Aperçu des produits pour anti-C-JUN (JUN) Anticorps

Human Jun Proto-Oncogene (JUN) interaction partners

1. the findings of this study indicated that luteolin effectively enhanced TRAILinitiated apoptosis, and that these effects were likely to be mediated by autophagy and JNKmediated DR5 expression.

2. CJun protein is overexpressed in glioma tissues and positively correlated with PDK1 levels.C-jun role in the epithelial-mesenchymal transition.

3. Herpes simplex virus type 2 infection could stimulate AP-1 activation via TLR4-MyD88/TRIF axis, and then feedback to up-regulate TLR4 expression in human genital epithelial cells.

4. The CCL17 SNP rs223828 is associated with increased risk of CAD, and this site may be a potential AP-1 binding site.

5. results suggested that four differentially expressed genes, Jun, Gal, Cd74, and C1qb, had the potential to serve as prognostic or predictive markers for neuropathic pain, suggesting a potential application in the improvement of prognostic tools and treatments.

6. High expression of c-Jun or Fra-1 was associated with poor prognosis in oral squamous cell carcinoma patients.

7. High c-Jun expression is associated with oral squamous cell carcinoma.

8. the present study demonstrated that the AP-1 complex may be a novel regulator of MANF transcriptional enhancement, and that MANF is a novel downstream target of AP-1, which may indicate a novel role of AP-1 in regulating inflammatory pathways.

9. USP6 is an enzyme that deubiquitinates c-Jun and regulates its downstream cellular functions.USP6 regulates the stability of the c-Jun protein in an enzyme activity-dependent manner.

10. data indicated that miR-139-5p was down-regulated in the hearts of Hypertrophic cardiomyopathy patients and that it inhibited cardiac hypertrophy by targetting c-Jun expression.

11. this study identified an essential Jun/miR-22/HuR regulatory axis in CRC (the working model is summarised in Fig. 8) and highlighted the vital role of HuR and miR-22 in CRC proliferation and migration.

12. a novel cascade mediated by AP-1 and FOXF1 that regulates oncogene-induced senescence, is reported.

13. Multivalent Interactions with Fbw7 and Pin1 Facilitate Recognition of c-Jun by the Fbw7.

14. High AP-1 expression is associated with metastasis in colon cancer.

15. Our results suggest that extended AP-1 binding sites, together with adjacent binding sites for additional TFs, encode part of the information that governs transcription factor binding sites activity in the genome.

16. the expression of WIF-1 was low in GBC cells due to aberrant hypermethylation of its promoter region. Additionally, an alternative pathogenesis of GBC was indicated in which c-Jun causes hypermethylation of the WIF-1 promoter region, and represses the expression of WIF-1 through transcriptional regulation and interaction with DNMT1 as an early event in the tumorigenesis of GBC.

17. Mutant cellular AP-1 proteins promote expression of a subset of Epstein-Barr virus late genes in the absence of lytic viral DNA replication.

18. Secreted Ta9 has therefore, not only the ability to stimulate CD8+ T cells, but also the potential to activate AP-1-driven transcription and contribute to T. annulata-induced leukocyte transformation

19. MiR-216b directly targets c-Jun, thereby reducing AP-1-dependent transcription and sensitizing cells to ER stress-dependent apoptosis.

20. results suggest that c-Jun, p38 MAPK, PIK3CA/Akt, and GSK3 signaling involved in the effect of miR-203 on the proliferation of hepatocellular carcinoma cells.

Xenopus laevis Jun Proto-Oncogene (JUN) interaction partners

1. AP-1(c-Jun/FosB) may play a role in neurogenesis via the induction of FoxD5b expression during early vertebrate development

2. The cJun transcription factor bound to a variant cAMP response element in the promoter region of tlx3 and modulated transcription and regulated neurotransmitter phenotype via its transactivation domain

Zebrafish Jun Proto-Oncogene (JUN) interaction partners

1. These results support a role for trim69 in the development of the zebrafish brain through ap-1 pathway.

2. CPEB-1 control of c-Jun mRNA translation regulates GH gene expression and resulting downstream signaling events (e.g., synaptic plasticity) in the mouse hippocampus.

