BAIT

UBQLN2

Chap1, Dsk2, HRIHFB2157, Plic-2, Plic2, RP23-240F13.1
ubiquilin 2
GO Process (0)
GO Function (1)
GO Component (2)

Gene Ontology Molecular Function

Gene Ontology Cellular Component

Mus musculus
PREY

ATP6V1G1

1810024D14Rik, AA960677, ATP6J, Atp6g1, VAG1, Vma10
ATPase, H+ transporting, lysosomal V1 subunit G1
Mus musculus

Affinity Capture-Western

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 identified by Western blot with a specific polyclonal antibody or second epitope tag. This category is also used if an interacting protein is visualized directly by dye stain or radioactivity. Note that this differs from any co-purification experiment involving affinity capture in that the co-purification experiment involves at least one extra purification step to get rid of potential contaminating proteins.

Publication

ALS/FTD mutations in UBQLN2 impede autophagy by reducing autophagosome acidification through loss of function.

Wu JJ, Cai A, Greenslade JE, Higgins NR, Fan C, Le NTT, Tatman M, Whiteley AM, Prado MA, Dieriks BV, Curtis MA, Shaw CE, Siddique T, Faull RLM, Scotter EL, Finley D, Monteiro MJ

Mutations in UBQLN2 cause amyotrophic lateral sclerosis (ALS), frontotemporal dementia (FTD), and other neurodegenerations. However, the mechanism by which the UBQLN2 mutations cause disease remains unclear. Alterations in proteins involved in autophagy are prominent in neuronal tissue of human ALS UBQLN2 patients and in a transgenic P497S UBQLN2 mouse model of ALS/FTD, suggesting a pathogenic link. Here, we show UBQLN2 ... [more]

Proc Natl Acad Sci U S A Dec. 30, 2019; 117(26);15230-15241 [Pubmed: 32513711]

Throughput

  • Low Throughput

Curated By

  • BioGRID