BAIT

INO80

chromatin-remodeling ATPase INO80, L000004543, YGL150C
ATPase and nucleosome spacing factor; subunit of complex containing actin and actin-related proteins that has chromatin remodeling activity and 3' to 5' DNA helicase activity in vitro; promotes nucleosome shifts in the 3 prime direction; has a role in modulating stress gene transcription
Saccharomyces cerevisiae (S288c)
PREY

RPN11

MPR1, proteasome regulatory particle lid subunit RPN11, L000002976, L000002965, YFR004W
Metalloprotease subunit of 19S regulatory particle; part of 26S proteasome lid; couples the deubiquitination and degradation of proteasome substrates; involved, independent of catalytic activity, in fission of mitochondria and peroxisomes; protein abundance increases in response to DNA replication stress
UPS Project
Saccharomyces cerevisiae (S288c)

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

INO80 Chromatin Remodeler Facilitates Release of RNA Polymerase II from Chromatin for Ubiquitin-Mediated Proteasomal Degradation.

Lafon A, Taranum S, Pietrocola F, Dingli F, Loew D, Brahma S, Bartholomew B, Papamichos-Chronakis M

Stalling of RNA Polymerase II (RNAPII) on chromatin during transcriptional stress results in polyubiquitination and degradation of the largest subunit of RNAPII, Rpb1, by the ubiquitin proteasome system (UPS). Here, we report that the ATP-dependent chromatin remodeling complex INO80 is required for turnover of chromatin-bound RNAPII in yeast. INO80 interacts physically and functionally with Cdc48/p97/VCP, a component of UPS required for ... [more]

Mol. Cell Dec. 03, 2015; 60(5);784-96 [Pubmed: 26656161]

Throughput

  • Low Throughput

Additional Notes

  • Figure S1

Related interactions

InteractionExperimental Evidence CodeDatasetThroughputScoreCurated ByNotes
INO80 RPN11
Negative Genetic
Negative Genetic

Mutations/deletions in separate genes, each of which alone causes a minimal phenotype, but when combined in the same cell results in a more severe fitness defect or lethality under a given condition. This term is reserved for high or low throughput studies with scores.

High-0.25BioGRID
1933833

Curated By

  • BioGRID