◀ Back to EGF
AHSA1 — EGF
Text-mined interactions from Literome
Rebsamen et al., J Mol Cell Cardiol 2000
(Cardiomegaly) :
The results further show that
EGF activates Stat5, that this response requires
p38 MAPK stimulation, and it is negatively modulated by p42/44 MAPK
Stoll et al., Wound Repair Regen 2003
(MAP Kinase Signaling System) :
These data also indicate that autocrine heparin binding
epidermal growth factor expression is not
regulated by
p38
Cooper et al., Toxicol Appl Pharmacol 2004
:
In contrast,
p38 activation was
independent of
EGF receptor or Src-family kinase activity
Guo et al., World J Gastroenterol 2005
:
The data suggest that TPA and
EGF induced
p38 phosphorylation is through an autophosphorylation dependent mechanism ... Since p38 phosphorylation induced by TGF-beta1 plays an important role in caspase activation and apoptosis, TPA and
EGF induced
p38 phosphorylation may not be requisite for their anti-apoptotic function
Singh et al., Mol Cancer Ther 2006
(MAP Kinase Signaling System) :
Silibinin treatment under similar conditions also strongly inhibited
EGF induced ERK1/2, JNK1/2, and
p38K as well as Akt phosphorylation, and also suppressed EGF induced AP-1 and NF-kappaB activation
Wang et al., Invest Ophthalmol Vis Sci 2006
:
EGF induced changes in Erk1/2 and
p38 phosphorylation status are dependent on PP-mediated crosstalk
Browne et al., Biochem Biophys Res Commun 2008
:
ERK5 activation by either TGF-beta or
epidermal growth factor (EGF) was also
inhibited by the
p38 MAP kinase inhibitor, SB-202190
Lofgren et al., Breast Cancer Res 2011
(Breast Neoplasms...) :
Brk dependent signaling to p38 MAPK was recapitulated by Brk overexpression in the HC11 murine mammary epithelial cell (MEC) line and human MEC, while Brk knock-down in breast cancer cells blocked
EGF stimulated
p38 signaling
Hazzalin et al., Mol Cell Biol 1998
:
These data show that anisomycin behaves like a true signalling agonist and suggest that the anisomycin desensitized signalling component ( s ) is not involved in JNK/SAPK or
p38/RK activation by
EGF , bFGF, TNF-alpha, or TPA but may play a significant role in UV- and hyperosmolarity stimulated responses
Chan-Hui et al., Biochem J 1998
:
Kinase-inactive DeltaMAPKKK4 partly inhibited the
activation of
p38alpha , JNK1/2 and ERK2 induced by stress, tumour necrosis factor alpha or
epidermal growth factor , suggesting that MAPKKK4 might be physiologically involved in all three MAPK cascades