophrenia; no significant differences are found in the expression of Jun B or Jun D proteins.
- activator protein 1 and ERKs play crucial roles in FGF2-stimulated premature cranial suture closure
- The AP1 transcription factor c-jun is the prototypical nuclear effector of the JNK signal transduction pathway.
- Data suggest that overexpression and binding of JunB to the AP-1 site may relieve the repression of the core promoter by CD30 in Hodgkin-Redd Sternberg cells, which provide one basis for the constitutive overexpression of CD30 in Hodgkin's lymphoma
- The Ca2+-mediated increase in AP-1 binding may play an important role in upregulating AP-1-responsive gene expression, in stimulating pulmonary vascular cell proliferation and in pulmonary vascular remodeling in hypoxia-mediated pulmonary hypertension.
- transcription factors Sp1 and c-Jun have roles in regulation of keratin 16 gene expression by epidermal growth factor
- JUN has a role in androgen stimulation which blocks p53-dependent transactivation of the Fas gene, which can be blocked by androgen stimulation during radiation-induced Fas sensitization in prostate cancer cells
- c-Jun fails to act as a negative regulator for the cell survival of pancreatic cancer cells
- Findings strongly suggest that the AP-1/JNK signaling pathway has little or no impact on the generation of inflammatory mediators in neutrophils.
- c-fos and AP-1 are regulated by JNK and p38 MAPK
- NF-kappa B and AP-1 are required for basal MAT2A expression in HepG2 cells and mediate the increase in MAT2A expression in response to TNF-alpha
- 15d-PGJ2 covalently modifies c-Jun and directly inhibits the DNA binding activity of AP-1. In addition, 15d-PGJ2 can promote the oligomerization of a fraction of c-Jun through the formation of intermolecular disulfide bonds or 15d-PGJ2-bonded dimers.
- c-Jun activity is modified by the estrogen receptor in the stress response
- activator protein-1 is repressed by Notch-1 with C promoter-binding factor 1
- findings demonstrate that activator protein-1 activation in human smooth muscle cells in response to angiotensin II and platelet-derived growth factor-AA is mediated via generation of p22phox-dependent reactive oxygen species
- An inverse correlation between JUN and p27(Kip1) expression levels in breast cancer.
- DET1 promotes ubiquitination and degradation of c-Jun by assembling a multisubunit ubiquitin ligase containing DNA Damage Binding Protein-1 (DDB1), cullin 4A (CUL4A), Regulator of Cullins-1 (ROC1), and constitutively photomorphogenic-1
- AP1 and CHOP are induced by MEKK3 and have roles in TRAF7-related apoptosis
- Results suggest that in human HL60 cells the presence of the AP-1 signal acts as a survival factor that determines the outcome of myc-induced proliferation or apoptosis.
- the well characterized basic leucine zipper domain of c-Jun functions in transcriptional activation by binding to the N terminus of hsTAF1 to derepress transcription
- a dominant negative mutant of c-Jun activates the interleukin-6 promoter
- oxysterols induce specific AP-1 proteins, thereby activating involucrin, one of the genes required for epidermal differentiation.
- data illustrate that NF-kappaB orchestrates immediate-early effects of LPS signaling and controls secondary AP-1 activation to mount an appropriate biological response
- Overexpression of ZNF394 in the cell inhibits the transcriptional activities of c-Jun and AP-1 reporters.
- AP-1 and JNK have roles in reactive oxygen species activation in tobacco-induced mucin production in lung cells
- role in regulating interleukin-5 expression
- c-Jun has a role in regulating p73 function
- These results define a novel regulatory pathway linking the transcription factors c-Jun, HERP2, and GATA-1.
- Data describe a possible mechanism by which NF-kappa B regulates the expression of c-Fos and AP-1 by controlling the expression of Elk-1.
