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both nitrogen and carbon metabolism(passive) is influenced byPTSNtr activation
FADD ( Fas - associated protein with death domain ) and procaspase-8causingcaspase-8 activation
two signals(passive) is resulted byInflammasome activation
G - proteins and G - protein combined receptors involved with myometrial contraction G - protein combined receptorcan leadGPCR ) activation
the mitochondriacausedinflammasome activation
NLRP3leadsinflammasome activation
NLRP3contributesinflammasome activation
factorsinfluencinginflammasome activation
that have been shownto causeinflammasome activation
reactive oxygen species ( ROS ) productioncausinginflammasome - activation
Toll - like receptor agonistsmay also causemacrophage activation
by exposure of cells(passive) caused byJNK activation
by exposure of cells to(passive) caused byJNK activation
Stimulation of A549 cells with denbinobincausedJNK activation
by exposure of cells to environmental stress(passive) caused byJNK activation
exposure of cells to environmental stress(passive) caused byJNK activation
This associationcausesTRAF6 activation
Suppressors of a cold - sensitive mutation in yeast U4 RNA define five domains in the splicing factor Prp8influencespliceosome activation
by release of N - acetylglucosamine that is detected in the cytosol by the glycolytic enzyme hexokinase(passive) is caused byinflammasome activation
release of N - acetylglucosamine that is detected in the cytosol by the glycolytic enzyme hexokinase(passive) is caused byinflammasome activation
With this study we foundcausesinflammasome activation
by treatment with H2O2(passive) caused byJNK activation
treatment with H2O2(passive) caused byJNK activation
through the generation of ROS(passive) could be causedJNK activation
The binding of an agonistcausesGPCR activation
p53 overexpressiondoes ... causeJNK activation
both extracellular glutamate and intracellular glutathione(passive) can be influenced byMicroglial activation
the expression of constitutively active Ras or Raf(passive) caused byERK2 activation
by systemic morphine treatment(passive) caused byglial activation
IL-8 / CXCL8 ( subsequent to activation of upstream kinases(passive) caused bygIVaPLA2 activation
dietary factors(passive) are influenced bymicroglial activation
by proinflammatory cytokines(passive) caused byJNK activation
proinflammatory cytokines(passive) caused byJNK activation
Systemic cytokinescauseglial activation
cerebral ischemiacausesJNK activation
ASK1causesJNK activation
MAF - ULTRAcausesmacrophage activation
to demonstratecausesmicroglial activation
Any insult to the central nervous system ( CNS ) , including infection , trauma , or metabolic dysfunctioncausesmicroglial activation
Methamphetaminecausesmicroglial activation
to the processing of proinflammatory cytokines and pyroptotic cell death through the recruitment and activation of caspase 1leadsto the processing of proinflammatory cytokines and pyroptotic cell death through the recruitment and activation of caspase 1
to the activation of caspase-1 and the release of pro - inflammatory cytokinesleadsto the activation of caspase-1 and the release of pro - inflammatory cytokines
to caspase-1 activation , secretion of pro - inflammatory cytokines and hostleadsto caspase-1 activation , secretion of pro - inflammatory cytokines and host
to caspase-1 dependent production of the proinflammatory cytokinesleadsto caspase-1 dependent production of the proinflammatory cytokines
to production of proinflammatory cytokines and eventual cell deathleadsto production of proinflammatory cytokines and eventual cell death
to the production of proinflammatory cytokines and eventual cell deathleadsto the production of proinflammatory cytokines and eventual cell death
to maturation and secretion of the proinflammatory cytokines IL-1leadsto maturation and secretion of the proinflammatory cytokines IL-1
to release of the proinflammatory cytokines IL-1 andleadsto release of the proinflammatory cytokines IL-1 and
to release of the proinflammatory cytokines IL-1leadsto release of the proinflammatory cytokines IL-1
to the production of proinflammatory cytokines and the recruitment of immune cells , such as neutrophilsleadsto the production of proinflammatory cytokines and the recruitment of immune cells , such as neutrophils
to activation of caspase-1leadsto activation of caspase-1
to caspase-1 activationleadsto caspase-1 activation
to the processing and secretion of proinflammatory cytokinesleadsto the processing and secretion of proinflammatory cytokines
to the processing and secretion of the proinflammatory cytokinesleadsto the processing and secretion of the proinflammatory cytokines
to the processing of proinflammatory cytokines and pyroptotic cell deathleadsto the processing of proinflammatory cytokines and pyroptotic cell death
to angiogenesiscan leadto angiogenesis
IL-1 secretion and inflammatory cell infiltrationthen causesIL-1 secretion and inflammatory cell infiltration
to Caspase-1 cleavage and secretionleadingto Caspase-1 cleavage and secretion
to the maturation of caspase-1 and the processing of its substrates , IL-1 and IL-18leadsto the maturation of caspase-1 and the processing of its substrates , IL-1 and IL-18
to the maturation of caspase-1 and the processing of its substrates , IL-1 andleadsto the maturation of caspase-1 and the processing of its substrates , IL-1 and
to the maturation of caspase-1 and the processing of its substrates , IL-1leadsto the maturation of caspase-1 and the processing of its substrates , IL-1
to release of the potent inflammatory cytokine IL-1beta from infected macrophagesleadingto release of the potent inflammatory cytokine IL-1beta from infected macrophages
to maturation and secretion of the proinflammatoryleadsto maturation and secretion of the proinflammatory
to release of the proinflammatoryleadsto release of the proinflammatory
to cell death via pyroptosiscan leadto cell death via pyroptosis
to cleavage and release of IL-1beta and IL-18leadsto cleavage and release of IL-1beta and IL-18
to cleavage and release of IL-1beta andleadsto cleavage and release of IL-1beta and
to IL-1 ? release in human monocytes and macrophagesleadingto IL-1 ? release in human monocytes and macrophages
to the maturation of caspase-1 and the processing of its substrates , interleukin 1 ( IL-1 ) and IL-18leadsto the maturation of caspase-1 and the processing of its substrates , interleukin 1 ( IL-1 ) and IL-18
to the maturation of caspase-1 and the processing of its substratesleadsto the maturation of caspase-1 and the processing of its substrates
to secretion of caspase-1leadsto secretion of caspase-1
to IL-1 productionleadingto IL-1 production
to auto - activationleadsto auto - activation
to mitochondrial cell deathledto mitochondrial cell death
to pain reliefledto pain relief
to cell deathcan leadto cell death
to release of inflammatory cytokinesleadingto release of inflammatory cytokines
to the release of IL-18 , andleadsto the release of IL-18 , and
to IL-1Beta productionleadingto IL-1Beta production
to cleavage of pro - IL-1 andleadsto cleavage of pro - IL-1 and