Fanconi贫血蛋白FANCD2通过tankyrase1依赖的方式抑制TRF1多adp核糖基化。

Q4 Biochemistry, Genetics and Molecular Biology Genome Integrity Pub Date : 2011-02-12 DOI:10.1186/2041-9414-2-4
Alex Lyakhovich, Maria Jose Ramirez, Andres Castellanos, Maria Castella, Amanda M Simons, Jeffrey D Parvin, Jordi Surralles
{"title":"Fanconi贫血蛋白FANCD2通过tankyrase1依赖的方式抑制TRF1多adp核糖基化。","authors":"Alex Lyakhovich,&nbsp;Maria Jose Ramirez,&nbsp;Andres Castellanos,&nbsp;Maria Castella,&nbsp;Amanda M Simons,&nbsp;Jeffrey D Parvin,&nbsp;Jordi Surralles","doi":"10.1186/2041-9414-2-4","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>Fanconi anemia (FA) is a rare autosomal recessive syndrome characterized by developmental abnormalities, progressive bone marrow failure, and predisposition to cancer. The key FA protein FANCD2 crosstalks with members of DNA damage and repair pathways that also play a role at telomeres. Therefore, we investigated whether FANCD2 has a similar involvement at telomeres.</p><p><strong>Results: </strong>We reveal that FANCD2 may perform a novel function separate to the FANCD2/BRCA pathway. This function includes FANCD2 interaction with one of the telomere components, the PARP family member tankyrase-1. Moreover, FANCD2 inhibits tankyrase-1 activity in vitro. In turn, FANCD2 deficiency increases the polyADP-ribosylation of telomere binding factor TRF1.</p><p><strong>Conclusions: </strong>FANCD2 binding and inhibiting tankyrase-1PARsylation at telomeres may provide an additional step within the FA pathway for the regulation of genomic integrity.</p>","PeriodicalId":53596,"journal":{"name":"Genome Integrity","volume":"2 1","pages":"4"},"PeriodicalIF":0.0000,"publicationDate":"2011-02-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1186/2041-9414-2-4","citationCount":"25","resultStr":"{\"title\":\"Fanconi anemia protein FANCD2 inhibits TRF1 polyADP-ribosylation through tankyrase1-dependent manner.\",\"authors\":\"Alex Lyakhovich,&nbsp;Maria Jose Ramirez,&nbsp;Andres Castellanos,&nbsp;Maria Castella,&nbsp;Amanda M Simons,&nbsp;Jeffrey D Parvin,&nbsp;Jordi Surralles\",\"doi\":\"10.1186/2041-9414-2-4\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Background: </strong>Fanconi anemia (FA) is a rare autosomal recessive syndrome characterized by developmental abnormalities, progressive bone marrow failure, and predisposition to cancer. The key FA protein FANCD2 crosstalks with members of DNA damage and repair pathways that also play a role at telomeres. Therefore, we investigated whether FANCD2 has a similar involvement at telomeres.</p><p><strong>Results: </strong>We reveal that FANCD2 may perform a novel function separate to the FANCD2/BRCA pathway. This function includes FANCD2 interaction with one of the telomere components, the PARP family member tankyrase-1. Moreover, FANCD2 inhibits tankyrase-1 activity in vitro. In turn, FANCD2 deficiency increases the polyADP-ribosylation of telomere binding factor TRF1.</p><p><strong>Conclusions: </strong>FANCD2 binding and inhibiting tankyrase-1PARsylation at telomeres may provide an additional step within the FA pathway for the regulation of genomic integrity.</p>\",\"PeriodicalId\":53596,\"journal\":{\"name\":\"Genome Integrity\",\"volume\":\"2 1\",\"pages\":\"4\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2011-02-12\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://sci-hub-pdf.com/10.1186/2041-9414-2-4\",\"citationCount\":\"25\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Genome Integrity\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.1186/2041-9414-2-4\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q4\",\"JCRName\":\"Biochemistry, Genetics and Molecular Biology\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Genome Integrity","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1186/2041-9414-2-4","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"Biochemistry, Genetics and Molecular Biology","Score":null,"Total":0}
引用次数: 25

摘要

背景:范可尼贫血(FA)是一种罕见的常染色体隐性综合征,以发育异常、进行性骨髓衰竭和癌症易感为特征。关键FA蛋白FANCD2与DNA损伤和修复途径的成员串扰,也在端粒中发挥作用。因此,我们研究了FANCD2是否在端粒中有类似的参与。结果:我们发现FANCD2可能具有独立于FANCD2/BRCA通路的新功能。该功能包括FANCD2与端粒组分之一PARP家族成员tankyase -1的相互作用。此外,FANCD2在体外抑制tankyase -1活性。反过来,FANCD2缺陷增加了端粒结合因子TRF1的多adp核糖基化。结论:FANCD2结合和抑制端粒tankyase - 1parsylation可能在FA途径中为基因组完整性的调节提供了额外的步骤。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

摘要图片

摘要图片

摘要图片

查看原文
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
Fanconi anemia protein FANCD2 inhibits TRF1 polyADP-ribosylation through tankyrase1-dependent manner.

Background: Fanconi anemia (FA) is a rare autosomal recessive syndrome characterized by developmental abnormalities, progressive bone marrow failure, and predisposition to cancer. The key FA protein FANCD2 crosstalks with members of DNA damage and repair pathways that also play a role at telomeres. Therefore, we investigated whether FANCD2 has a similar involvement at telomeres.

Results: We reveal that FANCD2 may perform a novel function separate to the FANCD2/BRCA pathway. This function includes FANCD2 interaction with one of the telomere components, the PARP family member tankyrase-1. Moreover, FANCD2 inhibits tankyrase-1 activity in vitro. In turn, FANCD2 deficiency increases the polyADP-ribosylation of telomere binding factor TRF1.

Conclusions: FANCD2 binding and inhibiting tankyrase-1PARsylation at telomeres may provide an additional step within the FA pathway for the regulation of genomic integrity.

求助全文
通过发布文献求助,成功后即可免费获取论文全文。 去求助
来源期刊
Genome Integrity
Genome Integrity Biochemistry, Genetics and Molecular Biology-Genetics
自引率
0.00%
发文量
1
期刊最新文献
Transforming Healthcare: Artificial Intelligence (AI) Applications in Medical Imaging and Drug Response Prediction. Androgen Receptor Influenced Recurrence Score Correlation in Hormone Positive and HER2 Negative Breast Cancer Indian Patients: A Comparative Approach. Role of Mitogen-Activated Protein (MAP) Kinase Pathways in Metabolic Diseases. Therapeutic Fractional Doses of Ionizing Radiation Promote Epithelial-Mesenchymal Transition, Enhanced Invasiveness, and Altered Glycosylation in MCF-7 Breast Cancer Cells. The Detection of DNA Damage Response in MCF7 and MDA-MB-231 Breast Cancer Cell Lines after X-ray Exposure.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1