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Twist homolog 2

Twist2, Dermo-1
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, Twist. It is thought that during osteoblast development this protein may inhibit osteoblast maturation and maintain cells in a preosteoblast phenotype. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: PDE, E-cadherin, HAD, CAN, V1a
Papers on Twist2
3-Deazaneplanocin A suppresses aggressive phenotype-related gene expression in an oral squamous cell carcinoma cell line.
Yamazaki et al., Fukuoka, Japan. In Biochem Biophys Res Commun, Jan 2016
Finally, quantitative RT-PCR analysis demonstrated that genes involved in the aggressive phenotypes (TWIST2, EGFR, ACTA2, TGFB1, WNT5B, and APLIN) were down-regulated, whereas epithelial phenotype genes (CDH1, CLDN4, IVL, and TGM1) were up-regulated in SAS cells treated with DZNep.
Contribution of Underlying Connective Tissue Cells to Taste Buds in Mouse Tongue and Soft Palate.
Liu et al., Ann Arbor, United States. In Plos One, Dec 2015
Three independent mouse models were used for fate mapping of NC and NC derived connective tissue cells: (1) P0-Cre/R26-tdTomato (RFP) to label NC, NC derived Schwann cells and derivatives; (2) Dermo1-Cre/RFP to label mesenchymal cells and derivatives; and (3) Vimentin-CreER/mGFP to label Vimentin-expressing CT cells and derivatives upon tamoxifen treatment.
ALK inhibitor resistance in ALK(F1174L)-driven neuroblastoma is associated with AXL activation and induction of EMT.
George et al., Boston, United States. In Oncogene, Dec 2015
Although ectopic expression of AXL and TWIST2 individually in TAE684-sensitive parental cells led to the elevated expression of mesenchymal markers and invasive capacity, only AXL overexpression induced resistance to TAE684 as well.
Setleis syndrome due to inheritance of the 1p36.22p36.21 duplication: evidence for lack of penetrance.
Desnick et al., New York City, United States. In J Hum Genet, Nov 2015
The syndrome results from recessive mutations in the TWIST2 gene, encoding a basic helix-loop-helix transcription factor or de novo genomic duplication or triplication, which include 1.3 Mb at 1p36.22p36.21,
Mesenchymal fibroblast growth factor receptor signaling regulates palatal shelf elevation during secondary palate formation.
Ornitz et al., Saint Louis, United States. In Dev Dyn, Nov 2015
Here, we studied the role of mesenchymal fibroblast growth factor receptor (FGFR) signaling during palate development by conditional inactivation of Fgfrs using a mesenchyme-specific Dermo1-Cre driver.
Wntless spatially regulates bone development through β-catenin-dependent and independent mechanisms.
Williams et al., Grand Rapids, United States. In Dev Dyn, Oct 2015
RESULTS: In this study, we systemically evaluated how deletion of Wntless in different stages of osteochondral differentiation affected embryonic bone development, by crossing Wntless (Wls)-flox/flox mice with strains expressing cre recombinase behind the following promoters: Osteocalcin, Collagen 2a1, or Dermo1.
Detection of a Distinctive Genomic Signature in Rhabdoid Glioblastoma, A Rare Disease Entity Identified by Whole Exome Sequencing and Whole Transcriptome Sequencing.
Lee et al., Seoul, South Korea. In Transl Oncol, Aug 2015
Fusion gene analysis showed 14 candidate genes that may be functionally involved in R-GBM, including TWIST2, and UPK3BL.
Roles of dopamine receptors and their antagonist thioridazine in hepatoma metastasis.
Li et al., Shanghai, China. In Onco Targets Ther, 2014
It also inhibited cell migration via suppression of epithelial-mesenchymal transition (EMT)-related genes such as twist2 and E-cadherin.
Role of microRNA in epithelial to mesenchymal transition and metastasis and clinical perspectives.
Cano et al., Madrid, Spain. In Cancer Manag Res, 2013
The EMT triggering leads to the activation of a core of transcription factors (EMT-TFs) - SNAIL1/SNAIL2, bHLH (E47, E2-2, and TWIST1/TWIST2), and ZEB1/ZEB2 - that act as E-cadherin repressors and, ultimately, coordinate EMT.
