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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.
Inactivation of VHL gene direct angiogenesis in vascular endothelial cells, not vasculogenesis via Twist1 accumulation, was associated with hemangioblastoma neovascularization.
High TWIST1 expression is associated with Bladder Urothelial Carcinoma.
A significant correlation between mRNA levels of Twist1, fibronectin and vimentin was evident. Although their expression was inversely proportional, no association was observed between Twist1 and E-cadherin expression
miR-539 inhibited the EMT of TE3 cells by downregulating TWIST1, and TWIST1 was a target of miR-539.
Study demonstrated that TWIST protein expression was elevated in liver cancer tissue specimens and was positively correlated with MDR1 expression. Knockdown of TWIST increased the sensitivity of RHepG2 cells to antineoplastic agents through a reduction in MDR1 expression and drug efflux ability.
we demonstrate that HMGA2 is correlated with GC VM formation and that positivity for both HMGA2 and VM predicts a worse clinical outcome for GC patients. HMGA2 can directly target Twist1 and promote the expression of Twist1 and VE-cadherin.
Study provides evidence that genetic variants in SNAI1 and TWIST1 are associated with breast cancer (BC) and ovarian cancer (OC) susceptibility and suggests a synergistic effect of those related loci on BC/OC risk.
These results suggested that EPN3 enhances the migration and invasion of glioblastoma cells by activating the transcription factors Slug, Twist and ZEB1, but not Snail 1 or ZEB2, to induce EMT in glioma cells; EPN3 involvement in the Notch and WNT/betacatenin signaling pathways may contribute to this process.
As potential molecular markers for bladder carcinoma, both TWIST1 and LASS2 transcripts seem to play role during the tumorigenesis and development of bladder cancer.
Authors found that swainsonine inhibits cell invasion and EMT in the esophageal carcinoma cells by downregulation of Twist1 and deactivation of the PI3K/AKT signaling pathway.
The administration of si-Twist1 cancelled the effect of miR-203 inhibitor on cell proliferation, apoptosis, invasion, and migration. These demonstrated that miR-203 may function as a tumor-suppressive microRNA in BCa by negatively targeting Twist1.
Expression levels of MACC1, CD44, Twist1, and KiSS-1 are related to duration of overall survival among patients with colonic adenocarcinoma.
Data identified Twist1 and CD44 as novel REST targeted genes and provide new insight into the epigenetic regulation of Twist1 and CD44 by REST.
TWIST1 promotes catabolic reactions by inducing MMP3 expression through 5hmC gain in MMP3 promoter via regulation of TET1.
The results support the role of TWIST in carcinogenesis, development of oral squamous cell carcinoma, and its metastasis to lymph nodes.
TWIST1-miR-214 pathway in the control of migration and invasion of lung adenocarcinoma.
the SDF1/CXCR4 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.
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 up-regulating STAT3 activation and subsequent TWIST1 expression, leading to prostate cancer migration.
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.
TLR4 signaling via NANOG cooperates with STAT3 to activate Twist1 and promote formation of tumor-initiating stem-like cells in livers of mice.
studies suggested that the Twist1 transcription in GC cells might be regulated through potential cooperation of DNA methylation, histone modification in complex with Sp1 binding to CpG-rich regions within the exon 1 region
Study shows that Twist1 plays a pivotal role in the TNF mediated suppression of E-box dependent transactivation of Period genes and Dbp. Thereby Twist1 may provide a link between the immune system and the circadian timing system.
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)