ALKBH5 regulates cardiomyocyte proliferation and heart regeneration by demethylating the mRNA of YTHDF1
N -methyladenosine (m A) RNA modification, a dynamic and reversible process, is essential for tissue development and pathogenesis. However, the potential involvement of m A in the regulation of cardiomyocyte (CM) proliferation and cardiac regeneration remains unclear. In this study, we aimed to inve...
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| Veröffentlicht in: | Theranostics 2021, Vol.11 (6), p.3000-3016 |
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| creator | Han, Zhenbo Wang, Xiuxiu Xu, Zihang Cao, Yang Gong, Rui Yu, Yang Yu, Ying Guo, Xiaofei Liu, Shenzhen Yu, Meixi Ma, Wenya Zhao, Yiming Xu, Juan Li, Xingda Li, Shuainan Xu, Yan Song, Ruijie Xu, Binbin Yang, Fan Bamba, Djibril Sukhareva, Natalia Lei, Hong Gao, Manqi Zhang, Wenwen Zagidullin, Naufal Zhang, Ying Yang, Baofeng Pan, Zhenwei Cai, Benzhi |
| description | N
-methyladenosine (m
A) RNA modification, a dynamic and reversible process, is essential for tissue development and pathogenesis. However, the potential involvement of m
A in the regulation of cardiomyocyte (CM) proliferation and cardiac regeneration remains unclear. In this study, we aimed to investigate the essential role of m
A modification in heart regeneration during postnatal and adult injury.
In this study, we identified the downregulation of m
A demethylase ALKBH5, an m6A "eraser" that is responsible for increased m
A methylation, in the heart after birth. Notably,
knockout mice exhibited decreased cardiac regenerative ability and heart function after neonatal apex resection. Conversely, forced expression of ALKBH5 via adeno-associated virus-9 (AAV9) delivery markedly reduced the infarct size, restored cardiac function and promoted CM proliferation after myocardial infarction in juvenile (7 days old) and adult (8-weeks old) mice. Mechanistically, ALKBH5-mediated m
A demethylation improved the mRNA stability of YTH N
-methyladenosine RNA-binding protein 1 (YTHDF1), thereby increasing its expression, which consequently promoted the translation of Yes-associated protein (YAP). The modulation of ALKBH5 and YTHDF1 expression in human induced pluripotent stem cell-derived cardiomyocytes consistently yielded similar results.
Taken together, our findings highlight the vital role of the ALKBH5-m
A-YTHDF1-YAP axis in the regulation of CMs to re-enter the cell cycle. This finding suggests a novel potential therapeutic strategy for cardiac regeneration. |
| doi_str_mv | 10.7150/thno.47354 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_7806463</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2598241582</sourcerecordid><originalsourceid>FETCH-LOGICAL-c406t-2a29db856c430c2ebb4e62f7846d4621c7f1dc5d891ea8964b736a5085274ae43</originalsourceid><addsrcrecordid>eNpdkU1rFEEQhhtRTIi5-AOkwYsIG_u7ey7CGhNXXBQkHjw1PT01OxNmujfdPcL8-8yaD6J1qaLq4eUtXoReU3KmqSQfShfimdBcimfomBpuVloJ8vzJfIROc74mSwnCKlq9REecC6mkkcdot95--7SROMFuGlyBjL1LTR_HOfq5AN6nOPQtJFf6GLALDe7ApXLgITys6xk3MELp5kWiDztcOsDjz-9rHFv8-2rz-ZK-Qi9aN2Q4ve8n6NflxdX5ZrX98eXr-Xq78oKosmKOVU1tpPKCE8-grgUo1mojVCMUo163tPGyMRUFZyolas2Vk8RIpoUDwU_Qxzvd_VSP0HgIJbnB7lM_ujTb6Hr77yX0nd3FP1YbooTii8C7e4EUbybIxY599jAMLkCcsmVCG62ripgFffsfeh2nFJb3LJOVYYJKwxbq_R3lU8w5QftohhJ7iNAeIrR_I1zgN0_tP6IPgfFbz0-XjQ</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2598241582</pqid></control><display><type>article</type><title>ALKBH5 regulates cardiomyocyte proliferation and heart regeneration by demethylating the mRNA of YTHDF1</title><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>PubMed