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Validated All-in-One™ qPCR Primer for SALL1(NM_002968.2) Search again
Powered by BiozBy 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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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 protein encoded by this gene is a zinc finger transcriptional repressor and may be part of the NuRD histone deacetylase complex (HDAC). Defects in this gene are a cause of Townes-Brocks syndrome (TBS) as well as bronchio-oto-renal syndrome (BOR). Two transcript variants encoding different isoforms have been found for this gene. [provided by RefSeq].
Gene References into function
- Mutation in Townes-Brocks syndrome. Product is a transcriptional repressor which interacts with TRF1/PIN2 and localizes to pericentromeric heterochromatin.
- binding of proteins SALL1, UBE2I and SUMO-1
- sall1 enhances the canonical Wnt signaling by localizing to heterochromatin
- analysis of SALL1 mutations in Townes-Brocks syndrome
- Sall1 is essential for ureteric bud invasion, the initial key step for metanephros development
- there is a different contribution of SALL1 gene function to mouse and human embryonic development
- Data show that SALL1 contains two repression domains, one located at the extreme N-terminus of the protein and the other in the central region.
- SALL1 is a likely target gene for SIX1 during kidney development
- There is an enhancer element in the SALL1 gene.
- SALL1 gene, mutations of which result in the Townes-Brocks phenotype, is expressed in the developing kidney.
- SALL1 and GLI3 may have roles in limb malformation and are affected by nonsense-mediated decay
- analysis of one sporadic case of Townes-Brocks syndrome for SALL1 gene mutations and review of the literature [review]
- truncated SALL1 protein is expressed in cells derived from a TBS patient
- This case increases the demand to examine all children with Townes-Brocks Syndrome (TBS) for ophthalmic abnormalities.