推荐产品
生物来源
mouse
质量水平
偶联物
unconjugated
抗体形式
purified from hybridoma cell culture
抗体产品类型
primary antibodies
克隆
HRD1-5, monoclonal
表单
buffered aqueous solution
分子量
antigen ~70 kDa
种属反应性
human
浓度
~1.0 mg/mL
技术
immunoprecipitation (IP): 5-10 μg using lysates of human HEK-293T cells
western blot: 2-4 μg/mL using whole extracts of HEK-293T cells over-expressing human HRD1/SYVN1
同位素/亚型
IgG1
UniProt登记号
运输
dry ice
储存温度
−20°C
靶向翻译后修饰
unmodified
基因信息
human ... SYVN1(84447)
一般描述
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.
免疫原
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.
应用
Anti-HRD1/SYVN1 antibody, Mouse monoclonal has been used in immunoblotting and immunoprecipitation.
生化/生理作用
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.
外形
0.01M 磷酸缓冲盐溶液,pH 7.4,含 15mM 叠氮化钠。
免责声明
Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.
未找到合适的产品?
试试我们的产品选型工具.
储存分类代码
10 - Combustible liquids
闪点(°F)
Not applicable
闪点(°C)
Not applicable
法规信息
常规特殊物品
A de novo 0.57 Mb microdeletion in chromosome 11q13.1 in a patient with speech problems, autistic traits, dysmorphic features and multiple endocrine neoplasia type 1.
European Journal of Medical Genetics, 54, e461-e464 (2011)
ER signaling in unfolded protein response
Life Sciences, 74(2-3), 199-205 (2003)
Pharmacological basis research on neurodegenerative disease treatment of human novel endoplasmic reticulum protein HRD1
Japanese Journal of Pharmacology, 133, 252-256 (2009)
Hrd1 facilitates tau degradation and promotes neuron survival.
Current Molecular Medicine, 12, 138-152 (2012)
Genes & development, 17(19), 2436-2449 (2003-09-17)
Rheumatoid arthritis (RA) is one of the most critical articular diseases with synovial hyperplasia followed by impairment of quality of life. However, the mechanism(s) that regulates synovial cell outgrowth is not fully understood. To clarify its mechanism(s), we carried out
我们的科学家团队拥有各种研究领域经验,包括生命科学、材料科学、化学合成、色谱、分析及许多其他领域.
联系技术服务部门