Absence of cyclin-dependent kinase inhibitor p27 or p18 increases efficiency of iPSC generation without induction of iPSC genomic instability
Mechanisms underlying the generation of induced pluripotent stem cells (iPSC) and keeping iPSC stability remain to be further defined. Accumulated evidences showed that iPSC reprogramming may be controlled by the cell-division-rate-dependent model. Here we reported effects of absence of mouse p27 or...
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| Veröffentlicht in: | Cell death & disease 2019-03, Vol.10 (4), p.271-271, Article 271 |
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| creator | Zhan, Zhiyan Song, Lili Zhang, Weiwei Gu, Haihui Cheng, Haizi Zhang, Yingwen Yang, Yi Ji, Guangzhen Feng, Haizhong Cheng, Tao Li, Yanxin |
| description | Mechanisms underlying the generation of induced pluripotent stem cells (iPSC) and keeping iPSC stability remain to be further defined. Accumulated evidences showed that iPSC reprogramming may be controlled by the cell-division-rate-dependent model. Here we reported effects of absence of mouse
p27
or
p18
on iPSC generation efficiency and genomic stability. Expression levels of cyclin-dependent kinases inhibitors (CDKIs), p21, p27, and p18 decreased during iPSC reprogramming. Like
p21
loss,
p27
or
p18
deficiency significantly promoted efficiency of iPSC generation, whereas ectopic expression of p27, p18, or treatment with CDK2 or CDK4 inhibitors repressed the reprogramming rate, suggesting that CDKIs-regulated iPSC reprogramming is directly related with their functions as CDK inhibitors. However, unlike
p21
deletion, absence of
p27
or
p18
did not increase DNA damage or chromosomal aberrations during iPSC reprogramming and at iPSC stage. Our data not only support that cell cycle regulation is critical for iPSC reprogramming, but also reveal the distinction of CDKIs in somatic cell reprogramming. |
| doi_str_mv | 10.1038/s41419-019-1502-8 |
| format | Article |
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p27
or
p18
on iPSC generation efficiency and genomic stability. Expression levels of cyclin-dependent kinases inhibitors (CDKIs), p21, p27, and p18 decreased during iPSC reprogramming. Like
p21
loss,
p27
or
p18
deficiency significantly promoted efficiency of iPSC generation, whereas ectopic expression of p27, p18, or treatment with CDK2 or CDK4 inhibitors repressed the reprogramming rate, suggesting that CDKIs-regulated iPSC reprogramming is directly related with their functions as CDK inhibitors. However, unlike
p21
deletion, absence of
p27
or
p18
did not increase DNA damage or chromosomal aberrations during iPSC reprogramming and at iPSC stage. Our data not only support that cell cycle regulation is critical for iPSC reprogramming, but also reveal the distinction of CDKIs in somatic cell reprogramming.</description><identifier>ISSN: 2041-4889</identifier><identifier>EISSN: 2041-4889</identifier><identifier>DOI: 10.1038/s41419-019-1502-8</identifier><identifier>PMID: 30894510</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>13/1 ; 13/100 ; 13/109 ; 13/2 ; 13/21 ; 13/31 ; 14/34 ; 14/35 ; 38/39 ; 38/77 ; 631/532/2064/2158 ; 631/532/2435 ; 631/80/82/23 ; Animals ; Antibodies ; Biochemistry ; Biomedical and Life Sciences ; Cell Biology ; Cell Culture ; Cell cycle ; Cell Division - genetics ; Cellular Reprogramming - genetics ; Chromosome Aberrations ; Clonal deletion ; Cyclin-dependent kinase ; Cyclin-dependent kinase 2 ; Cyclin-Dependent Kinase 2 - antagonists & inhibitors ; Cyclin-dependent kinase 4 ; Cyclin-Dependent Kinase 4 - antagonists & inhibitors ; Cyclin-Dependent Kinase Inhibitor p18 - deficiency ; Cyclin-Dependent Kinase Inhibitor p18 - genetics ; Cyclin-Dependent Kinase Inhibitor p18 - metabolism ; Cyclin-dependent kinase inhibitor p21 ; Cyclin-Dependent Kinase Inhibitor p21 - deficiency ; Cyclin-Dependent Kinase Inhibitor p21 - genetics ; Cyclin-Dependent Kinase Inhibitor p21 - metabolism ; Cyclin-dependent kinase inhibitor p27 ; Cyclin-Dependent Kinase Inhibitor p27 - deficiency ; Cyclin-Dependent Kinase Inhibitor p27 - genetics ; Cyclin-Dependent Kinase Inhibitor p27 - metabolism ; Cyclin-dependent kinases ; DNA damage ; Ectopic expression ; Efficiency ; Enzyme inhibitors ; Fibroblasts - metabolism ; Genomic instability ; Genomic Instability - genetics ; Immunology ; Induced Pluripotent Stem Cells - metabolism ; Kinases ; Life Sciences ; Mice ; Mice, Inbred C57BL ; Mice, Inbred NOD ; Mice, Knockout ; Mice, SCID ; Pluripotency ; Stem cell transplantation ; Stem cells ; Transduction, Genetic</subject><ispartof>Cell death & disease, 2019-03, Vol.10 (4), p.271-271, Article 271</ispartof><rights>The Author(s) 2019</rights><rights>This work is published under http://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><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c470t-85ae7efe8b20218b49fda9bf5d66cdb8d827386229e8574cfd6d7a7d684a2293</citedby><cites>FETCH-LOGICAL-c470t-85ae7efe8b20218b49fda9bf5d66cdb8d827386229e8574cfd6d7a7d684a2293</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6426969/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6426969/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,27901,27902,41096,42165,51551,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30894510$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhan, Zhiyan</creatorcontrib><creatorcontrib>Song, Lili</creatorcontrib><creatorcontrib>Zhang, Weiwei</creatorcontrib><creatorcontrib>Gu, Haihui</creatorcontrib><creatorcontrib>Cheng, Haizi</creatorcontrib><creatorcontrib>Zhang, Yingwen</creatorcontrib><creatorcontrib>Yang, Yi</creatorcontrib><creatorcontrib>Ji, Guangzhen</creatorcontrib><creatorcontrib>Feng, Haizhong</creatorcontrib><creatorcontrib>Cheng, Tao</creatorcontrib><creatorcontrib>Li, Yanxin</creatorcontrib><title>Absence of cyclin-dependent kinase inhibitor p27 or p18 increases efficiency of iPSC generation without induction of iPSC genomic instability</title><title>Cell death & disease</title><addtitle>Cell Death Dis</addtitle><addtitle>Cell Death Dis</addtitle><description>Mechanisms underlying the generation of induced pluripotent stem cells (iPSC) and keeping iPSC stability remain to be further defined. Accumulated evidences showed that iPSC reprogramming may be controlled by the cell-division-rate-dependent model. Here we reported effects of absence of mouse
p27
or
p18
on iPSC generation efficiency and genomic stability. Expression levels of cyclin-dependent kinases inhibitors (CDKIs), p21, p27, and p18 decreased during iPSC reprogramming. Like
p21
loss,
p27
or
p18
deficiency significantly promoted efficiency of iPSC generation, whereas ectopic expression of p27, p18, or treatment with CDK2 or CDK4 inhibitors repressed the reprogramming rate, suggesting that CDKIs-regulated iPSC reprogramming is directly related with their functions as CDK inhibitors. However, unlike
p21
deletion, absence of
p27
or
p18
did not increase DNA damage or chromosomal aberrations during iPSC reprogramming and at iPSC stage. Our data not only support that cell cycle regulation is critical for iPSC reprogramming, but also reveal the distinction of CDKIs in somatic cell reprogramming.