- results suggest that the modulation of p38 and c-jun may play an important role in the differentiation and proliferation of human endometrial cells
- transcriptional activities of ElK-1 and AP-1 are inhibited by TRIM45, a novel human RBCC/TRIM protein
- c-Jun is phosphorylated by the human vaccinia-related kinase 1 (VRK1) and cooperates with the N-terminal kinase of c-Jun (JNK)
- there is a novel association between TRAF2 and TRAF3 that is mediated by unique portions of each protein and that specifically regulates activation of NF-kappaB, but not AP-1
- functional binding sites for NF-kappaB and AP-1 in the human beta-defensin-2 promoter are required for induction of hBD-2 through E. coli Nissle 1917
- The visualization of ubiquitinated Jun in living cells has uncovered a lysosomal pathway for Jun degradation that involves ubiquitination by Itch/AIP4.
- Trx may regulate cell cycle and growth through a novel modulation of AP-1 activity and p27Kip1 degradation with Jab1
- c-jun, junD, junB, and c-fos and Notch2 are expressed in splenic marginal zone lymphoma
- expression of AP-1-dependent genes is inhibited by the cJun dominant negative; the AP-1 blockade does not affect mRNA ERalpha expression or estrogen induction of estrogen-responsive element activity
- Cooperation of CD99 engagement with suboptimal TCR/CD3 signals resulted in enhanced CD4+ T cell proliferation, elevated expression of CD25 and GM1, increased apoptosis, augmented activation of JNK, and increased AP-1 activation
- COBRA1 may directly modulate AP-1 pathway and, therefore, may play important roles in cell proliferation, differentiation, apoptosis, and oncogenesis.
- evidence for an substance P-mediated induction of AP-1, which may contribute to the expression of pro-inflammatory cytokines
- Glucocorticoid receptor mutant is able to distinguish between NF-kappaB and AP-1 repression.
- induction of Smad7 gene expression by UV irradiation is mediated via induction of the transcription factor AP-1 in human skin fibroblasts
- c-Jun plays an important role in epidermal differentiation by negatively regulating the human involucrin gene.
- molecular mechanisms underlying ligand-dependent signaling in the ER/AP-1 pathway
- enhanced expression of c-Jun in basal and suprabasal keratinocytes might contribute to the pathogenesis of psoriasis.
- p300 is essential for SENP1 to enhance c-Jun-dependent transcription because SENP1 can desumoylate the CRD1 domain of p300, thereby releasing the cis-repression of CRD1 on p300
- Overexpression of a transfected gene encoding YB-1 in human HeLa cervical carcinoma cells significantly represses the transactivation of a minimal AP-1 reporter construct in response to the tumour promoter PMA.
- p38alpha and -beta mediate UV-induced, AP-1-mediated, c-Fos phosphorylation
- Shear stress induces lipocalin-type prostaglandin D synthase expression by transcriptional activation through the AP-1 binding site
- Prolactin and estrogen cooperatively enhance the activity of AP-1 in in breast cancer cells.
- JUN-dependent expression of PTN and SDF-1 in fibroblasts has a role in keratinocyte proliferation
- MMP-9 activity is inhibited by ascochlorin through suppression of AP-1-dependent induction of MMP-9 gene expression
- Activation of TrkA gene expression by methylation was considered to be caused by the direct interference of c-Jun binding to the negatively regulating AP-1-like site.
- hepatopoietin association with thioredoxin constitutes a redox signal transduction in activation of AP-1/NF-kappaB
- The proto-oncogene c-jun ia novel target gene of Aryl hydrocarbon receptor.
- Erg and Jun proteins interact in living cells
- TNF-alpha-induced CD44 expression was regulated by AP-1 through the activation of the CaMK-II pathway, whereas LPS-induced CD44 transcription was regulated specifically by Egr-1 through JNK activation.
- Overexpression of ZNF446 in COS-7 cells inhibits the transcriptional activities of SRE and AP-1.
- In conclusion, this study has demonstrated for the first time that sodium lactate and LPS exert synergistic effect on MMP and cytokine expression through NF-kappaB and MAPK pathways.
- chlorogenic acid stimulates Nrf2, inhibits activator protein-1, NF-kappaB, and MAPKs and induces phase 2 detoxifying enzyme activity
- Activation of both NF-kappaB and AP-1 may be required for ICH-1L/S-induced apoptosis in hepatocellular carcinoma(HCC), but not for Fas/FasL-mediated apoptosis. NF-kappaB and AP-1 may play important roles in pathogenesis of human HCC.
