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anti-Mouse (Murine) TCF7L2 Antibodies:
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Human Monoclonal TCF7L2 Primary Antibody for IHC (p), ELISA - ABIN520776
da Silva Xavier, Loder, McDonald, Tarasov, Carzaniga, Kronenberger, Barg, Rutter: TCF7L2 regulates late events in insulin secretion from pancreatic islet beta-cells. in Diabetes 2009
Show all 2 Pubmed References
Human Polyclonal TCF7L2 Primary Antibody for ICC, IF - ABIN446586
Kwon, Leibovitch, Bansal, Pereira, Chung, Ariztia, Zelent, Farias, Waxman: Targeted interference of SIN3A-TGIF1 function by SID decoy treatment inhibits Wnt signaling and invasion in triple negative breast cancer cells. in Oncotarget 2017
Tcf7l2 required for the effects of Lkb1 deletion on insulin secretion in the mouse beta cell. Tcf7l2, lies on a pathway through which LKB1 acts in the beta cell to restrict insulin secretion.
This work identified Tcf7L2 as the principal transcription factor mediating canonical Wnt signalling in the embryonic neocortex.
TCF7L2 protein is increased during adipogenesis in 3T3-L1 cells and primary adipocyte stem cells and that TCF7L2 expression is required for the regulation of Wnt signaling during adipogenesis.
Data (including data from studies in transgenic mice) suggest that inactivation of Tcf7l2 in pancreatic pericytes is associated with impaired expression of genes required for pancreatic beta-cell function and maturity of isolated pancreatic islets. Transgenic mice in which Tcf7l2 is selectively inactivated in pancreatic pericytes exhibit glucose intolerance.
TCF7L2 does not affect oligodendrocyte precursor cells during remyelination.
the inhibition of beta-catenin's TCF-dependent transcriptional activity, independent of its protein expression level, retains the naive ground state pluripotency in mouse embryonic stem cells.
Findings demonstrate an alpha cell-autonomous role for Tcf7l2 in the control of pancreatic glucagon secretion and the maintenance of alpha cell mass and function.
Suggest transcription factor 7-like 2 is a possible regulator of glucagon-like peptide 1 receptor expression in endothelial/smooth muscle cells in diabetic mice.
along with the elevation of miR-17-5p expression in mouse epididymal fat tissue in response to high fat diet consumption, allowed us to suggest that miR-17-5p is among central switches of adipogenic differentiation
TCF7L2 mediates canonic Wnt/beta-catenin signaling and c-Myc upregulation during abnormal cardiac remodeling in heart failure and suppression of Wnt/beta-catenin to c-Myc axis can be explored for preventing and treating heart failure.
These findings suggest a unique role for Tcf7l2 in generating distinct neuronal phenotypes from homogeneous progenitor population.
Tcf7l2 may be involved in maintenance of stem/progenitor cells properties.
results indicate that miR-181a-5p promotes 3T3-L1 preadipocyte differentiation and adipogenesis through regulating TGFbeta/Smad and Wnt signaling pathway by directly targeting Smad7 and Tcf7l2
Tcf7l2 protein levels decline upon initiation of endocrine differentiation in vivo, disclosing the downregulation of this factor in the developing endocrine compartment.
Kaiso and Sox10 sequentially interact with Tcf7l2 to coordinate the maturation of oligodendrocyte.
Tcf7l2 plays a cell autonomous role in the control of beta cell function and mass, serving as an important regulator of gene expression and islet cell coordination
Tcf7l2 is regulating proinsulin expression directly via Isl1, Ins1 and indirectly via MafA, NeuroD1 and Pdx1.
Transcription factor 7-like 2 positively regulates neonatal and postnatal mouse oligodendrocyte differentiation during developmental myelination and remyelination in a manner independent of the Wnt/beta-catenin signaling pathway.
TCF7L2 expressed in the pancreatic beta cells plays a crucial role in glucose metabolism through regulation of the beta cell mass.
Marked expression of TCF7L2 in oligodendrocytes is restricted to a well defined time period during developmental myelination in human and mouse central nervous system tissue samples.
Tcf7l2 is essential for lateralized fate selection by habenular neurons that can differentiate along two alternative pathways, thereby leading to major neural circuit asymmetries.
Dorsal and ventral habenulae develop in different regions of prosomere 2. In the process of ventral habenula formation, functional tcf7l2 gene activity is required and in its absence, ventral habenular neurons do not develop.
In embryos, the tcf4 gene is highly regulated at the level of RNA splicing such that the variant proteins that are produced contain or lack domains proposed to be essential in repression or activation of transcription.
Study underscores the involvement of Tcf4 in maintaining proliferative self-renewal in the intestine throughout life.
This study reveals that Tcf4 (tcf7l2) is the major effector of Wnt signaling in the intestine during zebrafish organogenesis.
