Recombinant Mouse Transcription factor AP-1(Jun)

1. NOS1 inhibition prevents nuclear translocation of the AP1 transcription factor subunits. PMID: 29605772
2. these results highlight the metabolic oversight of the nerve injury response via the regulation of JUN activity by O-GlcNAcylation, a pathway that could be important in the neuropathy associated with diabetes and aging. PMID: 30012597
3. These results suggest JUN and DDIT3 are independently regulated pro-death signaling molecules in retinal ganglion cells and together account for the vast majority of apoptotic signaling in retinal ganglion cells after axonal injury PMID: 28969695
4. persistent distention/stretch on colonic smooth muscle cells could suppress SCF production probably through Ca(2+) -ERK-AP-1-miR-34c deregulation. PMID: 28580775
5. Jun is a major regulator of RGC somal degeneration after glaucomatous ocular hypertensive injury. These results suggest in glaucomatous neurodegeneration, JNK-JUN signaling has a major role as a pro-death signaling pathway between axonal injury and somal degeneration. PMID: 28726785
6. Loss of epidermal AP1 reduces filaggrin level, alters chemokine expression and produces an ichthyosis-related phenotype. PMID: 28569792
7. Study provide evidence that c-jun expression is regulated by WDR13. PMID: 28222755
8. The positive feedback regulation of OCT4 and c-JUN, resulting in the continuous expression of oncogenes such as c-JUN, seems to play a critical role in the determination of the cell fate decision from induced pluripotent stem cells to cancer stem cells in liver cancer. PMID: 27341307
9. In transgenic mice with graded elevation of Schwann cell c-Jun, high c-Jun elevation is a potential pathogenic mechanism because it inhibits myelination. There was no link between c-Jun elevation and tumorigenesis. Modest c-Jun elevation, which is beneficial for regeneration, is well tolerated during Schwann cell development and in the adult and is compatible with restoration of myelination and function after injury. PMID: 29109239
10. Overall, our results provide the first evidence that HDAC6 is capable of inducing expression of pro-inflammatory genes by regulating the ROS-MAPK-NF-kappaB/AP-1 pathways and serves as a molecular target for inflammation. PMID: 27208785
11. c-jun expression patterns suggest that c-jun has a pivotal role in the proliferation of embryonic neural precursor cells, but it has also other roles in adult neurogenesis PMID: 28091742
12. Data show that miR-200b and miR-200c could directly bind the 3' UTR of JUN, and JUN activated the transcription of srebp1 to increase lipid accumulation. PMID: 27166182
13. transgenic mice overexpressing sPLA2 -IIA keratinocytes showed enhanced activation of EGFR and JNK1/2 that led to c-Jun activation. PMID: 27299855
14. ths work provides transcriptional catalog for the developing inner circular smooth muscle and suggests that cJun regulates gene expression in the ICM downstream of Hh signaling. PMID: 26930384
15. Jun is required to upregulate a programme of genes associated with cell adhesion as Embryonic stem cells exit the pluripotent ground state. PMID: 26850660
16. ANXA11 level regulates lymph node metastases and 5-FU resistance of Hca-P murine hepatocarcinoma cells via c-Jun pathway PMID: 26908448
17. Taken together, these findings indicate that LT reduces c-Jun protein levels via two distinct mechanisms, thereby inhibiting critical cell functions, including cellular proliferation. PMID: 28893904
18. Ca(2+) signaling pathway increases Nr4a1 expression in MA-10 Leydig cells, at least in part, by enhancing the recruitment of coactivator most likely through the MEF2, AP1, and CREB transcription factors thus demonstrating an important interplay between the Ca(2+) and cAMP pathways in regulating Nr4a1 expression. PMID: 26647388
19. we performed cotransfections of AP-1 expression plasmids with different mouse Gja1 promoter/luciferase reporter constructs within TM3 Leydig and TM4 Sertoli cells.We showed that a functional cooperation between cJun and cFos activates Gja1 expression and requires an AP-1 DNA regulatory element located between -132 and -26 bp PMID: 28903063
20. AP1 factors are important regulators of adult taste cell renewal and their downregulation negatively impacts taste maintenance. PMID: 27787515
21. these data indicate that MEF2 and AP-1 confer antagonistic regulation of Hspb7 gene expression in skeletal muscle, with implications for autophagy and muscle atrophy. PMID: 27632998
22. results suggest that fibroblasts, c-Jun, and IGF-1 play key roles in mediating stromal-epithelial interactions that are required for the therapeutic effects of finasteride in benign prostate epithelial cells PMID: 28196103
23. These findings highlight a key role of the TLR4-NOS1-AP1 signaling axis in regulating macrophage polarization PMID: 28013342
