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CALM1 — KRAS
Pathways - manually collected, often from reviews:
-
KEGG Long-term potentiation:
CALM1/CALM2/CALM3/CALML3/CALML5/CALML6
→
HRAS/KRAS/NRAS
(protein-protein, activation)
Protein-Protein interactions - manually collected from original source literature:
Studies that report less than 10 interactions are marked with *
-
IRef Biogrid Interaction:
CALM1
—
KRAS
(physical association, affinity chromatography technology)
Villalonga et al., Mol Cell Biol 2001*
-
IRef Biogrid Interaction:
CALM1
—
KRAS
(direct interaction, pull down)
Villalonga et al., Mol Cell Biol 2001*
-
IRef Biogrid Interaction:
CALM1
—
KRAS
(direct interaction, pull down)
Sidhu et al., Biochem Biophys Res Commun 2003*
-
IRef Biogrid Interaction:
CALM1
—
KRAS
(direct interaction, two hybrid)
Sidhu et al., Biochem Biophys Res Commun 2003*
-
IRef Hprd Interaction:
CALM1
—
KRAS
(two hybrid)
Villalonga et al., Mol Cell Biol 2001*, Sidhu et al., Biochem Biophys Res Commun 2003*
-
IRef Hprd Interaction:
CALM1
—
KRAS
(in vivo)
Villalonga et al., Mol Cell Biol 2001*, Sidhu et al., Biochem Biophys Res Commun 2003*
-
IRef Hprd Interaction:
CALM1
—
KRAS
(in vitro)
Villalonga et al., Mol Cell Biol 2001*, Sidhu et al., Biochem Biophys Res Commun 2003*
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