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Human TCF7L2 Protein expressed in Wheat germ - ABIN1322376
Shitashige, Satow, Honda, Ono, Hirohashi, Yamada: Regulation of Wnt signaling by the nuclear pore complex. in Gastroenterology 2008
TCF7L2 protein is increased during adipogenesis in 3T3-L1 cells and primary adipocyte stem cells and th (show INS Proteins)at 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 (show HNF4A Proteins)-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 (show GCG Proteins) 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 (show GLP1R Proteins) 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 (show WNT2 Proteins)/beta-catenin (show CTNNB1 Proteins) signaling and c-Myc (show MYC Proteins) upregulation during abnormal cardiac remodeling in heart failure and suppression of Wnt (show WNT2 Proteins)/beta-catenin (show CTNNB1 Proteins) to c-Myc (show MYC Proteins) 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.
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 (show WNT2 Proteins) signaling in the intestine during zebrafish organogenesis.
XTcf4 has no repressive role but is required to activate expression of Xnr3 and chordin (show CHRD Proteins) in organizer cells at the gastrula stage
regulation of XTcf-4 by canonical wnt (show WNT2 Proteins)-signaling is directly controlled by binding to and activating a consensus Lef/Tcf (show HNF4A Proteins) binding site within its own promoter
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.
Type 1 diabetes mellitus patients carriers of the TCF7L2 variant had a milder immunologic and metabolic phenotype at type 1 diabetes diagnosis, which could be partly driven by type 2 diabetes-like pathogenic mechanisms.
The SNPs in TCF7L2 and HHEX were genotyped by polymerase chain reaction-restriction fragment length polymorphism. There were no significant differences in the distribution of genotypes and alleles between polycystic ovary syndrome cases and controls
TCF7L2 mRNA expression is downregulated in humans with impaired glucose tolerance and adipocyte insulin (show INS Proteins) resistance.
PGC-1alpha induction during differentiation is required for both mitochondrial biogenesis and commitment to the hepatocytic lineage, and TCF7L2 repression is sufficient to increase PGC-1alpha expression, mitochondrial biogenesis and OXPHOS activity.
Silencing the tcf4 (show TCF4 Proteins) gene confers sensitivity to oxaliplatin in colorectal cancer cells.
GRbeta bound to the N-terminus domain of TCF-4 (show TCF4 Proteins) its influence on Wnt (show WNT2 Proteins) signaling required both ligand- and DNA-binding domains. This is enough to maintain the TCF (show HNF4A Proteins)/LEF activity at a high level in the absence of beta-catenin (show CTNNB1 Proteins) stabilization.
TRIB2 (show TRIB2 Proteins) negatively regulates Wnt (show WNT2 Proteins) activity through a reduction in protein stability of TCF4 (show TCF4 Proteins) and beta-Catenin (show CTNNB1 Proteins)
CtBP physically interacted with TCF-4, and this interaction was significantly inhibited in the presence of MTOB. The above findings point to a novel role of CtBPs in the promotion of CSC growth and self-renewal
findings report an independent confirmation of the association of the TCF7L2 (show TCF4 Proteins) gene with milk yield and composition traits.
Genes implied in human type 2 diabetes development, TCF7L2, WFS1 (show WFS1 Proteins), FTO (show FTO Proteins), SLC30A8 (show SLC30A8 Proteins), and GCKR (show GCKR Proteins), 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