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Qaagi - Book of Why

Causes

Effects

the ability of diabetic DAMPsto triggerinflammasome activation

this receptor alone ... insufficientto triggerinflammasome activation

the ability of α - synuclein ( α - synto triggerinflammasome activation

Link to article on publisher 's site 26100496 Iracheta - Vellve , Arvin ; Petrasek , Jan ; Satishchandran , Abhishek ; Gyongyosi , Benedek ; Saha , Banishree ; Kodys , Karen ; Fitzgerald , Katherine A. ; Kurt - Jones , Evelyn A. ; and Szabo , Gyongyi , " Inhibition of sterile danger signals , uric acid and ATPpreventsinflammasome activation

that vacuolar escape / cytosolic localization is necessaryto triggerinflammasome activation

hypoxia(passive) caused bycalpain activation

the ability of dengue virus viroporin NS2A and NS2Bto triggerinflammasome activation

failure of the Ad5 vector aloneto triggerinflammasome activation

that the cytoprotective effects of celastrol are a result of its ability to inhibit the proteasome pathwaythereby preventinginflammasome activation

Kuhn A , Brow D. Suppressors of a cold - sensitive mutation in yeast U4 RNA define five domains in the splicing factor Prp8influencespliceosome activation

Select item 1092446514.Suppressors of a cold - sensitive mutation in yeast U4 RNA define five domains in the splicing factor Prp8influencespliceosome activation

Select item 1092446520.Suppressors of a cold - sensitive mutation in yeast U4 RNA define five domains in the splicing factor Prp8influencespliceosome activation

Lacroix S. P2X4 receptorsinfluenceinflammasome activation

Leukocytes P2X4 receptorsinfluenceinflammasome activation

2012 ) P2X4 receptorsinfluenceinflammasome activation

different danger signals(passive) triggered byInflammasome activation

Kuhn A. N. , Brow D. A. , 2000 Suppressors of a cold - sensitive mutation in yeast U4 RNA define five domains in the splicing factor Prp8influencespliceosome activation

blockade of Ca2 + influxpreventingcalpain activation

Together these data describe an unexpected and important difference in the ability of avirulent Fn and virulent SchuS4to triggerinflammasome activation

at low ATP(passive) is preventedSpliceosome activation

activation of bombesin receptors on the pancreatic acinar cellcauseszymogen activation

Thus additional signaling pathways may act independently or with Ca2 +to causezymogen activation

authors Lucia Mori Mycobacterium tuberculosispreventsinflammasome activation

Esp1 overexpression ... sufficientto triggerCdc14 activation

both the intrinsic and extrinsic pathways(passive) triggered byhemostatic activation

both ATP and L. monocytogenes(passive) triggered byinflammasome activation

the ATP levels ... an extenttriggeredinflammasome activation

Accumulation of misfolded proteinscausedinflammasome activation

tumors sharing common pathwaysleadingmekerk activation

LPS+ATP and Salmonella infectionto triggerinflammasome activation

metabolic stress products ( uric acid crystals , ATP , etc . ) and exogenous agents such as asbestoscan ... triggerinflammasome activation

A single amino acid mutationcan provokeBRAF activation

all known activators including MSU ( 13–15(passive) triggered byinflammasome activation

Supporting this idea , other crystals such such as silica and uric acid have been shownto triggerinflammasome activation

two signals via Toll - like receptors ( TLRs ) activation by endogenous or exogenous danger signals ( 29(passive) is resulted byInflammasome activation

ROS within mitochondria must initiate the mitochondrial cascade upstreamcausinginflammasome activation

poitn mutations in the kinase domain of the met proto - oncogene(passive) caused byOnkogenic activation

point mutations in the kinase domain of the met proto - oncogene(passive) caused byOnkogenic activation

Supporting this idea , other crystals such such as silica[8 ] and uric acid[9 ] have been shownto triggerinflammasome activation

direct intervention on mitochondria using a ligand of the mitochondrial benzodiazepin receptor or a protonophorecausesDEVDase activation

to activation of also HSF1leadsto activation of also HSF1

to release of the potent inflammatory cytokine IL-1beta from infected macrophagesleadingto release of the potent inflammatory cytokine IL-1beta from infected macrophages

to the maturation of caspase-1 and the processing of its substrates , IL-1β and IL-18leadsto the maturation of caspase-1 and the processing of its substrates , IL-1β and IL-18

release of IL-1βwill causerelease of IL-1β

to maturation and secretion of the proinflammatory cytokines IL-1β and IL-18 , which initiate early inflammatory responsesleadsto maturation and secretion of the proinflammatory cytokines IL-1β and IL-18 , which initiate early inflammatory responses

to the maturation of caspase-1 and processing of IL1βleadsto the maturation of caspase-1 and processing of IL1β

