Pages that link to "Q24535880"
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The following pages link to Nonsense and frameshift mutations in ZFHX1B, encoding Smad-interacting protein 1, cause a complex developmental disorder with a great variety of clinical features (Q24535880):
Displaying 35 items.
- Mowat-Wilson syndrome (Q21202963) (← links)
- Angelman syndrome: a review of the clinical and genetic aspects (Q24678174) (← links)
- SIP1/ZEB2 induces EMT by repressing genes of different epithelial cell-cell junctions (Q24814569) (← links)
- Churchill, a zinc finger transcriptional activator, regulates the transition between gastrulation and neurulation (Q28505236) (← links)
- Mice lacking ZFHX1B, the gene that codes for Smad-interacting protein-1, reveal a role for multiple neural crest cell defects in the etiology of Hirschsprung disease-mental retardation syndrome (Q28508181) (← links)
- Complementary expression pattern of Zfhx1 genes Sip1 and deltaEF1 in the mouse embryo and their genetic interaction revealed by compound mutants (Q28508407) (← links)
- Expression of the SMADIP1 gene during early human development (Q34144195) (← links)
- Organization of the mouse Zfhx1b gene encoding the two-handed zinc finger repressor Smad-interacting protein-1. (Q34246918) (← links)
- Origin and spread of the 1278insTATC mutation causing Tay-Sachs disease in Ashkenazi Jews: genetic drift as a robust and parsimonious hypothesis (Q34290326) (← links)
- A genome-wide association study identifies potential susceptibility loci for Hirschsprung disease (Q34331688) (← links)
- ZFHX1B mutations in patients with Mowat-Wilson syndrome (Q34597855) (← links)
- Genetic basis of Hirschsprung disease: implications in clinical practice (Q35563834) (← links)
- miR-200b mediates post-transcriptional repression of ZFHX1B. (Q35902048) (← links)
- Genitourinary anomalies in Mowat-Wilson syndrome with deletion/mutation in the zinc finger homeo box 1B gene (ZFHX1B). Report of three Italian cases with hypospadias and review (Q36134746) (← links)
- Epithelial-mesenchymal transition in development and cancer: role of phosphatidylinositol 3' kinase/AKT pathways (Q36313178) (← links)
- The developmental etiology and pathogenesis of Hirschsprung disease. (Q36951687) (← links)
- Highly conserved upstream sequences for transcription factor genes and implications for the regulatory network (Q37693845) (← links)
- Functional conservation of zinc-finger homeodomain gene zfh1/SIP1 in Drosophila heart development (Q38309940) (← links)
- Clinical utility gene card for: Mowat-Wilson syndrome (Q38413219) (← links)
- Zebrafish sip1a and sip1b are essential for normal axial and neural patterning (Q39687372) (← links)
- Interaction between Smad-interacting protein-1 and the corepressor C-terminal binding protein is dispensable for transcriptional repression of E-cadherin (Q40652239) (← links)
- ZEB2 gene mutation and duplication of 22q11.23 in Mowat-Wilson syndrome (Q41929813) (← links)
- A SHH-responsive signaling center in the forebrain regulates craniofacial morphogenesis via the facial ectoderm (Q42938802) (← links)
- Genetic interactions and modifier genes in Hirschsprung's disease (Q43010652) (← links)
- Phenotype and genotype of 87 patients with Mowat-Wilson syndrome and recommendations for care (Q47210500) (← links)
- BMP4 signaling mediates Zeb family in developing mouse tooth. (Q48651171) (← links)
- miR-200b regulates cell migration via Zeb family during mouse palate development (Q51823158) (← links)
- Neural crest-specific removal of Zfhx1b in mouse leads to a wide range of neurocristopathies reminiscent of Mowat-Wilson syndrome (Q51904000) (← links)
- Further delineation of the phenotype associated with heterozygous mutations in ZFHX1B. (Q51948432) (← links)
- XSIP1 is essential for early neural gene expression and neural differentiation by suppression of BMP signaling. (Q52087092) (← links)
- Generation of the floxed allele of the SIP1 (Smad-interacting protein 1) gene for Cre-mediated conditional knockout in the mouse. (Q52123529) (← links)
- Polymicrogyria in a 10-month-old boy with Mowat-Wilson syndrome. (Q53493173) (← links)
- CHARGE-like presentation, craniosynostosis and mild Mowat-Wilson Syndrome diagnosed by recognition of the distinctive facial gestalt in a cohort of 28 new cases (Q56266848) (← links)
- The single nucleotide polymorphisms in Smad-interacting protein 1 gene contribute to its ectopic expression and susceptibility in Hirschsprung's disease (Q87372179) (← links)
- Mutations in Smad-interacting protein 1 gene are responsible for absence of its expression in Hirschsprung's disease (Q88222530) (← links)