anti-Basic Leucine Zipper Transcriptional Factor ATF-Like 3 (BATF3) Antibodies

Human Basic Leucine Zipper Transcriptional Factor ATF-Like 3 (BATF3) interaction partners

1. Circular RNA circ_0034642/miR-1205/BATF3 pathway may play an important role in glioma.

2. The authors identified highly significant associations with better melanoma overall survival for rs6673928, impacting IL19 expression (HR, 0.56; 95% CI, 0.41-0.77; P = 0.0002) and rs6695772, controlling the expression of BATF3 (HR, 1.64; 95% CI, 1.19-2.24; P = 0.0019).

3. Basic Leucine Zipper ATF-Like Transcription Factor 3 (BATF3), an AP-1 family transcription factor, is a glucocorticoid receptor coregulator whose interaction with glucocorticoid receptor is modulated by the lever arm.

4. Batf3-dependent dendritic cells elicit the rejection of cells and grafts expressing mismatched minor histocompatibility antigens.

5. correlation of transcriptional repression by p21(SNFT) with changes in DNA.NF-AT complex interactions

6. overexpression of p21SNFT in HepG2 cells leads to repression of matrix metalloproteinase-1 by 70-80%

Mouse (Murine) Basic Leucine Zipper Transcriptional Factor ATF-Like 3 (BATF3) interaction partners

1. this study demonstrates a role for BATF3 in TH9 differentiation and T-cell-driven mucosal pathologies

2. These results underscore a specific role for Batf3-dependent dendritic cells in regulating priming and expansion of effector CD8(+) T cells necessary for host resistance against acute respiratory vaccinia virus infection.

3. The transcription factor Batf3 inhibits the differentiation of regulatory T cells in the periphery. We found that expression of Batf3 was selectively low in Treg cells but not in effector CD4 T (Teff) cells and that ectopic expression of Batf3 caused a marked reduction in the number of Foxp3+ Treg cells. Batf3 acts as a fate-decision factor with respect to Tconv versus Tregs by restraining Treg differentiation.

4. in contrast to adult mice, Batf3-dependent dendritic cells were absolutely required for generating rotavirus-specific CD8+ T-cell responses in neonates

5. Batf3(-/-) mice remained competent for skin graft rejection and delayed hypersensitivity, and retained a CD8(+) dendritic cell population.

6. Lack of Batf3/CD103(+) dendritic cells within the tumor microenvironment dominantly resists the effector phase of an anti-tumor T cell response, contributing to immune escape.

7. study reports that Batf3 is critical for accumulation of CD103(+) DCs in the kidney and tongue at steady state, for their expansion during systemic and oropharyngeal candidiasis, and for tissue-specific production of IL-12 in kidney but not tongue during systemic and oropharyngeal candidiasis, respectively

8. this study shows that Batf3 promotes priming of CD8+ T cells regardless of the location of Salmonella enterica antigen

9. Batf3 deficiency is not critical for the generation of CD8alpha dendritic cells.

10. Data indicte that interferon regulatory factor 8 (IRF8) expression becomes dependent on transcription factor Batf3.

11. IL-12 production by Batf3-dependent CD103+ dendritic cells is crucial for maintenance of local Th1 immunity against L. major infection.

12. The basic leucine zipper ATF-like 3 (BATF3)- dendritic cell lineage is enriched in the lungs of asthma-protected mice and strictly required for protection.

13. Irf8 expression in DC9 cells led to an increase in Batf3 transcript levels.When coexpressed with Irf8, Batf3 & Id2 had a synergistic effect on classical CD8alpha(+) DC development.

14. Batf3-dependent DCs in the renal lymph node presented antigen that had been concentrated in the kidney and used PD-L1 to induce apoptosis of cytotoxic T cells

15. A previously undescribed pathway by which CD8alpha+ Dendritic cells emerge independent of Id2, Nfil3, and Batf3, but dependent on Irf8.

16. Data show that targeting of antigen to Clec9A in batf3 null mice produced enhanced antibody responses.

17. Defective T effector priming and resistance to experimental autoimmune encephalitis (EAE) exhibited by Csf2rb(-/-) mice does not result from the absence of dermal CD11b(low/-)Langerin(+)CD103(+) dendritic cells.

18. study describes a transcription factor, Batf3, that controls development of CD8+ dendritic cells; dendritic cells from Batf3-/- mice were defective in cross-presentation, and Batf3-/- mice lacked virus-specific CD8+ T cell responses to West Nile virus