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1 ression of constitutively active Galpha(13), p115RhoGEF, or RhoA mimicked lysophosphatidic acid (LPA)
4 S interaction are preserved in the alpha(13)/p115RhoGEF interaction, there are also significant diffe
5 l cross-talk exerted from the LPA/Galpha(13)/p115RhoGEF/RhoA pathway to the beta(2)-adrenergic recept
6 IV collagen, whereas a constitutively active p115RhoGEF restored the arachidonic acid stimulation in
7 nstream mediators Galpha(12), Galpha(13) and p115RhoGEF regulated cell viability and was required for
8 eam RhoA activators including Galpha(13) and p115RhoGEF, with Galpha(13)-induced Rho.GTP loading inhi
9 beta(2)AR activation, both betaArrestin2 and p115RhoGEF translocate to the plasma membrane, with conc
10 unoblot analyses indicate that both CD44 and p115RhoGEF are expressed in MDA-MB-231 cells and that th
12 s, PDZ RhoGEF, which, together with LARG and p115RhoGEF, links the G(12/13) family of heterotrimeric
15 for Rho that includes PDZ-RhoGEF, LARG, and p115RhoGEF exhibits a unique structural feature consisti
16 olling the activity of PDZ-RhoGEF, LARG, and p115RhoGEF, which involves homo- and hetero-oligomerizat
17 tide exchange factor (GEF)), PDZ-RhoGEF, and p115RhoGEF augmented interaction between activated Galph
18 GEF within 1 min of thrombin stimulation and p115RhoGEF phosphorylation was dependent on PKCalpha.
22 tly stimulates the exchange activity of both p115RhoGEF and leukemia-associated RhoGEF but not PDZ-Rh
25 hrombin-mediated signaling or their effector p115RhoGEF involved in Rho activation caused MT disassem
26 on of the guanine nucleotide exchange factor p115RhoGEF, which contains a regulator of G-protein sign
28 specific guanine nucleotide exchange factor (p115RhoGEF) in human metastatic breast tumor cells (MDA-
29 ain of a guanine nucleotide exchange factor, p115RhoGEF, inhibited thrombin-dependent phosphorylation
30 specific guanine nucleotide exchange factors p115RhoGEF and LARG (leukemia-associated RhoGEF), fails
34 ed its ability to bind to p115RhoGEF, induce p115RhoGEF recruitment to the PM, and activate Rho-depen
37 ns (phospholipase C- inverted question mark, p115RhoGEF) and a growing family of regulators of G prot
40 om G alpha(13) to JNK requires activation of p115RhoGEF cascades, including p115RhoGEF itself, RhoA,
41 e data suggest that the exchange activity of p115RhoGEF is stimulated allosterically by Galpha(13) an
45 sing shortened RH-RhoGEF DH/PH constructs of p115RhoGEF/ARHGEF1, PDZ-RhoGEF (PRG)/ARHGEF11, and LARG/
46 C-epsilon nor inhibited by the RGS domain of p115RhoGEF but was blocked by expression of the RGS doma
47 ture of Galpha(13) bound to the RH domain of p115RhoGEF is also presented, which differs from a previ
49 e regulator of G protein signaling domain of p115RhoGEF to inhibit Galpha12 and Galpha13 during thymo
50 e regulator of G-protein signaling domain of p115RhoGEF, a GTPase activating protein for G12/13, also
51 lator of G protein signaling (RGS) domain of p115RhoGEF, a GTPase-activating protein for Galpha(12/13
52 for Galpha12 binding with the RGS domain of p115RhoGEF, a known G12-interacting protein that links G
53 or of G protein signaling (rgRGS) domains of p115RhoGEF and homologous exchange factors differ from t
54 of the constitutively active mutant form of p115RhoGEF (guanine nucleotide exchange factor) was foun
58 vated alpha(13) to induce the recruitment of p115RhoGEF to the plasma membrane (PM) and to activate R
59 scaffold protein that interacts with Net1 or p115RhoGEF, two Rho-specific guanine nucleotide exchange
60 pression of dominant negative p115-RhoGEF or p115RhoGEF-specific siRNA inhibited both RhoA activation
61 RGL-RhoGEFs) that includes PDZ-RhoGEF (PRG), p115RhoGEF, and LARG, thereby regulating cellular functi
62 anine nucleotide exchange factors (RhoGEFs) (p115RhoGEF, leukemia-associated RhoGEF, and PDZ-RhoGEF)
63 binding of HA to MDA-MB-231 cells stimulates p115RhoGEF-mediated RhoA signaling and Rho kinase (ROK)
64 mutations, when placed in the context of the p115RhoGEF molecule, produce deficiencies in GAP activit
67 Ser (G205S) retained its ability to bind to p115RhoGEF, induce p115RhoGEF recruitment to the PM, and
70 ho activation caused MT disassembly, whereas p115RhoGEF-specific negative regulator RGS preserved MT
71 can form homo- and hetero-oligomers, whereas p115RhoGEF can only homo-oligomerize, and that this inte
74 We observed that PKCalpha associated with p115RhoGEF within 1 min of thrombin stimulation and p115
77 strongly suggest that CD44 interaction with p115RhoGEF and ROK plays a pivotal role in promoting Gab