Twist1 is a basic helix-loop-helix domain-containing transcription factor. It forms homo- or hetero-dimers in order to bind the Nde1 E-box element and activate or repress its target genes. During development, Twist1 is essential for mesoderm specification and differentiation TWIST1 (Twist Family BHLH Transcription Factor 1) is a Protein Coding gene. Diseases associated with TWIST1 include Saethre-Chotzen Syndrome and Craniosynostosis 1.Among its related pathways are Adipogenesis and Notch-mediated HES/HEY network.Gene Ontology (GO) annotations related to this gene include DNA-binding transcription factor activity and protein heterodimerization activity
The protein encoded by this gene is a bHLH transcription factor and shares similarity with another bHLH transcription factor, Dermo1 (a.k.a. TWIST2). The strongest expression of this mRNA is in placental tissue; in adults, mesodermally derived tissues express this mRNA preferentially. Twist1 is thought to regulate osteogenic lineage TWIST1 and NY-ESO1 overexpression was significantly associated with stage of progression and size of tumors, respectively. A direct association between TWIST1 and NY-ESO1 mRNA expression was confirmed by induced ectopic expression of TWIST1 in ESCC cell lines KYSE-30 and YM-1. TWIST1-induced cells led to increase migration in ESCC cell line Twist1, through its carboxyl-terminal Twist-box, binds to the Sox9 high mobility group DNA-binding domain, inhibiting Sox9 transactivation potential. In chondrocyte precursor cells, Twist1, in a Twist-box-dependent manner, inhibits Sox9-dependent activation of chondrocyte marker gene expression by blocking Sox9-enhancer DNA association Bialek et al. (2004) determined that the Twist proteins transiently inhibit Runx2 (600211) function during skeletal development in mice. Twist1 and Twist2 were expressed in Runx2-expressing cells throughout the skeleton early during development, and osteoblast-specific gene expression occurred only after their expression decreased
TWIST1 function in vertebrates governs early mesodermal patterning and osteogenesis (5). Individuals with germ-line haploinsufficiency of the TWIST1 gene suffer from the hereditary disorder Saethre-Chotzen syndrome (acrocephakosyndactyly type III) characterized by premature craniosynostosis and limb, head, and face anomalies (6) Thus Twist1 and Etv genes might function in the same genetic pathway. To test this, we crossed Twist1 CC/+ mice with Etv4 and Etv5 null mutant mice ( Livet et al., 2002 , Lu et al., 2009 ) to progressively reduce Etv gene dosage, as Etv4 and Etv5 have overlapping functions ( Lu et al., 2009 , Mao et al., 2009 , Zhang et al., 2009 ) One-stop service from gene synthesis and vector construction to protein expression and purification. Multiple protein expression systems: bacterial, yeast, baculovirus-insect and mammalian expression system. Multiple purification systems (30+) to choose. High R & D ability with over 1000 new proteins per year and quick problem-solving ability According to the gene expression profile, the top functions enriched in TPC-Twist1 cells were cellular movement, cellular growth and proliferation, and cell death and survival. Silencing of the top 10 upregulated genes reduced viability of TPC-Twist1 and of CAL62 cells. Silencing of COL1A1, KRT7, and PDZK1 also induced cell death
Twist-1 is upregulated by NSD2 and contributes to tumour dissemination and an epithelial-mesenchymal transition-like gene expression signature in t (4;14)-positive multiple myeloma. TWIST1 expression and clinical significance in type I endometrial cancer and premalignant lesions: A retrospective clinical study TWIST1 transcriptionally regulates several glycolytic genes in pancreatic cancer. TWIST1 is highly expressed in pancreatic cancer tissue and predicts a poor prognosis. AGR2 is required for Twist1-induced proliferation, migration, and invasion of breast cancer cells Background. The bHLH transcription factor TWIST1 plays a key role in the embryonic development and in tumorigenesis. Some loss-of-function mutations of the TWIST1 gene have been shown to cause an autosomal dominant craniosynostosis, known as the Saethre-Chotzen syndrome (SCS). Although the functional impacts of many TWIST1 mutations have been experimentally reported, little is known on the.
