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支持凝血酶激活的纤维蛋白溶解抑制剂在乳腺癌中的结构和功能特征的数据。

Data supporting the structural and functional characterization of Thrombin-Activatable Fibrinolysis Inhibitor in breast cancer.

作者信息

Fawzy Manal S, Toraih Eman A

机构信息

Department of Medical Biochemistry, Faculty of Medicine, Suez Canal University, Ismailia, Egypt.

Department of Histology and Cell Biology (Genetics Unit), Faculty of Medicine, Suez Canal University, Ismailia, Egypt.

出版信息

Data Brief. 2015 Nov 14;5:981-9. doi: 10.1016/j.dib.2015.10.043. eCollection 2015 Dec.

DOI:10.1016/j.dib.2015.10.043
PMID:26740968
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4675892/
Abstract

The data in this paper is related to the research article entitled "Thrombin-activatable fibrinolysis inhibitor Thr325Ile polymorphism and plasma level in breast cancer: A pilot study" (Fawzy et al., 2015) [1]. Many emerging studies have begun to unravel the pathophysiologic role of the fibrinolytic system in breast cancer (BC) progression (Zorio et al., 2008) [2]. Activation of the fibrinolytic plasminogen/plasmin system results in degradation of protein barriers, thereby mediating cell migration essential for tumor growth, angiogenesis, and dissemination (Castellino and Ploplis, 2005) [3]. In the current study, in silico data analysis of Thrombin-Activatable Fibrinolysis Inhibitor (TAFI) gene and protein has been done. Data have been retrieved from several databases mentioned in details in the text. Determination and analysis of the structural and functional impact of TAFI and its expression could help elucidate the contribution of the TAFI pathway to acquired hemostatic dysfunction and will form the basis of potential therapeutic strategies to manipulate this pathway. An inhibition of TAFI (e.g. by FXI inhibitors) will offer the therapeutic possibilities to improve the decreased fibrinolysis and increase the efficiency of fibrinolytic therapy in thrombotic disorders including cancer.

摘要

本文中的数据与题为《乳腺癌中凝血酶激活的纤维蛋白溶解抑制剂Thr325Ile多态性与血浆水平:一项初步研究》(Fawzy等人,2015年)[1]的研究文章相关。许多新出现的研究已开始揭示纤维蛋白溶解系统在乳腺癌(BC)进展中的病理生理作用(Zorio等人,2008年)[2]。纤维蛋白溶解纤溶酶原/纤溶酶系统的激活导致蛋白质屏障降解,从而介导肿瘤生长、血管生成和扩散所必需的细胞迁移(Castellino和Ploplis,2005年)[3]。在本研究中,已对凝血酶激活的纤维蛋白溶解抑制剂(TAFI)基因和蛋白质进行了计算机数据分析。数据已从文中详细提及的几个数据库中检索。确定和分析TAFI的结构和功能影响及其表达,有助于阐明TAFI途径对获得性止血功能障碍的作用,并将构成操纵该途径的潜在治疗策略的基础。抑制TAFI(例如通过FXI抑制剂)将为改善纤维蛋白溶解降低的情况以及提高包括癌症在内的血栓性疾病中纤维蛋白溶解治疗的效率提供治疗可能性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da0a/4675892/714e4f7a481f/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da0a/4675892/b852f7a87c7a/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da0a/4675892/8c1c8d59c65e/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da0a/4675892/428235198d89/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da0a/4675892/0076de15cb67/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da0a/4675892/d7b2a3e2df72/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da0a/4675892/714e4f7a481f/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da0a/4675892/b852f7a87c7a/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da0a/4675892/8c1c8d59c65e/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da0a/4675892/428235198d89/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da0a/4675892/0076de15cb67/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da0a/4675892/d7b2a3e2df72/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da0a/4675892/714e4f7a481f/gr6.jpg

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