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Human TCF4 Protein expressed in Wheat germ - ABIN1322369
Schenkel, Zloza, Li, Narasipura, Al-Harthi: Beta-catenin signaling mediates CD4 expression on mature CD8+ T cells. in Journal of immunology (Baltimore, Md. : 1950) 2010
A frameshift-causing partial TCF4 gene deletion was identified in an adult patient with mild ID and nonspecific facial dysmorphisms but without the typical features of Pitt-Hopkins syndrome. A nonsense variant within exon 8 was identified in a child presenting with a severe phenotype largely mimicking PTHS.
rs613872, rs17595731, and CTG repeat expansions in intronic region of TCF4 are associated with increased risk of sporadic late-onset FECD (zeige COL8a2 Proteine) in the Indian cohort studied
High TCF4 expression is associated with colorectal cancer.
Examination of X-ray structures of the closely related TCF3 (zeige TCF3 Proteine) and USF1 (zeige USF1 Proteine) bound to DNA suggests TCF3 (zeige TCF3 Proteine) can undergo a conformational shift to preferentially bind to 5hmC while the USF1 (zeige USF1 Proteine) basic region is bulkier and rigid precluding a conformation shift to bind 5hmC. These results greatly expand the regulatory DNA sequence landscape bound by TCF4.
Array-comparative genomic hybridization confirmed a de novo paternal deletion of the 15q11.2q13 region and exome sequencing identified a second mutational event in both girls, which was a novel variant c.145+1G>A affecting a TCF4 canonical splicing site inherited from the mosaic mother
The CTG18.1 repeat expansion may reduce gene expression of TCF4 and ZEB1, suggesting that a mechanism triggering a loss of function may contribute to FECD (zeige COL8a2 Proteine).
repeat expansion showed stronger association than the most significantly associated SNP, rs613872, in TCF4, with the disease in the Australian cohort
Although validation in additional patients is required, the findings suggest that the dysmorphic features and severe intellectual disability characteristic of PTHS are partially rescued by overexpression of those short TCF4 transcripts encoding a nuclear localization signal, a transcription activation domain, and the basic helix-loop-helix domain.
Altered DNA methylation (zeige HELLS Proteine) in TCF4 involves in the etiology of Bipolar disorder and Major Depressive disorder .
We found that the genotype "AG" of rs9320010 and "GA" of rs7235757 decreased SCZ risk. In the genetic model analysis, we also observed that the allele "A" of rs9320010 and "G" of rs7235757 were inversely related with the risk of SCZ in the dominant model. Our study indicated that rs9320010, rs7235757, and rs1452787 were prominently associated with SCZ.
Our findings indicate that H2O2 inhibits NaV1.5 (zeige SCN5A Proteine) expression by activating the Wnt/b-catenin signaling and beta-catenin (zeige CTNNB1 Proteine) interacts with TCF4 to transcriptionally suppress cardiac NaV1.5 (zeige SCN5A Proteine) expression.
Hdac2 (zeige HDAC2 Proteine) isoform-selective knockdown was sufficient to rescue memory deficits in Tcf4(+/-) mice.
We report that TCF4 comprises two transcriptional isoforms, both of which are required for optimal plasmacytoid DC development in vitro
these data identified E2A (zeige TCF3 Proteine) and E2-2 as central regulators of B cell immunity.
down-regulation of Id3 (zeige ID3 Proteine) in B cells is essential for releasing E2A (zeige TCF3 Proteine) and E2-2, which in a redundant manner are required for antigen-induced B cell differentiation.
TCF-4 as a co-activator of p65 (zeige NFkBP65 Proteine) in the potentiation of proinflammatory cytokine production in macrophages and aggravation of high-fat diet induced chronic inflammation and insulin (zeige INS Proteine) resistance in mice.
Data indicate that upregulation of E2-2 protein markedly attenuated the inhibitor of DNA-binding 1 (ID1 (zeige ID1 Proteine))-mediated increase in endothelial progenitor cells (EPCs) proliferation and migration.
We conclude that E2-2 inhibited EPC (zeige TCF21 Proteine) proliferation via suppressing their autophagy, and E2-2 regulated EPC (zeige TCF21 Proteine) autophagy by mediating the expression of ATG7 (zeige ATG7 Proteine).
demonstrated that Id1 (zeige ID1 Proteine) and E2-2 are critical regulators of EPCs function in vitro. Id1 (zeige ID1 Proteine) interacts with E2-2 and relieves the E2-2-mediated repression of FGFR1 (zeige FGFR1 Proteine) and VEGFR2 (zeige KDR Proteine) expression to modulate EPCs functions
TCF4 is a regulator of neuronal intrinsic excitability in part by repression of Kcnq1 (zeige KCNQ1 Proteine) and Scn10a (zeige SCN10A Proteine).
GRG5/AES (zeige AES Proteine) interacts with TCF4 (zeige TCF7L2 Proteine) and represses Wnt (zeige WNT2 Proteine)-mediated transcription both in human cells and zebrafish embryos.
Data indicte that Tcf-1 (zeige HNF1A Proteine) and Lef-1 (zeige LEF1 Proteine) exhibit a function in the axis induction assay, which is lacking in Tcf-3 (zeige TCF3 Proteine) and -4.
Tcf4 (zeige TCF7L2 Proteine) transcription factor cooperates in patterning the Xenopus brain.
This gene encodes transcription factor 4, a basic helix-loop-helix transcription factor. The encoded protein recognizes an Ephrussi-box ('E-box') binding site ('CANNTG') - a motif first identified in immunoglobulin enhancers. This gene is broadly expressed, and may play an important role in nervous system development. Defects in this gene are a cause of Pitt-Hopkins syndrome. Multiple alternatively spliced transcript variants that encode different proteins have been described.
SL3-3 enhancer factor 2
, class B basic helix-loop-helix protein 19
, immunoglobulin transcription factor 2
, Transcription factor 4 (Immunoglobulin transcription factor 2) (ITF-2) (MITF-2) (SL3-3 enhancer factor 2) (SEF-2) (Class A helix-loop-helix transcription factor ME2)
, class A helix-loop-helix transcription factor ME2
, immunoglobulin transcription factor-2
, R8f DNA-binding protein
, thyroglobulin promoter transcription factor TFE
, transcription factor 7-like 2 (T-cell specific, HMG-box)
, transcriptional factor 4
, helix-loop-helix transcription factor
, LOW QUALITY PROTEIN: transcription factor 4