MMP12‐dependent emphysemacausesMMP12‐dependent emphysema

to caspase-1 activation , release of the proinflammatory cytokines , IL-1β and IL-18 and cell death in a process termed pyroptosisleadsto caspase-1 activation , release of the proinflammatory cytokines , IL-1β and IL-18 and cell death in a process termed pyroptosis

to production of proinflammatory cytokines and eventual cell deathleadsto production of proinflammatory cytokines and eventual cell death

to flaccid paralysismay leadto flaccid paralysis

to Caspase-1–dependent mitochondrial damage and block of mitophagy | PNAS PNAS October 28leadsto Caspase-1–dependent mitochondrial damage and block of mitophagy | PNAS PNAS October 28

to significant increases in the formation of 5-LOX products including leukotriene B(4also ledto significant increases in the formation of 5-LOX products including leukotriene B(4

to the secretion of pro - inflammatory cytokines such as IL-1β and IL-18 , which stimulate the adaptive immune systemleadsto the secretion of pro - inflammatory cytokines such as IL-1β and IL-18 , which stimulate the adaptive immune system

to the maturation of caspase-1 and the processing of the processing 's substrates , IL-1βleadsto the maturation of caspase-1 and the processing of the processing 's substrates , IL-1β

the scope of differential gene expression(passive) triggered bythe scope of differential gene expression

in the cleavage of effector pro - inflammatory cytokines such as pro - IL-1β and pro - IL-18 [ 24resultingin the cleavage of effector pro - inflammatory cytokines such as pro - IL-1β and pro - IL-18 [ 24

caspase-1 cleavage and IL-1β secretioncausescaspase-1 cleavage and IL-1β secretion

to activation of caspase-1 , interleukinleadsto activation of caspase-1 , interleukin

to the maturation of caspase-1 and the processing of its substrates , interleukin 1leadsto the maturation of caspase-1 and the processing of its substrates , interleukin 1

to Caspase-1- dependent mitochondrial damage and block of mitophagy , Proc Natl Acad Sci U S A. , 2014 , 111(43leadsto Caspase-1- dependent mitochondrial damage and block of mitophagy , Proc Natl Acad Sci U S A. , 2014 , 111(43

to IL-1β secretion and host cell death as wellleadsto IL-1β secretion and host cell death as well

to long - term behavioral alterations in mice injected with lipopolysaccharidecontributesto long - term behavioral alterations in mice injected with lipopolysaccharide

to caspase-1-dependent mitochondrial damage and block of mitophagy , Proceedings of the National Academy of Sciences of the United States of America 111 ( 43leadsto caspase-1-dependent mitochondrial damage and block of mitophagy , Proceedings of the National Academy of Sciences of the United States of America 111 ( 43

to a Caspase-1–dependent block of mitophagyleadsto a Caspase-1–dependent block of mitophagy

to outer hair cell hyperpolarization and frequency - selective suppression of afferent sound transmissionleadsto outer hair cell hyperpolarization and frequency - selective suppression of afferent sound transmission

in the secretion of the potent inflammatory cytokineresultedin the secretion of the potent inflammatory cytokine

to secretion of pro - inflammatory interleukinleadingto secretion of pro - inflammatory interleukin

to Caspase-1-dependent mitochondrial damage and block of mitophagy , Proceedings of the National Academy of Sciences of the United States of America , 111 ( 2014 ) 15514 - 15519leadsto Caspase-1-dependent mitochondrial damage and block of mitophagy , Proceedings of the National Academy of Sciences of the United States of America , 111 ( 2014 ) 15514 - 15519

to pro‐IL‐1β and pro‐IL‐18 cleavage by caspase 1 , resulting in IL‐1β and IL‐18 secretionleadsto pro‐IL‐1β and pro‐IL‐18 cleavage by caspase 1 , resulting in IL‐1β and IL‐18 secretion

to inhibition of signalling by independently ligated receptors | Biochemical Society Transactions | Portland Press Conferenceleadsto inhibition of signalling by independently ligated receptors | Biochemical Society Transactions | Portland Press Conference

dual recruitment of NLRC4 and NLRP3 to the same macromolecular complex Man , Si Mingcausesdual recruitment of NLRC4 and NLRP3 to the same macromolecular complex Man , Si Ming

to the transcription of a plethora of target genes that promote physiological changes associated with chemo-/radioresistance , including increasing the ability of DNA repair , the inhibition of apoptosis , and alterations of the cellular metabolismleadsto the transcription of a plethora of target genes that promote physiological changes associated with chemo-/radioresistance , including increasing the ability of DNA repair , the inhibition of apoptosis , and alterations of the cellular metabolism

to caspase-1–dependent mitochondrial damage ( 16leadsto caspase-1–dependent mitochondrial damage ( 16

to severe inflammation and recruitment of neutrophilsmay contributeto severe inflammation and recruitment of neutrophils

in IL‐1β secretion , NF‐κB activation , and consequent IL‐15 productionresultingin IL‐1β secretion , NF‐κB activation , and consequent IL‐15 production

to the cleavage of pro - caspase-1 and the subsequent processing of the bioactive form of IL-1β andleadsto the cleavage of pro - caspase-1 and the subsequent processing of the bioactive form of IL-1β and

in lymphoma cell proliferation and tumor growthresultedin lymphoma cell proliferation and tumor growth

to cell death and systemic inflammationleadingto cell death and systemic inflammation

pyroptosis , a rapid , inflammatory cell death that is caspase-1 dependent ( 52 , 66can triggerpyroptosis , a rapid , inflammatory cell death that is caspase-1 dependent ( 52 , 66

to secretion of caspase-1leadsto secretion of caspase-1

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