Anti-HRD1/SYVN1 antibody, Mouse monoclonal

Monoclonal Anti-HRD1/SYVN1 (mouse IgG1 isotype) is derived from the hybridoma HRD1-5 produced by the fusion of mouse myeloma cells and splenocytes from BALB/c mice immunized with a synthetic peptide corresponding to the C-terminal region of human HRD1/SYVN1 conjugated to KLH. β-Hydroxy β-methylglutaryl-CoA (HMG-CoA) reductase degradation protein (HRD1)/synoviolin (SYVN1) is an endoplasmic reticulum (ER)-membrane resident E3 ubiquitin ligase. It has a five-transmembrane domain, a really interesting new gene (RING)-finger domain and a proline-rich domain.

Synoviolin 1 (SYVN1), also referred as 3-hydroxy-3-methylglutaryl-CoA reductase degradation protein 1 (HRD1), is encoded by the gene mapped to human chromosome 11q13.1. It is mainly expressed in liver, spleen, prostate and pancreas.

a synthetic peptide corresponding to the C-terminal region of human HRD1/SYVN1, conjugated to KLH. The corresponding sequence differs by two amino-acids in rat and mouse.

Anti-HRD1/SYVN1 antibody, Mouse monoclonal has been used in immunoblotting and immunoprecipitation.

β-Hydroxy β-methylglutaryl-CoA (HMG-CoA) reductase degradation protein (HRD1)/synoviolin (SYVN1) protects against ER stress-induced apoptosis through ER stress-associated protein degradation (ERAD). The (RING)-finger domain mediates the transfer of ubiquitin from E2 to substrates. HRD1 expression is strongly induced by ER stress. It mediates proteasomal degradation via p53 tumor suppressor gene. Overexpression of HRD1 is implicated in the pathogenesis of rheumatoid arthritis.

Synoviolin 1 (SYVN1) plays a vital role in endoplasmic reticulum (ER)-associated degradation. The encoded protein acts as an E3 ubiquitin ligase and suppresses endoplasmic reticulum stress. It might also be involved in the protein quality control of optineurin (OPTN). Upregulated expression of the protein enhanced tau cytotoxicity and promoted cell survival in a study. SYVN1 interacts with Pael -R (substrate protein of familial Parkinson′s disease responsible gene Parkin) to promote neuronal cell death. It also increases degradation of APP (precursor of Alzheimer′s disease-causing protein amyloid β). SYVN1 activity is induced via inositol-requiring enzyme 1-X-box binding protein 1 (IRE1-XBP1) pathway. Therefore, drugs that enhance or suppress the expression of SYVN1, can be used as a therapeutic drugs for neurodegenerative diseases.

Solution in 0.01 M phosphate buffered saline, pH 7.4, containing 15 mM sodium azide.

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