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Human Monoclonal TCF4 Primary Antibody für 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
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Human Monoclonal TCF4 Primary Antibody für 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
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Human Monoclonal TCF4 Primary Antibody für 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 für 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 für 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 für 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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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 (zeige MAP2K1 Antikörper) 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 (zeige COL8a2 Antikörper) in the Indian cohort studied
Examination of X-ray structures of the closely related TCF3 (zeige TCF3 Antikörper) and USF1 (zeige USF1 Antikörper) bound to DNA suggests TCF3 (zeige TCF3 Antikörper) can undergo a conformational shift to preferentially bind to 5hmC while the USF1 (zeige USF1 Antikörper) 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 (zeige ZEB1 Antikörper), suggesting that a mechanism triggering a loss of function may contribute to FECD (zeige COL8a2 Antikörper).
repeat expansion showed stronger association than the most significantly associated SNP, rs613872, in TCF4, with the disease in the Australian cohort
Our findings indicate that H2O2 inhibits NaV1.5 (zeige SCN5A Antikörper) expression by activating the Wnt/b-catenin signaling and beta-catenin (zeige CTNNB1 Antikörper) interacts with TCF4 to transcriptionally suppress cardiac NaV1.5 (zeige SCN5A Antikörper) expression.
Hdac2 (zeige HDAC2 Antikörper) 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 Antikörper) and E2-2 as central regulators of B cell immunity.
down-regulation of Id3 (zeige ID3 Antikörper) in B cells is essential for releasing E2A (zeige TCF3 Antikörper) 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 Antikörper) in the potentiation of proinflammatory cytokine production in macrophages and aggravation of high-fat diet induced chronic inflammation and insulin (zeige INS Antikörper) resistance in mice.
Data indicate that upregulation of E2-2 protein markedly attenuated the inhibitor of DNA-binding 1 (ID1 (zeige ID1 Antikörper))-mediated increase in endothelial progenitor cells (EPCs) proliferation and migration.
We conclude that E2-2 inhibited EPC (zeige TCF21 Antikörper) proliferation via suppressing their autophagy, and E2-2 regulated EPC (zeige TCF21 Antikörper) autophagy by mediating the expression of ATG7 (zeige ATG7 Antikörper).
demonstrated that Id1 (zeige ID1 Antikörper) and E2-2 are critical regulators of EPCs function in vitro. Id1 (zeige ID1 Antikörper) interacts with E2-2 and relieves the E2-2-mediated repression of FGFR1 (zeige FGFR1 Antikörper) and VEGFR2 (zeige KDR Antikörper) expression to modulate EPCs functions
TCF4 is a regulator of neuronal intrinsic excitability in part by repression of Kcnq1 (zeige KCNQ1 Antikörper) and Scn10a (zeige SCN10A Antikörper).
GRG5/AES (zeige AES Antikörper) interacts with TCF4 (zeige TCF7L2 Antikörper) and represses Wnt (zeige WNT2 Antikörper)-mediated transcription both in human cells and zebrafish embryos.
Data indicte that Tcf-1 (zeige HNF1A Antikörper) and Lef-1 (zeige LEF1 Antikörper) exhibit a function in the axis induction assay, which is lacking in Tcf-3 (zeige TCF3 Antikörper) and -4.
Tcf4 (zeige TCF7L2 Antikörper) 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