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Human TGF-beta Activated Kinase 1/MAP3K7 Binding Protein 2 (TAB2) interaction partners

1. Data indicate an association between TAK1-binding protein 2 (TAB2) mutations and a connective tissue disorder with severe polyvalvular heart disease and subtle facial dysmorphism.

2. The combination of WES, genomic triangulation, and systems biology has uncovered perturbations in TGF-beta activated kinase 1 signaling as a novel pathogenic substrate for polyvalvular syndrome.

3. Data suggest that mRNA/protein levels of NLRP6 are down-regulated in synovial tissues and synoviocytes of rheumatoid arthritis (RA) patients compared to osteoarthritis patients; NLRP6 provides docking site to facilitate interaction between TAB2/3 and TRIM38 in RA synoviocytes in response to TNFalpha. (NLRP6 = ; TAB2/3 = transforming growth factor-b-activated kinase 1-binding protein 2/3; TRIM38 = tripartite motif 38)

4. A Novel Functional Domain of Tab2 Involved in the Interaction with Estrogen Receptor Alpha in Breast Cancer Cells

5. The expression of miR-155 target gene, TAB2, and the downstream gene, iNOS, were found to be inhibited in psoriatic dermal mesenchymal stem cells.

6. DK1 inhibits the formation of the TAK1-TAB2-TRAF6 complex and leads to the inhibition of TRAF6 ubiquitination.

7. Authors demonstrate that enterovirus 71 3C interacts with TAB2 and TAK1 and suppresses cytokine expression via cleavage of the TAK1 complex proteins.

8. SUMOylation may serve as a novel mechanism for the regulation of TAB2.

9. conclude that TRIM38 negatively regulates TNFalpha- and IL-1beta-induced signaling by mediating lysosome-dependent degradation of TAB2/3, two critical components in TNFalpha- and IL-1beta-induced signaling pathways

10. These data indicate that overexpression of TRIM22 may negatively regulate the TRAF6-stimulated NF-kappaB pathway by interacting with and degrading TAB2.

11. our data implicate Tab2 as a mediator of resistance to endocrine therapy and as a potential new target to reverse pharmacological resistance and potentiate antiestrogen action.

12. We found that endothelial TAK1 and TAB2, but not TAB1, were critically involved in vascular formation

13. MiR-23b suppresses IL-17-, tumor necrosis factor alpha (TNF-alpha)- or IL-1beta-induced NF-kappaB activation and inflammatory cytokine expression by targeting TAB2, TAB3 and IKK-alpha.

14. TAK1 and its adapter protein, TAB2, reciprocally regulate both TAK1- and ASK1-mediated signaling pathways to direct the activations of NF-kappaB and AP-1.

15. human TAB2 and TAB3, ubiquitin-chain sensory proteins involved in NF-kappaB signalling, are directly inactivated by enteropathogenic Escherichia coli NleE, a conserved bacterial type-III-secreted effector responsible for blocking host NF-kappaB signalling

16. These results point to the existence of an autophagy-stimulatory 'switch' whereby TAB2 and TAB3 abandon inhibitory interactions with Beclin 1 to engage in a stimulatory liaison with TAK1.

17. these studies show that the TAK1-TAB2-TAB3 signaling axis is critical for carcinoma-induced bone lesions, mediating expression of proinvasive and osteolytic factors.

18. microRNA-155 negatively regulates the expression of TAB2 and downstream IFN-gamma-inducible protein of 10 kDa as a negative feedback system.

19. The ability of human Trim5alpha to regulate TAB2 levels, to activate NF-kappaB, and to recognize retroviral capsids are genetically separable.

20. Co-expression of RelA and/or TAB2 markedly increased Tax-mediated NF-kappaB activation.

Mouse (Murine) TGF-beta Activated Kinase 1/MAP3K7 Binding Protein 2 (TAB2) interaction partners

1. Lipopolysaccharide-induced miR-155 promoted autophagy to increase osteoclast formation via decreased TAB2.

2. These findings support a regulatory role for TGF-beta-activated kinase 1 in governing downstream MAPKs/NF-kappaB signaling cascades in the macrophage activation in response to hyperglycemic insult

3. RNF4 negatively regulates NF-kappaB signaling by down-regulating TAB2

4. TAB1 and TAB2 are required for activated macrophages, making TAB1 and TAB2 effective targets to control inflammation by modulating macrophage survival.

5. Loss of Tab2 is associated with liver injury.

6. miR-155 inhibits the immunosuppressive capacity of MSCs by reducing iNOS expression by targeting TAB2.

7. TAB2 and TAB3 are essential for B cell activation leading to antigen-specific antibody responses, as well as B-1 and marginal zone B cell development.

8. We found that endothelial TAK1 and TAB2, but not TAB1, were critically involved in vascular formation

9. MiR-23b suppresses IL-17-, tumor necrosis factor alpha (TNF-alpha)- or IL-1beta-induced NF-kappaB activation and inflammatory cytokine expression by targeting TAB2, TAB3 and IKK-alpha.

10. Epithelial TAK1 activity is regulated through two unique, TAB1-dependent basal & TAB2-mediated stimuli-dependent mechanisms.

11. TAK1 and its adapter protein, TAB2, reciprocally regulate both TAK1- and ASK1-mediated signaling pathways to direct the activations of NF-kappaB and AP-1.

12. Wnt3a stimulation led to an increase in the interaction of TAB2 with NLK and the formation of a TAK1.TAB2.NLK complex, suggesting that this TAK1-TAB2-NLK pathway may constitute a negative feedback mechanism for canonical Wnt signaling.

13. TAB2 not only activates TAK1 but also plays an essential role in the deactivation of TAK1 by recruiting PP6 through a polyubiquitin chain-dependent mechanism

14. analysis of a mechanism for the recognition of Lys 63-linked polyubiquitin chains by TAB2 and TAB3 NZF domains in which diubiquitin units are specifically recognized by a single NZF domain

15. the expression of mouse TAB2 in the E11 dorsal aorta endothelium suggests a role for mTAB2 in hematopoietic stem cell emergence and/or regulation

16. TAB2 is essential for embryonic development through prevention of liver apoptosis but not for the IL-1 receptor-mediated signaling pathway.

17. multifunctional signaling molecule, both IL-1-dependent TRAF6 ubiquitination and assembly of the IL-1 signaling complex

18. TAB2 expression pattern shows striking similarities with previously reported IL-1 receptor expression and NFkappaB activation patterns

Zebrafish TGF-beta Activated Kinase 1/MAP3K7 Binding Protein 2 (TAB2) interaction partners

1. a critical, dosage-sensitive role during development was demonstrated by the cardiac defects observed upon titrated knockdown of tab2 expression in zebrafish embryos