Product: Twist1 Antibody
Catalog: AF4009
Description: Rabbit polyclonal antibody to Twist1
Application: WB IHC IF/ICC
Reactivity: Human, Mouse, Rat
Prediction: Pig, Bovine, Chicken, Xenopus
Mol.Wt.: 29 kd; 21kD(Calculated).
Uniprot: Q15672
RRID: AB_2835337

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Product Info

Source:
Rabbit
Application:
WB 1:500-1:2000, IHC 1:50-1:200, IF/ICC 1:100-1:500
*The optimal dilutions should be determined by the end user.
*Tips:

WB: For western blot detection of denatured protein samples. IHC: For immunohistochemical detection of paraffin sections (IHC-p) or frozen sections (IHC-f) of tissue samples. IF/ICC: For immunofluorescence detection of cell samples. ELISA(peptide): For ELISA detection of antigenic peptide.

Reactivity:
Human,Mouse,Rat
Prediction:
Pig(100%), Bovine(100%), Chicken(100%), Xenopus(100%)
Clonality:
Polyclonal
Specificity:
Twist1 Antibody detects endogenous levels of total Twist1.
RRID:
AB_2835337
Cite Format: Affinity Biosciences Cat# AF4009, RRID:AB_2835337.
Conjugate:
Unconjugated.
Purification:
The antiserum was purified by peptide affinity chromatography using SulfoLink™ Coupling Resin (Thermo Fisher Scientific).
Storage:
Rabbit IgG in phosphate buffered saline , pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol. Store at -20 °C. Stable for 12 months from date of receipt.
Alias:

Fold/Unfold

ACS3; B-HLH DNA binding protein; bHLHa38; BPES2; BPES3; Class A basic helix-loop-helix protein 38; CRS; CRS1; CSO; H-twist; OTTHUMP00000116043; SCS; TWIST; Twist basic helix loop helix transcription factor 1; Twist family bHLH transcription factor 1; Twist homolog 1 (Drosophila); Twist homolog 1; TWIST homolog of drosophila; Twist related protein 1; Twist-related protein 1; TWIST1; TWST1_HUMAN;

Immunogens

Immunogen:
Uniprot:
Gene(ID):
Expression:
Q15672 TWST1_HUMAN:

Subset of mesodermal cells.

Description:
Acts 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.
Sequence:
MMQDVSSSPVSPADDSLSNSEEEPDRQQPPSGKRGGRKRRSSRRSAGGGAGPGGAAGGGVGGGDEPGSPAQGKRGKKSAGCGGGGGAGGGGGSSSGGGSPQSYEELQTQRVMANVRERQRTQSLNEAFAALRKIIPTLPSDKLSKIQTLKLAARYIDFLYQVLQSDELDSKMASCSYVAHERLSYAFSVWRMEGAWSMSASH

Predictions

Predictions:

Score>80(red) has high confidence and is suggested to be used for WB detection. *The prediction model is mainly based on the alignment of immunogen sequences, the results are for reference only, not as the basis of quality assurance.

Species
Results
Score
Pig
100
Bovine
100
Xenopus
100
Chicken
100
Horse
0
Sheep
0
Dog
0
Zebrafish
0
Rabbit
0
Model Confidence:
High(score>80) Medium(80>score>50) Low(score<50) No confidence

PTMs - Q15672 As Substrate

Site PTM Type Enzyme
S6 Phosphorylation P28482 (MAPK1)
S18 Phosphorylation P68400 (CSNK2A1)
S20 Phosphorylation P68400 (CSNK2A1)
K38 Ubiquitination
S42 Phosphorylation P31749 (AKT1)
S45 Phosphorylation
S68 Phosphorylation Q15759 (MAPK11) , P45983 (MAPK8) , Q16539 (MAPK14) , P28482 (MAPK1) , P27361 (MAPK3)
K73 Acetylation
S102 Phosphorylation
Y103 Phosphorylation
T121 Phosphorylation
S123 Phosphorylation P31749 (AKT1)
T137 Phosphorylation
K142 Ubiquitination
S144 Phosphorylation
K145 Ubiquitination

Research Backgrounds

Function:

Acts 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. Represses the activity of the circadian transcriptional activator: NPAS2-ARNTL/BMAL1 heterodimer (By similarity).

Subcellular Location:

Nucleus.

Extracellular region or secreted Cytosol Plasma membrane Cytoskeleton Lysosome Endosome Peroxisome ER Golgi apparatus Nucleus Mitochondrion Manual annotation Automatic computational assertionSubcellular location
Tissue Specificity:

Subset of mesodermal cells.