Central</source><source>PubMed Central Open Access</source><creator>Han, Zhenbo ; Wang, Xiuxiu ; Xu, Zihang ; Cao, Yang ; Gong, Rui ; Yu, Yang ; Yu, Ying ; Guo, Xiaofei ; Liu, Shenzhen ; Yu, Meixi ; Ma, Wenya ; Zhao, Yiming ; Xu, Juan ; Li, Xingda ; Li, Shuainan ; Xu, Yan ; Song, Ruijie ; Xu, Binbin ; Yang, Fan ; Bamba, Djibril ; Sukhareva, Natalia ; Lei, Hong ; Gao, Manqi ; Zhang, Wenwen ; Zagidullin, Naufal ; Zhang, Ying ; Yang, Baofeng ; Pan, Zhenwei ; Cai, Benzhi</creator><creatorcontrib>Han, Zhenbo ; Wang, Xiuxiu ; Xu, Zihang ; Cao, Yang ; Gong, Rui ; Yu, Yang ; Yu, Ying ; Guo, Xiaofei ; Liu, Shenzhen ; Yu, Meixi ; Ma, Wenya ; Zhao, Yiming ; Xu, Juan ; Li, Xingda ; Li, Shuainan ; Xu, Yan ; Song, Ruijie ; Xu, Binbin ; Yang, Fan ; Bamba, Djibril ; Sukhareva, Natalia ; Lei, Hong ; Gao, Manqi ; Zhang, Wenwen ; Zagidullin, Naufal ; Zhang, Ying ; Yang, Baofeng ; Pan, Zhenwei ; Cai, Benzhi</creatorcontrib><description>N
-methyladenosine (m
A) RNA modification, a dynamic and reversible process, is essential for tissue development and pathogenesis. However, the potential involvement of m
A in the regulation of cardiomyocyte (CM) proliferation and cardiac regeneration remains unclear. In this study, we aimed to investigate the essential role of m
A modification in heart regeneration during postnatal and adult injury.
In this study, we identified the downregulation of m
A demethylase ALKBH5, an m6A "eraser" that is responsible for increased m
A methylation, in the heart after birth. Notably,
knockout mice exhibited decreased cardiac regenerative ability and heart function after neonatal apex resection. Conversely, forced expression of ALKBH5 via adeno-associated virus-9 (AAV9) delivery markedly reduced the infarct size, restored cardiac function and promoted CM proliferation after myocardial infarction in juvenile (7 days old) and adult (8-weeks old) mice. Mechanistically, ALKBH5-mediated m
A demethylation improved the mRNA stability of YTH N
-methyladenosine RNA-binding protein 1 (YTHDF1), thereby increasing its expression, which consequently promoted the translation of Yes-associated protein (YAP). The modulation of ALKBH5 and YTHDF1 expression in human induced pluripotent stem cell-derived cardiomyocytes consistently yielded similar results.
Taken together, our findings highlight the vital role of the ALKBH5-m
A-YTHDF1-YAP axis in the regulation of CMs to re-enter the cell cycle. This finding suggests a novel potential therapeutic strategy for cardiac regeneration.</description><identifier>ISSN: 1838-7640</identifier><identifier>EISSN: 1838-7640</identifier><identifier>DOI: 10.7150/thno.47354</identifier><identifier>PMID: 33456585</identifier><language>eng</language><publisher>Australia: Ivyspring International Publisher Pty Ltd</publisher><subject>Cardiac function ; Cardiomyocytes ; Cell cycle ; Heart ; Kinases ; Plasmids ; Protein expression ; Proteins ; Research Paper ; Rodents ; Stem cells</subject><ispartof>Theranostics, 2021, Vol.11 (6), p.3000-3016</ispartof><rights>The author(s).</rights><rights>2021. This work is published under https://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>The author(s) 