24. Data suggest that Sf1 and c-jun interact and cooperate to activate the Fdx1 promoter in MA-10 (tumorigenic cell line) and TM3 (non-tumorigenic cell line) Leydig cells; such activation requires different regulatory elements located between -124 and -306 bp of Fdx1 promoter and involves recruitment of Sf1 to this region. (Sf1 = splicing factor 1; c-jun = proto-oncogene c-jun; Fdx1 = ferredoxin 1) PMID: 28274746
25. NF-kappaB and c-Jun coregulate lipopolysaccharide-induced Fra-1 transcription. PMID: 27286066
26. BATF/JUN-B and BATF/C-JUN complexes play important roles in OA cartilage destruction through regulating anabolic and catabolic gene expression in chondrocytes. PMID: 27147707
27. this study shows that c-Jun regulates the activation state of macrophages and promotes arthritis via differentially regulating cyclooxygenase-2 and arginase-1 levels PMID: 28298526
28. PLIO treatment inhibited nuclear factorkappaB (NFkappaB) nuclear translocation in B16F10 cells. In addition, PLIO treatment inhibited the phosphorylation of c-Jun Nterminal kinases and AKT PMID: 27666322
29. Anxa5 mediates the in vitro malignant behaviours of murine hepatocarcinoma Hca-F cells via ERK2/c-Jun/p-c-Jun(Ser73) and ERK2/E-cadherin pathways. PMID: 27697636
30. These findings indicate that c-Jun has important functions during HBV-associated tumorigenesis by promoting hepatocyte proliferation as well as progression of dysplasia PMID: 26470729
31. The TLR4 pathway may play an important role in regulating AP-1 activation PMID: 26803521
32. These observations suggest that the antiinflammatory properties of crebanine may stem from the inhibition of proinflammatory mediators via suppression of the NF-kappaB, AP-1, MAPKs, and Akt signaling pathways. PMID: 26499331
33. In a model of heavy metal poisoning, copper contamination of drinking water (as can occur with corrosion in aging plumbing systems) up-regulates binding of transcription factor AP-1 in neurons of brain, even in low concentrations. PMID: 23719850
34. Transplant-induced reactivation of murine cytomegalovirus immediate early gene expression is associated with recruitment of NF-kappaB and AP-1 to the major immediate early promoter. PMID: 26795571
35. ERK contributes to the morphine-induced hyperalgesia by regulating the activation of c-JUN PMID: 26165762
36. These results indicate that both NF-kappaB and c-Jun/AP-1 are involved in regulating anti-beta2GPI-induced expression of prothrombotic and proinflammatory molecules in vivo. PMID: 26829121
37. Tumorigenesis by Meis1 overexpression is accompanied by a change of DNA target-sequence specificity which allows binding to the AP-1 element. PMID: 26259236
38. BMP7 and FGF9 coordinately regulate AP-1 transcription to promote G1-S cell cycle progression and nephron progenitor cells proliferation. PMID: 26634297
39. Our findings conclude that pharmacological actions of CoQ0 are mediated via inhibition of NFkappaB/AP-1 activation and induction of Nrf2/ARE-signaling. PMID: 26548719
40. Taken together, our results suggest that LPS induces PDK4 expression and alters glucose metabolism via the JNK pathway. PMID: 26740179
41. In the heterologous mouse model loss of c-Jun expression led to ablation of dissemination of Theileria annulata-infected and transformed macrophages. PMID: 25375322
42. Our results demonstrate that c-Jun can suppress adipocyte differentiation through the down-regulation of KLF15 at the transcriptional level. PMID: 26692489
43. the regulation of synaptic-vesicle (SV) recycling via early endosomes by the interdependent regulation of AP-2-mediated endocytosis and AP-1/sigma1B-mediated SV reformation, is reported. PMID: 25128028
44. A reciprocal antagonism between the MITF and c-Jun interconnects inflammation-induced dedifferentiation with pro-inflammatory cytokine responsiveness of melanoma cells favouring myeloid cell recruitment. PMID: 26530832
45. Data indicate that Sp1 and AP-1-related factors are involved in the regulation of MFG-E8 gene transcription by targeting their binding sites in the 5'-flanking region under physiological and inflammatory states. PMID: 25711369
46. Data show that p38 MAP Kinase (p38MAPK)-shRNA transfection and the p38MAPK inhibitor SB203580 significantly inhibited activator protein-1 (AP-1) activity. PMID: 25966080
47. AS-IV effectively inhibits LPS-induced acute inflammatory responses by modulating NF-kappaB and AP-1 signaling pathways PMID: 25960613
48. suggest that TLR-mediated Sesn2 induction is dependent on AP-1, Nrf2, and the inhibition of ubiquitin-mediated degradation of Sesn2 and might protect cells against endotoxin toxicity PMID: 25637945
49. Dioxin exposure markedly inhibited c-Jun phosphorylation in Map3k1-deficient embryonic eyelid epithelium, suggesting that dioxin-induced AHR pathways can synergize with gene mutations to inhibit MAP3K1 signaling. PMID: 26109068
50. The NF-kappaB-to-AP-1 switch is a protective mechanism to ensure timely transition from endothelial barrier injury to repair, accelerating barrier restoration following MOI. PMID: 24986487

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KEGG: mmu:16476

STRING: 10090.ENSMUSP00000054270

UniGene: Mm.275071