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A mutation in T-box of TBX1 was identified in an animal model of DiGeorge Syndrome; it's the DNA binding domain for transcription activity.
Data show that beta-catenin (show CTNNB1 ELISA Kits) was increased in expression when Tbx1 was inactivated, suggesting that there may be a negative feedback loop between canonical Wnt (show WNT2 ELISA Kits) and Tbx1.
Results show that loss of Tbx1 disrupts corticogenesis in mice by promoting premature neuronal differentiation in the medio-lateral embryonic cortex, which gives rise to the somatosensory cortex; altered polarity in both radially migrating excitatory neurons and tangentially migrating inhibitory interneurons; mesoderm-specific inactivation of Tbx1 is sufficient to recapitulate the brain phenotype
Tbx1 is required for the patterning but not timing of CA stem development and a Tbx1 reporter allele is expressed in myocardium adjacent to the left but not right CA stem.
Cell orientation is biased towards the shelf distal edge in the mid-palate of wild-type embryos but is essentially random in the Tbx1(-/-) mutant shelves
Suggest LITAF (show LITAF ELISA Kits) as regulatory of pro-inflammatory and pro-fibrogenic pattern in non-alcoholic fatty liver disease.
These results suggest that TBX1 plays a role in maintaining a progenitor state in VEGFR2 (show KDR ELISA Kits)+ cells.
Tbx1 is required upstream of key myogenic genes needed for core mesoderm cell survival and fate, between E9.5 and E10.5, resulting in formation of the branchiomeric muscles.
Tbx1 binds to the miR (show MLXIP ELISA Kits)-96 promoter and represses miR (show MLXIP ELISA Kits)-96 expression.
Loss of Tbx1 in mouse (Tbx1(-/-)) results in skeletal abnormalities similar to those of cleidocranial dysplasia in humans.
Studied expression, function, and regulation of T-box transcription factor (TBX1), in human parathyroid adult normal and tumor tissues.
A genome wide are study to identify acute kidney injury risk in critically ill patients identified a locus on chromosome 22 found 140kb upstream of TBX1, and may affect pathways that contribute to AKI pathophysiology.
The results clearly suggest a possible etiologic association between the TBX1 deletion and Tetralogy of Fallot.
TBX1 loss-of-function mutation with enhanced susceptibility to double outlet right ventricle (DORV (show GDF1 ELISA Kits)) and ventricular septal defect (VSD)in humans, which provides novel insight into the molecular mechanism underlying Congenital heart disease (CHD (show CHDH ELISA Kits)).
SNPs in three genes CYP26B1 rs2241057, CISD1 rs2251039, rs2590370, and TBX1 rs4819522 were involved in six potential pathways to influence serum prostate-specific antigen levels.
TBX1 T-box domain binds DNA as two distinct monomers.
TBX1 isoform C is the biologically essential variant and that TBX1 mutations are associated with a wide phenotypic spectrum, including most of 22q11.2DS phenotypes.
Findings indicate an association between TBX1 variations and fetal CTD. The results also demonstrate the power of array CGH to further scrutinize the critical gene(s) of del22q11.2 syndrome responsible for heart defects.
Observations suggest that TBX1 loss-of-function mutation may be involved in the pathogenesis of isolated conotrucal heart defects (CTDs)in patients without 22q11.2 deletion.
Results show that TBX1 regulates brain angiogenesis through the DLL4 (show DLL4 ELISA Kits)/Notch1 (show NOTCH1 ELISA Kits)-VEGFR3 (show FLT4 ELISA Kits) regulatory axis.
Tbx1 controls the morphogenesis of pharyngeal pouch epithelia through mesodermal Wnt11r (show WNT11 ELISA Kits) and Fgf8a.
Conservation of Tbx1 function in zebrafish second heart field biology.
Her9 represses neurogenic fate downstream of Tbx1 and retinoic acid signaling in the inner ear.
Tbx1 might play an essential role in the development of pharyngeal neural crest cells in zebrafish. Cardiac performance is impaired by Tbx1 knock down in zebrafish.
Retinoic acid could produce an altered Tbx1 expression pattern in zebrafish embryos.
This newly identified tbx1 expression pattern in cardiac regions other than the cardiac outflow tract offers a new insight into the role of the tbx1 transcription factor in cardiac development.
Probable role in regulating transcription of specific genes. May regulate through NFKB1 the expression of the CCL2/MCP-1 chemokine. May play a role in tumor necrosis factor alpha (TNF- alpha) gene expression.
, T-box protein 1
, T-box transcription factor 1
, T-box transcription factor TBX1
, LITAF-like protein
, LPS-induced TNF-alpha factor homolog
, Nedd4 WW domain-binding protein 3
, estrogen-enhanced transcript protein
, lipopolysaccharide-induced tumor necrosis factor-alpha factor homolog
, T-box 1 transcription factor C
, Testis-specific T-box protein
, testis-specific T-box protein
, van gogh