• Publications
  • Influence
Ca2+ sensitivity of smooth muscle and nonmuscle myosin II: modulated by G proteins, kinases, and myosin phosphatase.
TLDR
It is suggested that the RhoA/ROK pathway is constitutively active in a number of organs under physiological conditions; its aberrations play major roles in several disease states, particularly impacting on Ca2+ sensitization of smooth muscle in hypertension and possibly asthma and on cancer neoangiogenesis and cancer progression. Expand
Signal transduction and regulation in smooth muscle
TLDR
Abnormalities of these regulatory mechanisms and isoform variations may contribute to diseases of smooth muscle, and the G-protein-coupled inhibition of protein phosphatase is also likely to be impor-tant in regulating non-muscle cell functions mediated by cytoplasmic myosin II. Expand
Signal transduction by G‐proteins, Rho‐kinase and protein phosphatase to smooth muscle and non‐muscle myosin II
TLDR
Ca2+ sensitization by the Rho/Rho‐kinase pathway contributes to the tonic phase of agonist‐induced contraction in smooth muscle, and abnormally increased activation of myosin II by this mechanism is thought to play a role in diseases such as high blood pressure and cancer cell metastasis. Expand
Smooth Muscle Differentiation Marker Gene Expression Is Regulated by RhoA-mediated Actin Polymerization*
TLDR
The results of these studies indicate that in SMC, RhoA-dependent regulation of the actin cytoskeleton selectively regulates SMC differentiation marker gene expression by modulating SRF-dependent transcription and suggest that RHoA signaling may serve as a convergence point for the multiple signaling pathways that regulate SMC differentiate. Expand
Calcium release and ionic changes in the sarcoplasmic reticulum of tetanized muscle: an electron-probe study
TLDR
The unchanged distribution of a permeant anion, chloride, argues against the existence of a large and sustained transSR potential during tetanus, if the chloride permeability of the in situ SR is as high as suggested by measurements on fractionated SR. Expand
The effects of the Rho‐kinase inhibitor Y‐27632 on arachidonic acid‐, GTPγS‐, and phorbol ester‐induced Ca2+‐sensitization of smooth muscle
TLDR
It is concluded that AA induces Ca2+‐sensitization through dual mechanisms, one mediated by Rho‐kinase (or a related kinase), and (ii) Rho'kinase is not required for phorbol ester‐induced Ca2‐s Sensitization. Expand
SARCOPLASMIC RETICULUM AND EXCITATION-CONTRACTION COUPLING IN MAMMALIAN SMOOTH MUSCLES
TLDR
The presence of both thick and thin myofilaments and of rough SR in smooth muscles supports the dual, contractile and morphogenetic, function of smooth muscle. Expand
The contractile apparatus of vascular smooth muscle: intermediate high voltage stereo electron microscopy.
TLDR
Intermediate high voltage stereo electron microscopy of rabbit portal-anterior mesenteric vein smooth muscle showed that thick filaments are 2·2 μm long and have tapered ends, which could contribute to the ability of smooth muscle to develop equal or greater tension than striated muscle. Expand
Myosin light chain phosphatase activities and the effects of phosphatase inhibitors in tonic and phasic smooth muscle.
TLDR
The results suggest that the HMMosphatases of smooth muscle have properties common to type 1 protein phosphatases, but are inhibited only partially by high concentrations of inhibitor-2, and that the lower HMM phosphatase activity of tonic smooth muscle may contribute to its greater sensitivity toosphatase inhibitors and its slower rate of relaxation. Expand
Arachidonic acid inhibits myosin light chain phosphatase and sensitizes smooth muscle to calcium.
TLDR
It is concluded that AA may act as a messenger-promoting protein phosphorylation through direct inhibition of the form of protein phosphatase(s) that dephosphorylate MLC20 in vivo. Expand
...
1
2
3
4
5
...