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Mechanosensitive channel mechanisms

The molecular nature of the neuronal receptors is now becoming understood with the advent of molecular biological techniques. The molecular structure of the mechanosensitive channels has been established only recently. In principle mechanosensitive channels must be opened by mechanical deformation of the neural membrane in which they are em-... [Pg.62]

Figure 2. A proposed model demonstrating several different prominent calcium-related pathways whose activity may be altered in dystrophic muscle. Increased activity of mechanosensitive channels (MS) and store-activated channels (SOC), which are likely derived from the same gene product (TRPC), and the calcium leak channel, which could represent a proteolyzed TRPC SOC channel. Decreased mechanical coupling between L-type VGCC and ryanodine receptors may increase basal calcium release from calcium stores (not shown). Further, increased IP, and IP, receptor levels may also enhance basal and stimulated calcium-induced calcium release (CICR) from calcium stores. Calcium store depletion can increase translocation of SOCs from intracellular vesicles to the sarcolemma. Finally, the relationship between increased membrane fragility and tearing is less certain, but calcium influx through sarcolemmal tears could lead to calcium-dependent proteolysis and increased activity of calcium leak channels, as well as proteolysis of other targets, and increased release of calcium from intracellular stores through CICR. This model is not meant to be comprehensive, and other calcium-related molecules are discussed in the text... Figure 2. A proposed model demonstrating several different prominent calcium-related pathways whose activity may be altered in dystrophic muscle. Increased activity of mechanosensitive channels (MS) and store-activated channels (SOC), which are likely derived from the same gene product (TRPC), and the calcium leak channel, which could represent a proteolyzed TRPC SOC channel. Decreased mechanical coupling between L-type VGCC and ryanodine receptors may increase basal calcium release from calcium stores (not shown). Further, increased IP, and IP, receptor levels may also enhance basal and stimulated calcium-induced calcium release (CICR) from calcium stores. Calcium store depletion can increase translocation of SOCs from intracellular vesicles to the sarcolemma. Finally, the relationship between increased membrane fragility and tearing is less certain, but calcium influx through sarcolemmal tears could lead to calcium-dependent proteolysis and increased activity of calcium leak channels, as well as proteolysis of other targets, and increased release of calcium from intracellular stores through CICR. This model is not meant to be comprehensive, and other calcium-related molecules are discussed in the text...
Franco-Obregon, A., and Lansman, J.B., 2002, Changes in mechanosensitive channel gating following mechanical stimulation in skeletal muscle myotubes from the mdx mouse, J Physiol, 539, pp 391-407. [Pg.457]

Perozo E et al (2002) Open channel structure of MscL and the gating mechanism of mechanosensitive channels. Nature 418 942-948... [Pg.181]

The past few years have witnessed significant advances in establishing the gating mechanism of prokaryotic mechanosensitive channels, particularly the recent characterization of the open state of MscL (Sukharev et al., 2001a Perozo et al., 2002a) and the identification and initial... [Pg.205]

Martinac B. Eorce from hpids physical principles of gating mechanosensitive channels by mechanical force revealed by chemical manipulation of cellular membranes. Chem Educat. [Pg.970]

Perozo E, Cortes DM, Sompornpisut P. Kloda A, Martinac B. Structure of MscL in the open state and the molecular mechanism of gating in mechanosensitive channels. Nature 2002 418 942-948a. [Pg.971]

Perozo E, Rees DC. Structure and mechanism in prokaryotic mechanosensitive channels. Curr. Opinion Struct. Biol. 2003 13 432-442. Steinbacher S, Bass R, Strop P, Rees DC. Mechanosensitive Channel of Large Conductance (MscL). 2007. htp //www.rcsb.org/pdb/results/ results.do. [Pg.971]

Lee HS, Millward-Sadler SJ, Wright MO, Nuki G, Salter DM. 2000. Integrin and mechanosensitive ion channel-dependent tyrosine phosphorylation of focal adhesion proteins and beta-catenin in human articular chondrocytes after mechanical stimulation. J Bone Miner Res 15 1501-9. [Pg.557]

The pore-forming a 1 subunits Cay3.1-Cav3.3 are responsible for T-type Ca + currents and are considered LVA since they are activate at membrane potentials far more hyperpolarized than their HVA counterparts (Catterall et al. 2005). Intrigu-ingly, T-type Ca + channels are crucial for the normal function of mouse D-hair mechanosensitive fibers (Shin et al. 2003) that adapt rapidly to mechanical stimuli in a manner qualitatively similar to airway nodose A5 cough receptoT fibers (McAlexander et al. 1999). [Pg.142]

Matthews, B. D., D. R. Overby, R. Mannlx, and D. E. Ingber. 2006. Cellular adaptation to mechanical stress Role of integrins, Rho, cytoskeletal tension and mechanosensitive ion channels. / Cell Sci 119(Pt 3) 508-18. [Pg.472]


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