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Validated All-in-One™ qPCR Primer for SIAH1(NM_001006610.1) Search again
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:
Summary
This gene encodes a protein that is a member of the seven in absentia homolog (SIAH) family. The protein is an E3 ligase and is involved in ubiquitination and proteasome-mediated degradation of specific proteins. The activity of this ubiquitin ligase has been implicated in the development of certain forms of Parkinson's disease, the regulation of the cellular response to hypoxia and induction of apoptosis. Alternative splicing results in several additional transcript variants, some encoding different isoforms and others that have not been fully characterized. [provided by RefSeq].
Gene References into function
- Siah proteins function as E3 ubiquitin-protein ligases
- The Siah-1 gene promoter was cloned and the basic structure of the Siah-1 gene was determined.
- genetic regulation in tumor reversion
- structural analysis and interaction with Siah-interacting protein
- SIAH1 has been identified as a putative tumor suppressor gene for human hepatocellular carcinomas, with a correlation between its suppressed expression and tumor size and differentiation.
- PEG10 protein associated with SIAH1, a mediator of apoptosis, and overexpression of PEG10 decreased the cell death mediated by SIAH1.
- Siah-1 was found to abrogate the inhibitory effects of synphilin-1 on dopamine release
- A p53-binding site was identified in the siah-1b promoter, located at nucleotides -2155/-2103 relative to the translational start site.
- SIAH-mediated down regulation of alternative splicing may be an important developmental difference between otherwise highly conserved T-STAR proteins.
- role of interaction with AF4 and AF4.MLL fusion protein in t(4,11) pathobiology
- polycystin-1 is regulated by Siah-1 through the ubiquitin-dependent proteasome pathway.
- Siah-1L represents a new member of the human Siah family that is induced in response to p53 and plays an important role in the regulation of beta-catenin activity in tumor cells
- inactivating mutations of the Siah-1 may contribute to the development of gastric cancer through beta-catenin stabilization and apoptosis block
- Data show a signalling pathway in which nitric oxide generation that follows apoptotic stimulation elicits S-nitrosylation of GAPDH, which triggers binding to Siah1, nuclear translocation and apoptosis.
- SIP engages Siah1 by means of two elements, both of which are required for mediating beta-catenin destruction in cells
- GSK3beta modulates synphilin-1 ubiquitylation and cellular inclusion formation by SIAH
- analysis of the substrate binding site of Siah ubiquitin ligase
- genetic alterations of SIAH-1 do not significantly contribute to the pathogenesis of Parkinson disease
- HSiah1 lacks the self-regulatory catalytic activity displayed by the ring finger domain of hSiah2 in HEK293 cells.
- Such findings suggest that Siah ubiquitin ligases might play a role as up-stream regulators of both hydroxylases for HIF-1alpha.
- Siah-1S (splice variant S) displays a promotion effect on cells tumorigenicity
- Siah-1-mediated alpha-synuclein ubiquitination may play a critical role in Lewy body formation and Parkinson disease pathogenesis
- monoubiquitylation by SIAH1 and SIAH2 represents a possible trigger event for alpha-synuclein aggregation and Lewy body formation
- SIAH may offer a novel therapeutic target to halt tumor growth and ameliorate RAS-mediated pancreatic cancer.
- SIAH1-induced degradation of TRB3 represents a potential regulatory mechanism for TGF-beta signaling.
- SIAH-1 inhibition may represent a new therapeutic strategy in the treatment of human hepatocellular carcinoma.
- Results describe the control of HIPK2 stability by ubiquitin ligase Siah-1 and checkpoint kinases ATM and ATR.
