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anti-Human 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 Monoclonal TCF4 Primary Antibody for IHC (p), IP - ABIN264393
Barker, Huls, Korinek, Clevers: Restricted high level expression of Tcf-4 protein in intestinal and mammary gland epithelium. in The American journal of pathology 1999
Show all 5 Pubmed References
Human Monoclonal TCF4 Primary Antibody for IF, WB - ABIN393964
Eichhoff, Weeraratna, Zipser, Denat, Widmer, Xu, Kriegl, Kirchner, Larue, Dummer, Hoek: Differential LEF1 and TCF4 expression is involved in melanoma cell phenotype switching. in Pigment cell & melanoma research 2011
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
Human Polyclonal TCF4 Primary Antibody for IF, IP - ABIN2476691
Valenta, Lukas, Doubravska, Fafilek, Korinek: HIC1 attenuates Wnt signaling by recruitment of TCF-4 and beta-catenin to the nuclear bodies. in The EMBO journal 2006
Human Monoclonal TCF4 Primary Antibody for EMSA, IHC (p) - ABIN264394
Denys, Jadidizadeh, Amini Nik, Van Dam, Aerts, Alman, Cassiman, Tejpar: Identification of IGFBP-6 as a significantly downregulated gene by beta-catenin in desmoid tumors. in Oncogene 2004
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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 (show COL8a2 Antibodies) in the Indian cohort studied
High TCF4 expression is associated with colorectal cancer.
Examination of X-ray structures of the closely related TCF3 (show TCF3 Antibodies) and USF1 (show USF1 Antibodies) bound to DNA suggests TCF3 (show TCF3 Antibodies) can undergo a conformational shift to preferentially bind to 5hmC while the USF1 (show USF1 Antibodies) 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 (show ZEB1 Antibodies), suggesting that a mechanism triggering a loss of function may contribute to FECD (show COL8a2 Antibodies).
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 (show HELLS Antibodies) in TCF4 involves in the etiology of Bipolar disorder and Major Depressive disorder .
Our findings indicate that H2O2 inhibits NaV1.5 (show SCN5A Antibodies) expression by activating the Wnt/b-catenin signaling and beta-catenin (show CTNNB1 Antibodies) interacts with TCF4 to transcriptionally suppress cardiac NaV1.5 (show SCN5A Antibodies) expression.
Hdac2 (show HDAC2 Antibodies) 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 (show TCF3 Antibodies) and E2-2 as central regulators of B cell immunity.
down-regulation of Id3 (show ID3 Antibodies) in B cells is essential for releasing E2A (show TCF3 Antibodies) and E2-2, which in a redundant manner are required for antigen-induced B cell differentiation.
TCF-4 as a co-activator of p65 (show NFkBP65 Antibodies) in the potentiation of proinflammatory cytokine production in macrophages and aggravation of high-fat diet induced chronic inflammation and insulin (show INS Antibodies) resistance in mice.
Data indicate that upregulation of E2-2 protein markedly attenuated the inhibitor of DNA-binding 1 (ID1 (show ID1 Antibodies))-mediated increase in endothelial progenitor cells (EPCs) proliferation and migration.
We conclude that E2-2 inhibited EPC (show TCF21 Antibodies) proliferation via suppressing their autophagy, and E2-2 regulated EPC (show TCF21 Antibodies) autophagy by mediating the expression of ATG7 (show ATG7 Antibodies).
demonstrated that Id1 (show ID1 Antibodies) and E2-2 are critical regulators of EPCs function in vitro. Id1 (show ID1 Antibodies) interacts with E2-2 and relieves the E2-2-mediated repression of FGFR1 (show FGFR1 Antibodies) and VEGFR2 (show KDR Antibodies) expression to modulate EPCs functions
TCF4 is a regulator of neuronal intrinsic excitability in part by repression of Kcnq1 (show KCNQ1 Antibodies) and Scn10a (show SCN10A Antibodies).
GRG5/AES (show AES Antibodies) interacts with TCF4 (show TCF7L2 Antibodies) and represses Wnt (show WNT2 Antibodies)-mediated transcription both in human cells and zebrafish embryos.
Data indicte that Tcf-1 (show HNF1A Antibodies) and Lef-1 (show LEF1 Antibodies) exhibit a function in the axis induction assay, which is lacking in Tcf-3 (show TCF3 Antibodies) and -4.
Tcf4 (show TCF7L2 Antibodies) 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
, transcription factor 7-like 2
, transcription factor Tcf4
, LOW QUALITY PROTEIN: transcription factor 4