2021</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c406t-2a29db856c430c2ebb4e62f7846d4621c7f1dc5d891ea8964b736a5085274ae43</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7806463/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7806463/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,4010,27900,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/33456585$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Han, Zhenbo</creatorcontrib><creatorcontrib>Wang, Xiuxiu</creatorcontrib><creatorcontrib>Xu, Zihang</creatorcontrib><creatorcontrib>Cao, Yang</creatorcontrib><creatorcontrib>Gong, Rui</creatorcontrib><creatorcontrib>Yu, Yang</creatorcontrib><creatorcontrib>Yu, Ying</creatorcontrib><creatorcontrib>Guo, Xiaofei</creatorcontrib><creatorcontrib>Liu, Shenzhen</creatorcontrib><creatorcontrib>Yu, Meixi</creatorcontrib><creatorcontrib>Ma, Wenya</creatorcontrib><creatorcontrib>Zhao, Yiming</creatorcontrib><creatorcontrib>Xu, Juan</creatorcontrib><creatorcontrib>Li, Xingda</creatorcontrib><creatorcontrib>Li, Shuainan</creatorcontrib><creatorcontrib>Xu, Yan</creatorcontrib><creatorcontrib>Song, Ruijie</creatorcontrib><creatorcontrib>Xu, Binbin</creatorcontrib><creatorcontrib>Yang, Fan</creatorcontrib><creatorcontrib>Bamba, Djibril</creatorcontrib><creatorcontrib>Sukhareva, Natalia</creatorcontrib><creatorcontrib>Lei, Hong</creatorcontrib><creatorcontrib>Gao, Manqi</creatorcontrib><creatorcontrib>Zhang, Wenwen</creatorcontrib><creatorcontrib>Zagidullin, Naufal</creatorcontrib><creatorcontrib>Zhang, Ying</creatorcontrib><creatorcontrib>Yang, Baofeng</creatorcontrib><creatorcontrib>Pan, Zhenwei</creatorcontrib><creatorcontrib>Cai, Benzhi</creatorcontrib><title>ALKBH5 regulates cardiomyocyte proliferation and heart regeneration by demethylating the mRNA of YTHDF1</title><title>Theranostics</title><addtitle>Theranostics</addtitle><description>N
-methyladenosine (m
A) RNA modification, a dynamic and reversible process, is essential for tissue development and pathogenesis. However, the potential involvement of m
A in the regulation of cardiomyocyte (CM) proliferation and cardiac regeneration remains unclear. In this study, we aimed to investigate the essential role of m
A modification in heart regeneration during postnatal and adult injury.
In this study, we identified the downregulation of m
A demethylase ALKBH5, an m6A "eraser" that is responsible for increased m
A methylation, in the heart after birth. Notably,
knockout mice exhibited decreased cardiac regenerative ability and heart function after neonatal apex resection. Conversely, forced expression of ALKBH5 via adeno-associated virus-9 (AAV9) delivery markedly reduced the infarct size, restored cardiac function and promoted CM proliferation after myocardial infarction in juvenile (7 days old) and adult (8-weeks old) mice. Mechanistically, ALKBH5-mediated m
A demethylation improved the mRNA stability of YTH N
-methyladenosine RNA-binding protein 1 (YTHDF1), thereby increasing its expression, which consequently promoted the translation of Yes-associated protein (YAP). The modulation of ALKBH5 and YTHDF1 expression in human induced pluripotent stem cell-derived cardiomyocytes consistently yielded similar results.
Taken together, our findings highlight the vital role of the ALKBH5-m
A-YTHDF1-YAP axis in the regulation of CMs to re-enter the cell cycle. This finding suggests a novel potential therapeutic strategy for cardiac regeneration.</description><subject>Cardiac function</subject><subject>Cardiomyocytes</subject><subject>Cell cycle</subject><subject>Heart</subject><subject>Kinases</subject><subject>Plasmids</subject><subject>Protein expression</subject><subject>Proteins</subject><subject>Research Paper</subject><subject>Rodents</subject><subject>Stem