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Validated All-in-One™ qPCR Primer for SOX10(NM_006941.3) Search again
Product ID:
HQP017636
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
DOM, PCWH, SOX-10, WS2E, WS4, WS4C
Gene Description:
SRY-box transcription factor 10
Target Gene Accession:
NM_006941.3(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
This gene encodes a member of the SOX (SRY-related HMG-box) family of transcription factors involved in the regulation of embryonic development and in the determination of the cell fate.
Gene References into function
- novel mutations suggest a dominant negative role in Waardenburg-Shah syndrome
- Results show that the inhibition of the nuclear export of Sox10 led to decreased transactivation of transfected reporters and endogenous target genes, arguing that continuous nucleocytoplasmic shuttling is essential for the function of Sox10.
- Muations in SOX10 is associated with chronic intestinal pseudo-abstruction
- SOX10 mutation carriers in Hirschsprung's disease had a very long histologic transition and exhibited no gut caliber change
- SOX10 modulates alpha-melanocyte-stimulating hormone-triggered expression of microphthalmia-associated transcription factor in melanocytes
- The lack of normal SOX10 mediated activation of RET transcription may lead to intestinal aganglionosis, overexpression of genes coding for structural myelin proteins
- phenotype of Sox10Dom/+ mutants ranges over a continuum from severe aganglionosis to no detectable phenotype in the gut
- The SOX10 is highly expressed in unpigmented melanocyte precursors but are down-regulated upon differentiation.
- DNA methylation status of the SOX10 CpG island could be an epigenetic sign of oligodendrocyte dysfunction in schizophrenia.
- the transcriptional factor SOX10 is one of the key determinants of oligodendroglial differentiation
- identified an association of Sox10 with the N-myc interactor Nmi, which was mediated by the high-mobility group of Sox10 and the central region of Nmi; Nmi modulated the transcriptional activity of Sox10
- SOX10 protein is modified by sumoylation; three sumoylation consensus sites were found in the SOX10 protein, all of them are functional and modulate SOX10 activity.
- Results show that genetic variations in the SOX10 gene do not contribute to susceptibility to Japanese schizophrenia.
- pediatric and adult high grade tumors display strong nuclear staining for SOX10
- Sox10-regulated ErbB3 overexpression is a novel insight into the biology of pilocytic astrocytoma.
- SOX10 gene is related to the development of schizophrenia in a Japanese population.
- Failure to properly terminate SOX10 translation causes the generation of a deleterious functional domain that occurs because of translation of the normal 3'-UTR; the mutant fusion protein causes a severe neurological disease.
- investigation of the expression of Sox10 in other human tumors and in a number of gliomas. Sox10 expression was restricted to gliomas and melanomas.
- Neurological phenotypes reminiscent of that observed in Waardenburg syndrome types 2 affected patients with SOX10 deletions.
- A SOX10 "de novo" splice site mutation (c.698-2A > C) was identified in a severe type 4 Waardenburg syndrome without Hirschsprung disease.
- A de novo missense mutation in the gene encoding the SOX10 transcription factor in a Spanish sporadic case of Waardenburg syndrome type IV.
- Quantitative changes of enteric glia represented by SOX10 provide a basis for pathological assessment of glial proliferation and/or degeneration in the diseased gut.
- Waardenburg syndrome type II is caused by a heterozygous SOX10 frameshift mutation.
- Sox10 will serve as a more sensitive and specific marker for the diagnosis of melanocytic and schwannian tumors than S100 protein.
- Multiple sites belonging to 4 different genes (proteolipid protein, Sox10, extracellular superoxide dismutase, and pleiotrophin) were shown to directly interact with Sox10 by chromatin immunoprecipitation assay.