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TranscriptomicsTranscriptome analysis in primary fibroblasts from HOIL-1-deficient patients upon TNF-α or IL-1β stimulation
HOIL-1 deficient disease is a new early onset fatal autosomal recessive human disorder charaterized by chronic auto-inflammation, recurrent invasive bacterial infections and progressive muscular amylopectinosis. We studied the effect of TNF-α and IL-1β on transcriptional changes of primary fibrobla...
ORGANISM(S): Homo sapiens 
2012-10-28 | E-GEOD-40560 | biostudies-arrayexpress
GenomicsHOIL-1/RBCK1 promotes p53 degradation in Renal cancer cells
HOIL-1/RBCK1 promotes p53 degradation in Renal cancer cells
PRJNA490504 | ENA
TranscriptomicsTranscriptome analysis in peripheral blood mononuclear cells (PBMC) from HOIL-1-deficient patients upon TNF-α or IL-1β stimulation
HOIL-1 deficient disease is a new early onset fatal autosomal recessive human disorder charaterized by chronic auto-inflammation, recurrent invasive bacterial infections and progressive muscular amylopectinosis. We studied the effect of TNF-α and IL-1β on transcriptional changes of PBMCs from HOIL-1...
ORGANISM(S): Homo sapiens 
2012-10-28 | E-GEOD-40838 | biostudies-arrayexpress
TranscriptomicsTranscriptional analysis of whole blood, primary fibroblasts, and PBMCs upon TNF-alpha or IL-1beta stimulation from HOIL-1-deficient patients
This SuperSeries is composed of the following subset Series: GSE40560: Transcriptome analysis in primary fibroblasts from HOIL-1-deficient patients upon TNF-alpha or IL-1beta stimulation GSE40561: Transcriptional analysis of whole blood in patients with auto-inflammatory disorders GSE40838: Transcr...
ORGANISM(S): Homo sapiens 
2012-10-28 | E-GEOD-40752 | biostudies-arrayexpress
UnknownStructural basis for ubiquitylation by HOIL-1.
Not available
S-EPMC9853177 | biostudies-literature
ProteomicsCharacterize proteome-wide changes in protein abundance and ubiquitination during glucose starvation in wild-type and HOIL-1mut AC16 cardiomyocytesCharacterize proteome-wide changes in protein abundance and ubiquitination during glucose starvation in wild-type and HOIL-1mut AC16 cardiomyocytes
The cells expressing a truncated form of the E3 ubiquitin ligase HOIL-1 are hypersensitive to lethal metabolic stress. We hypothesize that alterations in ubiquitination or abundance of key substrates constitutes a mechanistic underpinning of this phenotype.
ORGANISM(S): Homo sapiens (Human) 
2026-03-13 | PXD046661 | Pride
Tmtpro Hoil-1 Ubiquitination 
UnknownSolution structure of the E3 ligase HOIL-1 Ubl domain.
Not available
S-EPMC3403446 | biostudies-literature
TranscriptomicsTranscriptome analysis in primary fibroblasts from HOIL-1-deficient patients upon TNF-α or IL-1β stimulation
HOIL-1 deficient disease is a new early onset fatal autosomal recessive human disorder charaterized by chronic auto-inflammation, recurrent invasive bacterial infections and progressive muscular amylopectinosis. We studied the effect of TNF-α and IL-1β on transcriptional changes of primary fibroblas...
ORGANISM(S): Homo sapiens 
2012-10-28 | GSE40560 | GEO
UnknownHOIL-1 ubiquitin ligase activity targets unbranched glucosaccharides and is required to prevent polyglucosan accumulation.
Not available
S-EPMC9016349 | biostudies-literature
UnknownThe RBR E3 ubiquitin ligase HOIL-1 can ubiquitinate diverse non-protein substrates in vitro.
Not available
S-EPMC11962058 | biostudies-literature
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