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An Unconventional Role of BMP-Smad1 Signaling in DNA Damage Response: A Mechanism for Tumor Suppression
ABSTRACT The genome is under constant attack by self‐produced reactive oxygen species and genotoxic reagents in the environment. Cells have evolved a DNA damage response (DDR) system to sense DNA damage, to halt cell cycle progression and repair the lesions, or to induce apoptosis if encountering ir...
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Published in: | Journal of cellular biochemistry 2014-03, Vol.115 (3), p.450-456 |
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container_title | Journal of cellular biochemistry |
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creator | Liu, Huijuan Bao, Dandan Xia, Xuechun Chau, Jenny Fung Ling Li, Baojie |
description | ABSTRACT
The genome is under constant attack by self‐produced reactive oxygen species and genotoxic reagents in the environment. Cells have evolved a DNA damage response (DDR) system to sense DNA damage, to halt cell cycle progression and repair the lesions, or to induce apoptosis if encountering irreparable damage. The best studied DDR pathways are the PIKK‐p53 and PIKK‐Chk1/2. Mutations in these genes encoding DDR molecules usually lead to genome instability and tumorigenesis. It is worth noting that there exist unconventional pathways that facilitate the canonical pathways or take over in the absence of the canonical pathways in DDR. This review will summarize on several unconventional pathways that participate in DDR with an emphasis on the BMP‐Smad1 pathway, a known regulator of mouse development and bone remodeling. J. Cell. Biochem. 115: 450–456, 2014. © 2013 Wiley Periodicals, Inc. |
doi_str_mv | 10.1002/jcb.24698 |
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The genome is under constant attack by self‐produced reactive oxygen species and genotoxic reagents in the environment. Cells have evolved a DNA damage response (DDR) system to sense DNA damage, to halt cell cycle progression and repair the lesions, or to induce apoptosis if encountering irreparable damage. The best studied DDR pathways are the PIKK‐p53 and PIKK‐Chk1/2. Mutations in these genes encoding DDR molecules usually lead to genome instability and tumorigenesis. It is worth noting that there exist unconventional pathways that facilitate the canonical pathways or take over in the absence of the canonical pathways in DDR. This review will summarize on several unconventional pathways that participate in DDR with an emphasis on the BMP‐Smad1 pathway, a known regulator of mouse development and bone remodeling. J. Cell. Biochem. 115: 450–456, 2014. © 2013 Wiley Periodicals, Inc.</description><identifier>ISSN: 0730-2312</identifier><identifier>EISSN: 1097-4644</identifier><identifier>DOI: 10.1002/jcb.24698</identifier><identifier>PMID: 24142423</identifier><language>eng</language><publisher>United States: Blackwell Publishing Ltd</publisher><subject>Animals ; Apoptosis - genetics ; Bone Morphogenetic Proteins - genetics ; Bone Morphogenetic Proteins - metabolism ; Bone Remodeling - genetics ; DNA Damage - genetics ; DNA Repair - genetics ; Gene Expression Regulation, Developmental ; Humans ; Mice ; Neoplasms - genetics ; Neoplasms - metabolism ; Neoplasms - pathology ; Reactive Oxygen Species - metabolism ; Signal Transduction - genetics ; Smad1 Protein - biosynthesis ; Smad1 Protein - genetics ; Smad1 Protein - metabolism</subject><ispartof>Journal of cellular biochemistry, 2014-03, Vol.115 (3), p.450-456</ispartof><rights>2013 Wiley