• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

面部皮肤黏膜静脉畸形可独立于TEK基因突变而发生,但可能与Src和p-Src的过度表达有关。

Facial cutaneo-mucosal venous malformations can develop independently of mutation of TEK gene but may be associated with excessive expression of Src and p-Src.

作者信息

Brahami Nabila, Subramaniam Selvakumar, Al-Ddafari Moudjahed Saleh, Elkaim Cecile, Harmand Pierre-Olivier, Sari Badr-Eddine, Lefranc Gérard, Aribi Mourad

机构信息

Laboratory of Applied Molecular Biology and Immunology, University of Tlemcen, Imama-Mansourah, Rocade # 2, PO Box: 262, Tlemcen, 13000, Algeria.

UMR U866 INSERM, University of Burgundy, 21000, Dijon, France.

出版信息

J Negat Results Biomed. 2017 Mar 20;16(1):9. doi: 10.1186/s12952-017-0072-5.

DOI:10.1186/s12952-017-0072-5
PMID:28316284
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5357811/
Abstract

We aimed to search for mutations in the germline and somatic DNA of the TEK gene and to analyze the expression level of Src and phospho-Src (p-Src) in tumor and healthy tissues from patients with facial cutaneo-mucosal venous malformations (VMCM). Eligible patients from twelve families and thirty healthy controls were recruited respectively at the Departments of Stomatology and Oral Surgery, and Transfusion Medicine of Tlemcen University Medical Centre. Immunoblot analyses of Src and p-Src were performed after direct DNA sequencing. No somatic or germline mutations were found in all the 23 exons and their 5' and 3' intronic flanking regions, except for one case in which a c.3025+20-3025+22 del mutation was highlighted at the intron 15, both in the germline and somatic DNA. Additionally, elevated expression levels of Src and p-Src were observed only in the patient with such mutation. However, when normalized to β-actin, the overall relative expression levels of both Src and p-Src were significantly increased in VMCM tissues when compared to healthy tissues (for both comparisons, p <0.001). In conclusion, we confirm the outcomes of our previous work suggesting that VMCM can develop independently of mutation of the TEK gene. Additionally, the results for Src activity are of particular interest in the context of specific targeted therapies and biological diagnosis. Nevertheless, such a conclusion should be confirmed through a mechanistic study and/or in a satisfactory number of patients.

摘要

我们旨在寻找TEK基因种系和体细胞DNA中的突变,并分析面部皮肤黏膜静脉畸形(VMCM)患者肿瘤组织和健康组织中Src和磷酸化Src(p-Src)的表达水平。分别从特莱姆森大学医学中心的口腔颌面外科和输血医学科招募了来自12个家庭的符合条件的患者和30名健康对照。在直接DNA测序后进行Src和p-Src的免疫印迹分析。在所有23个外显子及其5'和3'内含子侧翼区域均未发现体细胞或种系突变,只有1例在第15内含子中突出显示了一个c.3025+20-3025+22缺失突变,该突变在种系和体细胞DNA中均存在。此外,仅在有此类突变的患者中观察到Src和p-Src的表达水平升高。然而,与β-肌动蛋白标准化后,与健康组织相比,VMCM组织中Src和p-Src的总体相对表达水平均显著升高(两项比较均p<0.001)。总之,我们证实了我们之前工作的结果,表明VMCM可以独立于TEK基因突变而发生。此外,可以认为Src活性的结果在特定靶向治疗和生物学诊断方面具有特殊意义。然而,这一结论应通过机制研究和/或在足够数量的患者中得到证实。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3c8e/5357811/fa79ded28609/12952_2017_72_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3c8e/5357811/3ddd812ef5b2/12952_2017_72_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3c8e/5357811/f9f4713c5678/12952_2017_72_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3c8e/5357811/fa79ded28609/12952_2017_72_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3c8e/5357811/3ddd812ef5b2/12952_2017_72_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3c8e/5357811/f9f4713c5678/12952_2017_72_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3c8e/5357811/fa79ded28609/12952_2017_72_Fig3_HTML.jpg

