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抗肌动蛋白自身抗体与血小板的结合。

Binding of anti-actin autoantibodies to platelets.

作者信息

Bouvier C A, Gabbiani G, Ryan G B, Badonnel M C, Majno G, Lüscher E F

出版信息

Thromb Haemost. 1977 Apr 30;37(2):321-8.

PMID:406689
Abstract

Normal platelets incubated with anti-actin autoantibodies (AAA) (from the serum of patients with chronic aggressive hepatitis) do not show binding of these antibodies as seen by indirect immunofluorescence. AAA serum does not inhibit thrombin-induced clot retraction, despite the binding of the antibodies to platelets in the clot. Similarly, AAA serum does not affect "reversible" or "irreversible" aggregation (induced by ADP, collagen or epinephrine), despite the binding of the antibodies to platelet actin under such circumstances. AAA also bind to platelets when aggregation is inhibited by EDTA. The incubation of "reversibly" aggregated platelet with AAA results in a small but definite binding of AAA to platelets. These findings suggest that during "irreversible" and/or "reversible" aggregation, changes take place at the surface of platelets which expose the antigen at the surface of the cell.

摘要

用抗肌动蛋白自身抗体(AAA)(来自慢性侵袭性肝炎患者的血清)孵育正常血小板时,通过间接免疫荧光观察,未显示出这些抗体的结合。尽管抗体与凝块中的血小板结合,但AAA血清并不抑制凝血酶诱导的凝块回缩。同样,尽管在这种情况下抗体与血小板肌动蛋白结合,但AAA血清并不影响(由ADP、胶原蛋白或肾上腺素诱导的)“可逆”或“不可逆”聚集。当聚集被EDTA抑制时,AAA也会与血小板结合。用AAA孵育“可逆”聚集的血小板会导致AAA与血小板有少量但确定的结合。这些发现表明,在“不可逆”和/或“可逆”聚集过程中,血小板表面会发生变化,从而使细胞表面的抗原暴露出来。

相似文献

1
Binding of anti-actin autoantibodies to platelets.抗肌动蛋白自身抗体与血小板的结合。
Thromb Haemost. 1977 Apr 30;37(2):321-8.
2
Membrane changes associated with platelet activation. Exposure of actin on the platelet surface after thrombin-induced secretion.与血小板活化相关的膜变化。凝血酶诱导的分泌后肌动蛋白在血小板表面的暴露。
J Clin Invest. 1980 Jul;66(1):1-9. doi: 10.1172/JCI109821.
3
Inhibition of rat platelet aggregation by mycalolide-B, a novel inhibitor of actin polymerization with a different mechanism of action from cytochalasin-D.新型肌动蛋白聚合抑制剂Mycalolide-B对大鼠血小板聚集的抑制作用,其作用机制与细胞松弛素-D不同。
Thromb Haemost. 1998 Mar;79(3):614-9.
4
Molecular mechanisms of fibrin gel clot retraction by platelets and cultured tumor cells.血小板和培养的肿瘤细胞引起纤维蛋白凝胶凝块回缩的分子机制。
Pol J Pharmacol. 1996 May-Jun;48(3):341-3.
5
In vitro and in vivo functions of thrombin-treated platelets.凝血酶处理的血小板的体外和体内功能
Thromb Haemost. 1976 Feb 29;35(1):151-66.
6
Identification of human platelet membrane fibrinogen receptors by immunochemical techniques.通过免疫化学技术鉴定人血小板膜纤维蛋白原受体
Haematologia (Budap). 1984;17(3):387-98.
7
Binding of aggregated immunoglobulins to the human platelet Fc receptors: a mechanism of platelet to platelet bridging.聚集的免疫球蛋白与人血小板Fc受体的结合:血小板间桥联的一种机制。
Thromb Haemost. 1987 Dec 18;58(4):966-70.
8
Ca+2 mobilization and fibrinogen binding of platelets refractory to adenosine diphosphate stimulation.对二磷酸腺苷刺激无反应的血小板的钙离子动员和纤维蛋白原结合
J Lab Clin Med. 1985 Aug;106(2):111-22.
9
Functionally thrombasthenic state in normal platelets following the administration of ticlopidine.服用噻氯匹定后正常血小板的功能性血小板无力状态。
J Clin Invest. 1985 Feb;75(2):328-38. doi: 10.1172/JCI111705.
10
Stabilization of platelet-fibrinogen interactions: modulation by divalent cations.血小板 - 纤维蛋白原相互作用的稳定:二价阳离子的调节作用
J Lab Clin Med. 1993 Jan;121(1):135-41.

引用本文的文献

1
Low-temperature induction of calcium-dependent protein phosphorylation in blood platelets.血小板中钙依赖性蛋白磷酸化的低温诱导
J Cell Biol. 1980 Jul;86(1):280-5. doi: 10.1083/jcb.86.1.280.
2
Membrane changes associated with platelet activation. Exposure of actin on the platelet surface after thrombin-induced secretion.与血小板活化相关的膜变化。凝血酶诱导的分泌后肌动蛋白在血小板表面的暴露。
J Clin Invest. 1980 Jul;66(1):1-9. doi: 10.1172/JCI109821.