Mouse (Murine) Jun Proto-Oncogene (JUN) interaction partners

1. Bim is expressed in dopaminergic neurons and contributes to parkinsonian neurodegeneration. The transcriptional activation of Bim by c-Jun promotes MPTP-induced nigral dopaminergic neuron death. This study is significant because it precisely demonstrates a pro-death role of c-Jun/Bim upregulation in nigral dopaminergic neurons by using cell type-specific knockout mice.

2. High Jun is associated with tumourigenic transformation.

3. GnRH receptorexpression levels depend on JUN and are critical for reproductive function.

4. NOS1 inhibition prevents nuclear translocation of the AP1 transcription factor subunits.

5. 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.

6. 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

7. persistent distention/stretch on colonic smooth muscle cells could suppress SCF production probably through Ca(2+) -ERK-AP-1-miR-34c deregulation.

8. 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.

9. Loss of epidermal AP1 reduces filaggrin level, alters chemokine expression and produces an ichthyosis-related phenotype.

10. Study provide evidence that c-jun expression is regulated by WDR13.

11. 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.

12. 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.

13. 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.

14. 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

15. 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.

16. transgenic mice overexpressing sPLA2 -IIA keratinocytes showed enhanced activation of EGFR and JNK1/2 that led to c-Jun activation.

17. 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.

18. Jun is required to upregulate a programme of genes associated with cell adhesion as Embryonic stem cells exit the pluripotent ground state.

19. ANXA11 level regulates lymph node metastases and 5-FU resistance of Hca-P murine hepatocarcinoma cells via c-Jun pathway

20. Taken together, these findings indicate that LT reduces c-Jun protein levels via two distinct mechanisms, thereby inhibiting critical cell functions, including cellular proliferation.

Fruit Fly (Drosophila melanogaster) Jun Proto-Oncogene (JUN) interaction partners

1. Mir-8 modulates Drosophila C virus replication by negative regulation of dJun.

2. Tau and spectraplakin promote synapse formation and maintenance through Jun kinase and neuronal trafficking.

3. Jra recruits the HP1a/KDM4A complex to its gene body region upon osmotic stress to reduce H3K36 methylation levels and disrupt H3K36 methylation-dependent histone deacetylation

4. Data thus identify Atf3 as a new functional partner of Drosophila Jun during development.

5. study of multisite phosphorylation

6. Fos and Jun, the two components of AP1, are abundantly expressed in motor neurons; a model in which AP1 directly modulates NMJ plasticity processes through a cell autonomous pathway in the motor neuron is supported

7. Src, Jun N-terminal kinase, and STAT pathways are inhibited by Drosophila C-terminal Src kinase, which negatively regulates organ growth and cell proliferation

8. AP1 acts as a repressor by recruiting the deacetylase complex to terminate activation of a group of NF-kappaB target genes

9. We observed complex genetic interactions between mnn1 and jun in different developmental settings. Our data support the idea that one function of menin is to modulate Jun activity in a manner dependent on the cellular context.

10. AP-1 mediated synapse enhancement and its relationship to increases in synapse number, Ca2+ influx, Ca2+ sensitivity of vesicle fusion or synaptic vesicle number, were examined.

Pig (Porcine) Jun Proto-Oncogene (JUN) interaction partners

1. study highlights the role of AP1 in promoting the host gene expression profile that defines Ebola virus pathogenesis.

2. Porcine reproductive and respiratory syndrome virus -activated TAK-1 was essential for the activation of JNK and NF-kappaB pathways and IL-8 expression.

3. The effects of prostaglandin F2alpha administration on transcription factor AP-1 expression and the expression of downstream genes involved in luteolysis are reported.

Rabbit Jun Proto-Oncogene (JUN) interaction partners

1. ICAM1 and IL10 were upregulated in ventilator-induced lung injury. Nuclear transcription factor AP-1 may be responsible for this upregulation.

Cow (Bovine) Jun Proto-Oncogene (JUN) interaction partners

1. 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.

2. dynamic compression stimulates cell proliferation and proteoglycan synthesis in the presence of IL-1beta and/or inhibitors of the MAPKs and NFkappaB and AP-1 signalling pathways