In humans, Twist1 malfunction was first linked to Saethre-Chotzen syndrome and later identified to play an essential role in tumor initiation, stemness, angiogenesis, invasion, metastasis, and chemo-resistance in a variety of carcinomas, sarcomas, and hematological malignances The effects of TW loss of function (gene editing and knockdown) on inhibition of tumorigenicity of U87MG and GBM4 glioma stem cells were tested in orthotopic xenograft models and conditional knockdown in established flank xenograft tumors. TWIST1 regulates genes associated with ECM and PI3K signaling. (A) Heat map of GO categories of TW. Twist1, a basic helix-loop-helix transcription factor that regulates a number of genes involved in epithelial-to-mesenchymal transition (EMT), is upregulated in prostate cancer. Androgen regulation of Twist1 has been reported in a previous study Here, we identify transcription factor TWIST1 as a novel regulator of HSC maintenance through modulation of mitochondrial function. We demonstrate that Twist1 deletion results in significantly decreased lymphoid-biased HSC frequency, markedly reduced HSC dormancy and self-renewal capacity, and skewed myeloid differentiation in steady-state. In the present study, we showed a new function in the N-terminal of the TWIST1 protein. In conclusion, our study suggests that TWIST1 is involved in the etiology of VSD in the Chinese population. To the best of our knowledge, our study is the first to attempt to identify potential pathogenic mutations in the TWIST1 gene in patients with VSD
Previously, Twist1 was shown to transiently inhibit Runx2 function during early osteoblast differentiation by direct interaction with the Runx2 DNA-binding domain, thus precluding its sequence-specific association of with cognate binding sites in osteogenic target genes . During the double-positive phase of maturation in the thymus, all thymocytes destined to become single CD4 + or CD8 + circulating T lymphocytes express the CD4 promoter Replication of gene expression and DNA methylation in a second cohort identified TWIST1 gene expression, DNA methylation and protein expression as a cell marker of airway and parenchymal lung fibroblasts, with DNA methylation having 100% predictive discriminatory power
To further define TWIST1 functions in GBM we tested the impact of TWIST1 over-expression on invasion in vivo and its impact on gene expression. We found that TWIST1 significantly increased SNB19 and T98G cell line invasion in orthotopic xenotransplants and increased expression of genes in functional categories associated with adhesion. TWIST1 (TW) is a bHLH transcription factor (TF) and master regulator of the epithelial-to-mesenchymal transition (EMT). In vitro, TW promotes mesenchymal change, invasion, and self-renewal in glioblastoma (GBM) cells. However, the potential therapeutic relevance of TW has not been established through loss-of-function studies in human GBM cell. Gene ontology analysis of the genes associated with Twist1 binding regions in ECCs, limb buds, and PNST cells. A, B, C.ToppGene was utilized to perform GO analysis of the genes associated with Twist1 ChIP-seq peaks that are within 50 Kb of a transcriptional start site (TSS) of expressed genes in E12.5 ECCs (2191 genes), E10.5 limb buds (1622 genes), or PNST cells (110 genes) Twist1 and twist2 are well-conserved basic helix-loop-helix transcription factors (1,2).They dimerize with other basic helix-loop-helix proteins and bind to E-boxes in the promoter regions of their target genes ().The human twist proteins are highly homologous, although twist2 (previously Dermo1) is shorter than twist1 due to an NH 2-terminal truncation Twist1 Twist-related protein 1 (TWIST1) also known as class A basic helix-loop-helix protein 38 (bHLHa38) is a basic helix-loop-helix transcription factor that in humans is encoded by the TWIST1 gene. Twist1 is A master regulator of the epithelial to mesenchymal transition (EMT)
