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1
Hageman factor, platelets and polyphosphates: early history and recent connection. Hageman 因子、血小板和多聚磷酸盐:早期历史与近期关联。
J Thromb Haemost. 2010 Aug;8(8):1670-4. doi: 10.1111/j.1538-7836.2010.03893.x. Epub 2010 Apr 30.
2
Factor XII gene mutation in the Hageman family.哈格曼家族中的凝血因子XII基因突变。
J Thromb Haemost. 2011 Nov;9(11):2329-31. doi: 10.1111/j.1538-7836.2011.04508.x.
3
Platelet polyphosphates: the nexus of primary and secondary hemostasis.血小板多聚磷酸盐:初级和次级止血的交汇点。
Scand J Clin Lab Invest. 2011 Apr;71(2):82-6. doi: 10.3109/00365513.2010.550312.
4
Putting polyphosphates to the test: evidence against platelet-induced activation of factor XII.检验多聚磷酸盐:血小板诱导因子 XII 激活的证据。
Blood. 2013 Nov 28;122(23):3818-24. doi: 10.1182/blood-2013-05-499384. Epub 2013 Jul 29.
5
Factor XII Activation Promotes Platelet Consumption in the Presence of Bacterial-Type Long-Chain Polyphosphate In Vitro and In Vivo.因子 XII 的激活促进了体外和体内细菌型长链多聚磷酸盐存在时血小板的消耗。
Arterioscler Thromb Vasc Biol. 2018 Aug;38(8):1748-1760. doi: 10.1161/ATVBAHA.118.311193.
6
Platelet surface-associated activation and secretion-mediated inhibition of coagulation factor XII.血小板表面相关激活及分泌介导的凝血因子 XII 抑制作用
PLoS One. 2015 Feb 17;10(2):e0116665. doi: 10.1371/journal.pone.0116665. eCollection 2015.
7
Factor XII promotes blood coagulation independent of factor XI in the presence of long-chain polyphosphates.在长链多聚磷酸盐存在的情况下,因子 XII 可促进血液凝结,而无需因子 XI 的参与。
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The contact activation and kallikrein/kinin systems: pathophysiologic and physiologic activities.接触激活和激肽释放酶/激肽系统:病理生理和生理活性。
J Thromb Haemost. 2016 Jan;14(1):28-39. doi: 10.1111/jth.13194. Epub 2016 Jan 11.
9
Contact system revisited: an interface between inflammation, coagulation, and innate immunity.再探接触系统:炎症、凝血与天然免疫之间的一个界面
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Polyphosphate colocalizes with factor XII on platelet-bound fibrin and augments its plasminogen activator activity.多聚磷酸盐与血小板结合的纤维蛋白上的凝血因子XII共定位,并增强其纤溶酶原激活物活性。
Blood. 2016 Dec 15;128(24):2834-2845. doi: 10.1182/blood-2015-10-673285. Epub 2016 Sep 30.

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Cardiopulmonary bypass in a pediatric patient with factor XII deficiency.小儿 XII 因子缺乏症行体外循环。
J Extra Corpor Technol. 2024 Sep;56(3):125-127. doi: 10.1051/ject/2024021. Epub 2024 Sep 20.
2
An Update on Polyphosphate In Vivo Activities.体内多磷酸盐活性的最新研究进展。
Biomolecules. 2024 Aug 2;14(8):937. doi: 10.3390/biom14080937.
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Prolonged activated partial thromboplastin time secondary to factor XII deficiency in two surgical patients.两名外科手术患者因因子 XII 缺乏导致活化部分凝血活酶时间延长。
Oxf Med Case Reports. 2021 Mar 8;2021(3):omaa146. doi: 10.1093/omcr/omaa146. eCollection 2021 Mar.
4
Polyphosphate, Zn and high molecular weight kininogen modulate individual reactions of the contact pathway of blood clotting.多聚磷酸盐、锌和高分子量激肽原调节血液凝固接触途径的个体反应。
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Schistosomes can hydrolyze proinflammatory and prothrombotic polyphosphate (polyP) via tegumental alkaline phosphatase, SmAP.血吸虫可通过体表碱性磷酸酶SmAP水解促炎和促血栓形成的多聚磷酸盐(polyP)。
Mol Biochem Parasitol. 2019 Sep;232:111190. doi: 10.1016/j.molbiopara.2019.111190. Epub 2019 May 30.
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Factor XII Deficiency Mimicking Bleeding Diathesis: A Unique Presentation and Diagnostic Pitfall.模仿出血素质的因子 XII 缺乏症:一种独特的表现及诊断陷阱。
Cureus. 2018 Jun 15;10(6):e2817. doi: 10.7759/cureus.2817.
7
The search for new antithrombotic mechanisms and therapies that may spare hemostasis.寻找可能避免止血的新抗血栓形成机制和疗法。
Blood. 2018 Apr 26;131(17):1899-1902. doi: 10.1182/blood-2017-10-784074. Epub 2018 Feb 21.
8
Polyphosphate/platelet factor 4 complexes can mediate heparin-independent platelet activation in heparin-induced thrombocytopenia.多聚磷酸盐/血小板第4因子复合物可在肝素诱导的血小板减少症中介导不依赖肝素的血小板活化。
Blood Adv. 2016 Nov 22;1(1):62-74. doi: 10.1182/bloodadvances.2016000877. eCollection 2016 Nov 29.
9
The initiation and effects of plasma contact activation: an overview.血浆接触激活的起始与效应:综述
Int J Hematol. 2017 Mar;105(3):235-243. doi: 10.1007/s12185-016-2132-x. Epub 2016 Nov 15.
10
Polyphosphate as modulator of hemostasis, thrombosis, and inflammation.多聚磷酸盐作为止血、血栓形成和炎症的调节剂。
J Thromb Haemost. 2015 Jun;13 Suppl 1(0 1):S92-7. doi: 10.1111/jth.12896.

