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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
these results highlight TCF4 as a frequent cause of moderate to profound intellectual disabilities (ID) and broaden the clinical spectrum associated to TCF4 mutations to nonspecific ID.
TCF4 binding sites are found in a large number of neuronal genes that include many genetic risk factors for common neurodevelopmental disorders.
Expanded CTG.CAG repeats in the context of the third intron of TCF4 are transcribed and translated via non-ATG initiation, providing evidence for RAN translation in corneal endothelium of patients with Fuchs' endothelial corneal dystrophy (FECD).
Gene expression in the corneal endothelium of Fuchs endothelial corneal dystrophy patients with and without expansion of a trinucleotide repeat in TCF4
In conclusion, this study provides genetic and some preliminary functional evidence to support the view that the TCF4 (NM_001243232) p.Pro29Thr mutation causes familial SAK.
Hippo pathway transcription factor TEAD4 directly associates with the Wnt pathway transcription factor TCF4 via their DNA-binding domains, forming a complex on target genes. VGLL4 binds to this TEAD4-TCF4 complex to inhibit transactivation of both TCF4 and TEAD4.
these results from tumor xenograft modeling depict a link between altered TCF4 expression and breast cancer chemoresistance.
Long noncoding RNA AFAP1-AS1 enhances cell proliferation and invasion in osteosarcoma through regulating miR-4695-5p/TCF4-beta-catenin signaling.
we found that CypA binds beta-catenin and is recruited to Wnt target gene promoters. By increasing the interaction between beta-catenin and TCF4, CypA enhances transcriptional activity. Our results demonstrate that CypA enhances GIC stemness, self-renewal, and radioresistance through Wnt/beta-catenin signaling
Our results showed that the mRNA level of TCF4 may be associated with schizophrenia, its psychopathology, IQ and cognitive impairments in an Iranian group of patients with schizophrenia.
The formation of the beta-catenin/TCF4 complex was disrupted by HI-B1 due to the direct interaction of HI-B1 with beta-catenin. Colon cancer patient-derived xenograft (PDX) studies showed that a tumor with higher levels of beta-catenin expression was more sensitive to HI-B1 treatment, compared to a tumor with lower expression levels of beta-catenin
Expression of TCF4 at the mRNA and protein level may be significant in the etiology of recurrent depressive disorder and it is not dependent on sex and age.
Data show that silencing of immunoglobulin transcription factor 2 (ITF-2) by siRNA significantly enhanced susceptibility to the MEK inhibitor selumetinib (AZD6244) in resistant cells.
Expression of TCF4 in a neural progenitor cell line derived from the developing human cerebral cortex was reduced using RNA interference. Genes that were differentially expressed following TCF4 knockdown were highly enriched for involvement in the cell cycle. There was a nonsignificant trend for genetic association between the differentially expressed gene set and schizophrenia.
TCF4 knockdown promoted HepG-2 cell differentiation and inhibited tumor formation, and TCF4 could be the potential downstream target for clopidogrel therapy
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 in the Indian cohort studied
Black patients with Fuchs' dystrophy were less likely than white patients to demonstrate CTG18.1 allele expansion.
Examination of X-ray structures of the closely related TCF3 and USF1 bound to DNA suggests TCF3 can undergo a conformational shift to preferentially bind to 5hmC while the USF1 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 findings reveal the commitment and flexibility of E2-2high progenitor differentiation and imply that pertinent tuning machinery is present in the gut microenvironment.
TCF4 is broadly expressed in cortical and subcortical structures in the developing and adult mouse brain. Tcf4 haploinsufficiency in mice replicated structural brain anomalies observed in Pitt-Hopkins syndrome patients.
Our findings indicate that H2O2 inhibits NaV1.5 expression by activating the Wnt/b-catenin signaling and beta-catenin interacts with TCF4 to transcriptionally suppress cardiac NaV1.5 expression.
Hdac2 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 and E2-2 as central regulators of B cell immunity.
down-regulation of Id3 in B cells is essential for releasing E2A and E2-2, which in a redundant manner are required for antigen-induced B cell differentiation.
TCF-4 as a co-activator of p65 in the potentiation of proinflammatory cytokine production in macrophages and aggravation of high-fat diet induced chronic inflammation and insulin resistance in mice.
Data indicate that upregulation of E2-2 protein markedly attenuated the inhibitor of DNA-binding 1 (ID1)-mediated increase in endothelial progenitor cells (EPCs) proliferation and migration.
This study demonstrated that Tcf4tg mice displayed significantly delayed conditioning when pre-exposed to the conditioned stimulus (12 kHz) but not when pre-exposed to a different stimulus
We conclude that E2-2 inhibited EPC proliferation via suppressing their autophagy, and E2-2 regulated EPC autophagy by mediating the expression of ATG7.
demonstrated that Id1 and E2-2 are critical regulators of EPCs function in vitro. Id1 interacts with E2-2 and relieves the E2-2-mediated repression of FGFR1 and VEGFR2 expression to modulate EPCs functions
TCF4 is a regulator of neuronal intrinsic excitability in part by repression of Kcnq1 and Scn10a.
A disease-promoting role of E2-2 dependent pDCs in the pancreas.
Genetic disruption of Itf2 on the Apc(Min/+) background results in earlier death and a significant increase in tumor number and size in the small intestine.
Results show that binding of the transcription factor Tcf4 correlates with hypo-methylation and demonstrate that Tcf4 is one of the factors contributing to formation of differentially methylated regions.
Wnt/beta-catenin stimulation may repress BACE1 transcription via binding of TCF4 to BACE1 gene, and therefore, activation of the Wnt pathway may hold the key to new treatments of Alzheimer disease
study suggests that CREPT acts as an activator to promote transcriptional activity of the beta-catenin.TCF4 complex in response to Wnt signaling.
Dendritic cell-specific Tcf4 haplodeficiency ameliorated systemic lupus erythematosus-like disease caused by the overexpression of the endosomal RNA sensor Tlr7.
beta-catenin patterns zonal liver metabolism together with Tcf-4, Hnf-4alpha, and xenobiotic nuclear receptors.
GRG5/AES interacts with TCF4 and represses Wnt-mediated transcription both in human cells and zebrafish embryos.
XTcf-4C has been described as an essential factor for isthmus development.
Data indicte that Tcf-1 and Lef-1 exhibit a function in the axis induction assay, which is lacking in Tcf-3 and -4.
Tcf4 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