anti-Jun D Proto-Oncogene (JUND) Antibodies

Xenopus laevis Jun D Proto-Oncogene (JUND) interaction partners

1. identify AP-1(JunD/c-Fos) as a novel hematopoietic transcription factor and the requirement of AP-1(JunD/c-Fos) in BMP-4-induced hematopoiesis during Xenopus hematopoiesis.

Human Jun D Proto-Oncogene (JUND) interaction partners

1. Data indicate the mechanism underlying redox-regulation of AP-1 Fos/Jun transcription factors and suggest structural insight for therapeutic interventions targeting AP-1 proteins.

2. In T cells, after serum deprivation HBZ induces the expression of Delta JunD isoform. Unlike JunD, Delta JunD induces proliferation and transformation of cells. HBZ bypasses translational control of JunD uORF and favors the expression of Delta JunD. The truncated isoform Delta JunD has a central role in the oncogenic process leading to adult T-cell leukemia .

3. MiR-663a suppresses proliferation and invasion by targeting AP-1 component JunD in non-small cell lung cancer cells.

4. studies showed that down-regulation of JunD in response to TGF-beta treatment is mediated via the proteasomal degradation pathway.

5. CARMA1- and MyD88-dependent activation of Jun/ATF-type AP-1 complexes is a hallmark of ABC diffuse large B-cell lymphomas.

6. recombinant SERPINE2 induced a clear inhibition of MMP-13 expression in IL-1alpha-stimulated chondrocytes. This inhibitory effect is likely regulated through a pathway involving ERK 1/2, NF-kappaB and AP-1

7. miR-494 is a novel regulator of HNPC apoptosis induced by TNF-alpha

8. JunD activates miR-29b by enhancing its transcription and processing, which contribute to the inhibitory effect of JunD

9. Binding of specific AP-1 factors, we found JunD associated with the LILRB1 distal promoter.

10. Cells in contact with basement membrane undergo transient oscillations between two molecular states defined by their TGFBR3- JUND expression.

11. BAG3 stabilized JunD mRNA.

12. Jun proteins (pc-Jun and JunD) influence carcinogenesis and tumour progression, suggesting a significant role as prognostic predictors in human ovarian carcinoma.

13. This genotype-phenotype correlation study confirmed the lack of direct genotype-phenotype correlations. However, patients with mutations affecting the JunD interacting domain had a higher risk of death secondary to a MEN1 tumor

14. HTLV-1 bZIP factor(hbz) requires cellular JunD to upregulate HTLV-1 antisense transcription from the 3' long terminal repeat.

15. results demonstrate the presence of a common oncogenic cascade initiated by FRA2/JUND in CCR4-expressing mature T-cell malignancies such as ATLL and CTCLs

16. crystal structures of human menin in its free form and in complexes with MLL1 or with JUND, or with an MLL1-LEDGF heterodimer

17. Apoptosis induction by dominant negative JunD is due to induction of growth arrest and DNA damage inducible proteins (GADD) 45 alpha and 45 gamma proteins.

18. CDK4-mediated regulation of cell functions via c-Jun phosphorylation and AP-1 activation

19. JunD mediates, whereas c-Jun modulates, prostaglandin E2 activation of aromatase promoters

20. data indicate that JunD is an inhibitor of RHOH gene expression.

Cow (Bovine) Jun D Proto-Oncogene (JUND) 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.

Mouse (Murine) Jun D Proto-Oncogene (JUND) interaction partners

1. Differentiation-mediated activation of JunD results in enhanced TUBB4a expression in P19 embryonal carcinoma cells.

2. JunD provides protection in aging-induced endothelial dysfunction and may represent a novel target to prevent reactive oxygen species-driven vascular aging.

3. AP-1 composed with JunD and Fra2 protein plays a primary role in enhancing the transcription level of the CD11c gene in dendritic cells

4. Nfe2 modulates JunD binding to the Gcm1 promoter via acetylation

5. 5-HT2B blockade enhances liver regeneration by inhibiting induction of TGF-beta1 expression by hepatic stellate cells that is dependent on 5-HT, ERK and JunD.

6. CDK4-mediated regulation of cell functions via c-Jun phosphorylation and AP-1 activation

7. Downregulation of JunD and cyclin D1 expression in myofibroblasts may be important regarding the mechanism of action of MTA in Mdr2-/- mice

8. c-Jun, JunB, and JunD are not functionally equivalent and have both overlapping and independent functions in controlling cellular proliferation, cell-cycle arrest/senescence and the response to stress.

9. Study supports potential roles for jun D, jun B, and fra-1 in the dietary energy restriction regulation of AP-1 function in the Sencar mouse skin carcinogenesis model.

10. protects cells from p53-dependent senescence and apoptosis

11. Translation initiation from alternative AUG and non-AUG sites in human, mouse and rat.

12. Transcriptional activation of Ifi202 gene by Rb/JunD may be important for the regulation of cell growth and survival.

13. Data suggest that JunD is part of a regulatory network that controls proliferation to prevent pathological progression in chronic renal diseases.

14. regulatory role of JunD in T lymphocyte proliferation and Th cell differentiation

15. Menin-JunD interaction may negatively regulate the enhancing effect of menin on c-Jun-mediated transactivation

16. menin suppresses osteoblast maturation, in part, by inhibiting the differentiation actions of JunD

17. junD promotes both adaptive-protective and maladaptive hypertrophy in heart, depending on its expression levels.

18. JunD limits cardiomyocyte hypertrophy and protects the pressure-overloaded heart from cardiac apoptosis

19. stimulation of splenic B cells with IL-4 or IL-21 induced high Bcl6 expression with induction of junD

20. In conclusion, a signaling pathway for the development of fibrosis involves the regulation of TIMP-1 expression by phosphorylated JunD.