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Validated All-in-One™ qPCR Primer for ZEB1(NM_001128128.2) Search again
Product ID:
HQP067039
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
AREB6, BZP, DELTAEF1, FECD6, NIL2A, PPCD3, TCF8, ZFHEP, ZFHX1A
Gene Description:
zinc finger E-box binding homeobox 1
Target Gene Accession:
NM_001128128.2(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
ZEB1 encodes a zinc finger transcription factor that represses T-lymphocyte-specific IL2 gene (MIM 147680) expression by binding to a negative regulatory domain 100 nucleotides 5-prime of the IL2 transcription start site (Williams et al., 1991 [PubMed 1840704]).[supplied by OMIM].
Gene References into function
- ZEB1 plays a role in repressing E-cadherin and MUC1 in epithelial cells [ZEB-1]
- These data provide the first demonstration that Zfhep is post-translationally modified.
- Data show that ZEB-1/deltaEF1 and ZEB-2/SIP1 are regulators of transforming growth factor beta/bone morphogenetic protein signaling, with opposing effects on this pathway.
- while ZEB-1/deltaEF1 binds to p300 and promotes the formation of a p300-Smad transcriptional complex, ZEB-2/SIP1 acts as a repressor by recruiting CtBP
- an activator of transcription whose action may be DNA-context and cell-type specific, but not species specific.
- Data demonstrate that DNA methylation contributes to increased levels of p73 in Fanconi anemia cells by hampering the binding of the transcriptional repressor ZEB to an intronic regulatory region of the p73 gene.
- In colon cancer parients, the correlation between the expression of SNAIL and the downregulation of E-cadherin (CDH1) is lost when ZEB1 is overexpressed
- Levels of expression of CtBP and p300 are critical for the action of SNAIL and ZEB1, which have a pivotal role in levels of epithelial-mesenchymsal transitionin human colon carcinoma.
- zinc-finger-enhancer protein 1 (ZEB1) is the crucial transcriptional repressor of BM components in CRCs.
- The transcriptional repression of PKP3 by ZEB1 contributes to ZEB1-mediated disintegration of intercellular adhesion and epithelial to mesenchymal transition.
- Four novel pathogenic mutations were identified in four families; two deletions, one nonsense, and one duplication within exon 7 in the ZEB1 gene at 10p11.2. Czech patients were genotyped for a founder haplotype and lack of 20p11.2 locus segregation.
- Upregulation of ZEB1 is associated with colon and breast cancer progression
- The Zfhx1a-1 gene is autoregulated in part by negative feedback on its own promoter which is, in turn, modified by the availability of the negative dominant isoform Zfhx1a-2.
- TCF8 gene mutations are associated with Posterior polymorphous corneal dystrophy and abdominal hernia
- Based on these observations we suggest that bHLH factors recruit NFI to enhance skeletal muscle Na(+) channel expression.
- The identification of a novel missense mutation in only one of the patients implied that TCF8 does not play a significant role in the pathogenesis of FECD in this Chinese population.
- ZEB1 is a crucial promoter of malignant tumor progression.
- These results lead to a new hypothesis that Snail and ZEB1 are downstream of CCN6 and play a critical role in CCN6-mediated regulation of E-cadherin in breast cancer.
- Data show that miR-200 and -205 microRNAs cooperatively regulate expression of the E-cadherin transcriptional repressors ZEB1 (also known as deltaEF1) and SIP1 (also known as ZEB2), factors previously implicated in EMT and tumour metastasis.
- loss of expression of the miR-200 family members may play a critical role in the repression of E-cadherin by ZEB1 and ZEB2 during EMT, thereby enhancing migration and invasion during cancer progression.
- Down-regulation of TCF8 expression in ATLL cells was associated with resistance to TGF-beta1, a well-known characteristic of ATLL cells, suggesting that escape from TGF-beta1-mediated growth inhibition is important in the pathogenesis of ATLL
- These results indicate that ZEB1 triggers an microRNA-mediated feedforward loop that stabilizes the epithelial-mesenchymal transition and promotes invasion of cancer cells.
- ZEB1 may be a biomarker of aggressive endometrial cancers at high risk of recurrence.
- These data support the contention that high ZEB1 encourages gynecologic carcinoma progression.
- A double-negative feedback loop controlling ZEB1-SIP1 and miR-200 family expression.
- TCF8 activates R-Ras, another class of angiogenic regulator, to suppress angiogenesis by a mechanism other than a transcriptional attenuator.
- These findings suggest that Zeb1 represses T-cadherin expression and thus increases the invasive activity of gallbladder cancer.
- Integral role for TCF8 in the regulation of pathologic angiogenesis, and possible use of TCF8 as a target for therapeutic intervention in cancer.