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<dublin_core schema="dc">
<dcvalue element="contributor" qualifier="author">An&#x20;Hue&#x20;Vy&#x20;Tran</dcvalue>
<dcvalue element="contributor" qualifier="author">Han,&#x20;Se&#x20;Hee</dcvalue>
<dcvalue element="contributor" qualifier="author">Kim,&#x20;Joon</dcvalue>
<dcvalue element="contributor" qualifier="author">Grasso,&#x20;Francesca</dcvalue>
<dcvalue element="contributor" qualifier="author">Kim,&#x20;In&#x20;San</dcvalue>
<dcvalue element="contributor" qualifier="author">Han,&#x20;Ye&#x20;Sun</dcvalue>
<dcvalue element="date" qualifier="accessioned">2024-01-20T01:03:50Z</dcvalue>
<dcvalue element="date" qualifier="available">2024-01-20T01:03:50Z</dcvalue>
<dcvalue element="date" qualifier="created">2021-09-05</dcvalue>
<dcvalue element="date" qualifier="issued">2017-07</dcvalue>
<dcvalue element="identifier" qualifier="issn">0730-2312</dcvalue>
<dcvalue element="identifier" qualifier="uri">https:&#x2F;&#x2F;pubs.kist.re.kr&#x2F;handle&#x2F;201004&#x2F;122589</dcvalue>
<dcvalue element="description" qualifier="abstract">Numerous&#x20;studies&#x20;have&#x20;implied&#x20;that&#x20;mutY&#x20;DNA&#x20;glycosylase&#x20;(MYH)&#x20;is&#x20;involved&#x20;in&#x20;the&#x20;repair&#x20;of&#x20;post-replicative&#x20;mispairs&#x20;and&#x20;plays&#x20;a&#x20;critical&#x20;role&#x20;in&#x20;the&#x20;base&#x20;excision&#x20;repair&#x20;pathway.&#x20;Recent&#x20;in&#x20;vitro&#x20;studies&#x20;have&#x20;shown&#x20;that&#x20;MYH&#x20;interacts&#x20;with&#x20;tumor&#x20;necrosis&#x20;factor&#x20;receptor&#x20;type&#x20;1-associated&#x20;death&#x20;domain&#x20;(TRADD),&#x20;a&#x20;key&#x20;effector&#x20;protein&#x20;of&#x20;tumor&#x20;necrosis&#x20;factor&#x20;receptor-1&#x20;(TNFR1)&#x20;signaling.&#x20;The&#x20;association&#x20;between&#x20;MYH&#x20;and&#x20;TRADD&#x20;is&#x20;reversed&#x20;during&#x20;tumor&#x20;necrosis&#x20;factor&#x20;alpha&#x20;(TNF-alpha)-&#x20;and&#x20;camptothecin&#x20;(CPT)-&#x20;induced&#x20;apoptosis,&#x20;and&#x20;enhanced&#x20;during&#x20;TNF-alpha-induced&#x20;survival.&#x20;After&#x20;investigating&#x20;the&#x20;role&#x20;of&#x20;MYH&#x20;interacts&#x20;with&#x20;various&#x20;proteins&#x20;following&#x20;TNF-alpha&#x20;stimulation,&#x20;here,&#x20;we&#x20;focus&#x20;on&#x20;MYH&#x20;and&#x20;TRADD&#x20;interaction&#x20;functions&#x20;innecroptosis&#x20;and&#x20;its&#x20;effects&#x20;to&#x20;related&#x20;proteins.&#x20;We&#x20;report&#x20;that&#x20;the&#x20;level&#x20;of&#x20;the&#x20;MYH&#x20;and&#x20;TRADD&#x20;complex&#x20;was&#x20;also&#x20;reduced&#x20;during&#x20;necroptosis&#x20;induced&#x20;by&#x20;TNF-alpha&#x20;and&#x20;zVAD-fmk.&#x20;In&#x20;particular,&#x20;we&#x20;also&#x20;found&#x20;that&#x20;MYH&#x20;is&#x20;a&#x20;biologically&#x20;important&#x20;necrosis&#x20;suppressor.&#x20;Under&#x20;combined&#x20;TNF-alpha&#x20;and&#x20;zVAD-fmk&#x20;treatment,&#x20;MYH-deficient&#x20;cells&#x20;were&#x20;induced&#x20;to&#x20;enter&#x20;the&#x20;necroptosis&#x20;pathway&#x20;but&#x20;primary&#x20;mouse&#x20;embryonic&#x20;fibroblasts&#x20;(MEFs)&#x20;were&#x20;not.&#x20;Necroptosis&#x20;in&#x20;the&#x20;absence&#x20;of&#x20;MYH&#x20;proceeds&#x20;via&#x20;the&#x20;inactivation&#x20;of&#x20;caspase-8,&#x20;followed&#x20;by&#x20;an&#x20;increase&#x20;in&#x20;the&#x20;formation&#x20;of&#x20;the&#x20;kinase&#x20;receptor-interacting&#x20;protein&#x20;1&#x20;(RIP1)-RIP3&#x20;complex.&#x20;Our&#x20;results&#x20;suggested&#x20;that&#x20;MYH,&#x20;which&#x20;interacts&#x20;with&#x20;TRADD,&#x20;inhibits&#x20;TNF-alpha&#x20;necroptotic&#x20;signaling.&#x20;Therefore,&#x20;MYH&#x20;inactivation&#x20;is&#x20;essential&#x20;for&#x20;necroptosis&#x20;via&#x20;the&#x20;downregulation&#x20;of&#x20;caspase-8.&#x20;(C)&#x20;2017&#x20;Wiley&#x20;Periodicals,&#x20;Inc.</dcvalue>