本文引用的文献

1
Platelet polyphosphates are proinflammatory and procoagulant mediators in vivo.血小板多聚磷酸盐是体内促炎和促凝的介质。
Cell. 2009 Dec 11;139(6):1143-56. doi: 10.1016/j.cell.2009.11.001.
2
Polyphosphate binds with high affinity to exosite II of thrombin.多聚磷酸盐与凝血酶的外位 II 以高亲和力结合。
J Thromb Haemost. 2010 Mar;8(3):548-55. doi: 10.1111/j.1538-7836.2009.03723.x. Epub 2009 Dec 11.
3
Platelet dense-granule secretion plays a critical role in thrombosis and subsequent vascular remodeling in atherosclerotic mice.血小板致密颗粒分泌在动脉粥样硬化小鼠的血栓形成及随后的血管重塑过程中起关键作用。
Circulation. 2009 Sep 1;120(9):785-91. doi: 10.1161/CIRCULATIONAHA.108.845461. Epub 2009 Aug 17.
4
Inorganic polyphosphate: essential for growth and survival.无机多聚磷酸盐:生长和生存所必需。
Annu Rev Biochem. 2009;78:605-47. doi: 10.1146/annurev.biochem.77.083007.093039.
5
The elusive physiologic role of Factor XII.因子 XII 难以捉摸的生理作用。
J Clin Invest. 2008 Sep;118(9):3006-9. doi: 10.1172/JCI36617.
6
Misfolded proteins activate factor XII in humans, leading to kallikrein formation without initiating coagulation.错误折叠的蛋白质在人体内激活因子 XII,导致激肽释放酶形成,而不启动凝血过程。
J Clin Invest. 2008 Sep;118(9):3208-18. doi: 10.1172/JCI35424.
7
Polyphosphate as a general procoagulant agent.多聚磷酸盐作为一种通用的促凝剂。
J Thromb Haemost. 2008 Oct;6(10):1750-6. doi: 10.1111/j.1538-7836.2008.03104.x. Epub 2008 Jul 28.
8
Polyphosphate enhances fibrin clot structure.多聚磷酸盐可增强纤维蛋白凝块结构。
Blood. 2008 Oct 1;112(7):2810-6. doi: 10.1182/blood-2008-03-145755. Epub 2008 Jun 10.
9
Factor VII-activating protease (FSAP): vascular functions and role in atherosclerosis.凝血因子VII激活蛋白酶(FSAP):血管功能及其在动脉粥样硬化中的作用
Thromb Haemost. 2008 Feb;99(2):286-9. doi: 10.1160/TH07-10-0640.
10
A tribute to Arthur Kornberg 1918-2007.向亚瑟·科恩伯格致敬 1918 - 2007。
Nat Struct Mol Biol. 2008 Jan;15(1):2-17. doi: 10.1038/nsmb0108-2.

Hageman 因子、血小板和多聚磷酸盐:早期历史与近期关联。

Hageman factor, platelets and polyphosphates: early history and recent connection.

机构信息

Fondation Franco Chinoise pour la Science et ses Applications, Paris, France.

出版信息

J Thromb Haemost. 2010 Aug;8(8):1670-4. doi: 10.1111/j.1538-7836.2010.03893.x. Epub 2010 Apr 30.

DOI:10.1111/j.1538-7836.2010.03893.x
PMID:20456750
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2965785/
Abstract

Platelet activation and blood coagulation are essential for hemostasis and contribute to a variety of other biological processes such as inflammation, complement activation and tissue repair. Factor (F)XII, originally called Hageman factor, plays an important role in the kallikrein-kinin system by activating prekallikrein. In the 1960s, a platelet activity that promoted FXII activation was identified but its biochemical nature remained unknown. Inorganic polyphosphates (poly P) are polymers that consist of many phosphate residues linked by phosphoanhydride bonds. These polymers exist in all living organisms. In bacteria, poly P is important for growth and survival. Recently, poly P has been identified in human platelet dense granules. Studied have shown that upon platelet activation and secretion, poly P activates FXII, indicating that it is most likely the elusive platelet FXII activator. Poly P also regulates coagulation and fibrinolysis. In this review, we focus on early studies of FXII and the identification of platelet FXII activation activity, and discuss recent findings of poly P in FXII activation and coagulation.

摘要

血小板激活和血液凝固对于止血至关重要,并有助于多种其他生物过程,如炎症、补体激活和组织修复。因子 (F)XII,最初称为 Hageman 因子,通过激活前激肽原在激肽释放酶-激肽系统中发挥重要作用。20 世纪 60 年代,发现了一种促进 FXII 激活的血小板活性,但它的生化性质仍然未知。无机多聚磷酸盐 (poly P) 是由通过磷酸酐键连接的许多磷酸基团组成的聚合物。这些聚合物存在于所有生物中。在细菌中,多聚 P 对于生长和存活很重要。最近,在人类血小板致密颗粒中发现了多聚 P。研究表明,血小板激活和分泌后,多聚 P 会激活 FXII,表明它很可能是难以捉摸的血小板 FXII 激活剂。多聚 P 还调节凝血和纤维蛋白溶解。在这篇综述中,我们重点介绍 FXII 的早期研究和血小板 FXII 激活活性的鉴定,并讨论多聚 P 在 FXII 激活和凝血中的最新发现。