The molecular mechanisms of MLKL-dependent and MLKL-independent necrosis
Abstract Necrosis, a type of unwanted and passive cell demise, usually occurs under the excessive external stress and is considered to be unregulated. However, under some special conditions such as caspase inhibition, necrosis is regulable in a well-orchestrated way. The term ‘regulated necrosis’ ha...
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| Veröffentlicht in: | Journal of molecular cell biology 2021-04, Vol.13 (1), p.3-14 |
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| creator | Li, Lu Tong, An Zhang, Qiangsheng Wei, Yuquan Wei, Xiawei |
| description | Abstract
Necrosis, a type of unwanted and passive cell demise, usually occurs under the excessive external stress and is considered to be unregulated. However, under some special conditions such as caspase inhibition, necrosis is regulable in a well-orchestrated way. The term ‘regulated necrosis’ has been proposed to describe such programed necrosis. Recently, several forms of necrosis, including necroptosis, pyroptosis, ferroptosis, parthanatos, oxytosis, NETosis, and Na+/K+-ATPase-mediated necrosis, have been identified, and some crucial regulators governing regulated necrosis have also been discovered. Mixed lineage kinase domain-like pseudokinase (MLKL), a core regulator in necroptosis, acts as an executioner in response to ligands of death receptor family. Its activation requires the receptor-interacting protein kinases, RIP1 and RIP3. However, MLKL is only involved in necroptosis, i.e. MLKL is dispensable for necrosis. Therefore, this review is aimed at summarizing the molecular mechanisms of MLKL-dependent and MLKL-independent necrosis. |
| doi_str_mv | 10.1093/jmcb/mjaa055 |
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Necrosis, a type of unwanted and passive cell demise, usually occurs under the excessive external stress and is considered to be unregulated. However, under some special conditions such as caspase inhibition, necrosis is regulable in a well-orchestrated way. The term ‘regulated necrosis’ has been proposed to describe such programed necrosis. Recently, several forms of necrosis, including necroptosis, pyroptosis, ferroptosis, parthanatos, oxytosis, NETosis, and Na+/K+-ATPase-mediated necrosis, have been identified, and some crucial regulators governing regulated necrosis have also been discovered. Mixed lineage kinase domain-like pseudokinase (MLKL), a core regulator in necroptosis, acts as an executioner in response to ligands of death receptor family. Its activation requires the receptor-interacting protein kinases, RIP1 and RIP3. However, MLKL is only involved in necroptosis, i.e. MLKL is dispensable for necrosis. Therefore, this review is aimed at summarizing the molecular mechanisms of MLKL-dependent and MLKL-independent necrosis.</description><identifier>ISSN: 1759-4685</identifier><identifier>ISSN: 1674-2788</identifier><identifier>EISSN: 1759-4685</identifier><identifier>DOI: 10.1093/jmcb/mjaa055</identifier><identifier>PMID: 33064829</identifier><language>eng</language><publisher>United States: Oxford University Press</publisher><subject>Animals ; Humans ; Necroptosis ; Necrosis - pathology ; Protein Kinases - metabolism ; Reviews</subject><ispartof>Journal of molecular cell biology, 2021-04, Vol.13 (1), p.3-14</ispartof><rights>The Author(s) (2020). Published by Oxford University Press on behalf of Journal of Molecular Cell Biology , IBCB, SIBS, CAS. 2020</rights><rights>The Author(s) (2020). Published by Oxford University Press on behalf of Journal of Molecular Cell Biology, IBCB, SIBS, CAS.</rights><rights>The Author(s) (2020). Published by Oxford University Press on behalf of , IBCB, SIBS, CAS. 2020</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c416t-46f85229fe6b2685fcd87a5471b2f0b35f35c505baf140156f753c597fddac5e3</citedby><cites>FETCH-LOGICAL-c416t-46f85229fe6b2685fcd87a5471b2f0b35f35c505baf140156f753c597fddac5e3</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/PMC8035999/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8035999/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,1604,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/33064829$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Wu, Jiarui</contributor><creatorcontrib>Li, Lu</creatorcontrib><creatorcontrib>Tong, An</creatorcontrib><creatorcontrib>Zhang, Qiangsheng</creatorcontrib><creatorcontrib>Wei, Yuquan</creatorcontrib><creatorcontrib>Wei, Xiawei</creatorcontrib><title>The molecular mechanisms of MLKL-dependent and MLKL-independent necrosis</title><title>Journal of molecular cell biology</title><addtitle>J Mol Cell Biol</addtitle><description>Abstract
