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Displaying 20 of 26 results for "SEL1L"
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  1. Sel1L is Indispensable for Mammalian ERAD, ER Homeostasis and Survival BioProject

    ID: PRJNA230475

    Keywords: Transcriptome or Gene expression

    Access Type: download

  2. Sel1L is Indispensable for Mammalian ERAD, ER Homeostasis and Survival ArrayExpress

    ID: E-GEOD-52929

    Description: Sel1L is an adaptor protein for the E3 ligase Hrd1 involved in endoplasmic reticulum-associated degradation (ERAD). Its physiologic...

  3. The ER-Associated Degradation Adapter Protein Sel1L Regulates Triglyceride Metabolism via Lipoprotein Lipase BioProject

    ID: PRJNA244933

    Keywords: Transcriptome or Gene expression

    Access Type: download

  4. Crystal structure of mouse SEL1L PDB

    ID: PDB:5B26

    Description: Protein sel-1 homolog 1

  5. Sel1L is Indispensable for Mammalian ERAD, ER Homeostasis and Survival OmicsDI

    ID: E-GEOD-52929

    Date Released: 06-03-2014

    Description: Sel1L is an adaptor protein for the E3 ligase Hrd1 involved in endoplasmic reticulum-associated degradation (ERAD). Its physiologic...

  6. The ER-Associated Degradation Adapter Protein Sel1L Regulates Triglyceride Metabolism via Lipoprotein Lipase OmicsDI

    ID: E-GEOD-56918

    Date Released: 05-24-2015

    Description: Sel1L is an adaptor protein for the E3 ligase Hrd1 in the endoplasmic reticulum-associated degradation (ERAD), but its physiologica...

  7. The ER-Associated Degradation Adapter Protein Sel1L Regulates Triglyceride Metabolism via Lipoprotein Lipase ArrayExpress

    ID: E-GEOD-56918

    Description: Sel1L is an adaptor protein for the E3 ligase Hrd1 in the endoplasmic reticulum-associated degradation (ERAD), but its physiologica...

  8. IRE1alpha is an endogenous substrate of endoplasmic reticulum-associated degradation OmicsDI

    ID: E-GEOD-70563

    Date Released: 12-01-2015

    Description: n response (UPR), is a bona fide substrate of the Sel1L-Hrd1 ERAD complex. Mechanistically, ERAD-mediated IRE1alpha degradation occurs in a Bip-dependent manner under basal conditions and is attenuated in response to ER stress. Both intramembrane hydrophilic residues of IRE1alpha and lectin protein OS9 are required for IRE1alpha degradation. ERAD deficiency causes IRE1alpha protein stabilization, accumulation and mild activation both in vitro and in vivo, leading to cellular hypersensitivity ...

  9. IRE1alpha is an endogenous substrate of endoplasmic reticulum-associated degradation ArrayExpress

    ID: E-GEOD-70563

    Description: n response (UPR), is a bona fide substrate of the Sel1L-Hrd1 ERAD complex. Mechanistically, ERAD-mediated IRE1alpha degradation occurs in a Bip-dependent manner under basal conditions and is attenuated in response to ER stress. Both intramembrane hydrophilic residues of IRE1alpha and lectin protein OS9 are required for IRE1alpha degradation. ERAD deficiency causes IRE1alpha protein stabilization, accumulation and mild activation both in vitro and in vivo, leading to cellular hypersensitivity ...

  10. IRE1alpha is an endogenous substrate of endoplasmic reticulum-associated degradation BioProject

    ID: PRJNA289019

    Keywords: Transcriptome or Gene expression

    Access Type: download

    dataset.description: n response (UPR), is a bona fide substrate of the Sel1L-Hrd1 ERAD complex. Mechanistically, ERAD-mediated IRE1alpha degradation occurs in a Bip-dependent manner under basal conditions and is attenuated in response to ER stress. Both intramembrane hydrophilic residues of IRE1alpha and lectin protein OS9 are required for IRE1alpha degradation. ERAD deficiency causes IRE1alpha protein stabilization, accumulation and mild activation both in vitro and in vivo, leading to cellular hypersensitivity ...
  11. A CRISPR-based screen identifies genes essential for West Nile virus-induced cell death ArrayExpress

    ID: E-GEOD-69666

    Description: ng the genes identified, seven genes, EMC2, EMC3, SEL1L, DERL2, UBE2G2, UBE2J2, and HRD1, stood out as having the strongest phenotype, whose knockout conferred strong protection against WNV-induced cell death with two different WNV strains and in three cell lines. Interestingly, knockout of these genes did not block WNV replication. Thus, these appear to be essential genes that link WNV replication to downstream cell death pathway(s). In addition, the fact that all of these genes belong to the endoplasmic reticulum-associated protein degradation (ERAD) pathway suggests that this might be the primary driver of WNV-induced cell death. Examination of sgRNA populations in survival 293FT cells...

