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  • Receptors
  • Thus, deposition of additional ECM components, expression of co-receptors for ECM, cleavage of adhesive proteins, and the architecture of the ECM microenvironment are different mechanisms for modulating cell responses to fibronectin matrix. (ox.ac.uk)
  • Various agonists (neurotransmitters, hormones, etc.) bind to specific receptors to activate contraction in smooth muscle. (biology-online.org)
  • IP 3 binds to specific receptors on the sarcoplasmic reticulum, causing release of activator calcium (Ca 2+ ). (biology-online.org)
  • cdc42
  • In addition, using biochemical activity assays for Rho-like GTPases, we show that the expression of beta1A, beta1D, or IL2R-beta1A in GE11 or GD25 cells triggers activation of both RhoA and Rac1, but not of Cdc42. (nih.gov)
  • Therefore we gencrated E.coli carrying cnf2 and cDNA of rhoA, cdc42, or rac1. (nii.ac.jp)
  • On the other hand, CNF1 inhiibited GTPasc activity of RhoA and Cdc42. (nii.ac.jp)
  • Western analysis of CNF2-modificd small GTPascs revealed that RhoA and Racl were immunolabeled with this antibody but not was Cdc42. (nii.ac.jp)
  • On the other hand, Western analysis of CNF1-modified small GTPascs showed that RhoA and Cdc42 were positive while Raci was negative. (nii.ac.jp)
  • Epithelial Cells
  • Tight junctions (TJ) govern ion and solute diffusion through the paracellular space (gate function), and restrict mixing of membrane proteins and lipids between membrane domains (fence function) of polarized epithelial cells. (rupress.org)
  • Two key structural features of transporting epithelial cells specify this function: restricted distributions of specific membrane proteins to functionally distinct membrane domains that face these compartments ( Rodriguez-Boulan and Nelson, 1989 ), and formation of an intercellular junctional complex ( Farquhar and Palade, 1963 ). (rupress.org)
  • Inhibition
  • Analysis in vitro confirms that treatment of cerebrovascular endothelial cells with recombinant ANXA1 restores cell polarity, cytoskeleton integrity, and paracellular permeability through inhibition of the small G protein RhoA. (ox.ac.uk)
  • antibody
  • Nitration of endogenous p190A and exogenously expressed proteins was determined with 3-N antibody. (nih.gov)
  • Analysis of overproduced RhoA modified by CNF2 indicated that CNF2 deamidated RhoA at 63rd Q and converted it to U.We also used polyclonal antibody raised against Switch H domain of Rho family GTPascs with substitution of 63rd (or 61st) Q as E.This antibody presumably recognizes CNF-modificd small GTPascs. (nii.ac.jp)
  • inhibitory
  • Growth inhibitory proteins in the central nervous system (CNS) block axon growth and regeneration by signaling to Rho, an intracellular GTPase. (nih.gov)
  • Actomyosin
  • When both GTPases are activated, the protrusive structures caused by Rac1-dependent actin reorganization are spatially restricted and periodically destabilized, causing ruffling by RhoA-induced actomyosin contractility.Depletion of srGAP1 overactivates Rac1 and inactivates RhoA, resulting in continuous spatiotemporal spreading of lamellipodia and a modal shift of intrinsic cell motility from random to directionally persistent.Thus srGAP1 is a key determinant of lamellipodial dynamics and cell migratory behavior. (nih.gov)
  • When both GTPases are activated, the protrusive structures caused by Rac1-dependent actin reorganization are spatially restricted and periodically destabilized, causing ruffling by RhoA-induced actomyosin contractility. (nih.gov)
  • cells
  • Both PS and anti-PSR antibodies stimulated membrane ruffling, vesicle formation, and "bystander" uptake of cells bound to the surface of the phagocyte. (nih.gov)
  • Expression of beta1 integrins in GE11 cells resulted in a decrease in cadherin and alpha-catenin protein levels accompanied by their redistribution from the cytoskeleton-associated fraction to the detergent-soluble fraction. (nih.gov)
  • Further, recognition of PS was found to be dependent on the presence of the PS receptor (PSR).Both PS and anti-PSR antibodies stimulated membrane ruffling, vesicle formation, and 'bystander' uptake of cells bound to the surface of the phagocyte.We propose that the phagocytosis of apoptotic cells requires two events: tethering followed by PS-stimulated, PSR-mediated macropinocytosis. (nih.gov)
  • In situ Rho-GTP detection revealed that both neurons and glial cells showed Rho activation at SCI lesion sites. (nih.gov)
  • 2002). Treatment with C3-05 not only blocked the increase in p75NTR protein levels after SCI, as detected by Western blot (Fig. 8 C), but also reduced the number of p75NTR-TUNEL-labeled cells (Fig. 8 B). These results suggest, that early on, Rho activation after SCI is mediated, at least in part, by p75NTR. (nih.gov)
  • The aim of this project was to undcrstand the molccular mcchanism how the cytotoxic necrotizing factor (CNF) produced by pathogccin Eschcrichia coli activate small (G-protein Rho and its relatcd families in culture cells. (nii.ac.jp)
  • The interaction of RhoE with ROCK I was confirmed by coimmunoprecipitation of the endogenous proteins, and the two proteins colocalized on the trans-Golgi network in COS-7 cells. (ucl.ac.uk)
  • Freeze-fracture EM and immunofluoresence microscopy revealed abnormal TJ strand morphology and protein (occludin, ZO-1) localization in RhoAV14 and Rac1V12 cells. (rupress.org)
  • However, TJ strand morphology and protein localization appeared normal in RhoAN19 and Rac1N17 cells. (rupress.org)
  • Expression levels and protein complexes of occludin and ZO-1 appeared normal in all mutant cells, although ZO-1 was more readily solubilized from RhoAV14-expressing cells with Triton X-100. (rupress.org)
  • induces
  • RhoE induces stress fiber disassembly in a variety of cell types, whereas RhoA stimulates stress fiber assembly. (ucl.ac.uk)
  • These data suggest that RhoE induces stress fiber disassembly by directly binding ROCK I and inhibiting it from phosphorylating downstream targets. (ucl.ac.uk)
  • Andrei Bakin (Roswell Park Cancer Institute, Buffalo, NY) presented a model of EMT whereby transforming growth factor β (TGF-β) induces EMT but the ensuing metastatic and invasive properties are rendered by oncogenic H-RasV12 inhibiting the binding of Smad transducers of TGF-β to the promoter of tropomyosin TPM1, leading to nuclear export of Smad4. (aacrjournals.org)
  • Depletion
  • Depletion of srGAP1 overactivates Rac1 and inactivates RhoA, resulting in continuous spatiotemporal spreading of lamellipodia and a modal shift of intrinsic cell motility from random to directionally persistent. (nih.gov)
  • permeability
  • We found that the GTPase-activating protein (GAP) p190RhoGAP-A was selectively nitrated at Tyr1105, resulting in impaired GAP activity and RhoA activation.Thrombin, a mediator of increased endothelial permeability, also induced nitration of p120-catenin-associated p190RhoGAP-A.Thus, eNOS-dependent nitration of p190RhoGAP-A represents a crucial mechanism for AJ disassembly and resultant increased endothelial permeability. (nih.gov)
  • dramatically
  • Although alpha 4 beta 1 does not naturally support strong cell interactions with a fibrin-fibronectin matrix, binding is dramatically enhanced by proteolytic cleavage of fibronectin. (ox.ac.uk)
  • membrane
  • In turn, membrane-bound APC allows the localization of the MACF1 to the cell membrane, which is required for microtubule capture and stabilization. (abcam.co.jp)