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Human Polyclonal SYVN1 Primary Antibody for IF, IHC (p) - ABIN388980
Kaneko, Koike, Saito, Kitamura, Okuma, Nomura: Loss of HRD1-mediated protein degradation causes amyloid precursor protein accumulation and amyloid-beta generation. in The Journal of neuroscience : the official journal of the Society for Neuroscience 2010
Show all 12 Pubmed References
Human Polyclonal SYVN1 Primary Antibody for ICC, IF - ABIN250959
Soundararajan, Wang, Melters, Pearce: Glucocorticoid-induced Leucine zipper 1 stimulates the epithelial sodium channel by regulating serum- and glucocorticoid-induced kinase 1 stability and subcellular localization. in The Journal of biological chemistry 2010
Show all 9 Pubmed References
Human Polyclonal SYVN1 Primary Antibody for WB - ABIN1882139
Kikkert, Doolman, Dai, Avner, Hassink, van Voorden, Thanedar, Roitelman, Chau, Wiertz: Human HRD1 is an E3 ubiquitin ligase involved in degradation of proteins from the endoplasmic reticulum. in The Journal of biological chemistry 2004
Show all 6 Pubmed References
Human Polyclonal SYVN1 Primary Antibody for WB - ABIN650702
Wang, Yu, Guo, Zuo, Fisher, Subjeck, Wang: Enhanced endoplasmic reticulum entry of tumor antigen is crucial for cross-presentation induced by dendritic cell-targeted vaccination. in Journal of immunology (Baltimore, Md. : 1950) 2013
Show all 4 Pubmed References
Human Polyclonal SYVN1 Primary Antibody for IHC (fro), IF (p) - ABIN671811
Yan, Zheng, Chen, Liu, Li, Hu, Pei, Li: Expression of endoplasmic reticulum stress-related factors in the retinas of diabetic rats. in Experimental diabetes research 2011
Show all 2 Pubmed References
Human Polyclonal SYVN1 Primary Antibody for IHC (p), ELISA - ABIN542737
Yamada, Ishihara, Tamura, Takahashi, Yamaguchi, Takei, Tokita, Satake, Tashiro, Katagiri, Aburatani, Miyazaki, Oka: WFS1-deficiency increases endoplasmic reticulum stress, impairs cell cycle progression and triggers the apoptotic pathway specifically in pancreatic beta-cells. in Human molecular genetics 2006
Human Polyclonal SYVN1 Primary Antibody for ELISA, IHC - ABIN4319849
Kaneko: [Possible involvement of HRD1 (ubiquitin E3 ligase) in neurodegenerative diseases]. in Nihon yakurigaku zasshi. Folia pharmacologica Japonica 2009
Human Polyclonal SYVN1 Primary Antibody for ICC, IF - ABIN4319847
Stadler, Rexhepaj, Singan, Murphy, Pepperkok, Uhlén, Simpson, Lundberg: Immunofluorescence and fluorescent-protein tagging show high correlation for protein localization in mammalian cells. in Nature methods 2013
This study showed that Herp stability was regulated by synoviolin through lysine ubiquitination-independent proteasomal degradation.
Hrd1 is an E3 ubiquitin ligase in human T cells.IHrd1 expression is increased in CD4-positive T cells from multiple sclerosis patients.
HRD1 prevents apoptosis in renal tubular epithelial cells by mediating eIF-2a ubiquitylation and degradation.
PADI4 interacted with SYVN1 directly and that overexpression of PADI4 suppressed the ubiquitination of proteins. Thus, a reduction in ER stress induced by PADI4 may abrogate the initiation of chronic RA by suppressing the proliferative signals of RA synoviocytes.
Amyloid beta oligomers modulate BACE1 through an XBP-1-dependent pathway involving HRD1.
findings support a model of Hrd1 complex formation, where the Hrd1 cytoplasmic domain and FAM8A1 have a central role in the assembly and activity of this ERAD machinery.
HSP70-Hrd1 axis represents a potential therapeutic target for restoring the oncorepressor activity of unstable lymphoma-associated Blimp-1 mutants.
this study proved that SYVN1 enhances SERPINA1(E342K)/ATZ degradation through SQSTM1-dependent autophagy and attenuates SERPINA1(E342K)/ATZ cytotoxicity.
Results demonstrated that overexpression of Hrd1 increased the proteasomal degradation and microtubule-dependent aggresome formation of OPTN in the microtubular organizing center, whereas knockdown of Hrd1 stabilized OPTN and inhibited aggresome formation of OPTN.
Data show that E3 ubiquitin ligase HRD1 (HRD1) decreased the protein level of S100A8 through ubiquitination.
Analysis of affinity-captured Hrd1 complexes from these cells by size-exclusion chromatography, immunodepletion, and absolute quantification mass spectrometry identified two major high-molecular-mass complexes with distinct sets of interacting proteins and variable stoichiometries, suggesting a hitherto unrecognized heterogeneity in the functional units of Hrd1-mediated protein degradation.
This study provides new knowledge of the CFTR biosynthetic pathway. It suggests that SYVN1 and FBXO2 represent two distinct multiprotein complexes that may degrade DeltaF508-CFTR in airway epithelia and identifies a new role for NEDD8 in regulating DeltaF508-CFTR ubiquitination.
