Actin modulation

Lewy bodies are typical in neuronal degeneration, which is accompanied by the presence of these eosinophilic intracellular inclusions of 5-25 pm diameter in a proportion of still surviving neurons. Lewy bodies contain neurofilament, tubulin, microtubule-associated proteins 1 and 2, and gelsolin, an actin-modulating protein. 

Yin, H.L. 1987. Gelsolin calcium-and polyphosphoinositide-regulated actin-modulating protein. B/oessoys 7, 176-179. 

The general picture of muscle contraction in the heart resembles that of skeletal muscle. Cardiac muscle, like skeletal muscle, is striated and uses the actin-myosin-tropomyosin-troponin system described above. Unlike skeletal muscle, cardiac muscle exhibits intrinsic rhyth-micity, and individual myocytes communicate with each other because of its syncytial nature. The T tubular system is more developed in cardiac muscle, whereas the sarcoplasmic reticulum is less extensive and consequently the intracellular supply of Ca for contraction is less. Cardiac muscle thus relies on extracellular Ca for contraction if isolated cardiac muscle is deprived of Ca, it ceases to beat within approximately 1 minute, whereas skeletal muscle can continue to contract without an extraceUular source of Ca +. Cyclic AMP plays a more prominent role in cardiac than in skeletal muscle. It modulates intracellular levels of Ca through the activation of protein kinases these enzymes phosphorylate various transport proteins in the sarcolemma and sarcoplasmic reticulum and also in the troponin-tropomyosin regulatory complex, affecting intracellular levels of Ca or responses to it. There is a rough correlation between the phosphorylation of Tpl and the increased contraction of cardiac muscle induced by catecholamines. This may account for the inotropic effects (increased contractility) of P-adrenergic compounds on the heart. Some differences among skeletal, cardiac, and smooth muscle are summarized in... 

The role of tyrosine kinase signaling in actin cytoskeleton regulation is well established (166-171), and certain steps in the activation pathways of both Rac 1 and RhoA, two molecules known to modulate actin function, may also require tyrosine kinase activity (172,173). In fact, two recent reports have also indicated... 

Gallucci RM, Lee EG, Tomasek JJ. IL-6 modulates alpha-smooth muscle actin expression in dermal fibroblasts from IL-6-deficient mice. J Invest Dermatol 2006 126(3) 561-568. 

Parker KE 1998 Modulation of ATP-gated non-selective cation channel (P2X1 receptor) activation and desensitization by the actin cytoskeleton. J Physiol 510 19—25... 

Hwang J-U, Suh SS, Yi H, Kim J, Lee Y. Actin filaments modulate both stomatal opening and inward K+ channel activities in guard cells of Vidafaba. Plant Physiol 1997 115 335-342. 

In human vaginal-cervical cells, the estrogen-induced increase in permeability is mediated in part by decreases in R, s that involve fragmentation of the cytoskeleton [23], The effects of estrogen on cytoskeletal organization involve modulation of both cortical actin [29] and myosin [45] (Figure 15.4A, C, D). 

Modulation of Actin Polymerization Estrogen vis-a-vis Aging Effects... 

In addition to its influence on protein—protein interactions, phosphorylation also affects protein structure and activity. One case involves a protein termed dematin headpiece (DHP), an actin-binding protein found in a variety of tissues including heart, brain, skeletal muscle, kidney, and lung." DHP is known to interact with Ras-guanine nucleotide exchange factor (Ras-GRF2) and this interaction can modulate MARK pathways, which can link the cytoskeleton and signaling pathways." ... 

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