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miR-130a-3p suppressed aggressive phenotype of Gastric Cancer cells partially by direct targeting and decreasing TBL1XR1 and subsequent epithelial-mesenchymal transition process.
These results suggest that a de novo TBL1XR1 point mutation could alter Wnt/beta-catenin signaling activity. Further studies are required to clarify the involvement of TBL1XR1 mutations in neuropsychiatric conditions.
High TBL1XR1 expression indicates poor disease-free survival of stage I-III colorectal cancer patients; beta-catenin signaling is critical for TBL1XR1-mediated colorectal cancer cells oncogenicity.
emonstrated that TBL1XR1 can regulate the expression of vascular endothelial growth factor C and epithelial-mesenchymal transition proteins
TBLR1 has a role in reducing apoptosis in prostate cancer under androgen deprivation
Targeted SUMOylation of TBL1 and TBLR1 may be a useful strategy for therapeutic treatment of androgen-independent prostate cancer.
The patient with Tyr446Cys mutation presents with a submucous cleft palate and hydronephrosis in addition to severe delays, hypotonia, dysmorphic findings and emerging scoliosis, consistent with previous reports.
TBL1XR1-microduplication syndrome is an intellectual disability/learning disability syndrome with associated incomplete penetrance autism spectrum disorders, hearing loss, and delay of puberty. Its phenotypic overlap indicates that it is a genomic sister-disorder to the 3q26.32 microdeletion syndrome
the twins described by Fitzsimmons had heterozygous mutations in the SACS gene, the gene responsible for autosomal recessive spastic ataxia of Charlevoix Saguenay as well as a heterozygous mutation in the TRPS1, the gene responsible in Trichorhinophalangeal syndrome type 1A TBL1XR1 mutation was identified in the patient described in 2009 as contributing to his cognitive impairment and autistic features..
TBL1XR1 contributes to GC tumorigenesis and progression through the activation of the beta-catenin/MMP7/EGFR/ERK signalling pathway and may act as a new therapeutic target for GC.
This study identifies a specific TBL1XR1 mutation as the cause of Pierpont syndrome. Deletions and other mutations in TBL1XR1 can cause autism. The marked differences between Pierpont patients with the p.Tyr446Cys mutation and individuals with other mutations and whole gene deletions indicate a specific, but as yet unknown, disease mechanism of the TBL1XR1 p.Tyr446Cys mutation.
High expressions of TBL1XR1 is associated with liver metastasis for early stage colorectal cancer.
In targeted sequencing, a disruptive mutation of TNFAIP3 was the most common alteration (54%), followed by mutations of TBL1XR1 (18%) and cAMP response element binding proteins (CREBBP) (17%).
TBL1XR1 overexpression may be an unfavorable prognostic factor for Epithelial Ovarian Cancer.
Integrating population variation and protein structural analysis is harnessed to improve clinical interpretation of missense mutations in WD40 domain-containing TBLR1 protein for the prognosis of developmental disabilities.
in splenic hemangioma with t(3;6)(q26;p21), the entire coding region of HMGA1 comes under the control of the TBL1XR1 promoter, bringing about dysregulation of HMGA1
These finding suggested that TBLR1 is likely to be a potential prognostic indicator and therapeutic target for HCC and that TBLR1 may be implicated in EMT of HCC cells.
Results show that upregulation of TBL1XR1 induces Nasopharyngeal Carcinoma cells resistance to cisplatin by activating the NF-kappaB pathway.
that TBL1XR1 haploinsufficiency can cause intellectual disability with a recognizable dysmorphism, without necessarily causing autistic behavior.
TBLR1 plays a key role in the development and progression of breast cancer cells via cyclin D1-transactivation and activation of the beta-catenin signaling pathway.
SMRT/N-CoR repressor complex is involved in gene regulation during sperm differentiation since members of this complex, in particular TBL1XR1, interact with SLY in postmeiotic male germ cells.
our data suggest that Setd5 is required for maintaining PGC-associated genes and Setd5-associated protein complexes containing Tbl1xr1 and Ctr9, which in turn are likely involved in regulating germ cell-related genes in mESCs
The cell autonomous transcriptional activity of TBLR1 controls multiple beta-adrenoceptor and postreceptor checkpoints in white adipocytes, thereby coordinating an integrated response of cAMP-dependent free fatty acid (FFA) mobilization.
TBLR1 and TBL1 have roles in specific nuclear receptor-mediated gene activation events
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.
transducin (beta)-like 1 X-linked receptor 1
, F-box-like/WD repeat-containing protein TBL1XR1
, f-box-like/WD repeat-containing protein TBL1XR1-like
, transducin (beta)-like 1X-linked receptor 1
, nuclear receptor co-repressor/HDAC3 complex subunit
, TBL1-related protein 1
, nuclear receptor corepressor/HDAC3 complex subunit TBLR1
, transducin beta-like 1X-related protein 1
, F-box-like/WD repeat protein TBL1XR1