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anti-Mouse (Murine) TBL1X Anticorps:
anti-Rat (Rattus) TBL1X Anticorps:
anti-Human TBL1X Anticorps:
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Human Polyclonal TBL1X Primary Antibody pour ELISA, WB - ABIN546798
Hoberg, Yeung, Mayo: SMRT derepression by the IkappaB kinase alpha: a prerequisite to NF-kappaB transcription and survival. dans Molecular cell 2004
These results suggest that TBL1X is needed for the full activation of TRH and TSHbeta gene promoters by unliganded thyroid hormone receptors.
TBL1 deficiency resulted in inhibition of fatty acid oxidation due to impaired functional cooperation with its heterodimerization partner TBL-related (TBLR) 1 and the nuclear receptor peroxisome proliferator-activated receptor (PPAR) alpha
TBLR1 and TBL1 have roles in specific nuclear receptor-mediated gene activation events
TBL1X mRNA and protein expression were significantly increased in the gestational diabetes mellitus placenta. TBL1X is a potential target of miR-138-5p contributed to the abnormal growth of the placenta by enhancing the proliferation of trophoblasts.
missense mutations in the gene for TBLR1 that are associated with intellectual disability also prevent MeCP2 binding
Targeted SUMOylation of TBL1 and TBLR1 may be a useful strategy for therapeutic treatment of androgen-independent prostate cancer.
TBL1X mutations are associated with central hypothyroidism and hearing loss.
Here, the authors show that transcriptional co-factor Transducin beta-like (TBL) 1 was over-expressed in both human and murine pancreatic ductal adenocarcinoma and TBL1 deficiency both prevented and reversed pancreatic tumor growth.
TBL1 is required to protect GPS2 from degradation, with methylation of GPS2 by arginine methyltransferase PRMT6 regulating the interaction with TBL1 and inhibiting proteasome-dependent degradation.
We localized proteins encoded by the top two regulated genes, TBL1X and USH1C, using immunohistochemistry to placental stem and anchoring villi associated with active contractile function.
TBL1 and TBLR1 are functionally redundant and essential for transcriptional repression by unliganded thyroid hormone receptors (TR) but not essential for transcriptional activation by liganded TR
Mutations within the LisH (LIS1 homology)motif of TBL 1X are likely to result in pathogenic consequences in genes associated with genetic diseases.
Wnt signalling induced the interaction between beta-catenin and TBL1-TBLR1, as well as their binding to Wnt target genes. Importantly, the recruitment of TBL1-TBLR1 and beta-catenin to Wnt target-gene promoters was mutually dependent on each other.
The protein encoded by this gene has sequence similarity with members of the WD40 repeat-containing protein family. The WD40 group is a large family of proteins, which appear to have a regulatory function. It is believed that the WD40 repeats mediate protein-protein interactions and members of the family are involved in signal transduction, RNA processing, gene regulation, vesicular trafficking, cytoskeletal assembly and may play a role in the control of cytotypic differentiation. This encoded protein is found as a subunit in corepressor SMRT (silencing mediator for retinoid and thyroid receptors) complex along with histone deacetylase 3 protein. This gene is located adjacent to the ocular albinism gene and it is thought to be involved in the pathogenesis of the ocular albinism with late-onset sensorineural deafness phenotype. Four transcript variants encoding two different isoforms have been found for this gene. This gene is highly similar to the Y chromosome TBL1Y gene.
F-box-like/WD repeat-containing protein TBL1X
, transducin (beta)-like 1X-linked
, transducin beta-like 1X
, F-box-like/WD repeat-containing protein TBL1X-like
, f-box-like/WD repeat-containing protein TBL1X-like
, transducin beta-like protein 1X
, transducin-beta-like protein 1, X-linked
, transducin beta-like 1