相似文献

1
Facial cutaneo-mucosal venous malformations can develop independently of mutation of TEK gene but may be associated with excessive expression of Src and p-Src.面部皮肤黏膜静脉畸形可独立于TEK基因突变而发生,但可能与Src和p-Src的过度表达有关。
J Negat Results Biomed. 2017 Mar 20;16(1):9. doi: 10.1186/s12952-017-0072-5.
2
Cutaneomucosal venous malformations are linked to the TIE2 mutation in a large Chinese family.皮肤黏膜静脉畸形与一个大型中国家族中的 TIE2 突变有关。
Exp Dermatol. 2012 Jun;21(6):456-7. doi: 10.1111/j.1600-0625.2012.01492.x.
3
Somatic mutations in exon 17 of the TEK gene in vascular tumors and vascular malformations.TEK 基因外显子 17 的体细胞突变与血管肿瘤和血管畸形。
J Vasc Surg. 2011 Dec;54(6):1760-8. doi: 10.1016/j.jvs.2011.06.098. Epub 2011 Oct 1.
4
Somatic mutations in angiopoietin receptor gene TEK cause solitary and multiple sporadic venous malformations.血管生成素受体基因TEK中的体细胞突变导致散发性单发性和多发性静脉畸形。
Nat Genet. 2009 Jan;41(1):118-24. doi: 10.1038/ng.272. Epub 2008 Dec 14.
5
Hereditary cutaneomucosal venous malformations are caused by TIE2 mutations with widely variable hyper-phosphorylating effects.遗传性皮肤黏膜静脉畸形是由 TIE2 突变引起的,具有广泛的高磷酸化作用。
Eur J Hum Genet. 2010 Apr;18(4):414-20. doi: 10.1038/ejhg.2009.193. Epub 2009 Nov 4.
6
Genetic landscape of common venous malformations in the head and neck.头颈部常见静脉畸形的遗传景观。
J Vasc Surg Venous Lymphat Disord. 2021 Jul;9(4):1007-1016.e7. doi: 10.1016/j.jvsv.2020.11.016. Epub 2020 Nov 26.
7
CD10 and CD34 as markers in vascular malformations with PIK3CA and TEK mutations.CD10 和 CD34 作为 PIK3CA 和 TEK 突变的血管畸形标志物。
Hum Pathol. 2020 May;99:98-106. doi: 10.1016/j.humpath.2020.04.001. Epub 2020 Apr 6.
8
Somatic Activating PIK3CA Mutations Cause Venous Malformation.体细胞激活型PIK3CA突变导致静脉畸形。
Am J Hum Genet. 2015 Dec 3;97(6):914-21. doi: 10.1016/j.ajhg.2015.11.011.
9
Lack of TEK Gene Mutation in Patients with Cutaneomucosal Venous Malformations from the North-Western Region of Algeria.阿尔及利亚西北部皮肤黏膜静脉畸形患者中TEK基因突变的缺失
Genet Res Int. 2013;2013:784789. doi: 10.1155/2013/784789. Epub 2013 Dec 9.
10
Functional assessment of two variants of unknown significance in TEK by endothelium-specific expression in zebrafish embryos.通过斑马鱼胚胎内皮细胞特异性表达来评估 TEK 中的两个意义未明变异体的功能。
Hum Mol Genet. 2021 Dec 17;31(1):10-17. doi: 10.1093/hmg/ddab196.

引用本文的文献

1
Effect and mechanism of apelin on lipopolysaccharide induced acute pulmonary vascular endothelial barrier dysfunction.apelin 对脂多糖诱导的急性肺血管内皮屏障功能障碍的作用及机制。
Sci Rep. 2023 Jan 27;13(1):1560. doi: 10.1038/s41598-023-27889-6.

本文引用的文献

1
Adaptive metabolic rewiring to chronic SFK inhibition.对慢性Src家族激酶抑制的适应性代谢重编程。
Oncotarget. 2016 Mar 17;8(40):66758-66768. doi: 10.18632/oncotarget.8146. eCollection 2017 Sep 15.
2
Gene control of tyrosine kinase TIE2 and vascular manifestations of infections.酪氨酸激酶TIE2的基因调控与感染的血管表现
Proc Natl Acad Sci U S A. 2016 Mar 1;113(9):2472-7. doi: 10.1073/pnas.1519467113. Epub 2016 Feb 16.
3
Phosphorylation of unique domains of Src family kinases.Src家族激酶独特结构域的磷酸化
Front Genet. 2014 Jun 30;5:181. doi: 10.3389/fgene.2014.00181. eCollection 2014.
4
Unusual splice site mutations disrupt FANCA exon 8 definition.异常剪接位点突变破坏了FANCA外显子8的界定。
Biochim Biophys Acta. 2014 Jul;1842(7):1052-8. doi: 10.1016/j.bbadis.2014.03.014. Epub 2014 Apr 1.
5
Lack of TEK Gene Mutation in Patients with Cutaneomucosal Venous Malformations from the North-Western Region of Algeria.阿尔及利亚西北部皮肤黏膜静脉畸形患者中TEK基因突变的缺失
Genet Res Int. 2013;2013:784789. doi: 10.1155/2013/784789. Epub 2013 Dec 9.
6
Phosphatidylethanolamine-binding protein 4 is associated with breast cancer metastasis through Src-mediated Akt tyrosine phosphorylation.磷酯酰乙醇胺结合蛋白 4 通过 Src 介导的 Akt 酪氨酸磷酸化与乳腺癌转移相关。
Oncogene. 2014 Sep 11;33(37):4589-98. doi: 10.1038/onc.2013.408. Epub 2013 Nov 25.
7
CD99 suppresses osteosarcoma cell migration through inhibition of ROCK2 activity.CD99 通过抑制 ROCK2 活性抑制骨肉瘤细胞迁移。
Oncogene. 2014 Apr 10;33(15):1912-21. doi: 10.1038/onc.2013.152. Epub 2013 May 6.
8
Western blot evaluation of siRNA delivery by pH-responsive peptides.通过pH响应肽进行小干扰RNA递送的蛋白质免疫印迹评估。
Methods Mol Biol. 2013;986:73-87. doi: 10.1007/978-1-62703-311-4_5.
9
Introns in UTRs: why we should stop ignoring them.UTR 中的内含子:我们为何不应再忽视它们。
Bioessays. 2012 Dec;34(12):1025-34. doi: 10.1002/bies.201200073. Epub 2012 Oct 26.
10
Thrombin-induced CCN2 expression in human lung fibroblasts requires the c-Src/JAK2/STAT3 pathway.凝血酶诱导人肺成纤维细胞中 CCN2 的表达需要 c-Src/JAK2/STAT3 途径。
J Leukoc Biol. 2013 Jan;93(1):101-12. doi: 10.1189/jlb.0911449. Epub 2012 Oct 29.