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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.
our study revealed a novel mechanism of the RBMS3/Twsit1/MMP2 axis in the regulation of invasion and metastasis of breast cancer
These studies provide direct experimental evidence supporting protumorigenic role of TWIST1 independent of invasion in vivo and the therapeutic relevance of targeting TWIST1 in human glioblastoma.
MiR-223 and miR-19a were found to regulate the expression of TWIST and Runx2, influence the RANKL-RANK pathway and the expression of MCP-1, and finally regulate the pathophysiological process of osteolytic bone destruction.
the regional hypomethylation of Twist gene promoter in ovarian ectopic endometrium and eutopic endometrium may cause over-expression of Twist protein, which may directly lead to the pathogenesis of endometriosis.
Ecadherin expression levels were regulated by the manifold, and UPF1, a potential tumor suppressor, may promote the EMT process in Huh7 HCC cells. The findings of the present study suggested that UPF1 expression levels affected the EMT process by targeting Ecadherin, Ncadherin, Vimentin and Twist.
Investigated twist family bHLH transcription factor 1 (Twist), snail family transcriptional repressor 1 (Snail) and E-cadherin in prognosis, recurrence-free survival and overall survival in completely resected N0 NSCLC patients. Found high expression of Twist and Snail and low expression of E-cadherin were associated with unfavourable prognosis.
High twist1 expression correlates with elevated ROR1 level and poor survival in breast cancer.
Tip60 mediates acetylation at Lys residues 73 and 76 of TWIST1, which are required for SPZ1-TWIST1 complex formation and cancer cell migration in vitro and in vivo. Ectopic SPZ1 and TWIST1 expression, but notTWIST1 alone, enhanced VEGF expression via BRD4, enhancing RNA-Pol II-dependent transcription and inducing metastasis. Acetylation in the SPZ1-TWIST1-BRD4 axis functions in the mediation of EMT and its regulation.
These new findings suggest an oncogenic role for concomitant expression of MAML1 and TWIST1 genes in head and neck squamous cell carcinoma invasion and metastasis
Twist1silencing or overexpression combined with ChR treatment did not affect NF-kappaBp65 levels, but also reduced or enhanced EMT and CSLC properties. Importantly, overexpressing Twist1 combined with ChR reversed the effects of NF-kappaBp65 knockdown and ChR.
C-Myc transcriptionally enhances MTDH (metadherin) expression and subsequently activates Twist1 expression to induce EMT.
Rap1b increased Twist 1 expression by targeting its promoter activity to induce proliferation and migration of hepatocellular carcinoma cells.
ilencing endogenous Ets1 by siRNA in mouse cell lines decreases Twist1 mRNA levels, decreases invasion, and increases cell growth. Ets1 and Twist1 are at the crossroad of several signaling pathways in cancer. Understanding their regulation may inform the development of therapies to impair lung tumor metastasis.
Twist-related protein 1 (TWIST1) was a target of miR-490-3p and participated in long non-coding RNA TP73 antisense RNA 1 (TP73-AS1)/miR-490-3p-modulated MDA-MB-231cell vasculogenic mimicry (VM) formation.
This study demonstrated that protease-activated receptor-1 (PAR1) can increase the expression of endothelial markers and enhance VM formation by upregulating Twist1 both in vitro and in vivo through thrombin binding.
The Epithelial-to-Mesenchymal Transition inducing factor TWIST1 drives expression of discoidin domain receptor 2 (DDR2), a receptor tyrosine kinase (RTK) that recognizes fibrillar collagen as ligand.
The upregulation of Twist is involved in Gli1 induced migration and invasion of hepatocellular carcinoma (HCC) cells.
MiR-495 inhibited proliferation and metastasis and promoted apoptosis by targeting Twist1 in GC cells.
These studies establish TWIST1 as a driver of resistance to EGFR TKIs and provide rationale for use of TWIST1 inhibitors or BCL2 inhibitors as means to overcome EMT-mediated resistance to EGFR TKIs.
These results suggest that Twist1 is an important upstream mediator of mutant Htt-induced neuronal death and may in part operate through epigenetic mechanisms.
we suggest that altered mandibular development may also contribute risk for cleft palate in TWIST1- and IRF6-related disorders.
Mouse genetics further reveal requirements for Twist1 and Tcf12 in both the frontal and parietal bones for suture patency, and to maintain putative progenitors in the coronal region
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) 42 phosphorylation is required for endothelial-to-mesenchymal transition through TGF-beta-Smad signaling in vitro and in the mouse lung gel implantation system.
Overall, hypoxia-induced activation of Twist/miR-214/E-cadherin axis is involved in the EMT of TECs, and anti-miR-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 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
RNF8-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 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 in 3T3-L1 mature adipocytes. This regulatory link enhanced the regulation of PPARgamma 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.
findings demonstrate that Twist-1, which maintains BMSC at an immature state, endows them with an increased capacity for supporting hematopoiesis via direct activation of CXCL12 gene expression.
Twist1, a target of canonical Wnt/beta-catenin signaling, also functions to maintain Wnt responsiveness and is a key effector for cranial bone fate selection and dermal condensation.
Findings indicate that Twist1 has a novel role in epithelial carcinogenesis by regulating proliferation of keratinocytes, including keratinocyte stem cells during tumor promotion.
Data show that administration of MVA-TWIST/TRICOM vaccine induces Twist transcription factor-specific T-cell responses.
we show that combinatorial loss of TCF12 and TWIST1 homologs in zebrafish also results in specific loss of the coronal suture
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)