Study shows that mir125b is up-regulated in osteoarthritis (OA) and inversely correlated with SYNV1 expression. Also, findings demonstrated that miR- 125b-5p could promote apoptosis of synovial cells through targeting the SYVN1 gene, and the excessive apoptosis of synovial cells could contribute to the development of OA.
HRD1 is a novel substrate for USP19. USP19 negatively regulates the ubiquitination of HRD1 and prevents it from undergoing proteasomal degradation.
Prion protein mutants inhibit Hrd1-mediated retrotranslocation of misfolded proteins by depleting misfolded protein sensor BiP.
OS-9, an ER-resident lectin, acts downstream of Grp94 to further recognize misfolded alpha1 subunits in a glycan-dependent manner. This delivers misfolded alpha1 subunits to the Hrd1-mediated ubiquitination and the valosin-containing protein-mediated extraction pathway.
These findings uncover a novel role for HRD1 in breast cancer.
The inherently unstable nature of the human SEL1L protein lies in its transmembrane domain, and that association of HRD1 with the SEL1L transmembrane domain restored its stability.
specific silencing of Derlin-2, p97 and HRD1 by shRNAs increases steady state levels of proinsulin. these ERAD constituents are critically involved in proinsulin degradation and may therefore also play a role in subsequent antigen generation.
Charcot-Marie-Tooth disease-related PMP22 is trapped in the endoplasmic reticulum by calnexin-dependent retention and Rer1-mediated early Golgi retrieval systems and partly degraded by the Hrd1-mediated endoplasmic reticulum-associated degradation system.
HRD1 is a liver metabolic regulator and a potential drug target for obesity, fatty liver disease, and insulin resistance associated with the metabolic syndrome
the KAT4 promoter was significantly activated by the transcriptional factors, NFE2related factor 2 and peroxisome proliferatoractivated receptor coactivator 1beta, which are targets of Syvn1induced degradation
Hrd1 is a positive regulator of T cells.Hrd1 is required for T-cell activation and differentiation.
Hrd1-null B cells exhibited high Fas expression during activation and rapidly underwent Fas-mediated apoptosis, which could be largely inhibited by FasL neutralization. Fas mutation in Hrd1 KO mice abrogated the increase in B-cell AICD. We identified Hrd1 as the first E3 ubiquitin ligase of the death receptor Fas and Hrd1-mediated Fas destruction as a molecular mechanism in regulating B-cell immunity.
This study implicates Endoplasmic reticulum (ER)-associated degradation mediated by Sel1L-Hrd1 as a key regulator of B cell development.
SYVN1 may play an important role in inhibiting ER stress, chronic inflammation, and vascular overgrowth associated with DR.
Data show that inositol requiring enzyme 1alpha (IRE1alpha), the sensor of the unfolded protein response (UPR), is a bona fide substrate of the Sel1L proten-Hrd1 protein endoplasmic reticulum (ER)-associated degradation (ERAD) complex.
Hrd1 is an essential component of the adaptive endoplasmic reticulum stress response in cardiac myocytes.
The results highlight a novel function for SYVN1 in the control of body weight and mitochondrial biogenesis through negative regulation of PGC-1b.
Data indicate that E3 ubiquitin-protein ligase Hrd1 catalyzed ubiquitination and degradation of the transcriptional suppressor B lymphocyte-induced maturation protein 1 (BLIMP1) to promote MHC-II antigen expression.
oxidative stress-induced HRD1 insolubilization might be involved in a vicious cycle of increased amyloid beta production and amyloid beta-induced oxidative stress in Alzheimer's disease pathogenesis.
results indicate that Hrd1 plays an important role in the maturation of collagen I in renal fibrosis, and that Sec23A pathway is required for ER-to-Golgi procollagen trafficking to promote collagen synthesis
Synoviolin up-regulates amyloid beta production by targeting a negative regulator of gamma-secretase, Rer1, for degradation.
HRD1 is colocated with the neural stem cell marker protein nestin and glial fibrillary acidic protein in the endoplasmic reticulum membrane of the NSCs of the subventricular zone (SVZ astrocytes) but in the cell nucleus of in the dentate gyrus
these results clearly suggest that both beta-TrCP- and Hrd1-dependent degradation mechanisms regulate the transcriptional activity of Nrf1 to maintain cellular homeostasis.
IL-17 induction of synoviolin may contribute at least in part to RA chronicity by prolonging the survival of RA FLS and immune cells in germinal centre reactions
collagen expression in LX-2 cells was upregulated by synoviolin overexpression, while synoviolin knockdown led to reduced collagen expression
This gene encodes a protein involved in endoplasmic reticulum (ER)-associated degradation. The encoded protein removes unfolded proteins, accumulated during ER stress, by retrograde transport to the cytosol from the ER. This protein also uses the ubiquitin-proteasome system for additional degradation of unfolded proteins. Sequence analysis identified two transcript variants that encode different isoforms.
E3 ubiquitin-protein ligase synoviolin
, HMG-coA reductase degradation 1 homolog
, synovial apoptosis inhibitor 1, synoviolin
, synoviolin 1
, HRD1 protein
, LOW QUALITY PROTEIN: E3 ubiquitin-protein ligase synoviolin
, E3 ubiquitin-protein ligase synoviolin B
, RING-type E3 ubiquitin transferase synoviolin B
, Synovial apoptosis inhibitor 1-B
, synovial apoptosis inhibitor 1-B
, RING-type E3 ubiquitin transferase synoviolin