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Frame-shift mutation in TWIST1 is associated with type 2 scurs syndrome.
Interaction with Snail1/2, and Twist function more generally, is regulated by GSK-3-beta-mediated phosphorylation of conserved sites in the WR domain.
Data identified Twist1 and CD44 (show CD44 Proteins) as novel REST targeted genes and provide new insight into the epigenetic regulation of Twist1 and CD44 (show CD44 Proteins) by REST.
TWIST1 promotes catabolic reactions by inducing MMP3 expression through 5hmC gain in MMP3 promoter via regulation of TET1.
TWIST1-miR (show MLXIP Proteins)-214 pathway in the control of migration and invasion of lung adenocarcinoma.
the SDF1 (show CXCL12 Proteins)/CXCR4 (show CXCR4 Proteins) signaling pathway is involved in Lowintensity pulsed ultrasoundpromoted periodontal ligament stem cell migration.
Findings suggest that cytoplasmic, rather than nuclear expression of Twist1 can be considered as a prognostic marker especially for patients with clear cell renal cell carcinoma (show MOK Proteins).
Chromatin immunoprecipitation (ChIP), quantitative ChIP and dual luciferase activity assays were used to confirm the binding of SOX6 to the promoter region of TWIST1.
we demonstrated a mechanistic cascade of TMPRSS4 (show TMPRSS4 Proteins) up-regulating STAT3 (show STAT3 Proteins) activation and subsequent TWIST1 expression, leading to prostate cancer migration.
In cancer patients, elevated levels of Twist1 are associated with greater degrees of muscle wasting.
Twist, E-cadherin (show CDH1 Proteins), and N-cadherin (show CDH2 Proteins) protein were differently expressed in endometrioid adenocarcinoma tissues and in normal endometrium which indicates their potential function for endometrioid adenocarcinoma development.
Three SNPs were associated with survival: rs2526614 (TWIST1) (genotype CA + AA, adjusted HR=0.58, 95%CI=0.37-0.93), rs6953766 (TWIST1) (genotype GG, crude HR=2.02, 95%CI=1.06-3.82, adjusted HR=2.14, 95%CI=1.07-4.25), and rs431073 (ZEB1) (genotype AC + CC, crude HR=1.62, 95%CI=1.01-2.59, adjusted HR=1.96, 95%CI=1.18-3.25).
Overexpression of Twist1 in mouse muscle progenitor cells, either constitutively during development or inducibly in adult animals, caused severe muscle atrophy with features reminiscent of cachexia.
This study evaluated the role of Twist1 in the expression of other epithelial-mesenchymal transition transcription factors in tumor cells, including tumor progression, intravasation, and metastasis.
The authors demonstrate that Twist1 serine (Ser (show SIGLEC1 Proteins)) 42 phosphorylation is required for endothelial-to-mesenchymal transition through TGF-beta (show TGFB1 Proteins)-Smad (show SMAD1 Proteins) signaling in vitro and in the mouse lung gel implantation system.
Overall, hypoxia-induced activation of Twist/miR (show MLXIP Proteins)-214/E-cadherin (show CDH1 Proteins) axis is involved in the EMT (show ITK Proteins) of TECs, and anti-miR (show MLXIP Proteins)-214 may be an attractive strategy to ameliorate the progression of renal fibrosis.
molecular and cellular processes that regulate dural Cerebral vein development in mammals and describe venous malformations in humans with craniosynostosis and TWIST1 mutations that are recapitulated in mouse models, are reported.
Methyltransferase G9A (show EHMT2 Proteins) Regulates Osteogenesis via Twist Gene Repression in mice.
this study shows that loss of Twist1 in collagen-producing cells leads to increased bleomycin-induced pulmonary fibrosis, which is mediated by increased expression of CXCL12 (show CXCL12 Proteins)
RNF8 (show RNF8 Proteins)-promoted Twist ubiquitination is required for Twist localization to the nucleus for subsequent epithelial-mesenchymal transition and cancer stem cells functions, thereby conferring chemoresistance.
These results indicate that Twist1 Ser42 phosphorylation contributes to the pathogenesis of bleomycin-induced pulmonary fibrosis through angiopoietin-Tie2 (show TEK Proteins) signaling.
the mesenchymal properties of the cranial mesoderm are likely to be regulated by a network of TWIST1 targets that influences the extracellular matrix and cell-matrix interactions, and collectively they are required for the morphogenesis of the craniofacial structures.
the ventral migration of Cranial neural crest cells (CNCCs) away from a source of Bmps in the dorsal ectoderm promotes ectomesenchyme development by relieving Id2a-dependent repression of Twist1 function.
twist1a and twist1b control skeletal development and dorsoventral patterning by regulating runx2b in zebrafish
These observations are consistent with a role for twist1 in craniofacial, vertebral, and early renal development.
Basic helix-loop-helix (bHLH) transcription factors have been implicated in cell lineage determination and differentiation. The protein encoded by this gene is a bHLH transcription factor and shares similarity with another bHLH transcription factor, Dermo1. The strongest expression of this mRNA is in placental tissue\; in adults, mesodermally derived tissues express this mRNA preferentially. Mutations in this gene have been found in patients with Saethre-Chotzen syndrome.
twist homolog 1
, twist transcription factor
, twist homolog 1 (acrocephalosyndactyly 3; Saethre-Chotzen syndrome)
, hypothetical protein
, twist-like protein
, twist-related protein 1
, twist-related protein
, B-HLH DNA binding protein
, TWIST homolog of drosophila
, class A basic helix-loop-helix protein 38
, charlie chaplin
, polydactyly EMS
, twist gene homolog 1
, twist 1
, twist homolog 1 (Drosophila)