- Histone deacetylase inhibitors suppress the induction of c-Jun and its target genes including COX-2
- 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
- Involucrin expression of keratinocytes is suppressed by roxithromycin through direct inhibition of AP-1 and indirect inhibition of NF-kappaB.
- Dysregulated c-jun expression may be involved in the acquisition of anchorage independence in the process of human lung carcinogenesis
- results show that heparin affin regulatory peptide (HARP) is important for human prostate cancer cell proliferation and migration and establish role of activator protein-1 in up-regulation of HARP expression by low concentrations of hydrogen peroxide
- deletion constructs of the promoter and mutational deletion of specific transcription factor binding sites indicated that Smad3/4 and AP-1 binding sites mediated the TGF-beta1 response on LTBP-3
- Vpr protein activates activator protein-1, c-Jun N-terminal kinase, and NF-kappaB and stimulates HIV-1 transcription in promonocytic cells and primary macrophages
- demonstrates an important role of AP-1 and a member of the Ets family in the transcriptional regulation of C3aR expression, a prerequisite for the ability of C3a to participate in immunomodulation and inflammation
- Galectin-3 up-regulation of MUC2 transcription occurs at the level of transcription through AP-1 activation in colon cancer cells
- in vitro signaling pathway assay revealed that the JEV NS2B-NS3 protease significantly inhibited the signaling pathway of activator protein 1(AP1), a member of the bZIP family.
- AP-1 is a key transcription factor that, in part, controls astrocyte-specific expression of genes including the ACT and GFAP genes
- Results suggest that VEGF induced by hyperbaric oxygen is through c-Jun/AP-1 activation, and through simultaneous activation of ERK and JNK pathways.
- gene is identified in proliferative diabetic retinopasathy.
- PPARalpha activators LY-171883 and WY-14,643 were able to diminish transcriptional induction of COX-2 and VEGF by inhibiting AP-1 (activator protein-1)-mediated transcriptional activation.
- The AP-1 site in the u-PAR promoter seems to be a less tumor-specific regulator than the Sp1 and AP-2 alpha.
- AP-1 is a mediator of bile acid-induced liver cell apoptosis
- Jab1 is an important effector that mediates a novel signal transduction pathway for PAR-2-dependent gene expression
- matrix metalloproteinase-1 expression is regulated by JNK through Ets and AP-1 promoter motifs
- SMAP2 functions in the retrograde, early endosome-to-trans golig network pathway in a clathrin- and AP-1-dependent manner.
- Tacrolimus or cyclosporine A act on human osteoclast precursors in rheumatoid arthritis patients by targeting the calcineurin-dependent NFAT pathway and activation pathway for c-Jun or MITF.
- The data demonstrate that c-Jun contributes to the promotion of cellular survival by regulating the expression of PTEN.
- results indicate that HIV-1 Tat interacts with NFAT, affecting its cooperation with AP-1, without altering independent binding of these transcription factors to DNA
- The effects of Cybr on nuclear factor of activated T cells and AP-1 are dependent on MAPK activation.
- PEA3 and c-Jun stimulate synergistically the HER2/neu gene transcription with p300
- transcription factor, AP-1, was studied for its potential role in the hypoxia-induced protection against apoptosis. Specific inhibition of AP-1 decreased the protection effect of hypoxia against etoposide-induced apoptosis
- CD226 promoters P1 and P2 are regulated by Ets-1 and AP-1
- TNF-alpha down-regulates human Cu/Zn superoxide dismutase 1 promoter via JNK/AP-1 signaling pathway
- Crn7 interacts with AP-1 and is required for the maintenance of Golgi morphology and protein export from the Golgi
- These results indicate AP1-mediated upregulation of Bcl-X(L) expression is critical for protection of human gastric adenocarcinoma cells against adriamycin-induced apoptosis.
