Gene interactions and pathways from curated databases and text-mining

◀ Back to PRKCB

INSR — PRKCB

Pathways - manually collected, often from reviews:

  • OpenBEL Selventa BEL large corpus: INSR → Calcium/Diacylglycerol/PRKCB complex (PRKCB) (decreases, PRKCB Activity)

    Evidence: PKCa, but not bI, g, or e isoforms, inhibited in vivo insulin receptor kinase activity
  • OpenBEL Selventa BEL large corpus: Calcium/Diacylglycerol/PRKCB complex (PRKCB) → INSR (increases)
    Evidence: acti-Fig. 3. PKCb in insulin signal-ing. Insulin-stimulated insulin receptor (IR) phosphorylates IRS1. IRS1 recruit various signaling molecules through SH2-phos-photyrosine interactions. IRS1-binding proteins containing an SH2 domain include Grb2, PI3K, SHP-2, and Nck. Insulin-induced ERK activation in L6 myocytes occurs largely through Raf-1 rather than Ras activation. In contrast, EGF-induced ERK acti-vation is dependent on Grb2/Sos-mediated Ras activation.
  • OpenBEL Selventa BEL large corpus: PRKCB → INSR (increases, INSR Activity, PRKCB Activity)
    Evidence: Modified assertion
  • OpenBEL Selventa BEL large corpus: INSR → PRKCB (decreases, PRKCB Activity, INSR Activity)
    Evidence: Modified assertion

Text-mined interactions from Literome

Ghanim et al., Diabetologia 2007 (Inflammation...) : The increase in SOCS3 but not IKBKB or PRKCB2 is related inversely to p-INSR-beta and might mediate the inhibition of p-INSR-beta
Kellerer et al., Diabetologia 1998 : No effect was seen with PKC gamma, epsilon, zeta and eta while the earlier observed insulin receptor kinase inhibition of PKC beta2 was further augmented ( 91 +/- 13 %, n = 7, p < 0.001 instead of 45 % without IRS-1 )