Journal ArticleDOI
Norepinephrine and GTP-γ-S increase myofilament Ca2+ sensitivity in α-toxin permeabilized arterial smooth muscle
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TLDR
It is concluded that NE or GTP-γ-S causes an increase in myofilament Ca 2+ sensitivity and that G protein may be involved in receptor signal transduction system.About:
This article is published in Biochemical and Biophysical Research Communications.The article was published on 1988-12-15. It has received 298 citations till now. The article focuses on the topics: Muscle contraction & Smooth muscle tissue.read more
Citations
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Journal ArticleDOI
Calcium channels, potassium channels, and voltage dependence of arterial smooth muscle tone
TL;DR: It is shown that voltage-dependent Ca channels in the steady state can be open and very sensitive to membrane potential changes in a range that occurs in resistance arteries with tone.
Journal ArticleDOI
Signaling mechanisms underlying the vascular myogenic response
Michael J. Davis,Michael A. Hill +1 more
TL;DR: The purpose of this review is to summarize and synthesize information regarding the cellular mechanism(s) underlying the myogenic response in blood vessels, with particular emphasis on arterioles.
Journal Article
Calcium Movements, Distribution, and Functions in Smooth Muscle
Hideaki Karaki,Hiroshi Ozaki,Masatoshi Hori,Minori Mitsui-Saito,Ken-ichi Amano,Ken-ichi Harada,Shigeki Miyamoto,Hiroshi Nakazawa,Kyung-Jong Won,Koichi Sato +9 more
TL;DR: Contraction of smooth muscle is regulated by the cytosolic Ca2+ level ([Ca2+]i)b, and the sensitivity of the contractile elements in response to changes in the environment surrounding the cell.
Journal ArticleDOI
Alpha-toxin of Staphylococcus aureus.
Sucharit Bhakdi,J Tranum-Jensen +1 more
TL;DR: Alpha-toxin, the major cytotoxic agent elaborated by Staphylococcus aureus, was the first bacterial exotoxin to be identified as a pore former and well-studied phenomena include the stimulation of arachidonic acid metabolism, triggering of granule exocytosis, and contractile dysfunction.
Journal ArticleDOI
Involvement of rho p21 in the GTP-enhanced calcium ion sensitivity of smooth muscle contraction
Ken-ichi Hirata,Akira Kikuchi,Takuya Sasaki,Shinya Kuroda,K Kaibuchi,Yoshiharu Matsuura,H. Seki,K. Saida,Yoshimi Takai +8 more
TL;DR: Results indicate that rhoA p21 is involved in the GTP gamma S-enhanced Ca2+ sensitivity of the smooth muscle contraction.
References
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Journal Article
Protein Measurement with the Folin Phenol Reagent
TL;DR: Procedures are described for measuring protein in solution or after precipitation with acids or other agents, and for the determination of as little as 0.2 gamma of protein.
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The role of protein kinase C in cell surface signal transduction and tumour promotion
TL;DR: Protein kinase C probably serves as a receptor for the tumour promoters and further exploration of the roles of this enzyme may provide clues for understanding the mechanism of cell growth and differentiation.
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Inositol trisphosphate, a novel second messenger in cellular signal transduction.
TL;DR: Diacylglycerol operates within the plane of the membrane to activate protein kinase C, whereas inositol trisphosphate is released into the cytoplasm to function as a second messenger for mobilizing intracellular calcium.
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Isoquinolinesulfonamides, novel and potent inhibitors of cyclic nucleotide dependent protein kinase and protein kinase C.
TL;DR: Both the holoenzyme and the catalytic subunit (or fragment), which is active without an enzyme activator, are susceptible to these compounds with a similar concentration dependency, thereby indicating that the inhibitory effect is attributed to the direct interaction of the compound with the active center of the enzyme but not with the enzymeactivator.
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Release of Ca2+ from a nonmitochondrial intracellular store in pancreatic acinar cells by inositol-1,4,5-trisphosphate.
TL;DR: It is reported here that micromolar concentrations of Ins1,4,5P3 release Ca2+ from a nonmitochondrial intracellular Ca2- store in pancreatic acinar cells, and the results strongly suggest that this is the same Ca1+ store that is released by acetylcholine.