- temporal and dose-dependent interference by an AP-1 family member, c-Jun, upon NF-1 proteins binding an NF-1 consensus site derived from JC virus promoter sequence
- JAB1 overexpression is involved in the pathogenesis of pancreatic cancer through JAB1-mediated p27 degradation and that control of JAB1 expression is a novel therapeutic target in patients with pancreatic adenocarcinomas.
- Elafin inhibits the lipopolysaccharide-induced production of monocyte chemoattractant protein-1 in monocytes by inhibiting AP-1 and NF-kappaB activation.
- Phosphorylated forms of MKK4, JNK, and c-Jun were detected in salivary infiltrating mononuclear cells of Sjogren's syndrome patients
- JNK1 and JNK2 differentially regulate TBP through Elk-1, controlling c-Jun expression and cell proliferation
- AP-1 protein degradation has roles in collagen gel-induced epithelial cell apoptosis
- hyperactive variants of p38alpha induce, whereas hyperactive variants of p38gamma suppress, activating protein 1-mediated transcription
- AMPK mediates IL-2 production by regulating NF-AT and AP-1activation during T cell stimulation.
- Apoptosis induced by osmotic stress was suppressed by overexpression of c-Jun, indicating that the downregulation of c-Jun promotes apoptosis.
- a non-classical mechanism by which VDR acts as a c-Jun/AP-1 target gene to modify c-Jun activity in stress response through increased protein expression independent of classical transcriptional regulations
- activating protein 1 has a role in the transcriptional regulation of the human FCGR2B promoter mediated by the -343 G -> C polymorphism associated with systemic lupus erythematosus
- These findings indicate the dephosphorylation of c-Jun C terminus is required for the c-Jun/Sp1 interaction and reveal that PP2B plays an important role in regulating c-Jun/Sp1 interaction in phorbol 12-myristate 13-acetate -induced gene expression.
- 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.
- Ral is activated upon BCR stimulation and mediates BCR-controlled activation of AP-1 and NFAT transcription factors.
- IL-10 promoter activity was ablated by mutating two nonpolymorphic binding sites for the AP-1 transcription factor, and in primary human T cells, SDF-1 costimulation enhances AP-1 binding to both of these sites
- MCJ is required in these cells to prevent c-Jun-mediated expression of ABCB1 and maintain drug response.
- c-Jun homodimers are recruited to the interleukin-1beta (IL-1beta) promoter in the absence of direct DNA binding via protein-protein interactions with DNA-anchored PU.1 and CCAAT/enhancer-binding protein beta (C/EBPbeta).
- We will summarize the current knowledge regarding the implication of AP-1 proteins in respiratory epithelium carcinogenesis, highlight the ongoing research, and consider the future perspectives of their potential therapeutic interest.
- IGF-1 induces phosphorylation and an increase of the AP1 complex, which is phosphorylated and binds to the pS2/TFF1 promoter, allowing recruitment of the chromatin remodeling factor Brg1 followed by binding of ERalpha via its interaction with c-Jun
- These results suggest that hLBH proteins may act as a transcriptional activator in mitogen-activated protein kinase signaling pathway to mediate cellular functions.
- 1alpha-25(OH)2DHT(3) blocks TNF-induced monocytic tissue factor expression by inhibition of AP1 and NF-kappa b.
- FasL-induced activator protein (AP)-1 activation is required for optimal IL-8 production.
- Absence of CFTR at the cell membrane leads to an intrinsic AP1 activity.
- 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.
- the interaction between the hinge region and the GAE domain underlies the autoregulation of GGA function in clathrin-mediated trafficking through competing with the accessory proteins and the AP-1 complex
- These data suggest that Src-induced u-PAR gene expression and invasion/intravasation in vivo is also mediated via AP-1 region -190/-171, especially bound with c-Jun phosphorylated at Ser(73/63).
- Changes in AP-1 composition and the level of participating NFAT proteins can differentially influence cytokine gene expression, resulting in biological consequences for the modulation and dynamics of the immune response.
- These results imply that c-Jun plays a pivotal role in the pathway that connects ligand-activated AR to elevated ETV1 expression, leading to enhanced expression of matrix metalloproteinases and prostate cancer cell invasion.
