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INSR — PRKCB
Pathways - manually collected, often from reviews:
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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
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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.
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OpenBEL Selventa BEL large corpus:
PRKCB
→
INSR
(increases, INSR Activity, PRKCB Activity)
Evidence: Modified assertion
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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 )