Rho GTPases and their effector proteins.

By Anne L Bishop, A. Hall. Biochemical Journal, 2000

2,074 citations recorded by the source corpus.

Subfields: Cell Biology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/74e1d9b5ac725cc0ef9804e2ccfd044ee87dda73

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Citations in the corpus

Rho kinase, a promising drug target for neurological disorders (2005, background): “RhoGTPases, a subfamily of the Ras superfamily of GTPases, function as molecular devices that control multiple signalling pathways in a very precise and coordinated way by switching between a biochemically inactive (GDP-bound) and an active (GTP-bound) stat”
Smad-dependent and Smad-independent pathways in TGF-β family signalling (2003, background): “Rac and Cdc42 regulate JNK and p38 MAPK pathway activation, presumably by directly interacting with MAPKKKs upstream of JNK and p38 MAPK, whereas Rho, Rac and Cdc42 affect the cytoskeletal organizatio”
The role of the Rho GTPases in neuronal development. (2005, background): “For more comprehensive reviews on Rho effectors, the reader is referred to the following references: Van Aelst and D’Souza-Schorey (1997); Bishop and Hall (2000); Gundersen (2002); Luo (2002); Bokoch (2003); Miki and Takenawa (2003); Riento and Ridley (2003); Burridge and Wennerberg (2004); Millard…”
Integrin-mediated activation of Cdc42 controls cell polarity in migrating astrocytes through PKCzeta. (2001, background): “The wound edge cells, originally fibroblast-like in p65PAK, MRCK, and MLK as well as structural proteins shape, adopted a highly elongated shape through the such as WASp and IQGAP (Bishop and Hall, 2000).”
GEF means go: turning on RHO GTPases with guanine nucleotide-exchange factors (2005, background): “In contrast to Rho · GDP, Rho · GTP actively transduces signals by interacting with downstream effector”
Transforming growth factor-beta1 mediates epithelial to mesenchymal transdifferentiation through a RhoA-dependent mechanism. (2001, neutral): “members identified to date (Bishop and Hall, 2000), the”
Hippocampal LTP is accompanied by enhanced F-actin content within the dendritic spine that is essential for late LTP maintenance in vivo. (2003, background): “…A, AMPAR is internalized (Zhou et al., 2001). which is known to be a key regulator of actin cytoskeleFurthermore, AMPAR internalization is blocked by jas- ton dynamics in a variety of cell types (for a review, see plakinolide, an F-actin-stabilizing reagent (Zhou et al., Bishop and Hall, 2000).”
Neurotrophins: roles in neuronal development and function. (2001, background): “These have been shown by many laboratories to involve small G proteins of the Cdc-42/Rac/Rho family, which regulate the polymerization and turnover of F-actin (reviewed in Kjoller & Hall 1999, Bishop & Hall 2000).”
Cell migration: Rho GTPases lead the way. (2004, background): “Once activated, Rho GTPases interact with cellular target proteins (effectors) to generate a downstream response (Bishop and Hall, 2000).”
Trk receptors: mediators of neurotrophin action. (2001, background): “These small G proteins control many facets of cell metabolism, but their rapid effects on morphology reflect their regulation of the actin cytoskeleton (reviewed in [49,50]).”
Rho GTPases: biochemistry and biology. (2005, background): “For the handful of targets that have been examined structurally, it appears that they exist in a closed inactive conformation that is relieved through GTPase binding (Bishop & Hall 2000).”
Filamins as integrators of cell mechanics and signalling (2001, background): “A good example of the potential of such macromolecular cooperation is the fact that FLNa binds to RHO FAMILY GTPASES and to some of their regulatory cofactors that are strongly implicated in the regulation of actin assembly and myosin activatio”