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HSP70 (show HSP70 Proteins)-Hrd1 axis represents a potential therapeutic target for restoring the oncorepressor activity of unstable lymphoma-associated Blimp-1 (show PRDM1 Proteins) mutants.
this study proved that SYVN1 enhances SERPINA1 (show SERPINA1 Proteins)(E342K)/ATZ degradation through SQSTM1 (show SQSTM1 Proteins)-dependent autophagy and attenuates SERPINA1 (show SERPINA1 Proteins)(E342K)/ATZ cytotoxicity.
Results demonstrated that overexpression of Hrd1 increased the proteasomal degradation and microtubule-dependent aggresome formation of OPTN (show OPTN Proteins) in the microtubular organizing center, whereas knockdown of Hrd1 stabilized OPTN (show OPTN Proteins) and inhibited aggresome formation of OPTN (show OPTN Proteins).
Data show that E3 ubiquitin ligase (show MUL1 Proteins) HRD1 (HRD1) decreased the protein level of S100A8 (show S100A8 Proteins) 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 (show CFTR Proteins) biosynthetic pathway. It suggests that SYVN1 and FBXO2 (show FBXO2 Proteins) represent two distinct multiprotein complexes that may degrade DeltaF508-CFTR (show CFTR Proteins) in airway epithelia and identifies a new role for NEDD8 (show NEDD8 Proteins) in regulating DeltaF508-CFTR (show CFTR Proteins) ubiquitination.
Study shows that mir125b is up-regulated in osteoarthritis (OA) and inversely correlated with SYNV1 expression. Also, findings demonstrated that miR (show MLXIP Proteins)- 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 (show PRNP Proteins) mutants inhibit Hrd1-mediated retrotranslocation of misfolded proteins by depleting misfolded protein sensor BiP (show GDF10 Proteins).
OS-9 (show OS9 Proteins), an ER-resident lectin, acts downstream of Grp94 (show HSP90B1 Proteins) 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 (show vcp Proteins)-mediated extraction pathway.
Hrd1-null B cells exhibited high Fas (show FAS Proteins) expression during activation and rapidly underwent Fas (show FAS Proteins)-mediated apoptosis, which could be largely inhibited by FasL (show FASL Proteins) neutralization. Fas (show FAS Proteins) mutation in Hrd1 KO mice abrogated the increase in B-cell AICD. We identified Hrd1 as the first E3 ubiquitin ligase (show MUL1 Proteins) of the death receptor Fas (show FAS Proteins) and Hrd1-mediated Fas (show FAS Proteins) destruction as a molecular mechanism in regulating B-cell immunity.
This study implicates Endoplasmic reticulum (ER)-associated degradation mediated by Sel1L (show SEL1L Proteins)-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 (show ERN1 Proteins)), the sensor of the unfolded protein response (UPR), is a bona fide substrate of the Sel1L (show SEL1L Proteins) 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 (show PGC Proteins)-1b.
Data indicate that E3 ubiquitin-protein ligase (show UBE2K Proteins) Hrd1 catalyzed ubiquitination and degradation of the transcriptional suppressor B lymphocyte-induced maturation protein 1 (BLIMP1 (show PRDM1 Proteins)) to promote MHC-II antigen expression.
oxidative stress-induced (show SQSTM1 Proteins) 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 (show SEC23A Proteins) pathway is required for ER-to-Golgi procollagen trafficking to promote collagen synthesis
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