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Validated All-in-One™ qPCR Primer for ZEB2(NM_014795.3) Search again
Product ID:
HQP117473
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
HSPC082, SIP-1, SIP1, SMADIP1, ZFHX1B
Gene Description:
zinc finger E-box binding homeobox 2
Target Gene Accession:
NM_014795.3(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
The SMADIP1 gene (also known as SIP1) is a member of the delta-EF1 (ZEB1; MIM 189909)/Zfh1 family of 2-handed zinc finger/homeodomain proteins. SMADIP1 interacts with receptor-mediated, activated full-length SMADs (see MIM 605568) (Verschueren et al., 1999 [PubMed 10400677]).[supplied by OMIM].
Gene References into function
- Conditional expression of SIP1 in E-cadherin-positive cells abrogates E-cadherin-mediated intercellular adhesion and induces invasion. SIP1 therefore appears to be a promoter of invasion in malignant epithelial tumors.
- nonsense and frameshift mutations in ZFHX1B, encoding Smad-interacting protein 1, cause a complex developmental disorder with a great variety of clinical features
- large-scale deletions and SMADIP1 truncating mutations in syndromic Hirschsprung disease with involvement of midline structures
- ZFHX1B may be an important gene for normal embryonic neural crest development. Findings indicate that Hirschsprung's disease can be regarded as a congenital malformation. Mutations were located at exon 8 of ZFHX1B in 3 of 4 cases.
- ZEB1 plays a role in repressing E-cadherin and MUC1 in epithelial cells [ZEB-1]
- SMADIP1 is observed in neural crest derived cells (peripheric nervous system, enteric nervous system, facial neurectoderm and cranial nerve ganglia), central nervous system, genital tubercle, muscles and kidneys in the developing human
- 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
- Review: Mowat-Wilson syndrome is the result of heterozygous deletions or truncating mutations of the ZFHX1B (SIP1) gene on chromosome 2q22
- ZFHX1B is strongly transcribed at an early stage in the developing peripheral and central nervous systems of both mice and humans, in all neuronal regions of the brains of 25-week human fetuses and adult mice, and in numerous nonneural tissues.
- SIP1 expression may be induced during hepatocellular cell carcinoma progression; SIP1 directly represses E-cad gene transcription and activates cancer invasion via upregulation of the MMP gene family
- Over expression of snail is associated with breast carcinoma aggressiveness
- ZFHX1B deletions, splice site or truncating mutations were detected in all 28 patients classified as typical Mowat-Wilson syndrome.
- SIP1 sumoylation by Pc2 attenuates transcriptional repression of E-cadherin
- Results suggest that SIP1 contributes to the loss of E-cadherin expression and that detection of SIP1 expression is a predictive and prognostic tool in clinical management of oral carcinomas.
- results therefore implicate SIP1 in the regulation of vimentin observed in the EMT associated with breast tumor cell migration, a pathway that may contribute to the metastatic progression of breast cancer
- Over 100 mutations have been described in patients with clinically typical MWS, who almost always have whole gene deletions or truncating mutations (nonsense or frameshift) of ZFHX1B, suggesting that haploinsufficiency is the basis of MWS pathology.
- This study identifies miR-200b as a post-transcriptional regulator of ZFHX1B and demonstrates the ability of miR-200b to affect the promoter activity of the ZFHX1B target gene E-cadherin.
- Molecular genetic analysis of ZFHX1B is important for a definite diagnosis of Mowat-Wilson syndrome, which has a wide phenotypic spectrum of congenital anomalies.
- over 100 deletions/mutations in zinc finger E-box binding protein 2 gene are seen in Mowat-Wilson Syndrome; Clinical features suggest ZEB2 gene activity in development of neural-crest derived cells, central nervous system, heart septation, and midline
- NuRD and Zfhx1b functionally interact, and defective NuRD recruitment by mutant human ZFHX1B can be a Mowat-Wilson syndrome-causing mechanism.
- Mowat--Wilson syndrome: the clinical report with the novel mutation in ZFHX1B (exon 8: c.2372del C; p.T791fsX816).
- 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.
- A double-negative feedback loop controlling ZEB1-SIP1 and miR-200 family expression.
- study describes two sisters with clinical features of Mowat-Wilson syndrome in whom the same nonsense mutation in the ZEB2 gene was found
- In conclusion, Multiplex Ligation-dependent Probe Amplification assessment of rearrangements in the RET proto-oncogene and in 3 other associated genes, ZEB2, EDN3 and GDNF did not show any variants in 80 sporadic Hirschsprung disease patients.