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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 indicate a mechanism in breast cancer cells that tripartite motif-containing 28 (show TRIM28 Proteins) protein (TRIM28 (show TRIM28 Proteins)) enhances metastasis by stabilizing TWIST1, suggesting that targeting TRIM28 (show TRIM28 Proteins) could be an efficacious strategy in breast cancer treatment.
Twist1 and Snail1 (show SNAI1 Proteins) expression levels were associated with lymphovascular space invasion, lymph node metastasis and histological grade in cervical squamous cell carcinoma.
gene TWIST1 showed no significant difference in expression between groups
the inhibition of Twist1 transfected with siRNA could enhance the irinotecan sensitivity in LoVo/CPT (show CHPT1 Proteins)-11R cells and downregulate the expression of vimentin (show VIM Proteins) and CD44 (show CD44 Proteins). Our data provide evidence that EMT (show ITK Proteins) and CSC-like phenotype induced by Twist1 contribute to acquire resistance to irinotecan and enhanced migration and invasion in colon cancer
TWIST1, in part via GAS6 (show GAS6 Proteins) and L1CAM (show L1CAM Proteins), led to higher expression and activation of Akt (show AKT1 Proteins) upon cisplatin treatment, and inhibition of Akt (show AKT1 Proteins) activation sensitized cells to cisplatin.
High Twist-1 expression, aberrant E-cadherin (show CDH1 Proteins) and high EZH2 (show EZH2 Proteins) expression in primary prostate cancer are considered as adverse prognostic markers of an aggressive tumor with high metastatic potential.
ADAM12 (show ADAM12 Proteins) is induced by Twist1 and plays a crucial role in tumor invasion and metastasis by regulating both invadopodia and focal adhesions
Taken together, these findings demonstrated that Twist was upregulated in high invasion and metastasis cell lines as well as invasive ductal carcinoma (IDC (show LMNA Proteins)) tissues companioned with downregulated expression of E-cadherin (show CDH1 Proteins) and ER, which provides important clues for the deeper study of breast cancer
The mechanism study revealed that ASLNC02525, as an RNA sponge, broke the negative regulation of twist1 by hsa (show CD24 Proteins)-miRNA-489-3p, and once ASLNC02525 was silenced, the highly expressed hsa (show CD24 Proteins)-miRNA489-3p regained its regulation on twist1 and inhibited the proliferation and invasion.
the results from the present study indicate that BaP (show PHB2 Proteins) enhances the epithelial-mesenchymal transition-associated migration of lung adenocarcinoma A549 cells by upregulating Twist1.
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.
TWIST1 expression promotes developmental angiogenesis by inducing endothelial cell proliferation and migration.
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)