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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.
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.
miR186 strongly inhibits cell motility, invasive, soft-agar colony formation, 3D culture growth and vasculogenic mimicry (VM) formation capacity, as well as the epithelial-to-mesenchymal transition (EMT (show ITK Proteins)) process by downregulation of its target Twist1.
NF-kappaB (show NFKB1 Proteins) signaling thus appears to play a critical role in promoting both castration resistance and enzalutamide resistance in PKC (show PRRT2 Proteins)/Twist1 signaling in prostate cancer.
miR (show MLXIP Proteins)-186 affects the proliferation, invasion and migration of human gastric cancer (GC) by inhibition of Twist1, and could be a tumor suppressor in GC development. Thus, miR (show MLXIP Proteins)-186 may be served as a candidate prognostic biomarker and target for new therapies in human gastric cancer.
Results have shown that the formation of a TWIST1- RELA (show NFkBP65 Proteins) complex is partially dependent on the well conserved W190, R191, and E193 residues of the TWIST1 WR domain, and that mutations at these positions reduce binding and downstream IL-8 (show IL8 Proteins) promoter activation.
In urothelial bladder carcinoma, TWIST1 expression positively correlated with KLF4 (show KLF4 Proteins). Metastasis-free survival was poorest in those with KLF4 (show KLF4 Proteins)/TWIST1 coexpression. KLF4 (show KLF4 Proteins) knockdown suppressed TWIST1 expression. KLF4 (show KLF4 Proteins) overexpression activated TWIST1 expression and restored EMT (show ITK Proteins) and metastatic phenotype. TWIST1 knockdown abolished KLF4 (show KLF4 Proteins)-faciliated EMT (show ITK Proteins) and metastatic feature without affecting KLF4 (show KLF4 Proteins) expression.
data provide the first evidence that T17M rhodopsin (show RHO Proteins) mutant disrupts C3 secretion via the induction of ROS (show ROS1 Proteins) and the suppression of TWIST1.
C-ROS-1 (show ROS1 Proteins) is involved in Bone marrow-derived mesenchymal stem/stromal cell fate switching between osteogenesis and adipogenesis, mediated via PI3K (show PIK3CA Proteins)/AKT (show AKT1 Proteins)/mTORC1 signalling.
Data show that twist-related protein 1 (Twist1) requires TGF-beta type-I receptor (TGFBR1 (show TGFBR1 Proteins))-activation for activation for epithelial-mesenchymal transition (EMT (show ITK Proteins))-induction.
High Twist1 expression is associated with mesenchymal to epithelial transition of breast cancer.
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.
TWIST1 expression promotes developmental angiogenesis by inducing endothelial cell proliferation and migration.
There was a possible regulatory link between Twist 1 and PPARgamma (show PPARG Proteins) in 3T3-L1 mature adipocytes. This regulatory link enhanced the regulation of PPARgamma (show PPARG Proteins) and may be a functional mechanism of Twist 1 regulation of adipocyte physiology and pathology
ur study revealed the dynamic Twist localization within the early stage of embryo. The results are discussed in terms of potential roles of Twist1 in the processes of lineage segregation, hatching, and implantation in post-compaction embryos and in blastocysts.
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)