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PADI4 (显示 PADI4 蛋白) interacted with SYVN1 directly and that overexpression of PADI4 (显示 PADI4 蛋白) suppressed the ubiquitination of proteins. Thus, a reduction in ER stress induced by PADI4 (显示 PADI4 蛋白) may abrogate the initiation of chronic RA by suppressing the proliferative signals of RA synoviocytes.
Amyloid beta oligomers modulate BACE1 (显示 BACE 蛋白) through an XBP-1 (显示 XBP1 蛋白)-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 (显示 HSP70 蛋白)-Hrd1 axis represents a potential therapeutic target for restoring the oncorepressor activity of unstable lymphoma-associated Blimp-1 (显示 PRDM1 蛋白) mutants.
this study proved that SYVN1 enhances SERPINA1 (显示 SERPINA1 蛋白)(E342K)/ATZ degradation through SQSTM1 (显示 SQSTM1 蛋白)-dependent autophagy and attenuates SERPINA1 (显示 SERPINA1 蛋白)(E342K)/ATZ cytotoxicity.
Results demonstrated that overexpression of Hrd1 increased the proteasomal degradation and microtubule-dependent aggresome formation of OPTN (显示 OPTN 蛋白) in the microtubular organizing center, whereas knockdown of Hrd1 stabilized OPTN (显示 OPTN 蛋白) and inhibited aggresome formation of OPTN (显示 OPTN 蛋白).
Data show that E3 ubiquitin ligase (显示 MUL1 蛋白) HRD1 (HRD1) decreased the protein level of S100A8 (显示 S100A8 蛋白) 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 (显示 CFTR 蛋白) biosynthetic pathway. It suggests that SYVN1 and FBXO2 (显示 FBXO2 蛋白) represent two distinct multiprotein complexes that may degrade DeltaF508-CFTR (显示 CFTR 蛋白) in airway epithelia and identifies a new role for NEDD8 (显示 NEDD8 蛋白) in regulating DeltaF508-CFTR (显示 CFTR 蛋白) ubiquitination.
Study shows that mir125b is up-regulated in osteoarthritis (OA) and inversely correlated with SYNV1 expression. Also, findings demonstrated that miR (显示 MLXIP 蛋白)- 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-null B cells exhibited high Fas (显示 FAS 蛋白) expression during activation and rapidly underwent Fas (显示 FAS 蛋白)-mediated apoptosis, which could be largely inhibited by FasL (显示 FASL 蛋白) neutralization. Fas (显示 FAS 蛋白) mutation in Hrd1 KO mice abrogated the increase in B-cell AICD. We identified Hrd1 as the first E3 ubiquitin ligase (显示 MUL1 蛋白) of the death receptor Fas (显示 FAS 蛋白) and Hrd1-mediated Fas (显示 FAS 蛋白) destruction as a molecular mechanism in regulating B-cell immunity.
This study implicates Endoplasmic reticulum (ER)-associated degradation mediated by Sel1L (显示 SEL1L 蛋白)-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 (显示 ERN1 蛋白)), the sensor of the unfolded protein response (UPR), is a bona fide substrate of the Sel1L (显示 SEL1L 蛋白) 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 (显示 PGC 蛋白)-1b.
Data indicate that E3 ubiquitin-protein ligase (显示 UBE2K 蛋白) Hrd1 catalyzed ubiquitination and degradation of the transcriptional suppressor B lymphocyte-induced maturation protein 1 (BLIMP1 (显示 PRDM1 蛋白)) to promote MHC-II antigen expression.
oxidative stress-induced (显示 SQSTM1 蛋白) 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.
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