- Amino acid residues required for physical and cooperative transcriptional interaction of STAT3 and API-1 proteins c-Jun and c-Fos.
- The AP-1 factor regulates the expression of cyclin D and E2F (the latter in turn regulates E2F-downstream genes), leading to cell cycle progression and breast cancer cell proliferation.
- Ras/MAPK cascade acts as the upstream signaling for AP-1 activation and IL-8 expression in toxin A-stimulated intestinal epithelial cells.
- We conclude that Jab1 expression may lead to down-regulation of the negative cell cycle regulator p27(Kip1), pointing to a possible mechanism that promotes hepatocarcinogenesis.
- c-Jun nuclear import is mediated by multiple transport receptors
- These results suggest that SKAP55 modulates signal transduction from the T cell antigen receptor to Ras by binding to RasGRP1.
- The present study confirms that overexpression of c-Jun contributes to metastasis of breast cancer.
- Dimerization with the Jun proteins inhibits c-Fos nuclear exit.
- These data suggest that stromally expressed c-Jun may promote prostatic epithelial proliferation through IGF-1 as a paracrine signal that, in turn, can promote prostate epithelial proliferation.
- results suggest that HPE-induced IL-8 secretion occurs via activation of JNK/SAPK and transcription factors NF-kappaB and AP-1 in PMA-differentiated THP-1 cells
- Results show that Plk3 mediates UV irradiation-induced c-Jun activation by phosphorylating c-Jun, suggesting that Plk3 plays an important role in mediating programmed cell death of corneal epithelial cells after UV irradiation.
- Transactivation by AP-1 increased luciferase expression 85-fold, in the absence of stimulation. Synergistic interactions were demonstrated between Ets1, GATA-3 and AP-1.
- overexpression of c-Jun is associated with invasiveness and metastasis in breast cancer
- c-Jun may sense the strength of genotoxic stress through DNA-damage dependent phosphorylation of T95, which in turn augments c-Jun transactivation by JNKs.
- These findings demonstrate that c-Jun/AP-1 is hepatoprotective during acute hepatitis by regulating nos2/nitric oxide expression and thus functionally antagonizes the cell death-promoting functions of JNK.
- Calcineurin stabilizes c-Jun by dephosphorylating c-Jun at Ser-243 to enhance its tumorigenic ability
- dynamic changes of the COP1/COP1D ratio provide an additional level of regulation of the half-life of the substrates of this E3 ligase under homeostatic or pathological conditions
- HSP90 stabilizes c-Jun protein, and so increases the total activity of c-Jun in HEK293 cells.
- AP-1 and NF-kappaB transcription factors are activated and EGF-R is expressed in these cells and associated with COX-2 and VEGF production
- ER stress increases MTHFR expression and IRE1 and c-Jun mediate this activation
- Nef binding to the MHC-I cytoplasmic tail stabilizes the interaction of a tyrosine in the MHC-I cytoplasmic tail with the natural tyrosine binding pocket in AP-1
- Basic fibroblast growth factor-induced neuronal differentiation of mouse bone marrow stromal cells requires FGFR-1, MAPK/ERK, and transcription factor AP-1
- analysis of a cross-talk between AP-1 and NF-kappaB
- 17beta-estradiol induces ERRalpha gene expression in MCF-7 cells through active recruitment of co-activators and release of co-repressors when ERRalpha and AP1 bind and ERalpha is tethered to the multiple hormone-response element
- in addition to its transcriptional effects, c-Jun regulates rRNA processing and nucleolar compartmentalization of the rRNA processing protein DDX21
- study has demonstrated a robust augmentation by high glucose of lipopolysaccharide (LPS)-stimulated CD14 antigen expression through activator protein-1 (AP-1) and nuclear factor kappaB (NFkappaB)
- Sp1 recruits ATF3, c-Jun, and STAT3 to obtain the requisite synergistic effect in neuronal injury through DINE neuronal injury-inducible gene
- results reveal that especially NRF-1, along with AP-1 and, to a minor extent, an Sp1 site, is essential for human CAPNS1 promoter activity and gene expression
- Results suggest that secretogranin II represents a key AP-1-regulated protein that counteracts nitric oxide toxicity and mediates neuronal differentiation of neuroblastoma cells.
