Identifiers
NAME:ERK*:MEK*:_beta_-Arrestin2*
References
su_mpk1_mpk1_re86( Survival ):
The internalised GPCR receptor will finally be recycled into the cell membrane or be sent to lysosome for degradation (not modelled).
PMID:19565474
su_mpk1_mpk1_re87( Survival ):
Upon activation scaffold proteins serve as platforms in which ERK dimers are assembled forming complexes capable of interacting with and activating cognate cytoplasmic substrates.
Beta-ARRESTIN prevents the translocation of ERK into the nucleus thereby reducing phosphorylation of nuclear substrates and consequently MODULE:MAPK -dependent gene expression.
PMID:18775330 PMID:19091303
su_mpk1_mpk1_re192( Survival ):
MEK is continuously dephosphorylated by PP2A (PPP2CA) whose activity is stimulated by P38: P38 activity increases the physical association between PP2A and MEK/ERK complex. A direct interaction between P38 and ERK has been proposed as a mechanism to inhibit ERK phosphorylation. AP-1 mediated gene expression inhibits ERK phosphorylation.
PMID:18039929
Identifiers
NAME:ERK*:MEK*:_beta_-Arrestin2*
References
su_mpk1_mpk1_re87( Survival ):
Upon activation scaffold proteins serve as platforms in which ERK dimers are assembled forming complexes capable of interacting with and activating cognate cytoplasmic substrates.
Beta-ARRESTIN prevents the translocation of ERK into the nucleus thereby reducing phosphorylation of nuclear substrates and consequently MODULE:MAPK -dependent gene expression.
PMID:18775330 PMID:19091303
su_mpk1_mpk1_re94( Survival ):
RSK2 is a well known ERK substrate in the cytoplasm and has been shown to undergo autophosphorylation after ERK phosphorylation.
RSKs interact with ERK and dissociate upon activation.
Results suggested that KSR1 was the scaffold utilised by ERK1/2 for activating cPLA2 but not RSK1.
PMID:15239952 PMID:15187187 PMID:19114553
→ MEK*:_beta_-Arrestin2*@Cytoplasm + ERK*@Cytoplasm
→ GPCR*:GRK*@Early Endosomes + ERK*|pho|pho:MEK*|pho|pho:_beta_-Arrestin2*@Early Endosomes + RAF1@Cytoplasm
+ ERK*|pho|pho@Cytoplasm → ERK*|pho|pho|hm2:MEK*|pho|pho:_beta_-Arrestin2*@Cytoplasm