BAIT

NUM1

PAC12, L000001287, YDR150W
Protein required for nuclear migration; component of the mitochondria-ER-cortex-ancor (MECA); required for the association of mitochondria with the cell cortex and for accurate distribution of mitochondrial network; interacts with Mdm36p to link the ER and motochondria at the cortex; localizes to the mother cell cortex and the bud tip; may mediate interactions of dynein and cytoplasmic microtubules with the cell cortex
GO Process (5)
GO Function (1)
GO Component (4)

Gene Ontology Biological Process

Gene Ontology Molecular Function

Gene Ontology Cellular Component

Saccharomyces cerevisiae (S288c)
PREY

TAO3

PAG1, YIL129C
Component of the RAM signaling network; is involved in regulation of Ace2p activity and cellular morphogenesis, interacts with protein kinase Cbk1p and also with Kic1p
GO Process (3)
GO Function (0)
GO Component (4)

Gene Ontology Biological Process

Gene Ontology Cellular Component

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

Mitochondria-ER-PM contacts regulate mitochondrial division and PI(4)P distribution.

Casler JC, Harper CS, White AJ, Anderson HL, Lackner LL

The mitochondria-ER-cortex anchor (MECA) forms a tripartite membrane contact site between mitochondria, the endoplasmic reticulum (ER), and the plasma membrane (PM). The core component of MECA, Num1, interacts with the PM and mitochondria via two distinct lipid-binding domains; however, the molecular mechanism by which Num1 interacts with the ER is unclear. Here, we demonstrate that Num1 contains a FFAT motif ... [more]

J Cell Biol Sep. 02, 2024; 223(9); [Pubmed: 38781029]

Throughput

  • High Throughput

Related interactions

InteractionExperimental Evidence CodeDatasetThroughputScoreCurated ByNotes
TAO3 NUM1
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-0.182BioGRID
1990475

Curated By

  • BioGRID