◀ Back to HRAS
HRAS — SOS2
Pathways - manually collected, often from reviews:
-
KEGG Focal adhesion:
SOS1/SOS2
→
HRAS
(protein-protein, activation)
-
KEGG Gap junction:
SOS1/SOS2
→
HRAS/KRAS/NRAS
(protein-protein, activation)
-
KEGG Natural killer cell mediated cytotoxicity:
SOS1/SOS2
→
HRAS/KRAS/NRAS
(protein-protein, activation)
-
KEGG Fc epsilon RI signaling pathway:
SOS1/SOS2
→
HRAS/KRAS/NRAS
(protein-protein, activation)
-
KEGG Neurotrophin signaling pathway:
SOS1/SOS2
→
HRAS/KRAS/NRAS
(protein-protein, activation)
-
KEGG Regulation of actin cytoskeleton:
SOS1/SOS2
→
HRAS/KRAS/MRAS/NRAS/RRAS/RRAS2
(protein-protein, activation)
-
KEGG Insulin signaling pathway:
SOS1/SOS2
→
HRAS/KRAS/NRAS
(protein-protein, activation)
-
KEGG MAPK signaling pathway:
SOS1/SOS2
→
HRAS/KRAS/MRAS/NRAS/RRAS/RRAS2
(protein-protein, activation)
-
KEGG GnRH signaling pathway:
SOS1/SOS2
→
HRAS/KRAS/NRAS
(protein-protein, activation)
-
KEGG Hepatitis C:
SOS1/SOS2
→
HRAS/KRAS/NRAS
(protein-protein, activation)
-
KEGG Pathways in cancer:
SOS1/SOS2
→
HRAS/KRAS/NRAS
(protein-protein, activation)
-
KEGG Endometrial cancer:
SOS1/SOS2
→
HRAS/KRAS/NRAS
(protein-protein, activation)
-
KEGG Glioma:
SOS1/SOS2
→
HRAS/KRAS/NRAS
(protein-protein, activation)
-
KEGG Glioma:
SOS1/SOS2
→
HRAS/KRAS/NRAS
(protein-protein, activation)
-
KEGG Prostate cancer:
SOS1/SOS2
→
HRAS/KRAS/NRAS
(protein-protein, activation)
-
KEGG Chronic myeloid leukemia:
SOS1/SOS2
→
HRAS/KRAS/NRAS
(protein-protein, activation)
-
KEGG Acute myeloid leukemia:
SOS1/SOS2
→
HRAS/KRAS/NRAS
(protein-protein, activation)
-
KEGG Non-small cell lung cancer:
SOS1/SOS2
→
HRAS/KRAS/NRAS
(protein-protein, activation)
-
KEGG ErbB signaling pathway:
SOS1/SOS2
→
HRAS/KRAS/NRAS
(protein-protein, activation)
-
KEGG Chemokine signaling pathway:
SOS1/SOS2
→
HRAS/KRAS/NRAS
(protein-protein, activation)
-
NCI Pathway Database Regulation of Ras family activation:
HRAS/GDP complex (HRAS)
→
GRB2/SOS2 complex (GRB2-SOS2)
(modification, collaborate)
Gureasko et al., Nature structural & molecular biology 2008, Yang et al., J Biol Chem 1995*, Nielsen et al., Mol Cell Biol 1997*
Evidence: assay
-
WikiPathways Angiopoietin Like Protein 8 Regulatory Pathway:
SOS1/SOS2/GRB2
→
HRAS
(activation)
-
WikiPathways Chemokine signaling pathway:
SOS1/SOS2
→
HRAS/KRAS/NRAS
(activation)
-
WikiPathways DNA Damage Response (only ATM dependent):
Complex of GRB2-SOS1-SOS2
→
HRAS/KRAS/NRAS
(activation)
Protein-Protein interactions - manually collected from original source literature:
Studies that report less than 10 interactions are marked with *
-
IRef Bind Interaction:
SOS2
—
HRAS
Margarit et al., Cell 2003*
-
IRef Bind Interaction:
SOS2
—
HRAS
Margarit et al., Cell 2003*, Sondermann et al., Cell 2004*
-
IRef Bind_translation Interaction:
SOS2
—
HRAS
(x-ray crystallography)
Margarit et al., Cell 2003*
-
IRef Bind_translation Interaction:
SOS2
—
HRAS
(x-ray crystallography)
Margarit et al., Cell 2003*, Sondermann et al., Cell 2004*
-
IRef Hprd Interaction:
SOS2
—
HRAS
(in vitro)
Margarit et al., Cell 2003*
-
IRef Ophid Interaction:
SOS2
—
HRAS
(aggregation, interologs mapping)
Brown et al., Bioinformatics 2005
Text-mined interactions from Literome
Sondermann et al., Cell 2004
:
The recent discovery that
Ras*GTP is an allosteric
activator of
SOS indicated that the regulation of SOS is more complex than originally envisaged
Langlois et al., J Biol Chem 1995
:
Insulin and epidermal growth factor receptors transmit signals for cell proliferation and gene regulation through formation of active GTP bound
p21ras mediated by the guanine nucleotide exchange factor
Sos ... These data suggest that a negative feedback loop exists whereby activation of the Raf/MEK/MAP kinase cascade by
p21ras causes
Sos phosphorylation and, therefore, Sos/Grb2 dissociation, limiting the duration of p21ras activation by growth factors
Schneider et al., Eur J Immunol 1995
(Second Messenger Systems) :
T cell antigen CD28 binds to the
GRB-2/SOS complex,
regulators of
p21ras
D'Ambrosio et al., Eur J Immunol 1996
:
In view of previous studies which demonstrated p21ras co-capping with ligated BCR, the data presented here suggest that Ig-alpha/beta- and SHC tyrosine phosphorylation dependent recruitment of the Grb2/Sos complex to the receptor can occur and may provide a mechanism by which the nucleotide exchange activity of
Sos could
mediate activation of BCR localized
p21ras
Byrne et al., Oncogene 1996
(Pheochromocytoma) :
p21Ras activation by the guanine nucleotide exchange factor Sos,
requires the
Sos/Grb2 interaction and a second ligand dependent signal involving the Sos N-terminus ... It has been suggested that a key event in growth factor induced
p21Ras activation by the guanine nucleotide exchange factor
Sos , is the recruitment of Sos to the plasma membrane by its interaction with the adaptor protein Grb2 ... To clarify the
role of the
Sos/Grb2 interaction in ligand stimulated
p21Ras activation, we have utilised the observation that overexpression of the Sos C-terminal domain can effectively inhibit p21Ras dependent signalling in three different mammalian systems