cells</subject><issn>1838-7640</issn><issn>1838-7640</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>BENPR</sourceid><recordid>eNpdkU1rFEEQhhtRTIi5-AOkwYsIG_u7ey7CGhNXXBQkHjw1PT01OxNmujfdPcL8-8yaD6J1qaLq4eUtXoReU3KmqSQfShfimdBcimfomBpuVloJ8vzJfIROc74mSwnCKlq9REecC6mkkcdot95--7SROMFuGlyBjL1LTR_HOfq5AN6nOPQtJFf6GLALDe7ApXLgITys6xk3MELp5kWiDztcOsDjz-9rHFv8-2rz-ZK-Qi9aN2Q4ve8n6NflxdX5ZrX98eXr-Xq78oKosmKOVU1tpPKCE8-grgUo1mojVCMUo163tPGyMRUFZyolas2Vk8RIpoUDwU_Qxzvd_VSP0HgIJbnB7lM_ujTb6Hr77yX0nd3FP1YbooTii8C7e4EUbybIxY599jAMLkCcsmVCG62ripgFffsfeh2nFJb3LJOVYYJKwxbq_R3lU8w5QftohhJ7iNAeIrR_I1zgN0_tP6IPgfFbz0-XjQ</recordid><startdate>2021</startdate><enddate>2021</enddate><creator>Han, Zhenbo</creator><creator>Wang, Xiuxiu</creator><creator>Xu, Zihang</creator><creator>Cao, Yang</creator><creator>Gong, Rui</creator><creator>Yu, Yang</creator><creator>Yu, Ying</creator><creator>Guo, Xiaofei</creator><creator>Liu, Shenzhen</creator><creator>Yu, Meixi</creator><creator>Ma, Wenya</creator><creator>Zhao, Yiming</creator><creator>Xu, Juan</creator><creator>Li, Xingda</creator><creator>Li, Shuainan</creator><creator>Xu, Yan</creator><creator>Song, Ruijie</creator><creator>Xu, Binbin</creator><creator>Yang, Fan</creator><creator>Bamba, Djibril</creator><creator>Sukhareva, Natalia</creator><creator>Lei, Hong</creator><creator>Gao, Manqi</creator><creator>Zhang, Wenwen</creator><creator>Zagidullin, Naufal</creator><creator>Zhang, Ying</creator><creator>Yang, Baofeng</creator><creator>Pan, Zhenwei</creator><creator>Cai, Benzhi</creator><general>Ivyspring International Publisher Pty Ltd</general><general>Ivyspring International Publisher</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>2021</creationdate><title>ALKBH5 regulates cardiomyocyte proliferation and heart regeneration by demethylating the mRNA of YTHDF1</title><author>Han, Zhenbo ; Wang, Xiuxiu ; Xu, Zihang ; Cao, Yang ; Gong, Rui ; Yu, Yang ; Yu, Ying ; Guo, Xiaofei ; Liu, Shenzhen ; Yu, Meixi ; Ma, Wenya ; Zhao, Yiming ; Xu, Juan ; Li, Xingda ; Li, Shuainan ; Xu, Yan ; Song, Ruijie ; Xu, Binbin ; Yang, Fan ; Bamba, Djibril ; Sukhareva, Natalia ; Lei, Hong ; Gao, Manqi ; Zhang, Wenwen ; Zagidullin, Naufal ; Zhang, Ying ; Yang, Baofeng ; Pan, Zhenwei ; Cai, Benzhi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c406t-2a29db856c430c2ebb4e62f7846d4621c7f1dc5d891ea8964b736a5085274ae43</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Cardiac function</topic><topic>Cardiomyocytes</topic><topic>Cell cycle</topic><topic>Heart</topic><topic>Kinases</topic><topic>Plasmids</topic><topic>Protein expression</topic><topic>Proteins</topic><topic>Research Paper</topic><topic>Rodents</topic><topic>Stem cells</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Han, Zhenbo</creatorcontrib><creatorcontrib>Wang, Xiuxiu</creatorcontrib><creatorcontrib>Xu, Zihang</creatorcontrib><creatorcontrib>Cao, Yang</creatorcontrib><creatorcontrib>Gong, Rui</creatorcontrib><creatorcontrib>Yu, Yang</creatorcontrib><creatorcontrib>Yu, Ying</creatorcontrib><creatorcontrib>Guo, Xiaofei</creatorcontrib><creatorcontrib>Liu, Shenzhen</creatorcontrib><creatorcontrib>Yu, Meixi</creatorcontrib><creatorcontrib>Ma, Wenya</creatorcontrib><creatorcontrib>Zhao, Yiming</creatorcontrib><creatorcontrib>Xu, Juan</creatorcontrib><creatorcontrib>Li, Xingda</creatorcontrib><creatorcontrib>Li, Shuainan</creatorcontrib><creatorcontrib>Xu, Yan</creatorcontrib><creatorcontrib>Song, Ruijie</creatorcontrib><creatorcontrib>Xu, Binbin</creatorcontrib><creatorcontrib>Yang, Fan</creatorcontrib><creatorcontrib>Bamba, Djibril</creatorcontrib><creatorcontrib>Sukhareva, Natalia</creatorcontrib><creatorcontrib>Lei, Hong</creatorcontrib><creatorcontrib>Gao, Manqi</creatorcontrib><creatorcontrib>Zhang, Wenwen</creatorcontrib><creatorcontrib>Zagidullin, Naufal</creatorcontrib><creatorcontrib>Zhang, Ying</creatorcontrib><creatorcontrib>Yang, Baofeng</creatorcontrib><creatorcontrib>Pan, Zhenwei</creatorcontrib><creatorcontrib>Cai, Benzhi</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Theranostics</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Han, Zhenbo</au><au>Wang, Xiuxiu</au><au>Xu, Zihang</au><au>Cao, Yang</au><au>Gong, Rui</au><au>Yu, Yang</au><au>Yu, Ying</au><au>Guo, Xiaofei</au><au>Liu, Shenzhen</au><au>Yu, Meixi</au><au>Ma, Wenya</au><au>Zhao, Yiming</au><au>Xu, Juan</au><au>Li, Xingda</au><au>Li, Shuainan</au><au>Xu, Yan</au><au>Song, Ruijie</au><au>Xu, Binbin</au><au>Yang, Fan</au><au>Bamba, Djibril</au><au>Sukhareva, Natalia</au><au>Lei, Hong</au><au>Gao, Manqi</au><au>Zhang, Wenwen</au><au>Zagidullin, Naufal</au><au>Zhang, Ying</au><au>Yang, Baofeng</au><au>Pan, Zhenwei</au><au>Cai, Benzhi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>ALKBH5 regulates cardiomyocyte proliferation and heart regeneration by demethylating the mRNA of YTHDF1</atitle><jtitle>Theranostics</jtitle><addtitle>Theranostics</addtitle><date>2021</date><risdate>2021</risdate><volume>11</volume><issue>6</issue><spage>3000</spage><epage>3016</epage><pages>3000-3016</pages><issn>1838-7640</issn><eissn>1838-7640</eissn><abstract>N
-methyladenosine (m
A) RNA modification, a dynamic and reversible process, is essential for tissue development and pathogenesis. However, the potential involvement of m
A in the regulation of cardiomyocyte (CM) proliferation and cardiac regeneration remains unclear. In this study, we aimed to investigate the essential role of m
A modification in heart regeneration during postnatal and adult injury.
In this study, we identified the downregulation of m
A demethylase ALKBH5, an m6A "eraser" that is responsible for increased m
A methylation, in the heart after birth. Notably,
knockout mice exhibited decreased cardiac regenerative ability and heart function after neonatal apex resection. Conversely, forced expression of ALKBH5 via adeno-associated virus-9 (AAV9) delivery markedly reduced the infarct size, restored cardiac function and promoted CM proliferation after myocardial infarction in juvenile (7 days old) and adult (8-weeks old) mice. Mechanistically, ALKBH5-mediated m
A demethylation improved the mRNA stability of YTH N
-methyladenosine RNA-binding protein 1 (YTHDF1), thereby increasing its expression, which consequently promoted the translation of Yes-associated protein (YAP). The modulation of ALKBH5 and YTHDF1 expression in human induced pluripotent stem cell-derived cardiomyocytes consistently yielded similar results.
Taken together, our findings highlight the vital role of the ALKBH5-m
A-YTHDF1-YAP axis in the regulation of CMs to re-enter the cell cycle. This finding suggests a novel potential therapeutic strategy for cardiac regeneration.</abstract><cop>Australia</cop><pub>Ivyspring International Publisher Pty Ltd</pub><pmid>33456585</pmid><doi>10.7150/thno.47354</doi><tpages>17</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Theranostics, 2021, Vol.11 (6), p.3000-3016 |
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| language | eng |
| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_7806463 |
| source | Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central; PubMed Central Open Access |
| subjects | Cardiac function Cardiomyocytes Cell cycle Heart Kinases Plasmids Protein expression Proteins Research Paper Rodents Stem cells |
| title | ALKBH5 regulates cardiomyocyte proliferation and heart regeneration by demethylating the mRNA of YTHDF1 |
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