e_re778

Reaction state_transition e_re778 map

PIP5K1*@Cytoplasm map PIP5K1*@Cytoplasm map

Reaction regulators:

Physical_stimulation
  1. GTP:​RAC1@Cytoplasm map



References
RAC1 modulates cytoskeleton remodeling by activating ARFP2 and PIP5K1
PMID:10679324
Rac-associated PIP 5-kinase as the PIP 5-kinase isoforms alpha and beta.
When added to permeabilized platelets, PIP 5-kinase alpha induced actin filament uncapping and assembly.
PIP 5-kinase alpha is a critical mediator of thrombin- and Rac-dependent actin assembly.
PMID:14681219
PIP5K catalyzes the formation of the phospholipid, phosphatidylinositol 4,5-bisphosphate PIP2
RhoA and Rac1 bind and activate PIP5K.
3 isoforms of type I PIP5K (alpha,beta, and gamma) have been identified
RhoA and Rac1, as well as Cdc42, but not RalA and Rap1A, markedly stimulate PIP2 synthesis by all three PIP5K isoforms expressed in human embryonic kidney 293 cells, both in vitro and in vivo.
RhoA-stimulated PIP2 synthesis by the PIP5K isoforms was mediated by the RhoA effector, Rho kinase.
Stimulation of PIP5K isoforms by Rac1 and Cdc42 was apparently independent of and additive with RhoA- and Rho-kinase
RhoA, and to a lesser extent Rac1, but not Cdc42, interacted in a nucleotide-independent form with all three PIP5K isoforms.
Binding of PIP5K isoforms to GTP-bound, but not GDP-bound, RhoA could be displaced by Rho-kinase, suggesting a direct and constitutive PIP5K-Rho GTPase binding, which, however, does not trigger PIP5K activation.
Synthesis of PIP2 by the three PIP5K isoforms is controlled by RhoA, acting via Rho-kinase, as well as Rac1 and Cdc42, implicating that regulation of PIP2 synthesis has a central position in signaling by these three Rho GTPases.

Confidence
REF=2 FUNC=4


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