XTcf4 has no repressive role but is required to activate expression of Xnr3 and chordin in organizer cells at the gastrula stage
regulation of XTcf-4 by canonical wnt-signaling is directly controlled by binding to and activating a consensus Lef/Tcf binding site within its own promoter
REVIEW about mechanism by which genetic variation may alter diabetes risk
The type 2 diabetes-associated TCF7L2 locus influences progression of islet autoimmunity in type 1 diabetes, with differential effects by autoantibody specificity and interaction by obesity/overweight.
The results of this study demonstrated that TCF7L2 is associated with type 2 diabetes mellitus in the Chinese Korean ethnicity population.
FECD has the potential to be a model for treating many trinucleotide repeat diseases and targeting the TCF4 expansion with ASOs represents a promising therapeutic strategy to prevent and treat FECD.
Studied the role of transcription factor 7 like 2 (TCF7L2) single nucleotide polymorphisms (SNPs) in genetic predisposition to diabetes mellitus type 2.
rs7074440 was identified as a candidate functional SNP linked with genome-wide association studies-lead SNP for type 2 diabetes, which directly binds to C-FOS to alter TCF7L2 gene expression.
The presence of the rs12255372 and rs7903146 TCF7L2 gene variants plays an important role in the development of T2DM among individuals with metabolic syndrome.
Transfection of LS174T cells showed that the VTI1A promoter is highly active compared to the TCF7L2 promoter, and that CDX2 activates transcription of VTI1A.
Studied association of single nucleotide polymorphisms in Transcription factor 7-like 2 (TCF7L2) gene and genetic predisposition to type 2 diabetes in nonobese patients.
The meta-analysis suggested that TCF7L2 polymorphism rs7903146 was significantly associated with type 2 diabetes mellitus in Caucasian, East Asian, South Asian and other ethnicities. [Meta-analysis]
The responses of insulin and HOMA-IR to ALE supplementation have shown an interaction with single-nucleotide polymorphism rs7903146 in TCF7L2.
The two varients of the gene TCF7L2 are important genetic risk factors for the T2D development in the Han ethnic group in China.
In conclusion, homozygous TT allele carriers show altered postprandial triglyceride response, mainly influencing very low density lipoproteins and high density lipoproteins subclasses suggesting a genotype-mediated effect on hepatic lipid regulation.
a considerable connection of DEFB1 and TCF7L2 gene polymorphisms with nephrolithiasis
stable knockdown of FOXO3, NCOA3, and TCF7L2 restored growth in low glucose but reduced MEK/MAPK phosphorylation, reduced anchorage-independent growth, and modulated expressions of GLUT1 and Ras pathway related proteins.
Study showed the association of TCF7L2 SNPs (rs7903146, rs12255372, and rs10885406) with high total cholesterol/high-density lipoproteins ratio. Findings highlight the influence of TCF7L2 SNPs on altered lipid profile in the Balinese, which may further link to the risk of cardiovascular diseases.
TCF7L2 rs7903146 polymorphism may be associated with the susceptibility to diabetic nephropathy in Chinese Han population, but rs290487 is not. The strong linkage disequilibrium existed between the 2 single nucleotide polymorphisms and haplotype T-T (rs7903146-rs290487) increased the susceptibility to diabetic nephropathy.
the T risk allele of the rs7903146 in the TCF7L2 gene increases the risk of type 2 diabetes, was determined.
Common variation at TCF7L2 influences acute responses to both glipizide and metformin in people without diabetes and highlight altered incretin signaling as a potential mechanism by which TCF7L2 variation increases T2D risk.
No correlation between the studied polymorphisms of the TCF7L2 gene and GDM was observed.
findings report an independent confirmation of the association of the TCF7L2 gene with milk yield and composition traits.
Genes implied in human type 2 diabetes development, TCF7L2, WFS1, FTO, SLC30A8, and GCKR, were mapped on Sus scrofa chromosomes 14, 8, 6, 4, and 3, respectively. Only TCF7L2 was significantly associated with five fat traits in pigs.
This gene encodes a high mobility group (HMG) box-containing transcription factor that plays a key role in the Wnt signaling pathway. The protein has been implicated in blood glucose homeostasis. Genetic variants of this gene are associated with increased risk of type 2 diabetes. Several transcript variants encoding multiple different isoforms have been found for this gene.
transcription factor 7-like 2 (T-cell specific, HMG-box)
, HMG box transcription factor 4
, T-cell factor 4
, T-cell-specific transcription factor 4
, transcription factor 7-like 2
, transcription factor 7-like 2, T-cell specific, HMG-box
, transcription factor tcf4
, T-cell factor XTCF-4A
, transcription factor Tcf4
, T-cell factor-4 variant A
, T-cell factor-4 variant B
, T-cell factor-4 variant C
, T-cell factor-4 variant D
, T-cell factor-4 variant E
, T-cell factor-4 variant F
, T-cell factor-4 variant G
, T-cell factor-4 variant H
, T-cell factor-4 variant I
, T-cell factor-4 variant J
, T-cell factor-4 variant K
, T-cell factor-4 variant L
, T-cell factor-4 variant M
, T-cell factor-4 variant X2