Loading ...
exercise ’s abilityto triggersympathoadrenergic activation
The ability of SGKto preventJNK activation
A viral or bacterial an infection within any ganglia or paragangliacausesglial 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
the ability of diabetic DAMPsto triggerinflammasome activation
this receptor alone ... insufficientto triggerinflammasome activation
a compoundpreventedCB1R activation
different danger signals(passive) triggered byInflammasome activation
that vacuolar escape / cytosolic localization is necessaryto triggerinflammasome activation
failure of the Ad5 vector aloneto triggerinflammasome activation
In the present study , cotreatment of cells with the caspase inhibitor Z - VAD - FMK , which abrogated GSE - induced activation of caspases and apoptosis , has failedto preventJNK activation
the mutant form of the gene ( an oncogenecausesunrestrained activation
HIV infection or HIV - induced microbial translocation(passive) caused byaberrant activation
the reversible ATP - competitive inhibitor of JNK SP600125 and this perturbation of JNK activation(passive) is ... prevented byJNK activation
Implanted HCV core proteincausedglial activation
the ability of α - synuclein ( α - synto triggerinflammasome activation
Lacroix S. P2X4 receptorsinfluenceinflammasome activation
2012 ) P2X4 receptorsinfluenceinflammasome activation
Leukocytes P2X4 receptorsinfluenceinflammasome activation
feeding of a high - fat diet(passive) caused byJNK activation
the ability of dengue virus viroporin NS2A and NS2Bto triggerinflammasome activation
proinflammatory cytokines ( 49(passive) caused byJNK activation
other forms of environmental stress(passive) caused byJNK activation
that lack of Jedi1 in the DRG leads to decreased SGC engulfment of dead neuronscausingglial activation
DN caspase-8 or CrmApreventcaspase-8 activation
“ damage signals(passive) triggered byglial activation
inflammatory signalsto contributeglial activation
the bacterial signalstriggerinflammasome activation
these two stimuli(passive) triggered byJNK activation
Microbial strategiesto preventinflammasome activation
that the cytoprotective effects of celastrol are a result of its ability to inhibit the proteasome pathwaythereby preventinginflammasome activation
A decrease of ATPmay triggerPLA2 activation
exposure of cells to environmental stress(passive) caused byJNK activation
osmotic shock and UV radiation(passive) caused byJNK activation
Gómez - Nicola , D Interleukin 15 expression in the CNS : blockade of its activitypreventsglial activation
a model ( Fig . 6 ) in whichcould triggerGPCR activation
Together these data describe an unexpected and important difference in the ability of avirulent Fn and virulent SchuS4to triggerinflammasome activation
environmental stimuli such as starvation(passive) triggered byJNK activation
a wide variety of stimuli(passive) is triggered byInflammasome activation
both ATP and L. monocytogenes(passive) triggered byinflammasome activation
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 KYNA effects on the previously reported decrease of brain extracellular glutamate levels and reduction of excitatory transmissionmay contributeto KYNA effects on the previously reported decrease of brain extracellular glutamate levels and reduction of excitatory transmission
to rapid remodeling of the actin cytoskeleton , inhibition of proliferation , induction of differentiation , andledto rapid remodeling of the actin cytoskeleton , inhibition of proliferation , induction of differentiation , and
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 maturation of caspase-1 and processing of IL1βleadsto maturation of caspase-1 and processing of IL1β
to FcR - γ - dependent recruitment and phosphorylation of Sykleadsto FcR - γ - dependent recruitment and phosphorylation of Syk
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
atrial fibrillation in obstructive sleep apnea 11triggeringatrial fibrillation in obstructive sleep apnea 11
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
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
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
cys - LT formation through PMNL - endothelial cell transcellular synthesis ... resulting in increased coronary resistance and cardiac damagecausescys - LT formation through PMNL - endothelial cell transcellular synthesis ... resulting in increased coronary resistance and cardiac damage
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 cell death and systemic inflammationleadingto cell death and systemic inflammation
renal sodium and water retention secondary to arterial underfillingcausingrenal sodium and water retention secondary to arterial underfilling
to host tissue damageleadingto host tissue damage
caspase-1 cleavage and IL-1β secretioncausescaspase-1 cleavage and IL-1β secretion
synergistic hepatocyte apoptosis ( 2011causingsynergistic hepatocyte apoptosis ( 2011
to release of the potent inflammatory cytokine IL-1beta from infected macrophagesleadingto release of the potent inflammatory cytokine IL-1beta from infected macrophages
The potent immune response(passive) could be influenced byThe potent immune response
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 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 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
to caspase-1–dependent mitochondrial damage ( 16leadsto caspase-1–dependent mitochondrial damage ( 16
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
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 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
in IL‐1β secretion , NF‐κB activation , and consequent IL‐15 productionresultingin IL‐1β secretion , NF‐κB activation , and consequent IL‐15 production
to caspase‐1‐dependent processing of cytosolic pro‐IL‐1βleadsto caspase‐1‐dependent processing of cytosolic pro‐IL‐1β
to hyper - phosphorylation and the subsequent destabilization of retinoblastoma protein ( Rbcontributesto hyper - phosphorylation and the subsequent destabilization of retinoblastoma protein ( Rb
to secretion of caspase-1leadsto secretion of caspase-1
the process of cell death(passive) triggered bythe process of cell death
in cell death and consequent secretion of both IL-1β and IL-1α through different mechanismsresultsin cell death and consequent secretion of both IL-1β and IL-1α through different mechanisms