The Hand2 gene dosage effect in developmental defects and human congenital disorders.
Shiroishi et al., Tsukuba, Japan. In Curr Top Dev Biol, 2013
Mutations of the TWIST1 and TWIST2 genes are involved in human diseases.
Coexpression of hypoxia-inducible factor-2α, TWIST2, and SIP1 may correlate with invasion and metastasis of salivary adenoid cystic carcinoma.
Liang et al., Chengdu, China. In J Oral Pathol Med, 2012
Elevated expression of TWIST2 can contribute to invasion and metastasis of adenoid cystic carcinoma (ACC), and there might be some correlation between the hypoxia microenvironment and epithelial-mesenchymal transition in ACC.
Epigenetic inactivation of TWIST2 in acute lymphoblastic leukemia modulates proliferation, cell survival and chemosensitivity.
Strathdee et al., Newcastle upon Tyne, United Kingdom. In Haematologica, 2012
This study suggests a dual role for epigenetic inactivation of TWIST2 in acute lymphoblastic leukemia, initially through altering cell growth and survival properties and subsequently by increasing resistance to chemotherapy.
Correlation of TWIST2 up-regulation and epithelial-mesenchymal transition during tumorigenesis and progression of cervical carcinoma.
Wang et al., Wuhan, China. In Gynecol Oncol, 2012
TWIST2 overexpression was linked to cervix cancer progression, which makes it a promising marker for determining the metastatic potential.
Overexpression of TWIST2 correlates with poor prognosis in head and neck squamous cell carcinomas.
Maestro et al., Italy. In Oncotarget, 2011
upregulation of TWIST2, correlated with poor differentiation grade and shorter survival and identifies a subset of node-positive oral cavity/pharynx cancer patients with very poor prognosis
Setleis syndrome in Mexican-Nahua sibs due to a homozygous TWIST2 frameshift mutation and partial expression in heterozygotes: review of the focal facial dermal dysplasias and subtype reclassification.
Desnick et al., Mexico. In J Med Genet, 2011
Mexican-Nahua sibs with facial and ophthalmologic features of FFDD type III were evaluated. Genomic DNAs were isolated for sequencing of the TWIST2 gene. The affected sibs were homozygous for a novel TWIST2 frameshift mutation, c.168delC (p.S57AfsX45).
Hedgehog target genes: mechanisms of carcinogenesis induced by aberrant hedgehog signaling activation.
Katoh et al., Japan. In Curr Mol Med, 2009
Hedgehog signals upregulate BCL2 and CFLAR to promote cellular survival, SNAI1 (Snail), SNAI2 (Slug), ZEB1, ZEB2 (SIP1), TWIST2, and FOXC2 to promote epithelial-to-mesenchymal transition, and PTHLH (PTHrP) to promote osteolytic bone metastasis.
Hedgehog signaling, epithelial-to-mesenchymal transition and miRNA (review).
Katoh et al., Japan. In Int J Mol Med, 2008
SNAI1 (Snail), SNAI2 (Slug), SNAI3, ZEB1, ZEB2 (SIP1), KLF8, TWIST1, and TWIST2 are EMT regulators repressing CDH1 gene encoding E-cadherin.
Focal preauricular dermal dysplasia: distinctive congenital lesions with a bilateral and symmetric distribution.
Tallerås et al., Oslo, Norway. In Eur J Med Genet, 2006
No mutations in the TWIST2 gene were found in DNA extracted from peripheral leukocytes in the two children who were investigated.
TWIST2 demonstrates differential methylation in immunoglobulin variable heavy chain mutated and unmutated chronic lymphocytic leukemia.
Plass et al., Columbus, United States. In J Clin Oncol, 2005
Epigenetic silencing of TWIST2 in mutated Ig V(H)is associated with chronic lymphocytic leukemia
Twist regulates cytokine gene expression through a negative feedback loop that represses NF-kappaB activity.
Olson et al., Dallas, United States. In Cell, 2003
Mice homozygous for a twist-2 null allele or doubly heterozygous for twist-1 and -2 alleles show elevated expression of proinflammatory cytokines, resulting in perinatal death from cachexia.
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