◀ Back to CALM2
CALM2 — KRAS
Pathways - manually collected, often from reviews:
-
KEGG Long-term potentiation:
CALM1/CALM2/CALM3/CALML3/CALML5/CALML6
→
HRAS/KRAS/NRAS
(protein-protein, activation)
-
NCI Pathway Database Regulation of Ras family activation:
KRAS isoform 4B/GTP complex (KRAS)
→
KRAS isoform 4B/GTP/Ca2+/CaM complex (KRAS-CALM2)
(modification, collaborate)
Fivaz et al., J Cell Biol 2005*
Evidence: physical interaction
-
NCI Pathway Database Regulation of Ras family activation:
KRAS isoform 4B/GTP complex (KRAS)
→
Ca2+/CaM complex (CALM2)
(modification, collaborate)
Fivaz et al., J Cell Biol 2005*
Evidence: physical interaction
-
NCI Pathway Database Regulation of Ras family activation:
KRAS isoform 4B/GTP/Ca2+/CaM complex (KRAS-CALM2)
→
Ca2+/CaM complex (CALM2)
(modification, collaborate)
Fivaz et al., J Cell Biol 2005*
Evidence: physical interaction
-
NCI Pathway Database Regulation of Ras family activation:
KRAS isoform 4B/GTP complex (KRAS)
→
KRAS isoform 4B/GTP/Ca2+/CaM complex (KRAS-CALM2)
(modification, collaborate)
Fivaz et al., J Cell Biol 2005*
Evidence: physical interaction
-
NCI Pathway Database Regulation of Ras family activation:
KRAS isoform 4B/GTP complex (KRAS)
→
Ca2+/CaM complex (CALM2)
(modification, collaborate)
Fivaz et al., J Cell Biol 2005*
Evidence: physical interaction
-
NCI Pathway Database Regulation of Ras family activation:
KRAS isoform 4B/GTP/Ca2+/CaM complex (KRAS-CALM2)
→
Ca2+/CaM complex (CALM2)
(modification, collaborate)
Fivaz et al., J Cell Biol 2005*
Evidence: physical interaction
Text-mined interactions from Literome
Villalonga et al., Mol Cell Biol 2001
:
Furthermore,
calmodulin inhibition preferentially
activated K-Ras
Villalonga et al., J Biol Chem 2002
:
In vitro experiments showed that the phosphorylation of
K-Ras by PKC was
inhibited by
calmodulin , suggesting that calmodulin dependent modulation of K-Ras phosphorylation by PKC could be the mechanism underlying K-Ras activation in fibroblasts treated with TPA plus W13
Lopez-Alcalá et al., J Biol Chem 2008
:
Furthermore, using a K-Ras with impaired binding to calmodulin but with membrane localization, we could demonstrate in striatal neurones that interaction between K-Ras and
calmodulin was not
required for Golgi
K-Ras translocation induced by Ca ( 2+ ) influx