Zinc Finger and BTB Domain Containing 7B (ZBTB7B) ELISA试剂盒

Human Zinc Finger and BTB Domain Containing 7B (ZBTB7B) interaction partners

1. Authors show that the transcription factor ThPOK binds cooperatively with NF-kappaB to NRCs and mediates their physical proximity with the IFNB1 gene via its ability to oligomerize when bound to DNA.

2. a novel pathway by which TIP60 and ThPOK synergistically suppresses Eomes function and IFNgamma production, which could contribute to the regulation of inflammation.

3. ThPOK may be considered a central regulator of the earliest events in the immune system during colorectal cancer development, decreasing the immune response against cancer cells.

4. The distal regulatory element (DRE) in the Thpok gene also functions as a transcriptional enhancer, with DNA sequences specifically responsible for thymic enhancer activity.

5. ThPOK transgene stably represses CD8 gene expression through the deacetylation of Cd8 loci in CD4 cell lineage commitment.

6. The p65 subunit of NF-kappaB inhibits COL1A1 gene transcription in human dermal and scleroderma fibroblasts through its recruitment on promoter by protein interaction with transcriptional activators (c-Krox, Sp1, and Sp3).

7. comparing the promoter regions of the Th-POK gene between human and mouse, the region 3600 base pairs upstream from the transcription initiation site of the Th-POK gene was highly conserved

8. impairment of Lck-mediated CD4 coreceptor signaling by Nef is an important in vivo mechanism of HIV-1 pathogenesis

9. Thymoma neoplastic epithelial cells can induce Th-POK expression in T-cell subsets similarly to the normal thymic epithelial cells. In addition, there was no significant difference in Runx3 expression in T-cell subsets between normal thymi and thymomas.

10. These data suggest that the regulation of COL1A1 gene transcription in human dermal fibroblasts involves a complex machinery that implicates at least three transcription proteins, hc-Krox, Sp1, and Sp3.

11. Chondroitin sulphate and its derived hydrolytic fragments (CSf) repress COL1A1 gene transcription through a -112/-61 bp sequence upstream the start site of transcription and imply hc-Krox and Sp1 transcription factors.

12. Runx and ThPOK role in mechanisms of lineage-specific gene regulation in the process of T-cell commitments[review]

Mouse (Murine) Zinc Finger and BTB Domain Containing 7B (ZBTB7B) interaction partners

1. Zbtb7b recruits the brown fat Blnc1/heterogeneous nuclear ribonucleoprotein U (hnRNPU) ribonucleoprotein complex to activate thermogenic gene expression in adipocytes.

2. Th-POK functions as an important feed-forward regulator of insulin signaling in mammary gland lactation.

3. epigenetic regulation through microRNA-133b-regulated Th-POK expression and signals provided by dendritic cells are fundamental for thymic NKT17 cell differentiation

4. this study shows that Thpok and LRF are redundantly required to maintain the size and functions of the postthymic Treg pool

5. Together, these results suggest a novel mechanism regulating endothelial PATZ1 expression based on the down-regulation of miR-24 expression caused by hyperglycemia. Interfering with PATZ1 expression via miRNAs or miRNA mimics could potentially represent a new way to target endothelial PATZ1-dependent signaling of vascular dysfunction in diabetes.

6. Runx3 is crucial for the phenotypic and functional changes observed in ThPok-deficient invariant natural killer T cells.

7. present evidence that ectopic ThPOK expression gives rise to a preleukemic and self-perpetuating DN4 lymphoma precursor population

8. Data indicate that transcription factors Thpok and LRF redundantly maintain CD4+ lineage integrity.

9. induction of SOCS-encoding genes is the main mechanism by which ThPOK imposes the CD4(+) lineage fate in the thymus

10. The role of TCF-1 and LEF-1 in the CD4-versus-CD8 lineage 'choice' was mediated in part by direct positive regulation of the transcription factor Th-POK

11. These findings imply that long-lasting T-cell receptor signals are needed to establish stable Thpok expression activity to commit to helper T-cell fate.

12. Gata3 promotes Cd4 expression in Thpok-deficient thymocytes.

13. Data indicate that Valpha14 invariant natural killer T (Valpha14i NKT) cells from Th-POK-mutant helper deficient (hd/hd) mice have increased transcripts of genes normally expressed by Th17 and NKT17 cells.

14. ZBTB7B is a critical factor genetically predetermining the balance of effector subsets within the NKT cell population.

15. Th-POK and Runx3 transcription factors are reciprocally involved in the control of G1-phase progression, on which they exert their functions dependently.

16. T cells lacking Thpok, which only displayed LRF-dependent functions, contributed to multiple effector responses, both in vitro and in vivo, with the notable exception of Th2 cell responses that control extracellular parasites

17. comparing the promoter regions of the Th-POK gene between human and mouse, the region 3600 base pairs upstream from the transcription initiation site of the Th-POK gene was highly conserved

18. required for the differentiation of CD1d-restricted CD4+ NKT cells

19. impairment of Lck-mediated CD4 coreceptor signaling by Nef is an important in vivo mechanism of HIV-1 pathogenesis

20. Data show that ThPOK expression in gammadelta thymocytes is regulated by TCR signalling, that ThPOK is an important mediator of gammadelta T cell development/maturation, and that development of some gammadelta T cells depends on TCR engagement/signalling.