- activator protein-1 (AP-1) was activated through phosphorylation of cJun and cFos, induced by JNK and p38, respectively.
- analysis of the structural polymorphism of a 21-bp Pu.Py DNA segment within human c-jun protooncogene 3'-region, a potential target for triplex formation
- Transcriptional activation of the EGR-1 promoter by JNK-MKK7 or by IL-1 required a single upstream AP-1 site and three distal serum-response elements (SRE).
- Binding of Jun-Fos bZIP domains to both tetradecanoylphorbol acetate (TRE) and CRE response elements is under enthalpic control and accompanied by entropic penalty at physiological temperatures.
- c-Jun translocates B23 and ARF from the nucleolus after JNK activation by means of protein interactions
- Over-expression of RASSF1A inhibits the growth of SGC7901 cells by negatively regulating the AP-1 activity, the latter in turn negatively signals cell proliferation.
- Our results reveal a mechanism by which nuclear Dvl cooperates with c-Jun to regulate gene transcription stimulated by the canonical Wnt signaling pathway.
- Transcription factor AP-1 does not seem to have a significant role in the pathological process.
- activation protein 1 (AP-1) activates the miR-21 transcription in conjugation with the SWI/SNF complex
- AP-1 and AP-3 are involved in the formation of distinct types of clathrin-coated vesicles, each of which is characterized by the incorporation of specific cargo membrane proteins
- c-jun downregulation results in apoptosis-mediated anti-osteosarcoma activity
- A prominent role for ERK1/2 was shown in the TPA-induced activation of c-Jun regulating the Fra1 promoter.
- These data support the idea of an activator function of c-Jun that is executed by multiple mechanisms, including phosphorylation-dependent interaction with p65 NF-kappaB and HDAC3 at the level of chromatin.
- Phosphorylation deficient c-jun was less able to recruit PCAF to AP-1 sites.
- Activation of c-Jun by the p53-dependent PI-3K/Akt/ERK pathway is responsible for B(a)P-induced cell cycle alternations in human embryo lung fibroblasts.
- GPR30-mediated inhibition of urothelial cell proliferation is the result of decreased cyclin D1 by down-regulation of activation protein-1 signaling.
- Increased intracellular ROS generation in peripheral blood monocytes of diabetic patients is involved in the pathogenesis of diabetic nephropathy via activation of AP-1.
- The preliminary results showed that AC3-33 is an important novel gene related to supress AP-1 activity.
- These findings suggest that deregulation of AP-1 expression in primary cutaneous T-cell lymphoma is the result of aberrant expression of JUNB and possible JUND
- Involvement of c-Jun in human liposarcoma growth: supporting data from clinical immunohistochemistry and DNAzyme efficacy.
- Interleukin (IL) 1beta induction of IL-6 is mediated by a novel phosphatidylinositol 3-kinase-dependent AKT/IkappaB kinase alpha pathway targeting activator protein-1
- Concluded that IL-6/sIL-6R enhances cathepsin B and L production via IL-6/sIL-6R-mediated Cav-1-JNK-AP-1 pathway in human gingival fibroblasts.
- ERK1/2 phosphorylation and c-Jun expression were significantly lowered in gastric cancer compared with the non-cancer adjacent tissues.
- an important role of CDCA4 in the context of transcriptional regulation and cell fate determination through the JUN oncogene
- Thrombin Stimulation of c-jun mRNA expression showed biphasic responses with two peaks after 1 and 8 hours of exposure.
- HRG-beta-induced MMP-7 expression was regulated by HER2-mediated AP-1 activation in MCF-7 cells.
- Phosphorylation of Thr-178 and Thr-184 in the TAK1 T-loop is required for interleukin (IL)-1-mediated optimal NFkappaB and AP-1 activation as well as IL-6 gene expression.
