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Validated All-in-One™ qPCR Primer for TWIST1(NM_000474.3) Search again
Product ID:
HQP018328
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
ACS3, BPES2, BPES3, CRS, CRS1, CSO, SCS, SWCOS, TWIST, bHLHa38
Gene Description:
twist family bHLH transcription factor 1
Target Gene Accession:
NM_000474.3(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Validated result:
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| A | B |
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Each All-in-One™ qPCR Primer is experimentally validated to yield a single dissociation curve peak and to generate a single amplification of the correct size for the targeted gene. A cDNA Pool, containing reverse transcript products of 8 different human tissue total RNA(Liver, Testis,Muscle,Thyroid,Brain,Spleen,Stomach,Small Intestine)),was used as the qPCR validation template. qPCR was performed using 0.2 µM primer with 2XAll-in-One™ qPCR Mix (Catalog#: QP001,QP002,QP004,QP005). Reactions were incubated for 10min. at 95°C, followed by 40 cycles of 95°C for 10 sec.; 60°C, 20 sec. and 72°C, 15sec. using Bio-Rad iQ5™ Instrument. At the end of the last cycle, temperature was increased from 72 to 95°C to produce a melting curve. Panel A: Validated Result for Amplification Curve; Panel B: Validated Result for Melting Curve. |
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Summary
Basic helix-loop-helix (bHLH) transcription factors have been implicated in cell lineage determination and differentiation.
Gene References into function
- new TWIST mutation (7p21) with variable eyelid manifestations supports locus homogeneity of BPES at 3q22
- Deletion of 18 nucleotides or insertion of three, 15, or 21 nucleotides was not consistently associated with clinical disease and was conclude that they are at most weakly pathogenic.
- Identified direct paternal transmission of a novel missense TWIST mutation in the highly conserved Helix II domain of this bHLH-family gene.
- Deficience causes skull osteoblast apoptosis due to increased TNFalpha expression and caspase-2 activation.
- Cooperative E-box regulation of human GLI1 by this protein and USF
- Characterization of a dominant negative C. elegans Twist mutant protein with implications for human Saethre-Chotzen syndrome
- inactivation reduces CBFA1/RUNX2 expression and DNA binding to the osteocalcin promoter in osteoblasts
- One variant is associated with Robinow-Sorauf syndrome.
- The risk for developmental delay in patients with deletions involving the TWIST gene is approximately 90%.
- novel role for TWIST, a basic helix-loop-helix protein, which plays a central role in cell type determination and differentiation, during generation of acquired resistance to taxol in a nasopharyngeal carcinoma cell line, HNE1-T3
- TWIST1 plays an essential role in tumor metastasis.
- Twist was highly and selectively expressed in T cells of patients with Sezary Syndrome.
- loss of HOXA5 expression could lead to the functional activation of Twist resulting in aberrant cell cycle regulation and promoting breast carcinogenesis
- A reporter assay with the p21 promoter demonstrated that Snail inhibited expression of p21 induced by E2A. Co-expression of Snail with Twist showed additive inhibitory effects.
- H-Twist overexpression in neuroblastomas is responsible for the inhibition of the ARF/p53 pathway involved in the Myc-dependent apoptotic response.
- Misregulation of Twist1 dimerization by post-translational mechanisms underlies phenotypes of individuals with Saethre-Chotzen syndrome
- This analysis further dissects the structure-function relationships of TWIST and corroborates with phenotypic observations of disease expressivity.
- TWIST gene is involved in high-grade pediatric osteosarcomas and is a new marker with a possible initial predictive value.
- Results have identified TWIST as a critical regulator of prostate cancer cell growth and suggest a potential therapeutic approach to inhibit the growth and metastasis of androgen-independent prostate cancer through inactivation of the TWIST gene.
- Overexpression of TWIST protein in a human glioma cell line significantly enhanced tumor cell invasion, a hallmark of high-grade gliomas.
- Twist1 is induced by canonical Wnt signaling and expression of Twist1 strongly inhibited chondrocyte gene expression.
- Twist over-expression induces angiogenesis in a mouse breast cancer model
- Twist may play an important role in the invasion and metastasis of nasopharyngeal carcinoma
- Dimer partner selection is an important mediator of Twist1 function in transgenic mice, providing a mechanistic understanding of craniosynostosis due to TWIST haploinsufficiency.
- This provides genetic evidence that Twist1, Msx2 and Efna4 function together in boundary formation and the pathogenesis of coronal synostosis.
- Twist overexpression plays a role in destabilizing the genome, thus promoting chromosomal instability.
