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TBL1 deficiency resulted in inhibition of fatty acid oxidation due to impaired functional cooperation with its heterodimerization partner TBL-related (TBLR) 1 (Montrer TBL1XR1 Anticorps) and the nuclear receptor peroxisome proliferator-activated receptor (Montrer PPARG Anticorps) (PPAR) alpha (Montrer PPARA Anticorps)
TBLR1 (Montrer TBL1XR1 Anticorps) and TBL1 have roles in specific nuclear receptor-mediated gene activation events
missense mutations in the gene for TBLR1 that are associated with intellectual disability also prevent MeCP2 binding
Targeted SUMOylation of TBL1 and TBLR1 (Montrer TBL1XR1 Anticorps) 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 (Montrer GNAT1 Anticorps) 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 (Montrer GPS2 Anticorps) from degradation, with methylation of GPS2 (Montrer GPS2 Anticorps) by arginine methyltransferase PRMT6 (Montrer PRMT6 Anticorps) regulating the interaction with TBL1 and inhibiting proteasome-dependent degradation.
We localized proteins encoded by the top two regulated genes, TBL1X and USH1C (Montrer USH1C Anticorps), using immunohistochemistry to placental stem and anchoring villi associated with active contractile function.
TBL1 and TBLR1 (Montrer TBL1XR1 Anticorps) are functionally redundant and essential for transcriptional repression by unliganded thyroid hormone (Montrer PTH Anticorps) receptors (TR) but not essential for transcriptional activation by liganded TR
Mutations within the LisH (LIS1 (Montrer PAFAH1B1 Anticorps) homology)motif of TBL 1X are likely to result in pathogenic consequences in genes associated with genetic diseases.
Wnt (Montrer WNT2 Anticorps) signalling induced the interaction between beta-catenin (Montrer CTNNB1 Anticorps) and TBL1-TBLR1 (Montrer TBL1XR1 Anticorps), as well as their binding to Wnt (Montrer WNT2 Anticorps) target genes. Importantly, the recruitment of TBL1-TBLR1 (Montrer TBL1XR1 Anticorps) and beta-catenin (Montrer CTNNB1 Anticorps) to Wnt (Montrer WNT2 Anticorps) 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