- nuclear c-Abl kinase can activate CSF-1 gene transcription by regulating AP-1 activity in the signaling events induced by L-selectin ligation.
- These results reveal a new AP-1 site within the TRAIL promoter functionally involved in TGF-beta-induced TRAIL expression and apoptosis in hepatomas.
- hypoxia/reoxygenation induces Plk3 activation instead of the JNK effect to directly phosphorylate and activate c-Jun, subsequently contributing to apoptosis in human corneal epithelial cells
- (62)EEEE(65) plays a stabilizing role in the formation of a ternary complex between Nef, the MHC-I cytoplasmic domain, and AP-1
- Activator protein-1 and smad proteins synergistically regulate human follicle-stimulating hormone beta-promoter activity.
- Smad4 mediates transcriptional regulation through three mechanisms: Smad4 binding to a functional SBE site in the LAMA3 promoter, Smad4 binding to AP1 (and Sp1) sites via interaction with AP1 family, and Smad4 impact on transcription of AP1 factors
- activation of JNK1/AP-1 and subsequent IL-8 induction in hyperoxia are mediated by intracellular reactive oxygen species
- c-Jun down-regulation-mediated apoptosis in osteosarcoma cells involved caspase-1, caspase-2, and caspase-8, but not the Fas/FasL pathway.
- The thermodynamics of heterodimerization of leucine zippers of Jun and Fos was characterized.
- a link between RhoA, JNK, c-Jun, and MMP2 activity that is functionally involved in the reduction in osteosarcoma cell invasion by the statin. This suggests a novel strategy targeting RhoA-JNK-c-Jun signaling to reduce osteosarcoma cell tumorigenesis.
- These results suggest that alpha5 gene expression is likely dictated by subtle alterations in the nuclear ratio of TFs that either repress (NFI) or activate (Sp1 and AP-1) alpha5 transcription in corneal epithelial cells.
- These data suggest that c-Jun-N terminal kinase pathways are involved in oxidative stress-induced dopaminergic neuronal degeneration and pretreatment with selegiline affords neuroprotection by inhibiting these cell death-signaling pathways.
- identify c-JUN and c-FOS as important regulators of human replication origin selection
- NDRG2 modulates intracellular signals to control cell cycle through the regulation of cyclin D1 expression via phosphorylation pathway and down-regulation of AP-1
- a novel function for Parkin in modulating the expression of Eg5 through the Hsp70-JNK-c-Jun signaling pathway.
- Peptidylarginine deiminase Intergenic Enhancer is a strong enhancer of the PADI3 promoter in Ca2+-differentiated epidermal keratinocytes, and requires bound AP-1 factors, namely c-Jun and c-Fos
- Epstein Barr virus EBNA1 enhances activity of the AP-1 transcription factor in nasopharyngeal carcinoma cells.
- Dose-dependent effects of rosmarinic acid on activator protein 1 activation of cyclooxygenase 2 in normal and neoplastic cells lines is reported.
- bZIP domains of the Jun transcription factor bind to DNA as monomers prior to folding and homodimerization
- These results reveal the molecular bases of the expression specificity of PADI1 and PADI3 during keratinocyte differentiation through a long-range enhancer and support a model of PADI gene regulation depending on c-Jun-JunD competition.
- bexarotene increased the occupancy of the identified enhancer element in IGFBP-6 gene by RXRalpha, RARbeta, cJun, cFos, and p300
- Fast regulation of AP-1 activity through interaction of lamin A/C, ERK1/2, and c-Fos at the nuclear envelope.
- AP-1 and PI3K/Akt pathways play an essential role in the growth of somenon-small cell lung cancer cells
- EGF induces uPAR expression via ERK-1/2, AP-1, and NF-kappaB signaling pathways and, in turn, stimulates cell invasiveness in human gastric cancer AGS cells
- 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.
- NF-kappaB repression and activation of AP-1 enhance apoptosis in prostate cancer cells
- ablation of AP-1 function disrupts the cellular transformation and proliferation mediated by this oncogene. Data illustrate a novel mechanism required to couple mitogenic signals to the AP-1 gene regulatory program