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IRS1 — PRKCZ

Pathways - manually collected, often from reviews:

• OpenBEL Selventa BEL large corpus: IRS1 → PRKCZ (directlyIncreases, IRS1 Activity)
  Evidence: 15516986;14583092;16129678
• KEGG Type II diabetes mellitus: PRKCZ → IRS1/IRS2/IRS4 (protein-protein, inhibition)
• WikiPathways Type II diabetes mellitus: PRKCZ → IRS1 (mim-inhibition)

Protein-Protein interactions - manually collected from original source literature:

Studies that report less than 10 interactions are marked with *

• IRef Hprd Interaction: IRS1 — PRKCZ (in vitro) Ravichandran et al., J Biol Chem 2001*
• IRef Hprd Interaction: IRS1 — PRKCZ (in vivo) Ravichandran et al., J Biol Chem 2001*

Text-mined interactions from Literome

Sedaghat et al., Am J Physiol Endocrinol Metab 2002 (Insulin Resistance) : A novel mechanistic model of postreceptor events including phosphorylation of insulin receptor substrate-1 , activation of phosphatidylinositol 3-kinase, and subsequent activation of downstream kinases Akt and protein kinase C-zeta is coupled with previously validated subsystem models of insulin receptor binding, receptor recycling, and GLUT4 translocation
Corbould et al., J Endocrinol 2007 (Insulin Resistance...) : In the glucose metabolic pathway of insulin signaling, treatment of cells with T 10 nmol/l did not alter insulin stimulated phosphorylation of insulin receptor substrate-1 or Akt, but insulin stimulated phosphorylation of protein kinase C (PKC) zeta was impaired