</description><subject>13/1</subject><subject>13/100</subject><subject>13/109</subject><subject>13/2</subject><subject>13/21</subject><subject>13/31</subject><subject>14/34</subject><subject>14/35</subject><subject>38/39</subject><subject>38/77</subject><subject>631/532/2064/2158</subject><subject>631/532/2435</subject><subject>631/80/82/23</subject><subject>Animals</subject><subject>Antibodies</subject><subject>Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Cell Biology</subject><subject>Cell Culture</subject><subject>Cell cycle</subject><subject>Cell Division - genetics</subject><subject>Cellular Reprogramming - genetics</subject><subject>Chromosome Aberrations</subject><subject>Clonal deletion</subject><subject>Cyclin-dependent kinase</subject><subject>Cyclin-dependent kinase 2</subject><subject>Cyclin-Dependent Kinase 2 - antagonists & inhibitors</subject><subject>Cyclin-dependent kinase 4</subject><subject>Cyclin-Dependent Kinase 4 - antagonists & inhibitors</subject><subject>Cyclin-Dependent Kinase Inhibitor p18 - deficiency</subject><subject>Cyclin-Dependent Kinase Inhibitor p18 - genetics</subject><subject>Cyclin-Dependent Kinase Inhibitor p18 - metabolism</subject><subject>Cyclin-dependent kinase inhibitor p21</subject><subject>Cyclin-Dependent Kinase Inhibitor p21 - deficiency</subject><subject>Cyclin-Dependent Kinase Inhibitor p21 - genetics</subject><subject>Cyclin-Dependent Kinase Inhibitor p21 - metabolism</subject><subject>Cyclin-dependent kinase inhibitor p27</subject><subject>Cyclin-Dependent Kinase Inhibitor p27 - deficiency</subject><subject>Cyclin-Dependent Kinase Inhibitor p27 - genetics</subject><subject>Cyclin-Dependent Kinase Inhibitor p27 - metabolism</subject><subject>Cyclin-dependent kinases</subject><subject>DNA damage</subject><subject>Ectopic expression</subject><subject>Efficiency</subject><subject>Enzyme inhibitors</subject><subject>Fibroblasts - metabolism</subject><subject>Genomic instability</subject><subject>Genomic Instability - genetics</subject><subject>Immunology</subject><subject>Induced Pluripotent Stem Cells - metabolism</subject><subject>Kinases</subject><subject>Life Sciences</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Inbred NOD</subject><subject>Mice, Knockout</subject><subject>Mice, SCID</subject><subject>Pluripotency</subject><subject>Stem cell transplantation</subject><subject>Stem cells</subject><subject>Transduction, Genetic</subject><issn>2041-4889</issn><issn>2041-4889</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNp1kd9qHCEUxofS0oQ0D9CbIvSmN9Oqo47eFMLSfxBoILkXR4-7prO61ZmWfYi-c51umm4DEUQ53-98evia5iXBbwnu5LvCCCOqxXUTjmkrnzSnFDPSMinV06P7SXNeyi2uq-sw5eJ5c9JhqRgn-LT5dTEUiBZQ8sju7Rhi62AH0UGc0LcQTQEU4iYMYUoZ7WiPloPIWrQZqloQeB9sqCb7xSRcXa_QGiJkM4UU0c8wbdI8Vd7N9k_lCErbYKtSJjOEMUz7F80zb8YC53fnWXPz8cPN6nN7-fXTl9XFZWtZj6dWcgM9eJADxZTIgSnvjBo8d0JYN0gnad9JQakCyXtmvROuN70Tkpla7M6a9wfb3Txswdk6azaj3uWwNXmvkwn6fyWGjV6nH1owKpRYDN7cGeT0fYYy6W0oFsbRREhz0ZQoTgVWilT09QP0Ns051ukWivEes55Xihwom1MpGfz9ZwjWS9z6ELeuceslbi1rz6vjKe47_oZbAXoASpXiGvK_px93_Q09tLe0</recordid><startdate>20190320</startdate><enddate>20190320</enddate><creator>Zhan, Zhiyan</creator><creator>Song, Lili</creator><creator>Zhang, Weiwei</creator><creator>Gu, Haihui</creator><creator>Cheng, Haizi</creator><creator>Zhang, Yingwen</creator><creator>Yang, Yi</creator><creator>Ji, Guangzhen</creator><creator>Feng, Haizhong</creator><creator>Cheng, Tao</creator><creator>Li, Yanxin</creator><general>Nature Publishing Group UK</general><general>Springer Nature B.V</general><scope>C6C</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>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88I</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M2P</scope><scope>M7P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20190320</creationdate><title>Absence of cyclin-dependent kinase inhibitor p27 or p18 increases efficiency of iPSC generation without induction of iPSC genomic instability</title><author>Zhan, Zhiyan ; Song, Lili ; Zhang, Weiwei ; Gu, Haihui ; Cheng, Haizi ; Zhang, Yingwen ; Yang, Yi ; Ji, Guangzhen ; Feng, Haizhong ; Cheng, Tao ; Li, Yanxin</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c470t-85ae7efe8b20218b49fda9bf5d66cdb8d827386229e8574cfd6d7a7d684a2293</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>13/1</topic><topic>13/100</topic><topic>13/109</topic><topic>13/2</topic><topic>13/21</topic><topic>13/31</topic><topic>14/34</topic><topic>14/35</topic><topic>38/39</topic><topic>38/77</topic><topic>631/532/2064/2158</topic><topic>631/532/2435</topic><topic>631/80/82/23</topic><topic>Animals</topic><topic>Antibodies</topic><topic>Biochemistry</topic><topic>Biomedical and Life Sciences</topic><topic>Cell Biology</topic><topic>Cell Culture</topic><topic>Cell cycle</topic><topic>Cell Division - genetics</topic><topic>Cellular Reprogramming - genetics</topic><topic>Chromosome Aberrations</topic><topic>Clonal deletion</topic><topic>Cyclin-dependent kinase</topic><topic>Cyclin-dependent kinase 2</topic><topic>Cyclin-Dependent Kinase 2 - antagonists & inhibitors</topic><topic>Cyclin-dependent kinase 4</topic><topic>Cyclin-Dependent Kinase 4 - antagonists & inhibitors</topic><topic>Cyclin-Dependent Kinase Inhibitor p18 - deficiency</topic><topic>Cyclin-Dependent Kinase Inhibitor p18 - genetics</topic><topic>Cyclin-Dependent Kinase Inhibitor p18 - metabolism</topic><topic>Cyclin-dependent kinase inhibitor p21</topic><topic>Cyclin-Dependent Kinase Inhibitor p21 - deficiency</topic><topic>Cyclin-Dependent Kinase Inhibitor p21 - genetics</topic><topic>Cyclin-Dependent Kinase Inhibitor p21 - metabolism</topic><topic>Cyclin-dependent kinase inhibitor p27</topic><topic>Cyclin-Dependent Kinase Inhibitor p27 - deficiency</topic><topic>Cyclin-Dependent Kinase Inhibitor p27 - genetics</topic><topic>Cyclin-Dependent Kinase Inhibitor p27 - metabolism</topic><topic>Cyclin-dependent kinases</topic><topic>DNA damage</topic><topic>Ectopic expression</topic><topic>Efficiency</topic><topic>Enzyme inhibitors</topic><topic>Fibroblasts - metabolism</topic><topic>Genomic instability</topic><topic>Genomic Instability - genetics</topic><topic>Immunology</topic><topic>Induced Pluripotent Stem Cells - metabolism</topic><topic>Kinases</topic><topic>Life Sciences</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Inbred NOD</topic><topic>Mice, Knockout</topic><topic>Mice, SCID</topic><topic>Pluripotency</topic><topic>Stem cell transplantation</topic><topic>Stem cells</topic><topic>Transduction, Genetic</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhan, Zhiyan</creatorcontrib><creatorcontrib>Song, Lili</creatorcontrib><creatorcontrib>Zhang, Weiwei</creatorcontrib><creatorcontrib>Gu, Haihui</creatorcontrib><creatorcontrib>Cheng, Haizi</creatorcontrib><creatorcontrib>Zhang, Yingwen</creatorcontrib><creatorcontrib>Yang, Yi</creatorcontrib><creatorcontrib>Ji, Guangzhen</creatorcontrib><creatorcontrib>Feng, Haizhong</creatorcontrib><creatorcontrib>Cheng, Tao</creatorcontrib><creatorcontrib>Li, Yanxin</creatorcontrib><collection>Springer Nature OA Free Journals</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><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>Biology Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</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>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</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 Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Science Database</collection><collection>Biological Science Database</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>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Cell death & disease</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhan, Zhiyan</au><au>Song, Lili</au><au>Zhang, Weiwei</au><au>Gu, Haihui</au><au>Cheng, Haizi</au><au>Zhang, Yingwen</au><au>Yang, Yi</au><au>Ji, Guangzhen</au><au>Feng, Haizhong</au><au>Cheng, Tao</au><au>Li, Yanxin</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Absence