Inflamasom: Perbedaan antara revisi
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Anggota famili POP (pyrin-only protein) termasuk POP116 dan POP216 mengeblok perakitan inflamasom dengan mengikat ASC dan menghambat perekrutan ASC ke NLRP3.<ref>{{Cite journal|last=de Almeida|first=Lucia|last2=Khare|first2=Sonal|last3=Misharin|first3=Alexander V.|last4=Patel|first4=Rajul|last5=Ratsimandresy|first5=Rojo A.|last6=Wallin|first6=Melissa C.|last7=Perlman|first7=Harris|last8=Greaves|first8=David R.|last9=Hoffman|first9=Hal M.|date=2015-08-18|title=The PYRIN Domain-only Protein POP1 Inhibits Inflammasome Assembly and Ameliorates Inflammatory Disease|url=https://pubmed.ncbi.nlm.nih.gov/26275995|journal=Immunity|volume=43|issue=2|pages=264–276|doi=10.1016/j.immuni.2015.07.018|issn=1097-4180|pmc=4666005|pmid=26275995}}</ref><ref>{{Cite journal|last=Ratsimandresy|first=Rojo A.|last2=Chu|first2=Lan H.|last3=Khare|first3=Sonal|last4=de Almeida|first4=Lucia|last5=Gangopadhyay|first5=Anu|last6=Indramohan|first6=Mohanalaxmi|last7=Misharin|first7=Alexander V.|last8=Greaves|first8=David R.|last9=Perlman|first9=Harris|date=2017-06-05|title=The PYRIN domain-only protein POP2 inhibits inflammasome priming and activation|url=https://pubmed.ncbi.nlm.nih.gov/28580931|journal=Nature Communications|volume=8|pages=15556|doi=10.1038/ncomms15556|issn=2041-1723|pmc=5465353|pmid=28580931}}</ref> Molekul regulator negatif yang menyasar pada penghabisan ion, fungsi mitokondria, dan pensinyalan ROS juga dapat mengeblok aktivasi inflamasom NLRP3. Misalnya, senyawa badan keton β-hidroksibutirat dapat menghambat inflamasi yang diperantarai inflamasom NLRP3 dengan mencegah penghabisan ion kalium.<ref>{{Cite journal|last=Youm|first=Yun-Hee|last2=Nguyen|first2=Kim Y.|last3=Grant|first3=Ryan W.|last4=Goldberg|first4=Emily L.|last5=Bodogai|first5=Monica|last6=Kim|first6=Dongin|last7=D'Agostino|first7=Dominic|last8=Planavsky|first8=Noah|last9=Lupfer|first9=Christopher|date=2015-03|title=The ketone metabolite β-hydroxybutyrate blocks NLRP3 inflammasome-mediated inflammatory disease|url=https://pubmed.ncbi.nlm.nih.gov/25686106|journal=Nature Medicine|volume=21|issue=3|pages=263–269|doi=10.1038/nm.3804|issn=1546-170X|pmc=4352123|pmid=25686106}}</ref>
Modifikasi pasca-translasi NLRP3, termasuk ubiquitinasi dan deubiquitinasi, juga dapat menekan atau mengaktifkan aktivasi inflamasom.<ref>{{Cite journal|last=Shim|first=Do-Wan|last2=Lee|first2=Kwang-Ho|date=2018-05-18|title=Posttranslational Regulation of the NLR Family Pyrin Domain-Containing 3 Inflammasome|url=https://www.frontiersin.org/article/10.3389/fimmu.2018.01054/full|journal=Frontiers in Immunology|volume=9|pages=1054|doi=10.3389/fimmu.2018.01054|issn=1664-3224|pmc=PMC5968104|pmid=29868015}}</ref> Selama langkah aktivasi, fosforilasi NLRP3 oleh protein kinase D (PKD) diperantarai Golgi pada Ser293 (atau Ser295 manusia) dapat memicu perakitan inflamasom.<ref>{{Cite journal|last=Zhang|first=Zhirong|last2=Meszaros|first2=Gergö|last3=He|first3=Wan-Ting|last4=Xu|first4=Yanfang|last5=de Fatima Magliarelli|first5=Helena|last6=Mailly|first6=Laurent|last7=Mihlan|first7=Michael|last8=Liu|first8=Yansheng|last9=Puig Gámez|first9=Marta|date=2017-09-04|title=Protein kinase D at the Golgi controls NLRP3 inflammasome activation|url=https://pubmed.ncbi.nlm.nih.gov/28716882|journal=The Journal of Experimental Medicine|volume=214|issue=9|pages=2671–2693|doi=10.1084/jem.20162040|issn=1540-9538|pmc=5584123|pmid=28716882}}</ref> Sebaliknya, fosforilasi NLRP3 oleh PKA pada Ser 291 mencit memperantarai regulasi negatif inflamasom NLRP3 yang diinduksi asam empedu.<ref>{{Cite journal|last=Guo|first=Chuansheng|last2=Xie|first2=Shujun|last3=Chi|first3=Zhexu|last4=Zhang|first4=Jinhua|last5=Liu|first5=Yangyang|last6=Zhang|first6=Li|last7=Zheng|first7=Mingzhu|last8=Zhang|first8=Xue|last9=Xia|first9=Dajing|date=2016-10-18|title=Bile Acids Control Inflammation and Metabolic Disorder through Inhibition of NLRP3 Inflammasome|url=https://pubmed.ncbi.nlm.nih.gov/27692610|journal=Immunity|volume=45|issue=4|pages=802–816|doi=10.1016/j.immuni.2016.09.008|issn=1097-4180|pmid=27692610}}</ref> Selain enzim fosforilasi, enzim deubiquitinasi juga terlibat dalam regulasi inflamasom. Misalnya, BRCC3 mendorong aktivasi inflamasi dengan men-deubiquitin NLRP3 pada domain LRR.<ref>{{Cite journal|last=Py|first=Bénédicte F.|last2=Kim|first2=Mi-Sung|last3=Vakifahmetoglu-Norberg|first3=Helin|last4=Yuan|first4=Junying|date=2013-01-24|title=Deubiquitination of NLRP3 by BRCC3 critically regulates inflammasome activity|url=https://pubmed.ncbi.nlm.nih.gov/23246432|journal=Molecular Cell|volume=49|issue=2|pages=331–338|doi=10.1016/j.molcel.2012.11.009|issn=1097-4164|pmid=23246432}}</ref> ABRO1, suatu komponen kompleks BRCC3, dapat meningkatkan aktivasi inflamasom NLRP3 dengan mengatur deubiquitinasi NLRP3 setelah induksi LPS.<ref>{{Cite journal|last=Ren|first=Guangming|last2=Zhang|first2=Xuanyi|last3=Xiao|first3=Yang|last4=Zhang|first4=Wen|last5=Wang|first5=Yu|last6=Ma|first6=Wenbing|last7=Wang|first7=Xiaohan|last8=Song|first8=Pan|last9=Lai|first9=Lili|date=2019-03-15|title=ABRO1 promotes NLRP3 inflammasome activation through regulation of NLRP3 deubiquitination|url=https://pubmed.ncbi.nlm.nih.gov/30787184|journal=The EMBO journal|volume=38|issue=6|pages=e100376|doi=10.15252/embj.2018100376|issn=1460-2075|pmc=6418445|pmid=30787184}}</ref>
==Peran pada kesehatan==
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