To further evaluate the TWIST1-mediated transcriptional regulation of KDR and SFRP4 during the transdifferentiation process, we used the gain- and loss-of-function approach by overexpression and/or silencing of TWIST1 gene that was confirmed by immunoblotting the expression of the tags Flag or GFP, KDR, SFRP4, and TWIST1 in transfected WJ-MSC. The transcription factor TWIST1 plays an important role in the epithelial-mesenchymal transition (EMT) process and in the migration, invasion and metastasis of cancer cells. OCT4, which is a homeobox transcription factor, has an important role in the self-renewal potential of cancer cells. Our aim here is to elucidate impact of ectopic expression of TWIST1 on OCT4 gene expression in. Plasmids and reagents. For MTDH knockdown, the sense and antisense shRNA oligonucleotides were annealed and cloned into the BglII and HindIII site of pSUPER.retro.puro (OligoEngine) as previously described ().The same method was used for TWIST1 and CBP knockdown. For MTDH overexpression, the human MTDH gene was cloned into the pcDNA3.1 vector with BamHI and EcoRI digestion
The expression and function of TWIST1 was studied in EC in both developing vasculature and during the initiation of atherosclerosis. In zebrafish, twist was expressed in early embryonic vasculature where it promoted angiogenesis by inducing EC proliferation and migration. In adult porcine and murine arteries, TWIST1 was expressed preferentially. Objectives TWIST1 is a member of the class B of basic helix-loop-helix transcription factors that regulates cell lineage determination and differentiation and has been implicated in epithelial-to-mesenchymal transition. Here, we aimed to investigate the role of TWIST1 for the activation of resident fibroblasts in systemic sclerosis (SSc). Methods The expression of Twist1 in fibroblasts was. TWIST1 functions as a negative regulator of epithelial gene expression and a positive regulator of mesenchymal gene expression, leading to induction of the EMT (15,27). In this study, TWIST1 was found to be upregulated in two LAD cell lines after hypoxic induction
TWIST1 prosurvival and proinvasive functions are also mediated by the transcriptional up-regulation of AKT2 (Cheng et al., 2007). Moreover, there is a correlation between Wnt signalling and TWIST1 (Howe et al., 2003), which were included in a poor prognosis gene signature during metastasis to lung (DiMeo et al., 2009) They also described three patients with confirmed de novo TWIST1 entire gene deletion but only one of those patients with an exclusively TWIST1 deletion with other genes as FERD3L or HDAC9. The authors also described several families with TWIST1 mutations and Saethre?Chotzen syndrome to mild nonsyndromic phenotypes. Therefore, the authors wrote. Addgene Alerts. Receive email alerts when new plasmids with this gene become available. Log in to subscribe to Addgene Alerts. Description twist basic helix-loop-helix transcription factor 1. Also known as M-Twi, M-Twist, Pde, Pluri, Ska, Ska10, Ska<m10J, Ska<m10Jus>, Twist, bHLHa, bHLHa38, pd, pdt. Species Mus musculus Tissue i. The Tissue Atlas contains information regarding the expression profiles of human genes both on the mRNA and protein level. The protein expression data from 44 normal human tissue types is derived from antibody-based protein profiling using immunohistochemistry. The green piechart indicates the level of reliability of the analyzed.
Sequencing of the TWIST1 gene identified a c.148_157dup (p.A56RfsX87) frame-shift mutation predicted to completely inactivate this gene. Genotyping 17 scurred and 20 horned founders of our pedigree as well as 48 unrelated horned controls revealed a perfect association between this mutation and the type 2 scurs phenotype JPX and Twist1 were coordinately upregulated in lung cancer tissues and cells. Since studies have shown that miR-33a-5p negatively regulates its target gene, Twist1 [16, 25], we aimed to further investigate the relationship between JPX and Twist1 in lung cancer. Twist1 expression was verified in 95 pairs of lung cancer tissues and adjacent tissues Structure-Function Studies of the bHLH Phosphorylation Domain of TWIST1 in Prostate Cancer Cells. Rajendra P. Gajula, Sivarajan T. Chettiar, Russell D. Williams, Katriana Nugent, Yoshinori Kato,.