of cyclin-dependent kinase inhibitor p27 or p18 increases efficiency of iPSC generation without induction of iPSC genomic instability</atitle><jtitle>Cell death & disease</jtitle><stitle>Cell Death Dis</stitle><addtitle>Cell Death Dis</addtitle><date>2019-03-20</date><risdate>2019</risdate><volume>10</volume><issue>4</issue><spage>271</spage><epage>271</epage><pages>271-271</pages><artnum>271</artnum><issn>2041-4889</issn><eissn>2041-4889</eissn><abstract>Mechanisms underlying the generation of induced pluripotent stem cells (iPSC) and keeping iPSC stability remain to be further defined. Accumulated evidences showed that iPSC reprogramming may be controlled by the cell-division-rate-dependent model. Here we reported effects of absence of mouse
p27
or
p18
on iPSC generation efficiency and genomic stability. Expression levels of cyclin-dependent kinases inhibitors (CDKIs), p21, p27, and p18 decreased during iPSC reprogramming. Like
p21
loss,
p27
or
p18
deficiency significantly promoted efficiency of iPSC generation, whereas ectopic expression of p27, p18, or treatment with CDK2 or CDK4 inhibitors repressed the reprogramming rate, suggesting that CDKIs-regulated iPSC reprogramming is directly related with their functions as CDK inhibitors. However, unlike
p21
deletion, absence of
p27
or
p18
did not increase DNA damage or chromosomal aberrations during iPSC reprogramming and at iPSC stage. Our data not only support that cell cycle regulation is critical for iPSC reprogramming, but also reveal the distinction of CDKIs in somatic cell reprogramming.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>30894510</pmid><doi>10.1038/s41419-019-1502-8</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Cell death & disease, 2019-03, Vol.10 (4), p.271-271, Article 271 |
| issn | 2041-4889 2041-4889 |
| language | eng |
| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_6426969 |
| source | MEDLINE; Nature Free; DOAJ Directory of Open Access Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central; Springer Nature OA Free Journals |
| subjects | 13/1 13/100 13/109 13/2 13/21 13/31 14/34 14/35 38/39 38/77 631/532/2064/2158 631/532/2435 631/80/82/23 Animals Antibodies Biochemistry Biomedical and Life Sciences Cell Biology Cell Culture Cell cycle Cell Division - genetics Cellular Reprogramming - genetics Chromosome Aberrations Clonal deletion Cyclin-dependent kinase Cyclin-dependent kinase 2 Cyclin-Dependent Kinase 2 - antagonists & inhibitors Cyclin-dependent kinase 4 Cyclin-Dependent Kinase 4 - antagonists & inhibitors Cyclin-Dependent Kinase Inhibitor p18 - deficiency Cyclin-Dependent Kinase Inhibitor p18 - genetics Cyclin-Dependent Kinase Inhibitor p18 - metabolism Cyclin-dependent kinase inhibitor p21 Cyclin-Dependent Kinase Inhibitor p21 - deficiency Cyclin-Dependent Kinase Inhibitor p21 - genetics Cyclin-Dependent Kinase Inhibitor p21 - metabolism Cyclin-dependent kinase inhibitor p27 Cyclin-Dependent Kinase Inhibitor p27 - deficiency Cyclin-Dependent Kinase Inhibitor p27 - genetics Cyclin-Dependent Kinase Inhibitor p27 - metabolism Cyclin-dependent kinases DNA damage Ectopic expression Efficiency Enzyme inhibitors Fibroblasts - metabolism Genomic instability Genomic Instability - genetics Immunology Induced Pluripotent Stem Cells - metabolism Kinases Life Sciences Mice Mice, Inbred C57BL Mice, Inbred NOD Mice, Knockout Mice, SCID Pluripotency Stem cell transplantation Stem cells Transduction, Genetic |
| title | Absence of cyclin-dependent kinase inhibitor p27 or p18 increases efficiency of iPSC generation without induction of iPSC genomic instability |
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