Key features and details
- Rabbit polyclonal to Twist
- Suitable for: ICC/IF
- Reacts with: Human
- Isotype: IgG
Product nameAnti-Twist antibody
See all Twist primary antibodies
DescriptionRabbit polyclonal to Twist
Tested applicationsSuitable for: ICC/IFmore details
Species reactivityReacts with: Human
Predicted to work with: Mouse, Chicken, Chimpanzee
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Storage instructionsShipped at 4°C. Store at +4°C short term (1-2 weeks). Upon delivery aliquot. Store at -20°C or -80°C. Avoid freeze / thaw cycle.
Storage bufferpH: 7.40
Preservative: 0.097% Sodium azide
Constituent: 0.0268% PBS
Concentration information loading...
PurityImmunogen affinity purified
The Abpromise guarantee
Our Abpromise guarantee covers the use of ab50581 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
Use a concentration of 1 - 2 µg/ml.
Use a concentration of 1 - 2 µg/ml.
FunctionActs as a transcriptional regulator. Inhibits myogenesis by sequestrating E proteins, inhibiting trans-activation by MEF2, and inhibiting DNA-binding by MYOD1 through physical interaction. This interaction probably involves the basic domains of both proteins. Also represses expression of proinflammatory cytokines such as TNFA and IL1B. Regulates cranial suture patterning and fusion. Activates transcription as a heterodimer with E proteins. Regulates gene expression differentially, depending on dimer composition. Homodimers induce expression of FGFR2 and POSTN while heterodimers repress FGFR2 and POSTN expression and induce THBS1 expression. Heterodimerization is also required for osteoblast differentiation.
Tissue specificitySubset of mesodermal cells.
Involvement in diseaseDefects in TWIST1 are a cause of Saethre-Chotzen syndrome (SCS) [MIM:101400]; also known as acrocephalosyndactyly type 3 (ACS3). SCS is a craniosynostosis syndrome characterized by coronal synostosis, brachycephaly, low frontal hairline, facial asymmetry, hypertelorism, broad halluces, and clinodactyly.
Defects in TWIST1 are the cause of Robinow-Sorauf syndrome (RSS) [MIM:180750]; also known as craniosynostosis-bifid hallux syndrome. RSS is an autosomal dominant defect characterized by minor skull and limb anomalies which is very similar to Saethre-Chotzen syndrome.
Defects in TWIST1 are the cause of craniosynostosis type 1 (CRS1) [MIM:123100]. Craniosynostosis consists of premature fusion of one or more cranial sutures, resulting in an abnormal head shape.
Sequence similaritiesContains 1 basic helix-loop-helix (bHLH) domain.
- Information by UniProt
- ACS3 antibody
- B-HLH DNA binding protein antibody
- bHLHa38 antibody
Human melanoma Mel15 cells were fixed and permeabilized with 4% paraformaldehyde followed by 0.1% Triton X-100. Fixed cells were stained with 2 µg/ml ab50581. The antibody was developed with Goat Anti-Rabbit IgG, Cy3 conjugate.
ab50581 staining Twist in human glioblastoma cells by Immunocytochemistry/ Immunofluorescence. The cells were fixed in paraformaldehyde, permeabilised in 0.1% Triton X-100 and then blocked using 0.5% BSA for 20 minutes. Samples were then incubated with primary antibody at 1/50 for 16 hours at 4°C. The secondary antibody used was a goat anti-rabbit IgG conjugated to Cy3® used at a 1/400 dilution.
ab50581 has been referenced in 108 publications.
- Wang K et al. Knockdown of MMP-1 inhibits the progression of colorectal cancer by suppressing the PI3K/Akt/c-myc signaling pathway and EMT. Oncol Rep 43:1103-1112 (2020). PubMed: 32323782
- Sun Q et al. HIF-1a or HOTTIP/CTCF Promotes Head and Neck Squamous Cell Carcinoma Progression and Drug Resistance by Targeting HOXA9. Mol Ther Nucleic Acids 20:164-175 (2020). PubMed: 32169804
- Cai X et al. USP18 deubiquitinates and stabilizes Twist1 to promote epithelial-mesenchymal transition in glioblastoma cells. Am J Cancer Res 10:1156-1169 (2020). PubMed: 32368392
- Aseervatham J & Ogbureke KUE Effects of DSPP and MMP20 Silencing on Adhesion, Metastasis, Angiogenesis, and Epithelial-Mesenchymal Transition Proteins in Oral Squamous Cell Carcinoma Cells. Int J Mol Sci 21:N/A (2020). PubMed: 32630820
- Chang S et al. MiR-3622a-3p acts as a tumor suppressor in colorectal cancer by reducing stemness features and EMT through targeting spalt-like transcription factor 4. Cell Death Dis 11:592 (2020). PubMed: 32719361