mechanism of Twist1 gene activity on cell invasion and metastasis of gastric carcinoma remain enigmatic. MicroRNAs (miRNAs) are important regulators and function as oncogenes or tumor suppressors by targeting the 3' untranslated region (UTR) of messenger RNA (mRNA) to induce mRNA degradation and suppression of translation[25, 26] Twist1 : twist homolog 1 (Drosophila) Twist1 : twist gene homolog 1 (Drosophila) Nomenclature updated to reflect human and mouse nomenclature: 1299863: APPROVED: 2005-01-20: Twist1 : twist gene homolog 1 (Drosophila) Twist : twist gene homolog, (Drosophila) Symbol and Name updated: 1299863: APPROVED: 2002-08-07: Twist : twist gene homolog. Languages. Български; Қазақ; Hrvatski; Slovák; Српски; عرب; Bahasa Indonesi Twist1, a highly conserved, basic helix‐loop‐helix transcription factor mapped at 7q21.2, has a bifunctional role, acting as an activator or a repressor, depending on post‐translational modifications and physiologic contexts. 29, 30 Twist1 induces gene transactivation through cis‐binding to E‐box regulatory regions, which are present. The bHLH transcription factor TWIST1 plays a key role in the embryonic development and in tumorigenesis. Some loss-of-function mutations of the TWIST1 gene have been shown to cause an autosomal dominant craniosynostosis, known as the Saethre-Chotzen syndrome (SCS). Although the functional impacts of many TWIST1 mutations have been experimentally reported, little is known on the molecular.
TWIST1 is a highly conserved bHLH class transcription factor with multiple functions. a TWIST1 functions in normal development and in small populations of adult stem cells, where it assists in wound healing. When reactivated in cancers, TWIST1 activates a transcriptional and protein binding program giving rise to EMT, and thus to metastases 19 TWIST1 is a master transcriptional regulator of the epithelial to mesenchymal transition (EMT) 20 and a high level of TWIST1 is a prognostic marker indicative of poor cancer outcomes. We 21 demonstrate that TWIST1 target genes are also downregulated in E2 positive N/Tert-1 cells Mutations affecting the b-HLH domain of the TWIST1 gene have been associated with Saethre-Chotzen syndrome, an autosomal dominant craniosynostosis disorder causing craniofacial and limb abnormalities (4,5). TWIST1 is upregulated in various human tumors and may play a role in EMT (epithelial-mesenchymal transition) and metastasis (6,7) Together these analyses identify multiple new genes involved in cell proliferation and migration that are differentially expressed in the developing heart valves, are responsive to Twist1 transcriptional function, and contain Twist1 responsive regulatory sequences View Twist1<tm2Bhr> allele: origin, molecular description, gene associations, and references
Results: To further define TWIST1 functions in GBM we tested the impact of TWIST1 over-expression on invasion in vivo and its impact on gene expression. We found that TWIST1 significantly increased SNB19 and T98G cell line invasion in orthotopic xenotransplants and increased expression of genes in functional categories associated with adhesion. expression of TWIST1, one of the master regulators of tumor metastasis. Conclusions: This study first indicates that miR-876-5p functions as a suppressor in regulating of GBM EMT by targeting TWSIT1, and it promise as a therapeu - tic target and prognostic marker for metastatic GBM. Keywords: miR-876-5p, glioma, invasion, TWIST1 Introductio behavior . TWIST1 is a basic helix-loop-helix (bHLH) multidomain transcription factor that binds to E-box- and D-box-regulated target genes resulting in the elaboration of an EMT transcriptional program [4-9].TWIST1functionsasadimer,eitherasahomodimer,TWIST1-TWIST1 (T-T), or as a heterodimer with E2A proteins (E12/E47)
Because TWIST1 mRNA expression levels were commonly and negatively correlated with FOXF2 expression in the basal-like breast cell lines (Figure 4A, B and C), we investigated whether TWIST1 is a transcriptional target of FOXF2. First, we performed a BLAST search for FOXF2 binding sites in the promoter region of the TWIST1 gene Benzo(a)pyrene (BaP), an important toxic component of cigarette smoke, can cause lung cancer and lead to the progression of lung cancer. In the present study, we investigated the effect of BaP on the migration of lung adenocarcinoma A549 cells. BaP (1 µM) promoted the migration of A549 cells in a time-dependent manner and upregulated the expression of the Twist family BHLH transcription.