Subunit Structure:

Efficient DNA binding requires dimerization with another bHLH protein. Homodimer or heterodimer with E proteins such as TCF3. ID1 binds preferentially to TCF3 but does not interact efficiently with TWIST1 so ID1 levels control the amount of TCF3 available to dimerize with TWIST1 and thus determine the type of dimer formed (By similarity).

Research Fields

· Human Diseases > Cancers: Overview > Proteoglycans in cancer.

References

1). Twist1 Regulates Vimentin through Cul2 Circular RNA to Promote EMT in Hepatocellular Carcinoma. CANCER RESEARCH, 2018 (PubMed: 29844124) [IF=11.2]

Application: IHC    Species: mouse    Sample: HCC tumor samples

(E, F) Twist1 and Vimentin expression in the tumor tissues of Twi-L+control, Twi-L+circ-10720, Twi-H+siRNA control and TwiH+si-circ-10720 groups were analyzed via IHC.

Application: WB    Species: human    Sample: HCC cells

Figure 2.| circ-10720 regulated by Twist1 exhibits oncogenic effects in HCC cells.(D) Western blot analysis of Twist1 and Cul2 protein levels in Twist1 overexpression or knockdown cells. Intensity of each band from biological triplicate experiments was quantified by densitometry with the Image J software with GAPDH as a normalizer. *P<0.05, **P<0.01, Student’s t-test.

Application: IHC    Species: human    Sample: tumor

Figure 4. |Intratumoral silencing of circ-10720 blocks the promotive effect of Twist1-mediated on Vimentin expression in a PDTX model of HCC. (E, F) Twist1 and Vimentin expression in the tumor tissues of Twi-L+control, Twi-L+circ-10720, Twi-H+siRNA control and TwiH+si-circ-10720 groups were analyzed via IHC. Each bar represents the mean ± SD for triplicate measurements of four xenografts in each group. **P<0.01, one-way ANOVA.

2). Salidroside improves the hypoxic tumor microenvironment and reverses the drug resistance of platinum drugs via HIF-1α signaling pathway. EBioMedicine, 2018 (PubMed: 30396856) [IF=11.1]

Application: WB    Species: human    Sample: PLC/PRF/5 cells

Fig. 3.|Sal reversed the drug resistance and inhibited HIF-1α signaling pathway. (I) Protein expression level of Twist1, Zeb1 and E-cadherin in PLC/PRF/5 cells treated hypoxia and hypoxia combined with Sal. Error bars represent the standard deviation of experiments performed in triplicate (*P b .05, **P b .01).

3). Hsp90β promotes aggressive vasculogenic mimicry via epithelial-mesenchymal transition in hepatocellular carcinoma. ONCOGENE, 2023 (PubMed: 30087438) [IF=8.0]

Application: WB    Species: human    Sample: SMMC-7721cells

Fig. 4| Hsp90β stabilize Twist1 and promotes its deubiquitination by combining with USP19. a Hsp90β knockdown decreases Twist1 stability. SMMC-7721 cells were transfected with the Hsp90βsiRNA for 24h and then were treated with CHX (100mg/ml) at the indicated time points. b SMMC-7721 cells transfected with Hsp90βsiRNA were treated with 10µM MG132 and followed by immuno-blotting using anti-Twist1 and Hsp90β.

Application: IHC    Species: human    Sample: tumor

Fig. 6 | Hsp90β promotes tumor growth and VM formation relied on Twist1 in vivo and Hsp90 inhibitor depresses the promotion effect.e, f Hsp90β, Twist1, VE-cadherin, E-cadherin, Vimentin,MMP2, and MMP9 expression levels were measured in tumor tissue of the control, Hsp90β overexpression, Hsp90β+ Twist1 siRNA,control shRNA, and Hsp90β knockdown groups by IHC.

4). RETRACTED ARTICLE: Hsp90β promotes aggressive vasculogenic mimicry via epithelial–mesenchymal transition in hepatocellular carcinoma. Oncogene, 2018 (PubMed: 30087438) [IF=8.0]

5). Molecular mechanism of albumin in suppressing invasion and metastasis of hepatocellular carcinoma. LIVER INTERNATIONAL, 2022 (PubMed: 34854209) [IF=6.7]

Application: WB    Species: Human    Sample: HepG2 and Huh7 cells

FIGURE 7 A, Representative images of the western blot results for uPAR, MMP2 and MMP9 in ALB knockdown HepG2 and Huh7 cells; B, Zymography analysis illustrates MMP2 and MMP9 activity in ALB knockdown HepG2 and Huh7 cells; C, Quantitative analysis results and representative images of the western blot results for the EMT‐associated markers, E‐cadherin, N‐cadherin, vimentin, Snail and Twist by western blot in ALB knockdown HepG2 and Huh7 cells; D, Quantification shows a significantly higher uPAR in HCC group with ALB <3.5 g/dL compared to ALB ≥3.5 g/dL (*P < .05); E, Scatterplot showing the correlation between plasma levels of ALB and uPAR. The vertical position represents the expression levels of uPAR (lg pg/mL)