  12. A CRISPR-based screen identifies genes essential for West Nile virus-induced cell death BioProject

    ID: PRJNA286127

    Keywords: Other

    Access Type: download

    dataset.description: ng the genes identified, seven genes, EMC2, EMC3, SEL1L, DERL2, UBE2G2, UBE2J2, and HRD1, stood out as having the strongest phenotype, whose knockout conferred strong protection against WNV-induced cell death with two different WNV strains and in three cell lines. Interestingly, knockout of these genes did not block WNV replication. Thus, these appear to be essential genes that link WNV replication to downstream cell death pathway(s). In addition, the fact that all of these genes belong to the endoplasmic reticulum-associated protein degradation (ERAD) pathway suggests that this might be the primary driver of WNV-induced cell death. Overall design: Examination of sgRNA populations in survival 293FT cells...
  13. The inducuction of UPR target genes in response to zinc depletion and serum starvation in HeLa cells. BioProject

    ID: PRJNA214661

    Keywords: Transcriptome or Gene expression

    Access Type: download

    dataset.description: stress through specific interactions with Derlin-1, which is a component of the ER-associated degradation machinery. Moreover, we recently demonstrated that this interaction is common to ALS-linked SOD1 mutants, and SOD1WT comprises a masked Derlin-1-binding region. We found that under serum starved and zinc-deficient conditions, SOD1WT adopts a mutant-like conformation that exposes the Derlin-1-binding region, suggesting that SOD1-Derlin-
  14. The inducuction of UPR target genes in response to zinc depletion and serum starvation in HeLa cells ArrayExpress

    ID: E-GEOD-49657

    Description: stress through specific interactions with Derlin-1, which is a component of the ER-associated degradation machinery. Moreover, we recently demonstrated that this interaction is common to ALS-linked SOD1 mutants, and SOD1WT comprises a masked Derlin-1-binding region. We found that under serum starved and zinc-deficient conditions, SOD1WT adopts a mutant-like conformation that exposes the Derlin-1-binding region, suggesting that SOD1-Derlin-

  15. IBD2_ASHGO UniProt:Swiss-Prot

    ID: Q754P2

    Description: Protein IBD2 Poly-Lys

  16. IBD2_VANPO UniProt:Swiss-Prot

    ID: A7TMZ9

    Description: Protein IBD2 His-rich

  17. The inducuction of UPR target genes in response to zinc depletion and serum starvation in HeLa cells. OmicsDI

    ID: E-GEOD-49657

    Date Released: 06-03-2014

    Description: stress through specific interactions with Derlin-1, which is a component of the ER-associated degradation machinery. Moreover, we recently demonstrated that this interaction is common to ALS-linked SOD1 mutants, and SOD1WT comprises a masked Derlin-1-binding region. We found that under serum starved and zinc-deficient conditions, SOD1WT adopts a mutant-like conformation that exposes the Derlin-1-binding region, suggesting that SOD1-Derlin-

  18. Transcription profiling of human Barretts oesophagus cell line CP-A hTERT treated with deoxycholic acid and primary bile acids ArrayExpress

    ID: E-GEOD-9768

    Description: nd 10 down-regulated at 2 hours (34 at 6 hours). 12 genes were identified and were subsequently assessed in patients with non-erosive reflux disease, oesophagitis, Barrett's oesophagus and oesophageal adenocarcinoma; Background and Aims: The major etiological risk factor for Barrett’s esophagus and esophageal adenocarcinoma is gastro-esophageal reflux. This study’s aim was to identify genes involved in the cellular response to components of reflux both in vitro and in patients with reflux-related disease. Methods: The Barrett’s cell line, CP-A hTERT, was exposed to media with acid, deoxycholic acid or a primary bile salt mixture. RNA expression was compared with controls on Affymetrix U133 Plus 2.0 arrays. 12 genes of interest were analysed by Rea...

  19. IBD2_YEAS7 UniProt:Swiss-Prot

    ID: A6ZRR9

    Description: Protein IBD2 Phosphoserine Phosphoserine Phosphothreonine

  20. A CRISPR-based screen identifies genes essential for West Nile virus-induced cell death OmicsDI

    ID: E-GEOD-69666

    Date Released: 08-20-2015

    Description: ng the genes identified, seven genes, EMC2, EMC3, SEL1L, DERL2, UBE2G2, UBE2J2, and HRD1, stood out as having the strongest phenotype, whose knockout conferred strong protection against WNV-induced cell death with two different WNV strains and in three cell lines. Interestingly, knockout of these genes did not block WNV replication. Thus, these appear to be essential genes that link WNV replication to downstream cell death pathway(s). In addition, the fact that all of these genes belong to the endoplasmic reticulum-associated protein degradation (ERAD) pathway suggests that this might be the primary driver of WNV-induced cell death. Examination of sgRNA populations in survival 293FT cells...


Displaying 20 of 26 results for "SEL1L"