Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:4.6.1.2 (guanylate cyclase)
 8,497 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Several mechanisms are used to control the behaviour of sea urchin spermatozoa while fertilizing eggs. These include discrete regulatory steps that modulate the sperm activation sequence from spawning to gamete membrane fusion. After release from the testis, sperm motility is instantaneously activated, by using intracellular pH as a throttle mechanism to control the rate of the dynein motor that catalyses axonemal bending. To support motility, energy is transported from the mitochondrion to the tail, by using a shuttle mechanism involving phosphocreatine diffusion. This shuttle employs a novel, endotriplicated, creatine kinase of Mr 140,000 in the flagellar axoneme as its terminus. The steering mechanism that determines where the spermatozoon swims is unknown, but may involve an egg peptide-induced guanylate cyclase activation, mediated by a cGMP-dependent Ca2+ channel, and attenuated by a plasma membrane cGMP phosphodiesterase. Upon arriving at the egg, which is identified by virtue of its proteoglycan coat (egg jelly), the spermatozoon undergoes a univesicular secretion that prepares it to fuse with the egg. This acrosome reaction involves several altered ionic fluxes in its mechanism, terminating in a massive Ca2+ uptake. If the spermatozoon is fortunate enough to fuse with an egg, a new member of the species is generated; if the acrosome reaction occurs without gamete fusion, the spermatozoon rapidly dies. All of these activation processes involve changes in the intracellular ionic milieu that are co-ordinated with altered enzyme activities, often in a causal fashion. Even with our current imperfect understanding of the process, a few of the steps in sperm activation may be defined by biochemical pathways that include specific modulatory control points.
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PMID:Molecular mechanisms of sea-urchin sperm activation before fertilization. 196

Nitric oxide (NO) has various roles in the skeletal musculature in both normal and pathological conditions. NO primarily activates soluble guanylate cyclase (sGC) and mediates subsequent intracellular signaling in target cells. We sought to identify the target cells of NO in the rat skeletal musculature, using subtypes of sGCalpha1 and sGCbeta1 antibodies. Immunohistochemistry revealed that both antibodies stained the same cells with round or oval shapes, having several long processes. The sGC-immunopositive cells co-expressed NG2 chondroitin sulfate proteoglycan, a marker of pericytes. The sGC-immunopositive cells were associated with capillaries and formed cellular networks with elongated cytoplasmic processes. sGCalpha1 and sGCbeta1 were not found in muscle sarcolemma that were stained by anti-dystrophin, or neuromuscular junctions, as detected by anti-synaptophysin. Based on these findings, we concluded that sGC immunoreactivity was specifically distributed in capillary pericytes. Pericytes in the skeletal musculature have been shown to be target cells of NO and are involved in the microvascular blood flow.
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PMID:The expression of soluble guanylate cyclase in the vasculature of rat skeletal muscle. 2000 48