◀ Back to MAPK14
MAPK14 — SHC1
Pathways - manually collected, often from reviews:
-
NCI Pathway Database IL2-mediated signaling events:
IL2/IL2R alpha/beta/gamma/JAK1/LCK/JAK3/SHC complex (IL2RA-IL2RB-IL2RG-IL2-JAK1-LCK-JAK3-SHC1)
→
p38alpha-beta-active (MAPK14/MAPK11)
(modification, activates)
Hunt et al., J Biol Chem 1999, Crawley et al., J Biol Chem 1997
Evidence: mutant phenotype, other species
-
NCI Pathway Database IL2-mediated signaling events:
IL2/IL2R alpha/beta/gamma/JAK1/LCK/JAK3/SHC complex (IL2RA-IL2RB-IL2RG-IL2-JAK1-LCK-JAK3-SHC1)
→
p38alpha-beta (MAPK14/MAPK11)
(modification, activates)
Hunt et al., J Biol Chem 1999, Crawley et al., J Biol Chem 1997
Evidence: mutant phenotype, other species
-
WikiPathways Hypothesized Pathways in Pathogenesis of Cardiovascular Disease:
SHC1
→
Complex of MAPK3-MAPK8-MAPK1-MAPK14
(activation)
Protein-Protein interactions - manually collected from original source literature:
Studies that report less than 10 interactions are marked with *
Text-mined interactions from Literome
Hunt et al., J Biol Chem 1999
:
Role of interleukin (IL)-2 receptor beta-chain subdomains and
Shc in p38
mitogen activated protein ( MAP ) kinase and p54 MAP kinase ( stress activated protein Kinase/c-Jun N-terminal kinase ) activation
Ursø et al., J Biol Chem 1999
:
In contrast, the IGF-I receptor chimera mediated more effective
Shc phosphorylation, association of Shc with Grb2, and
activation of
mitogen activated protein kinase compared with the insulin receptor chimera
Cousin et al., Biochem J 1999
:
Glucose ( > 3 mM ) independently increased tyrosine-phosphorylation mediated recruitment of growth-factor bound protein 2 (Grb2)/murine sons of sevenless-1 protein ( mSOS ) and PI3'K to insulin receptor substrate (IRS)-1 and IRS-2, as well as
SH2 containing protein (Shc) association with Grb2/mSOS and downstream
activation of
mitogen activated protein kinase and 70 kDa S6 kinase
Goetze et al., J Biol Chem 2000
:
Insulin binding to the insulin receptor (IR) triggers its autophosphorylation, resulting in phosphorylation of
Shc and the downstream
activation of p42/p44 extracellular signal regulated kinase 1/2
mitogen activated protein kinase ( ERK1/2 ), which mediates insulin induced proliferation in vascular smooth muscle cells ( VSMC )
Song et al., Mol Endocrinol 2002
(Breast Neoplasms) :
Overexpression of dominant negative
Shc blocked the effect of E2 on
MAPK , indicating a critical role of Shc in E2 action
Kornmann et al., Gastroenterology 2002
(Cell Transformation, Neoplastic...) :
In vitro, TAKA-1 cells stably transfected with FGFR-1 IIIc exhibited increased basal growth ; enhanced basal tyrosine phosphorylation of FGFR substrate-2 (FRS2),
Shc , and phospholipase Cgamma ; and increased
activation of mitogen activated protein kinase (
MAPK )
Chen et al., J Biol Chem 2002
:
Incubation of cells with the specific EGFR inhibitor AG4178 blocked MbetaCD induced phosphorylation of EGFR,
SHC , phospholipase C-gamma, and Gab-1 as well as
MAPK activation
Song et al., Proc Natl Acad Sci U S A 2004
:
Down-regulation of
Shc , ERalpha, or IGF-1R with specific small inhibitory RNAs all
blocked E2-induced
mitogen activated protein kinase phosphorylation
Crowe et al., BMC cancer 2004
(Carcinoma, Squamous Cell) :
FAK recruitment of paxillin to the cell membrane correlates with
Shc phosphorylation and
activation of
MAPK
Clemmons et al., Mol Endocrinol 2005
:
Shc activation
results in induction of
MAPK
Lieskovska et al., J Biol Chem 2006
(MAP Kinase Signaling System) :
Our previous studies have shown that IGF-I induced
Shc phosphorylation is
necessary for sustained activation of
MAPK and increased cell proliferation of SMCs, and both Shc and the tyrosine phosphatase SHP-2 must be recruited to the membrane protein SHPS-1 in order for Shc to be phosphorylated
Myers et al., Mol Cell Biol 1994
:
Coexpression of IRS-1 or IRS-1F-895 with the insulin receptor was required for insulin stimulated mitogenesis in 32-D cells, while expression of the insulin receptor alone was sufficient to mediate insulin stimulated tyrosine phosphorylation of
Shc and
activation of p21ras and
mitogen activated protein ( MAP ) kinase
Gunn-Moore et al., Biochem J 1997
:
Taken together, our data suggest that the apparent defect in
MAPK activation caused by the kinase insert may
result predominantly from an inhibition of high-affinity
Shc binding, although a role for PLC gamma and PtdIns 3-kinase can not be completely excluded
Gotoh et al., Mol Cell Biol 1997
:
Shc stimulates
Ras/mitogen activated protein kinase ( MAPK ) through forming a complex with Grb2 at the phosphorylated tyrosine ( Y ) residue 317
Seno et al., Growth Factors 1998
:
The refolded, modified rhCR-1 protein was found to be biologically active by its ability to inhibit beta-casein expression, to stimulate the tyrosine phosphorylation of
Shc and the
activation of
MAPK and by its capacity to facilitate branching growth of mouse mammary epithelial cells in type I collagen gels
Maru et al., J Cell Physiol 1998
:
Matrigel
induced long lasting tyrosine phosphorylation of
Shc , with recruitment of Grb-2 and microtubule associated protein kinase (
MAPK ) activation in both parental NP31 and NP31 transformed by ts-v-Ras, which was blocked by anti-beta1 integrin antibody
Lee et al., Pediatr Res 1998
:
Shc 52 is an
activator of Ras and
mitogen activated protein kinase , whereas Shc 66 antagonizes Ras activation