New PDF release: Mechanisms of Stimulus—Response Coupling in Platelets

By Neville Crawford (auth.), J. Westwick, M. F. Scully, D. E. MacIntyre, V. V. Kakkar (eds.)

Since its inception the study zone of platelet pharmacology has consistently been a energetic one and it's a attribute that new methods to the knowledge of platelet functionality are swiftly and carefully investigated. The depth of this job is attri­ butable, most likely, to an appreciation via learn staff within the box passable healing keep an eye on of platelet functionality has but to be discovered. additionally that if and whilst this challenge of con­ trolling platelet functionality is accomplished the advantages to scientific medication should be sizeable considering that platelets are recognized to be interested in a multiplicity of occasions coupled in the haemostatic mechanisms and inflammatory responses. Aberrations within the behaviour of plate­ shall we is a part of the aetiology of atherosclerosis, myocardial and cerebral infarction and thrombosis. At this day and age, study in platelet functionality is in a very swift country of flux. the hot findings of analysis employees energetic within the box and likewise staff investigating mechan­ isms of stimulus reaction coupling in different cells, have supplied fascinating insights into the generality of mechanisms occupied with the functionality of responsive cells. One may well itemize those advancements because the region of cellphone receptor/ligand interplay, induction of mobilephone­ ular reaction through protein phosphorylation and calcium flux. The mech­ anism of those latter occasions happens in the course of the task of phospho­ lipase producing brief intermediates. those intermediates might act as ionophores or enzyme activators or may perhaps, with regards to eico­ sanoids, make stronger and make irreversible the mobile response.

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Additional info for Mechanisms of Stimulus—Response Coupling in Platelets

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8xlO Rate constant of association 127 °C (M- 1 _ min-I) on Divalent requirement 0,26 x 10 6 0,40 x 10 yes yes yes partial Stabilization 6 MOLECULAR NATURE OF THE FIBRINOGEN RECEPTOR Two major surface membrane glycoproteins have been implicated in fibrinogen receptor function. GPIIb has a molecular weight of approximately 136,000 when non reduced and is made up with two disulfide linked subunits (GPIIb 0( = 116,000 and GPIIb(3 = 23,000). GP III consists of a single polypeptide chain of Mr = 95,000.

The molecule does not interact with non stimulated platelet, whereas binding is observed when the cell is challenged with ADP and the binding sites exhibit the characteristics of a receptor system 1-3. The interaction is saturable with respect to both ADP and fibrinogen concentration, divalent ion dependent, specific for the native molecule and occurs in buffer system as well as in a plasma milieu (Table 1) 4. We have established in the past that the binding of fibrinogen to this receptor system is part of a multisteps reaction which entails : 1) the initial stimulation of the cell, 2) the induction of the receptor, 3) the binding of fibrinogen and 4) the stabilization of the fibrinogen receptor complex 3.

39. N. 40. s. 41. G. 42. N. 43. J. inhibition by 2-a1ky1thio analogues of adenosine 5'-monophosphate and adenosine 5'-triphosphate of human platelet aggregation induced by adenosine 5'-diphosphate, Br. J. Pharmac. 75: 397 (1982). J. Czarnecki, M. S. Abbott, and B. R. Selman, Photoaffinity labeling with 2-azidoadenosine diphosphate of a tight nucleotide binding site on chloroplast coupling factor 1, Proc. Nat1. Acad. Sci. USA 79:7744 (1982). Burns to ck, and C. M. Brown, An introduction to purinergic receptors, in: "Purinergic Receptors: Receptors and Recognition Series B.

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