Following these experiments, expression of several important genes in hepatic and fibroblast function were monitored. Results show that, of the 7 fibroblast specific genes tested, Twist1 overexpression activated two genes, Prrx1 and Sema3a, in Fg14 hepatoma cells. However, the remaining 5 fibroblast genes were not affected A focus of our research program is the Saethre-Chotzen Syndrome, a disorder of development of the skull, face and limbs which is associated with mutations of the human TWIST1 gene. The research project is designed to investigate, in the laboratory mouse, the function of the Twist1 gene in a specific population of cells that participate in. The FGFR3 gene provides instructions for making a protein called fibroblast growth factor receptor 3. This protein is part of a family of four fibroblast growth factor receptors that share similar structures and functions. These proteins play a role in several important cellular processes, including regulation of cell growth and division (proliferation), determination of cell type, formation. RNA-Based TWIST1 Inhibition via Dendrimer Complex to Reduce Breast Cancer Cell Metastasis. James Finlay,1,2,3 Cai M. Roberts,1,2 Gina Lowe,1 Joana Loeza,4 John J. Rossi,2 and Carlotta A. Glackin 1. 1Department of Neurosciences, City of Hope Beckman Research Institute, 1500 East Duarte Road, Duarte, CA 91010, USA with increased IL-4 . From gene profiling studies, a unique gene expression phenotype of SS has been uncovered . Gene expression changes in SS, such as decreased expression of IFN-γ, and increased ex-pression of unique biomarker genes identified in SS such as TWIST1,andTOX are frequent and represent important features of CTCL [13-15]
Here, Twist1 deletion rescued the inhibition of bone formation by constitutive β-catenin activation . In addition to Twist1, Twist2 also contributes to repression of chondrocytic gene expression in the skull, which is consistent with previous reports that Twist family members can have overlapping functions (Sosic et al., 2003) Reconstitution of p62 in p62 KO cells restored Twist1 abundance (Fig. 3D). p62 addition increased Twist1 protein stability in 293T cells (Fig. 3E), whereas it had no effect on the stability of Twist2 (Fig. S2A), another member of the Twist subfamily of bHLH proteins regulating gene expression in development and cancer . These findings. A synthesized peptide derived from human Twist1, corresponding to a region within N-terminal amino acids. Uniprot: >>Visit The Human Protein Atlas. Gene ID: Gene Name: TWIST1. Molecular Weight: Observed Mol.Wt.: 29kD. Predicted Mol.Wt.: 21kDa(Calculated).. Subcellular Location: Nucleus. Tissue Specificity: Q15672 TWST1_HUMAN: Subset of. For more info on TWIST1, check out the TWIST1 Infographic We have 30,000+ of these available, one for each gene! check them out. In this infographic you will see the following information for TWIST1: database IDs, super-family, protein function, synonyms, molecular weight, chromosomal locations, tissues of expression, subcellular locations, post translational modifications, and related.
TWIST1, a basic helix-loop-helix protein which acts as a transcriptional regulator, plays a central role in differentiation of mesodermal during embryogenesis. It is also implicated in tumorigenesis, invasion and metastasis. TWIST1 forms both homodimers (45KD) and heterodimers with E2A E proteins, and dimer partner selection is a critical.