<dcvalue element="language" qualifier="none">English</dcvalue>
<dcvalue element="publisher" qualifier="none">WILEY</dcvalue>
<dcvalue element="subject" qualifier="none">NF-KAPPA-B</dcvalue>
<dcvalue element="subject" qualifier="none">INDUCED&#x20;APOPTOSIS</dcvalue>
<dcvalue element="subject" qualifier="none">L929&#x20;CELLS</dcvalue>
<dcvalue element="subject" qualifier="none">PROGRAMMED&#x20;NECROSIS</dcvalue>
<dcvalue element="subject" qualifier="none">CASPASE&#x20;INHIBITORS</dcvalue>
<dcvalue element="subject" qualifier="none">SIGNALING&#x20;COMPLEX</dcvalue>
<dcvalue element="subject" qualifier="none">MOLECULAR&#x20;SWITCH</dcvalue>
<dcvalue element="subject" qualifier="none">DEATH&#x20;PATHWAYS</dcvalue>
<dcvalue element="subject" qualifier="none">RECEPTOR</dcvalue>
<dcvalue element="subject" qualifier="none">KINASE</dcvalue>
<dcvalue element="title" qualifier="none">MutY&#x20;DNA&#x20;Glycosylase&#x20;Protects&#x20;Cells&#x20;From&#x20;Tumor&#x20;Necrosis&#x20;Factor&#x20;Alpha-Induced&#x20;Necroptosis</dcvalue>
<dcvalue element="type" qualifier="none">Article</dcvalue>
<dcvalue element="identifier" qualifier="doi">10.1002&#x2F;jcb.25866</dcvalue>
<dcvalue element="description" qualifier="journalClass">1</dcvalue>
<dcvalue element="identifier" qualifier="bibliographicCitation">JOURNAL&#x20;OF&#x20;CELLULAR&#x20;BIOCHEMISTRY,&#x20;v.118,&#x20;no.7,&#x20;pp.1827&#x20;-&#x20;1838</dcvalue>
<dcvalue element="citation" qualifier="title">JOURNAL&#x20;OF&#x20;CELLULAR&#x20;BIOCHEMISTRY</dcvalue>
<dcvalue element="citation" qualifier="volume">118</dcvalue>
<dcvalue element="citation" qualifier="number">7</dcvalue>
<dcvalue element="citation" qualifier="startPage">1827</dcvalue>
<dcvalue element="citation" qualifier="endPage">1838</dcvalue>
<dcvalue element="description" qualifier="journalRegisteredClass">scie</dcvalue>
<dcvalue element="description" qualifier="journalRegisteredClass">scopus</dcvalue>
<dcvalue element="identifier" qualifier="wosid">000403051700023</dcvalue>
<dcvalue element="identifier" qualifier="scopusid">2-s2.0-85015198591</dcvalue>
<dcvalue element="relation" qualifier="journalWebOfScienceCategory">Biochemistry&#x20;&amp;&#x20;Molecular&#x20;Biology</dcvalue>
<dcvalue element="relation" qualifier="journalWebOfScienceCategory">Cell&#x20;Biology</dcvalue>
<dcvalue element="relation" qualifier="journalResearchArea">Biochemistry&#x20;&amp;&#x20;Molecular&#x20;Biology</dcvalue>
<dcvalue element="relation" qualifier="journalResearchArea">Cell&#x20;Biology</dcvalue>
<dcvalue element="type" qualifier="docType">Article</dcvalue>
<dcvalue element="subject" qualifier="keywordPlus">NF-KAPPA-B</dcvalue>
<dcvalue element="subject" qualifier="keywordPlus">INDUCED&#x20;APOPTOSIS</dcvalue>
<dcvalue element="subject" qualifier="keywordPlus">L929&#x20;CELLS</dcvalue>
<dcvalue element="subject" qualifier="keywordPlus">PROGRAMMED&#x20;NECROSIS</dcvalue>
<dcvalue element="subject" qualifier="keywordPlus">CASPASE&#x20;INHIBITORS</dcvalue>
<dcvalue element="subject" qualifier="keywordPlus">SIGNALING&#x20;COMPLEX</dcvalue>
<dcvalue element="subject" qualifier="keywordPlus">MOLECULAR&#x20;SWITCH</dcvalue>
<dcvalue element="subject" qualifier="keywordPlus">DEATH&#x20;PATHWAYS</dcvalue>
<dcvalue element="subject" qualifier="keywordPlus">RECEPTOR</dcvalue>
<dcvalue element="subject" qualifier="keywordPlus">KINASE</dcvalue>
<dcvalue element="subject" qualifier="keywordAuthor">mutY&#x20;DNA&#x20;GLYCOSYLASE&#x20;(MYH)</dcvalue>
<dcvalue element="subject" qualifier="keywordAuthor">TUMOR&#x20;NECROSIS&#x20;FACTOR&#x20;RECEPTOR&#x20;TYPE&#x20;1-ASSOCIATED&#x20;DEATH&#x20;DOMAIN&#x20;(TRADD)</dcvalue>
<dcvalue element="subject" qualifier="keywordAuthor">TUMOR&#x20;NECROSIS&#x20;FACTOR&#x20;ALPHA&#x20;(TNF-alpha)</dcvalue>
<dcvalue element="subject" qualifier="keywordAuthor">NECROPTOSIS</dcvalue>
</dublin_core>