Periodicals, Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4908-c9b1dde7cd91984704009dd33c5216670aa3d22bfec28e311745488e6e3aee123</citedby><cites>FETCH-LOGICAL-c4908-c9b1dde7cd91984704009dd33c5216670aa3d22bfec28e311745488e6e3aee123</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24142423$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Liu, Huijuan</creatorcontrib><creatorcontrib>Bao, Dandan</creatorcontrib><creatorcontrib>Xia, Xuechun</creatorcontrib><creatorcontrib>Chau, Jenny Fung Ling</creatorcontrib><creatorcontrib>Li, Baojie</creatorcontrib><title>An Unconventional Role of BMP-Smad1 Signaling in DNA Damage Response: A Mechanism for Tumor Suppression</title><title>Journal of cellular biochemistry</title><addtitle>J. Cell. Biochem</addtitle><description>ABSTRACT
The genome is under constant attack by self‐produced reactive oxygen species and genotoxic reagents in the environment. Cells have evolved a DNA damage response (DDR) system to sense DNA damage, to halt cell cycle progression and repair the lesions, or to induce apoptosis if encountering irreparable damage. The best studied DDR pathways are the PIKK‐p53 and PIKK‐Chk1/2. Mutations in these genes encoding DDR molecules usually lead to genome instability and tumorigenesis. It is worth noting that there exist unconventional pathways that facilitate the canonical pathways or take over in the absence of the canonical pathways in DDR. This review will summarize on several unconventional pathways that participate in DDR with an emphasis on the BMP‐Smad1 pathway, a known regulator of mouse development and bone remodeling. J. Cell. Biochem. 115: 450–456, 2014. © 2013 Wiley Periodicals, Inc.</description><subject>Animals</subject><subject>Apoptosis - genetics</subject><subject>Bone Morphogenetic Proteins - genetics</subject><subject>Bone Morphogenetic Proteins - metabolism</subject><subject>Bone Remodeling - genetics</subject><subject>DNA Damage - genetics</subject><subject>DNA Repair - genetics</subject><subject>Gene Expression Regulation, Developmental</subject><subject>Humans</subject><subject>Mice</subject><subject>Neoplasms - genetics</subject><subject>Neoplasms - metabolism</subject><subject>Neoplasms - pathology</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>Signal Transduction - genetics</subject><subject>Smad1 Protein - biosynthesis</subject><subject>Smad1 Protein - genetics</subject><subject>Smad1 Protein - metabolism</subject><issn>0730-2312</issn><issn>1097-4644</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><recordid>eNqN0U9v0zAYBnALgVgpHPgCyBIXOGTzfyfcug42pnWgtRNHy3XelJTEDnYD7Nvj0W0HJCQu9sG_95H1Pgi9pOSQEsKOtm59yISqykdoQkmlC6GEeIwmRHNSME7ZAXqW0pYQUlWcPUUHTFDBBOMTtJl5fO1d8D_A79rgbYevQgc4NPh48blY9rameNlu8kPrN7j1-ORyhk9sbzeAryANwSd4h2d4Ae6r9W3qcRMiXo19PpfjMERIKec-R08a2yV4cXdP0fWH96v5WXHx6fTjfHZROFGRsnDVmtY1aFdXtCqFJiL_ua45d5JRpTSxlteMrRtwrAROqRZSlCUo4BaAMj5Fb_a5QwzfR0g707fJQddZD2FMhkoiOVclrf6HCiH1rZ-i13_RbRhj3klWopRaMallVm_3ysWQUoTGDLHtbbwxlJjbokwuyvwpKttXd4njuof6Qd43k8HRHvxsO7j5d5I5nx_fRxb7iTbt4NfDhI3fjNJcS_Pl8tQszpU4m8uVWfHfAxSoYQ</recordid><startdate>201403</startdate><enddate>201403</enddate><creator>Liu, Huijuan</creator><creator>Bao, Dandan</creator><creator>Xia, Xuechun</creator><creator>Chau, Jenny Fung Ling</creator><creator>Li, Baojie</creator><general>Blackwell Publishing Ltd</general><general>Wiley Subscription Services, Inc</general><scope>BSCLL</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QL</scope><scope>7QP</scope><scope>7QR</scope><scope>7T7</scope><scope>7TK</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>M7N</scope><scope>P64</scope><scope>7X8</scope><scope>7TM</scope></search><sort><creationdate>201403</creationdate><title>An Unconventional Role of BMP-Smad1 Signaling in DNA Damage Response: A Mechanism for Tumor Suppression</title><author>Liu, Huijuan ; Bao, Dandan ; Xia, Xuechun ; Chau, Jenny Fung Ling ; Li, Baojie</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4908-c9b1dde7cd91984704009dd33c5216670aa3d22bfec28e311745488e6e3aee123</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Animals</topic><topic>Apoptosis - genetics</topic><topic>Bone Morphogenetic Proteins - genetics</topic><topic>Bone Morphogenetic Proteins - metabolism</topic><topic>Bone Remodeling - genetics</topic><topic>DNA Damage - genetics</topic><topic>DNA Repair - genetics</topic><topic>Gene Expression Regulation, Developmental</topic><topic>Humans</topic><topic>Mice</topic><topic>Neoplasms - genetics</topic><topic>Neoplasms - metabolism</topic><topic>Neoplasms - pathology</topic><topic>Reactive Oxygen Species - metabolism</topic><topic>Signal Transduction - genetics</topic><topic>Smad1 Protein - biosynthesis</topic><topic>Smad1 Protein - genetics</topic><topic>Smad1 Protein - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Liu, Huijuan</creatorcontrib><creatorcontrib>Bao, Dandan</creatorcontrib><creatorcontrib>Xia, Xuechun</creatorcontrib><creatorcontrib>Chau, Jenny Fung Ling</creatorcontrib><creatorcontrib>Li, Baojie</creatorcontrib><collection>Istex</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Neurosciences Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><collection>Nucleic Acids Abstracts</collection><jtitle>Journal of cellular biochemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Liu, Huijuan</au><au>Bao, Dandan</au><au>Xia, Xuechun</au><au>Chau, Jenny Fung Ling</au><au>Li, Baojie</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>An Unconventional Role of BMP-Smad1 Signaling in DNA Damage Response: A Mechanism for Tumor Suppression</atitle><jtitle>Journal of cellular biochemistry</jtitle><addtitle>J. Cell. Biochem</addtitle><date>2014-03</date><risdate>2014</risdate><volume>115</volume><issue>3</issue><spage>450</spage><epage>456</epage><pages>450-456</pages><issn>0730-2312</issn><eissn>1097-4644</eissn><abstract>ABSTRACT
The genome is under constant attack by self‐produced reactive oxygen species and genotoxic reagents in the environment. Cells have evolved a DNA damage response (DDR) system to sense DNA damage, to halt cell cycle progression and repair the lesions, or to induce apoptosis if encountering irreparable damage. The best studied DDR pathways are the PIKK‐p53 and PIKK‐Chk1/2. Mutations in these genes encoding DDR molecules usually lead to genome instability and tumorigenesis. It is worth noting that there exist unconventional pathways that facilitate the canonical pathways or take over in the absence of the canonical pathways in DDR. This review will summarize on several unconventional pathways that participate in DDR with an emphasis on the BMP‐Smad1 pathway, a known regulator of mouse development and bone remodeling. J. Cell. Biochem. 115: 450–456, 2014. © 2013 Wiley Periodicals, Inc.</abstract><cop>United States</cop><pub>Blackwell Publishing Ltd</pub><pmid>24142423</pmid><doi>10.1002/jcb.24698</doi><tpages>7</tpages></addata></record> |
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subjects | Animals Apoptosis - genetics Bone Morphogenetic Proteins - genetics Bone Morphogenetic Proteins - metabolism Bone Remodeling - genetics DNA Damage - genetics DNA Repair - genetics Gene Expression Regulation, Developmental Humans Mice Neoplasms - genetics Neoplasms - metabolism Neoplasms - pathology Reactive Oxygen Species - metabolism Signal Transduction - genetics Smad1 Protein - biosynthesis Smad1 Protein - genetics Smad1 Protein - metabolism |
title | An Unconventional Role of BMP-Smad1 Signaling in DNA Damage Response: A Mechanism for Tumor Suppression |
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