Use your antibodies-online credentials, if available.
Il n’y a pas de produits dans votre liste de comparaison.
Votre panier est vide.
ZBTB7B encodes a zinc finger-containing transcription factor that acts as a key regulator of lineage commitment of immature T-cell precursors.
Showing 2 out of 2 products:
a novel pathway by which TIP60 (Montrer KAT5 Kits ELISA) and ThPOK synergistically suppresses Eomes (Montrer EOMES Kits ELISA) function and IFNgamma production, which could contribute to the regulation of inflammation.
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.
The distal regulatory element (DRE) in the Thpok gene also functions as a transcriptional enhancer, with DNA sequences specifically responsible for thymic enhancer activity.
ThPOK transgene stably represses CD8 (Montrer CD8A Kits ELISA) gene expression through the deacetylation of Cd8 (Montrer CD8A Kits ELISA) loci in CD4 (Montrer CD4 Kits ELISA) cell lineage commitment.
The p65 subunit of NF-kappaB (Montrer NFKB1 Kits ELISA) inhibits COL1A1 (Montrer COL1A1 Kits ELISA) gene transcription in human dermal and scleroderma fibroblasts through its recruitment on promoter by protein interaction with transcriptional activators (c-Krox, Sp1 (Montrer PSG1 Kits ELISA), and Sp3 (Montrer SP3 Kits ELISA)).
impairment of Lck (Montrer LCK Kits ELISA)-mediated CD4 (Montrer CD4 Kits ELISA) coreceptor signaling by Nef is an important in vivo mechanism of HIV-1 pathogenesis
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 (Montrer RUNX3 Kits ELISA) expression in T-cell subsets between normal thymi and thymomas.
These data suggest that the regulation of COL1A1 (Montrer COL1A1 Kits ELISA) gene transcription in human dermal fibroblasts involves a complex machinery that implicates at least three transcription proteins, hc-Krox, Sp1 (Montrer PSG1 Kits ELISA), and Sp3 (Montrer SP3 Kits ELISA).
Chondroitin sulphate and its derived hydrolytic fragments (CSf (Montrer CSF2 Kits ELISA)) repress COL1A1 (Montrer COL1A1 Kits ELISA) gene transcription through a -112/-61 bp sequence upstream the start site of transcription and imply hc-Krox and Sp1 (Montrer PSG1 Kits ELISA) transcription factors.
Runx and ThPOK role in mechanisms of lineage-specific gene regulation in the process of T-cell commitments[review]
this study shows that Thpok and LRF (Montrer ZBTB7A Kits ELISA) are redundantly required to maintain the size and functions of the postthymic Treg pool
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.
Runx3 (Montrer RUNX3 Kits ELISA) is crucial for the phenotypic and functional changes observed in ThPok-deficient invariant natural killer T cells.
present evidence that ectopic ThPOK expression gives rise to a preleukemic and self-perpetuating DN4 lymphoma precursor population
Data indicate that transcription factors Thpok and LRF (Montrer ZBTB7A Kits ELISA) redundantly maintain CD4 (Montrer CD4 Kits ELISA)+ lineage integrity.
induction of SOCS-encoding genes is the main mechanism by which ThPOK imposes the CD4 (Montrer CD4 Kits ELISA)(+) lineage fate in the thymus
The role of TCF-1 (Montrer HNF1A Kits ELISA) and LEF-1 (Montrer LEF1 Kits ELISA) in the CD4 (Montrer CD4 Kits ELISA)-versus-CD8 (Montrer CD8A Kits ELISA) lineage 'choice' was mediated in part by direct positive regulation of the transcription factor Th-POK
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.
Gata3 (Montrer GATA3 Kits ELISA) promotes Cd4 (Montrer CD4 Kits ELISA) expression in Thpok-deficient thymocytes.
Data indicate that Valpha14 invariant natural killer T (Valpha14i NKT (Montrer CTSL1 Kits ELISA)) cells from Th-POK-mutant helper deficient (hd/hd (Montrer HTT Kits ELISA)) mice have increased transcripts of genes normally expressed by Th17 and NKT17 cells.
This gene encodes a zinc finger-containing transcription factor that acts as a key regulator of lineage commitment of immature T-cell precursors. It is necessary and sufficient for commitment of CD4 lineage, while its absence causes CD8 commitment. It also functions as a transcriptional repressor of type I collagen genes. Alternatively spliced transcript variants have been found for this gene.
T-helper-inducing POZ/Krueppel-like factor
, krueppel-related zinc finger protein cKrox
, zinc finger and BTB domain containing 15
, zinc finger and BTB domain-containing protein 7B
, zinc finger protein 67 homolog
, zinc finger protein 857B
, zinc finger protein Th-POK
, T helper-inducing POZ/Krueppel factor
, Vzinc finger and BTB domain containing 7B
, zinc finger protein 67
, zinc finger and BTB domain containing 7B
, kruppel-related zinc finger protein hcKrox