- These results implicate Twist proteins in regulation of TNFalpha production by antiinflammatory factors and pathways, and provide a mechanism by which type I IFNs and Axl receptors suppress inflammatory cytokine production.
- Twist may act as a negative regulator of osteoblastic differentiation in periodontal ligament cells
- Twist haploinsufficiency results in decreased Cbl-mediated PI3K degradation in osteoblasts.
- Patients with TWIST gene mutations may have more ophthalmic abnormalities, including more strabismus, ptosis, NLDO, astigmatism, vertical deviations, and amblyopia compared with patients with FGFR3 gene mutations.
- suggest critical implication of the CCT repeats in association with Sp1 and Sp3 factors in sustaining expression of the TWIST1 gene in mesenchymal cells
- Twist, a novel oncogene, is upregulated in pancreatic cancer
- Induction of Twist by a human viral oncoprotein LMP1 directly contributes to the metastatic nature of nasopharyngeal carcinoma.
- Twist is a positive transcriptional regulator of AKT2 expression;Twist-AKT2 signaling is involved in promoting invasive ability and survival of breast cancer cells.
- Some TWIST1 mutations in the RUNX2 binding site are associated with craniosynostosis.
- TWIST may serve as a prognostic marker for high-grade prostatic cancer in humans; up-regulation of TWIST with aberrant expression of E-cadherin may predict development of metastatic disease.
- Data suggest that Twist-1 and -2 play an important role in NF-kappaB-dependent chemoresistance.
- no evidence that mosaicism for mutations, normally associated with syndromal forms of craniosynostosis, occur in single suture craniosynostosis
- findings suggest that reduced expression of TWIST suppresses the multistep process of peritoneal dissemination (detachment from the primary lesion, adhesion to MCs and invasion of MCs.
- Twist regulates cell motility and invasion in gastric cancer cell lines, probably through the N-cadherin and fibronectin production
- TWIST plays a key role in the continuous proliferation of immortalized cells. Over-expression of TWIST results in down-regulation of p14(ARF), which leads to the impairment of DNA damage checkpoint in response to genotoxic stress.
- TWIST1 was frequently observed in the bone marrow of breast cancer patients before chemotherapy; expression of TWIST1 correlated with the rapid occurrence of distant metastasis or local progression, within 1 year from initial diagnosis
- TWIST may be a useful prognostic marker and target for gastric cancer therapy.
- analysis of transcriptional activation by the proto-oncogene Twist1
- Twist was found in cell membrane and cytoplasm of cervical cancers.High expression predicted poor survival; it was a significant prognostic factor in radiation-sensitive squamous cell carcinomas but not in radiation-resistant adenocarcinomas.
- Results identified TWIST1 loci showing significant differential DNA methylation levels between tumor and non-tumor lung and highly significant hypermethylation in adenocarcinoma.
- Twist may play an important role in the angiogenesis and metastasis of hepatocellular carcinoma.
- Using transient promoter assays, we show that Twist can down-regulate E-cadherin promoter activity by up to two folds.
- Both YB-1 and Twist expression could induce tumor progression, promoting cell growth and driving oncogenesis in various cancers.
- TWIST microdeletion is associated with Saethre-Chotzen phenotype and a complex rearrangement involving chromosomes 2 and 7
- a key signalling pathway involving HIF-1alpha and TWIST promotes metastasis in response to intratumoural hypoxia
- These data indicate that MSX2 plays a crucial role in pancreatic cancer development by inducing changes consistent with epithelial to mesenchymal transition through enhanced expression of Twist 1.
- STAT3, Twist, and AKT2 form a functional signaling axis to regulate pivotal oncogenic properties of cancer cells
- summary of the effects of FGFR2 and Twist genetic mutations resulting in altered osteoblast phenotype and premature cranial fusion based on analysis in human syndromic craniosynostosis [review]
- high expression level of Twist is closely associated with more aggressive behaviors of human hepatocellular carcinoma
- thrombin up-regulates Twist, which is required for thrombin-induced angiogenesis as measured by endothelial cell migration, Matrigel tubule formation, and tumor angiogenesis
- Twist proteins promote malignant conversion and metastatic dissemination.
- Th lymphocytes from the inflamed joint or gut tissue of patients with rheumatic diseases, Crohn's disease or ulcerative colitis expressed high levels of twist1.
- In human melanoma cells, MFG-E8 knockdown attenuated Akt and Twist signaling and thereby compromised tumor cell survival, EMT, and invasive ability
- TWIST1 promoter methylation is significantly more prevalent in malignant compared with healthy breast tissue.