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anti-Human TCF4 Antibodies:
anti-Mouse (Murine) TCF4 Antibodies:
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Human Monoclonal TCF4 Primary Antibody for IF, ELISA - ABIN520754
Tanaka, Itoh, Nishiyama, Takezawa, Kurihara, Itoh, Kato: Inhibition of endothelial cell activation by bHLH protein E2-2 and its impairment of angiogenesis. in Blood 2010
Show all 3 Pubmed References
Human Polyclonal TCF4 Primary Antibody for IHC, IHC (p) - ABIN4358095
Saegusa, Hashimura, Kuwata: Sox4 functions as a positive regulator of β-catenin signaling through upregulation of TCF4 during morular differentiation of endometrial carcinomas. in Laboratory investigation; a journal of technical methods and pathology 2012
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we observed that the beta-catenin/TCF4 complex mediates NRF3 expression by binding directly to the WRE site.
Structural basis for preferential binding of human TCF4 to DNA containing 5-carboxylcytosine has been described.
We found CTG repeat length to be a useful adjunct indicator which may be used to counsel a Fuchs' Endothelial Corneal Dystrophy (FECD) patient regarding his or her risk of significant clinical progression and keratoplasty over the next 10 years. There was more rapid clinical progression of FECD amongst patients who harbor an expanded TCF4 CTG18.1 allele (i.e. L40 group), during the first 5 years.
a serine determining the transcriptional activity of TCF-4 in lung carcinoma cells, was identified.
We confirmed that rs613872 in the TCF4 gene is strongly and statistically associated with late-onset FECD in a Greek population.
rs1273263 is a potential regulator of TCF4 expression, and might be associated with schizophrenia.
Our findings showed that TCF4 mRNA is upregulated in the corneal endothelium of patients with Fuchs' endothelial corneal dystrophy.
Study identify TCF4 as a key regulator of neural stem cells (NSCs). TCF4 interacts with Mediator, colocalizes with Mediator at super enhancers and regulates neurogenic transcription factor genes with super enhancers and broad H3K4me3 domains. Data suggest that high binding-affinity for Mediator is an important organizing feature in the transcriptional network that determines NSC identity.
Our large German cohort demonstrated a significant association between the risk allele G in rs613872 and FECD, irrespective of TNR expansion, although this risk allele was more frequent in Fuchs endothelial corneal dystrophy cases with TNR expansion than without.
The rs8766 in TCF4 was selected for genotyping. rs8766 allele and genotype frequencies were not significantly different between case and control groups and a significant association cannot be suggested for the selected SNP for schizophrenia.
We observed instability of the TCF4 triplet repeat expansion in nearly a third of parent-child transmissions. Large mutant CTG18.1 alleles are prone to contraction, whereas intermediate mutant alleles tend to expand when unstably transmitted. Intergenerational instability of TCF4 repeat expansion has implications on FECD disease inheritance.
in cell fractions with erythroid lineage potential, TCF4 is expressed less in MDS patients than in healthy controls. This correlates with the low overall Hb levels seen in MDS patients compared with healthy individuals and is consistent with the positive impact of TCF4 on erythroid development while not having impact on white colonies.
Thirteen genes within the 108 loci had both a TCF4 binding site +/-10kb and were differentially expressed in siRNA knockdown experiments of TCF4, suggesting direct TCF4 regulation. These findings confirm TCF4 as an important regulator of neural genes and point toward functional interactions with potential relevance for schizophrenia (SCZ).
In contrast to HEB and E2A, which facilitate AML1-ETO-mediated leukemogenesis, E2-2 compromises the function of the AML1-ETO-containing transcription factor complex and negatively regulates leukemogenesis.
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.
Tcf4 is involved in synaptic plasticity in mature neurons.
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.
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