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anti-Human TWIST1 Antibodies:
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Human Monoclonal TWIST1 Primary Antibody for ICC, IF - ABIN2668516
Ezponda, Popovic, Shah, Martinez-Garcia, Zheng, Min, Will, Neri, Kelleher, Yu, Licht: The histone methyltransferase MMSET/WHSC1 activates TWIST1 to promote an epithelial-mesenchymal transition and invasive properties of prostate cancer. in Oncogene 2013
Show all 5 Pubmed References
Human Polyclonal TWIST1 Primary Antibody for ELISA, ICC - ABIN6267722
Yang, Lian, Sun, Qi, Ding, Zhang: High nuclear expression of Twist1 in the skeletal extramedullary disease of myeloma patients predicts inferior survival. in Pathology, research and practice 2016
Show all 4 Pubmed References
Human Monoclonal TWIST1 Primary Antibody for IP, RNAi - ABIN563296
Saito, Murata-Kamiya, Hirayama, Ohba, Hatakeyama: Conversion of Helicobacter pylori CagA from senescence inducer to oncogenic driver through polarity-dependent regulation of p21. in The Journal of experimental medicine 2010
Show all 3 Pubmed References
Human Monoclonal TWIST1 Primary Antibody for ELISA, WB - ABIN1098133
Yu, Li, Lu, Tian, Ma, Wang, Xu: Down-regulation of TWIST decreases migration and invasion of laryngeal carcinoma Hep-2 cells by regulating the E-cadherin, N-cadherin expression. in Journal of cancer research and clinical oncology 2011
Show all 2 Pubmed References
Human Polyclonal TWIST1 Primary Antibody for IF, WB - ABIN6149715
Ju, Chen, Deng, Liu, Wang, Wang, Nie, Wang, Ding, Yao, Gui, Li, Xu, Ma, Song, Kvansakul, Zen, Zhang, Luo, Fang, Huang, Allis, Tan, Zeng, Wei, Zhao: NatD promotes lung cancer progression by preventing histone H4 serine phosphorylation to activate Slug expression. in Nature communications 2018
Show all 2 Pubmed References
Human Polyclonal TWIST1 Primary Antibody for IF, WB - ABIN6689284
Du, Fang, Chen, Teng, Xiao, Xie, Jin, Wang: Effect of silencing the T‑Box transcription factor TBX2 in prostate cancer PC3 and LNCaP cells. in Molecular medicine reports 2018
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Human Monoclonal TWIST1 Primary Antibody for IP, ELISA - ABIN521172
Cosset, Hamdan, Jeanpierre, Voeltzel, Sagorny, Hayette, Mahon, Dumontet, Puisieux, Nicolini, Maguer-Satta: Deregulation of TWIST-1 in the CD34+ compartment represents a novel prognostic factor in chronic myeloid leukemia. in Blood 2011
Human Polyclonal TWIST1 Primary Antibody for CyTOF, FACS - ABIN4898987
Satelli, Mitra, Brownlee, Xia, Bellister, Overman, Kopetz, Ellis, Meng, Li: Epithelial-mesenchymal transitioned circulating tumor cells capture for detecting tumor progression. in Clinical cancer research : an official journal of the American Association for Cancer Research 2015
Human Monoclonal TWIST1 Primary Antibody for ICC, FACS - ABIN1724845
Weiss, Abel, Mayberry, Basile, Berger, Aplin: TWIST1 is an ERK1/2 effector that promotes invasion and regulates MMP-1 expression in human melanoma cells. in Cancer research 2012
Human Polyclonal TWIST1 Primary Antibody for IHC (p), IHC - ABIN189738
Jin, Ren, Macarak, Rosenbloom et al.: Pathobiological mechanisms of peritoneal adhesions: The mesenchymal transition of rat peritoneal mesothelial cells induced by TGF-β1 and IL-6 requires activation of Erk1/2 and Smad2 linker region ... in Matrix biology : journal of the International Society for Matrix Biology 2016
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.
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.
The simultaneous expression of TNC and Twist1 was significantly higher in stromal fibroblasts of gastric cancer than in noncancerous tissues.
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.
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)