Nature Communications (Apr 2017)
Structural insights into POT1-TPP1 interaction and POT1 C-terminal mutations in human cancer
- Cong Chen,
- Peili Gu,
- Jian Wu,
- Xianyun Chen,
- Shuangshuang Niu,
- Hong Sun,
- Lijie Wu,
- Na Li,
- Junhui Peng,
- Shaohua Shi,
- Cuiying Fan,
- Min Huang,
- Catherine C. L. Wong,
- Qingguo Gong,
- Chandan Kumar-Sinha,
- Rongguang Zhang,
- Lajos Pusztai,
- Rekha Rai,
- Sandy Chang,
- Ming Lei
Affiliations
- Cong Chen
- National Center for Protein Science Shanghai, State Key Laboratory of Molecular Biology, Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences
- Peili Gu
- Department of Laboratory Medicine, Yale School of Medicine
- Jian Wu
- National Center for Protein Science Shanghai, State Key Laboratory of Molecular Biology, Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences
- Xianyun Chen
- National Center for Protein Science Shanghai, State Key Laboratory of Molecular Biology, Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences
- Shuangshuang Niu
- National Center for Protein Science Shanghai, State Key Laboratory of Molecular Biology, Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences
- Hong Sun
- National Center for Protein Science Shanghai, State Key Laboratory of Molecular Biology, Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences
- Lijie Wu
- National Center for Protein Science Shanghai, State Key Laboratory of Molecular Biology, Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences
- Na Li
- National Center for Protein Science Shanghai, State Key Laboratory of Molecular Biology, Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences
- Junhui Peng
- National Laboratory for Physical Science at the Microscale and School of Life Sciences, University of Science and Technology of China
- Shaohua Shi
- National Center for Protein Science Shanghai, State Key Laboratory of Molecular Biology, Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences
- Cuiying Fan
- National Center for Protein Science Shanghai, State Key Laboratory of Molecular Biology, Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences
- Min Huang
- National Center for Protein Science Shanghai, State Key Laboratory of Molecular Biology, Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences
- Catherine C. L. Wong
- National Center for Protein Science Shanghai, State Key Laboratory of Molecular Biology, Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences
- Qingguo Gong
- National Laboratory for Physical Science at the Microscale and School of Life Sciences, University of Science and Technology of China
- Chandan Kumar-Sinha
- Department of Pathology, University of Michigan School of Medicine
- Rongguang Zhang
- National Center for Protein Science Shanghai, State Key Laboratory of Molecular Biology, Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences
- Lajos Pusztai
- Department of Medicine, Yale School of Medicine
- Rekha Rai
- Department of Laboratory Medicine, Yale School of Medicine
- Sandy Chang
- Department of Laboratory Medicine, Yale School of Medicine
- Ming Lei
- National Center for Protein Science Shanghai, State Key Laboratory of Molecular Biology, Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences
- DOI
- https://doi.org/10.1038/ncomms14929
- Journal volume & issue
-
Vol. 8,
no. 1
pp. 1 – 15
Abstract
Human telomeres are protected by a specialized shelterin complex composed of six proteins. Here the authors structurally characterize the interaction between the POT1-TPP1 shelterin component and identify mutations associated with genome instability and cancer that disrupt the POT1-TPP1 interaction.