Necrosis, a type of unwanted and passive cell demise, usually occurs under the excessive external stress and is considered to be unregulated. However, under some special conditions such as caspase inhibition, necrosis is regulable in a well-orchestrated way. The term ‘regulated necrosis’ has been proposed to describe such programed necrosis. Recently, several forms of necrosis, including necroptosis, pyroptosis, ferroptosis, parthanatos, oxytosis, NETosis, and Na+/K+-ATPase-mediated necrosis, have been identified, and some crucial regulators governing regulated necrosis have also been discovered. Mixed lineage kinase domain-like pseudokinase (MLKL), a core regulator in necroptosis, acts as an executioner in response to ligands of death receptor family. Its activation requires the receptor-interacting protein kinases, RIP1 and RIP3. However, MLKL is only involved in necroptosis, i.e. MLKL is dispensable for necrosis. Therefore, this review is aimed at summarizing the molecular mechanisms of MLKL-dependent and MLKL-independent necrosis.</description><subject>Animals</subject><subject>Humans</subject><subject>Necroptosis</subject><subject>Necrosis - pathology</subject><subject>Protein Kinases - metabolism</subject><subject>Reviews</subject><issn>1759-4685</issn><issn>1674-2788</issn><issn>1759-4685</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>TOX</sourceid><sourceid>EIF</sourceid><recordid>eNp9kEFPwyAYhonRuGXu5tn0pgfroPRr6cXELOqMNV7mmVAKrkuhtawm_ntZOue8yAXy8eTl5UHonOAbgjM6WxtZzMxaCAxwhMYkhSyMEwbHB-cRmjq3xn5RRinDp2hEKU5iFmVjtFiuVGCaWsm-Fl1glFwJWznjgkYHL_lzHpaqVbZUdhMIWw6jyv4OrZJd4yp3hk60qJ2a7vYJenu4X84XYf76-DS_y0MZk2TjC2kGUZRplRSRL6dlyVIBcUqKSOOCgqYgAUMhNIkxgUSnQCVkqS5LIUHRCbodctu-MKqUvkMnat52lRHdF29Exf_e2GrF35tPzjCFLMt8wNUuoGs-euU23FROqroWVjW941EMhEHqBXn0ekC3X3Sd0vtnCOZb_3zrn-_8e_zisNoe_rHtgcsBaPr2_6hvYRKQPg</recordid><startdate>20210410</startdate><enddate>20210410</enddate><creator>Li, Lu</creator><creator>Tong, An</creator><creator>Zhang, Qiangsheng</creator><creator>Wei, Yuquan</creator><creator>Wei, Xiawei</creator><general>Oxford University Press</general><scope>TOX</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>7X8</scope><scope>5PM</scope></search><sort><creationdate>20210410</creationdate><title>The molecular mechanisms of MLKL-dependent and MLKL-independent necrosis</title><author>Li, Lu ; Tong, An ; Zhang, Qiangsheng ; Wei, Yuquan ; Wei, Xiawei</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c416t-46f85229fe6b2685fcd87a5471b2f0b35f35c505baf140156f753c597fddac5e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Animals</topic><topic>Humans</topic><topic>Necroptosis</topic><topic>Necrosis - pathology</topic><topic>Protein Kinases - metabolism</topic><topic>Reviews</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Li, Lu</creatorcontrib><creatorcontrib>Tong, An</creatorcontrib><creatorcontrib>Zhang, Qiangsheng</creatorcontrib><creatorcontrib>Wei, Yuquan</creatorcontrib><creatorcontrib>Wei, Xiawei</creatorcontrib><collection>Oxford Journals Open Access Collection</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Journal of molecular cell biology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Li, Lu</au><au>Tong, An</au><au>Zhang, Qiangsheng</au><au>Wei, Yuquan</au><au>Wei, Xiawei</au><au>Wu, Jiarui</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The molecular mechanisms of MLKL-dependent and MLKL-independent necrosis</atitle><jtitle>Journal of molecular cell biology</jtitle><addtitle>J Mol Cell Biol</addtitle><date>2021-04-10</date><risdate>2021</risdate><volume>13</volume><issue>1</issue><spage>3</spage><epage>14</epage><pages>3-14</pages><issn>1759-4685</issn><issn>1674-2788</issn><eissn>1759-4685</eissn><abstract>Abstract
Necrosis, a type of unwanted and passive cell demise, usually occurs under the excessive external stress and is considered to be unregulated. However, under some special conditions such as caspase inhibition, necrosis is regulable in a well-orchestrated way. The term ‘regulated necrosis’ has been proposed to describe such programed necrosis. Recently, several forms of necrosis, including necroptosis, pyroptosis, ferroptosis, parthanatos, oxytosis, NETosis, and Na+/K+-ATPase-mediated necrosis, have been identified, and some crucial regulators governing regulated necrosis have also been discovered. Mixed lineage kinase domain-like pseudokinase (MLKL), a core regulator in necroptosis, acts as an executioner in response to ligands of death receptor family. Its activation requires the receptor-interacting protein kinases, RIP1 and RIP3. However, MLKL is only involved in necroptosis, i.e. MLKL is dispensable for necrosis. Therefore, this review is aimed at summarizing the molecular mechanisms of MLKL-dependent and MLKL-independent necrosis.</abstract><cop>United States</cop><pub>Oxford University Press</pub><pmid>33064829</pmid><doi>10.1093/jmcb/mjaa055</doi><tpages>12</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Humans Necroptosis Necrosis - pathology Protein Kinases - metabolism Reviews |
| title | The molecular mechanisms of MLKL-dependent and MLKL-independent necrosis |
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