搶嫗堛壢帟壢戝妛丂榁擭昦撪壢偺儂乕儉儁乕僕偱偡丅

尋媶偵偮偄偰

榁擭昦撪壢偺傕偆堦偮偺婄偼丄摦柆峝壔傪偼偠傔偲偡傞寣娗昦偺尋媶傪扴摉偡傞戝妛堾堛帟妛憤崌尋媶壢寣棳惂屼撪壢妛暘栰偱偡丅
慜恎偺媽戞俁撪壢偼憂棫摉弶偐傜摦柆峝壔尋媶傪儊僀儞僥乕儅偲偟搰杮懡婌梇丄慜戲廏寷丄徖栰摗晇偺俁戙偺嫵庼壓偱桪傟偨嬈愌傪偁偘偰偒傑偟偨丅寣棳惂屼撪壢暘栰偼媽戞俁撪壢偺弞娐婍摦柆峝壔尋媶僌儖乕僾偺堦晹偲帀幙丒摐戙幱僌儖乕僾傪曣懱偲偟偰敪懌偟傑偟偨丅摦柆峝壔偺尋媶偲恌椕偼傢傟傢傟偺廳梫側擟柋偱偡丅
暘巕惗暔妛偺恑曕偼堛妛惗暔妛尋媶偺奯崻傪庢傝彍偒偮偮偁傝傑偡丅摦柆峝壔傗榁壔偺尋媶傪恑傔偰偄偔偙偲偱堛妛惗暔妛慡懱偵塭嬁傪梌偊傞傛偆側桪傟偰惉壥傪偁偘傞偙偲偑偱偒傞偲巚偭偰偄傑偡丅

尋媶撪梕

丂丒帀幙丒摐戙幱堎忢傪拞怱偲偟偨摦柆峝壔徢偺暘巕嵶朎惗暔妛揑尋媶
丂丒帀幙丒摐戙幱堎忢傪拞怱偲偟偨惗妶廗姷昦偺椪彴塽妛揑尋媶
丂丒 摦柆峝壔徢偺愭抂揑恌抐帯椕偵娭偡傞尋媶 (椪彴寣娗堛妛)

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婎慴摦柆峝壔妛島嵗乮婑晅島嵗乯

丂丂弝嫵庼丂幝嶈徃暯
丂丂乽摐擜昦丄擣抦徢側偳榁壔偵傛傞昦婥偵嫟捠偟偨敪徢偺偟偔傒傪悽奅偱弶傔偰夝柧乿

亂尋媶撪梕亃
摦柆峝壔徢傗摐擜昦偲偄偭偨惗妶廗姷昦側偳偺奺庬幘姵偵嫟捠偡傞婎斦昦懺偲偟偰乽枬惈墛徢乿偑拲栚偝傟偰偄傑偡丅墛徢偼丄摐擜昦丄榁壔偵敽偭偰婲偙傞僀儞僗儕儞掞峈惈丄偁傞偄偼榁壔夁掱偦偺傕偺偵娭傢偭偰偄傞偲峫偊傜傟偰偄傑偡丅
巹偨偪偺尋媶幒偱偼丄墛徢斀墳摍偵傛傝惗惉偟偨堦巁壔拏慺偑僔僗僥僀儞巆婎偺僠僆乕儖婎傪捈愙S-僯僩儘僜壔偡傞丄東栿屻僞儞僷僋幙廋忺婡峔偵拝栚偟丄怴偨偵S-僯僩儘僜壔僞儞僷僋幙傪栐梾揑偐偮崅姶搙偵専弌偡傞曽朄傪妋棫偟傑偟偨丅杮尋媶幒偼丄S-僯僩儘僜壔偵傛傞嵶朎撪僔僌僫儖揱払傪柧傜偐偵偡傞偙偲偱丄摦柆峝壔敪徢偺儊僇僯僘儉傗儊僞儃儕僢僋僔儞僪儘乕儉偍傛傃摐擜昦敪徢梊杊偺偨傔偺怴偨側帯椕朄偍傛傃憂栻偺偨傔偺僞乕僎僢僩偺敪尒傪栚揑偲偟偰偄傑偡丅

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丂
丂(恾侾) 栰惗宆儅僂僗(嵍)偲旍枮摐擜昦(ob/ob)儅僂僗(塃)

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丂(恾俀) 怴偨偵奐敪偟偨S-僯僩儘僜壔僞儞僷僋幙栐梾揑専弌朄乮擇師尦揹婥塲摦憸乯丅娵偱埻傑傟偨晹暘偑丄旍枮偵傛丂丂丂丂偭偰憹壛偟偨S-僯僩儘僜壔僞儞僷僋幙偲梊憐偝傟傞

丂Inflammatory and stress signaling pathways have been highlighted as a major culprit of obesity-induced insulin resistance, diabetes, atherosclerosis, and aging. Protein S-nitrosylation, a covalent attachment of nitric oxide (NO) moiety (NO+) to reactive cysteine thiols, has emerged as the major mediator of diverse actions of NO.
We focus on the post-translational protein modification of S-nitrosylation, and we established a novel method to detect with high sensitivity and comprehensively S-nitrosylated proteins. The overall objectives of the research program are to clarify the roles of inducible nitric oxide synthase (iNOS), a major mediator of inflammation, and protein S-nitrosylation in the pathogenesis of obesity-induced insulin resistance and metabolic syndromes.

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擔杮岅丂丂丂ENGLISH

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