6). Long non‐coding RNA LINC01137 contributes to oral squamous cell carcinoma development and is negatively regulated by miR-22-3p. CELLULAR ONCOLOGY, 2021 (PubMed: 33797737) [IF=6.6]

Application: WB    Species: Human    Sample: HSC3 and Tca8113 cells

Fig. 3 LINC01137 downregulation inhibits OSCC cell migration and invasion. a Transwell chambers were used to detect the effect of LINC01137 knockdown on the migration of HSC3 and Tca8113 cells. n = 10 fields, **p < 0.01. b Transwell chambers precoated with Matrigel were used to detect the effect of LINC01137 knockdown on the invasion of HSC3 and Tca8113 cells. n = 10 fields, **p < 0.01. c Western blotting was performed to detect the expression of EMT related proteins (Vimentin, Snail, Twist, MMP-2 and MMP-9) after LINC01137 knockdown in HSC3 and Tca8113 cells. n = 3, *p < 0.05

7). Phenylpropenol ester and sesquiterpenoids with antimetastatic activities from the whole plants of Chloranthus japonicus. Arabian Journal of Chemistry, 2022 [IF=6.0]

8). Cytoplasmic p27 is a novel prognostic biomarker and oncogenic protein for nasopharyngeal carcinoma. Artificial Cells Nanomedicine and Biotechnology, 2020 (PubMed: 31884829) [IF=5.8]

9). γ-Glutamyl cyclotransferase contributes to endometrial carcinoma malignant progression and upregulation of PD-L1 expression during activation of epithelial-mesenchymal transition. International Immunopharmacology, 2020 (PubMed: 31757677) [IF=5.6]

Application: WB    Species: Human    Sample: endometrial carcinoma cells

Fig. 4. GGCT contributed to malignant biological behaviors of endometrial carcinoma cells during EMT activation. The expression of the EMT markers E-cadherin, N- cadherin, Vimentin, Twist, Snail, and Slug detected using western blot demonstrated the contribution of GGCT to the EMT process in endometrial carcinoma. This analysis was repeated three times (A, B). Immunohistochemical staining of the EMT markers E-cadherin, N-cadherin, Vimentin, Twist, Snail, and Slug in tumor tissues from the xenograft model demonstrated the contribution of GGCT to the EMT process in vivo (C). *p < 0.05.

Application: IHC    Species: Human    Sample: endometrial carcinoma cells

Fig. 4. GGCT contributed to malignant biological behaviors of endometrial carcinoma cells during EMT activation. The expression of the EMT markers E-cadherin, N- cadherin, Vimentin, Twist, Snail, and Slug detected using western blot demonstrated the contribution of GGCT to the EMT process in endometrial carcinoma. This analysis was repeated three times (A, B). Immunohistochemical staining of the EMT markers E-cadherin, N-cadherin, Vimentin, Twist, Snail, and Slug in tumor tissues from the xenograft model demonstrated the contribution of GGCT to the EMT process in vivo (C). *p < 0.05.

10). MicroRNA-181a regulates epithelial-mesenchymal transition by targeting PTEN in drug-resistant lung adenocarcinoma cells. INTERNATIONAL JOURNAL OF ONCOLOGY, 2015 (PubMed: 26323677) [IF=5.2]

Application: WB    Species: human    Sample: A549 cells

Figure 3. A549/DDP and A549/PTX cells showed molecular and morphological changes that were consistent with EMT. (A) microscopy at x200 magnification was used to assess cell morphology. The A549 cells (parental cells) had an epithelioid, rounded cobblestone appearance and there was limited formation of pseudopodia. A549/PTX and A549/DDP cells exhibited a spindle-shaped morphology and an increased formation of pseudopodia, indicating a loss of cell polarity. (B) E-cadherin, β-catenin, vimentin, MMP-2 and MMP-9 which are EMT-related proteins, were assessed in terms of expression levels. EMT-related transcription factors (Snail, Slug, Twist and ZEB1) were measured in A549/PTX and A549/DDP cells using western blot analysis. (C) The expression changes were confirmed at the mRNA level by qRT-PCR. Expression was standardized to the expression of GAPDH and normalized to 1.0 in the parental cells (compared with the parental A549 cells, means ± SEM, n=3, * P<0.05)

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