BAIT
HSPB1
CMT2F, HEL-S-102, HMN2B, HS.76067, HSP27, HSP28, Hsp25, SRP27
heat shock 27kDa protein 1
GO Process (21)
GO Function (7)
GO Component (8)
Gene Ontology Biological Process
- RNA metabolic process [TAS]
- cellular component movement [TAS]
- cellular response to vascular endothelial growth factor stimulus [IMP]
- gene expression [TAS]
- intracellular signal transduction [IMP]
- mRNA metabolic process [TAS]
- negative regulation of apoptotic process [TAS]
- negative regulation of oxidative stress-induced intrinsic apoptotic signaling pathway [ISS]
- negative regulation of protein kinase activity [ISS]
- platelet aggregation [IMP]
- positive regulation of angiogenesis [IMP]
- positive regulation of blood vessel endothelial cell migration [IMP]
- positive regulation of endothelial cell chemotaxis [IMP]
- positive regulation of endothelial cell chemotaxis by VEGF-activated vascular endothelial growth factor receptor signaling pathway [IMP]
- positive regulation of interleukin-1 beta production [ISS]
- positive regulation of tumor necrosis factor biosynthetic process [ISS]
- regulation of I-kappaB kinase/NF-kappaB signaling [ISS]
- regulation of translational initiation [TAS]
- response to unfolded protein [NAS]
- response to virus [IEP]
- retina homeostasis [IEP]
Gene Ontology Molecular Function
Gene Ontology Cellular Component
Homo sapiens
PREY
KIAA1217
SKT, RP11-324E23.1
KIAA1217
GO Process (1)
GO Function (0)
GO Component (1)
Gene Ontology Biological Process
Homo sapiens
Affinity Capture-MS
An interaction is inferred when a bait protein is affinity captured from cell extracts by either polyclonal antibody or epitope tag and the associated interaction partner is identified by mass spectrometric methods.
Publication
Neuropathy-causing mutations in HSPB1 impair autophagy by disturbing the formation of SQSTM1/p62 bodies.
HSPB1 (heat shock protein family B [small] member 1) is a ubiquitously expressed molecular chaperone. Most mutations in HSPB1 cause axonal Charcot-Marie-Tooth neuropathy and/or distal hereditary motor neuropathy. In this study we show that mutations in HSPB1 lead to impairment of macroautophagic/autophagic flux. In HSPB1 knockout cells, we demonstrate that HSPB1 is necessary for autophagosome formation, which was rescued upon ... [more]
Autophagy Dec. 01, 2018; 15(6);1051-1068 [Pubmed: 30669930]
Throughput
- High Throughput
Curated By
- BioGRID