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U4 RNA define five domains in the splicing factor Prp8influencespliceosome activation
intracellular ROSprovokesNLRP3 inflammasome activation
apoptotic mitochondriacausedNLRP3 inflammasome activation
several stimuli(passive) could be prompted byNlrp3 inflammasome activation
by the binding of TCDD(passive) caused byAhR activation
by the binding of TCDD(passive) caused by AhR activation
by the binding of dioxin(passive) caused byAhR activation
that have been shownto causeNLRP3 inflammasome activation
FADD ( Fas - associated protein with death domain ) and procaspase-8causingcaspase-8 activation
N. caninum infection(passive) caused byNLRP3 inflammasome activation
two signals(passive) is resulted byInflammasome activation
Some chemicals appearto causeactivation ofendonucleases
the oncogenic tyrosine kinase fusion proteincausesMAPK activation
the mitochondriacausedinflammasome activation
the genes encoding these proteins ... many of the stimulicauseMAPK activation
NLRP3leadsinflammasome activation
NLRP3contributesinflammasome activation
which results in its binding to TAK1causingTAK1 activation
by KRAS or BRAF mutation(passive) caused byMAPK activation
factorsinfluencinginflammasome activation
that have been shownto causeinflammasome activation
reactive oxygen species ( ROS ) productioncausinginflammasome - activation
So not all odorants that activate select ORswill causeCSDn activation
an oncogenic tyrosine kinase fusioncausesMAPK activation
ain an oncogenic tyrosine kinase fusion ... ; andcausesMAPK activation
who were evaluated in the ED at CSMCpromptedSTEMI activation
TRAF3 within the MyD88 complex is then degradedcausesTAK1 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
BCG vaccinecausesTh1 activation
by a CXCR4 antagonist(passive) caused byCXCR4 activation
by these mutations(passive) caused byATGL activation
epithelial injurycausesmyofibroblast activation
cytokinescould causeosteoclast activation
the mechanisms by whichcausesosteoclast activation
that binds RANK on osteoclastscausingosteoclast activation
pulmonary phthalate exposure ... likelyto causePPAR activation
Human pancreatic lipaseinfluencesinterfacial activation
the opposite switch from retraction to protractioncausesthe opposite switch from retraction to protraction
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 the production of proinflammatory cytokines and eventual cell deathleadsto the production of proinflammatory cytokines and eventual cell death
to production of proinflammatory cytokines and eventual cell deathleadsto 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
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-1leadsto the maturation of caspase-1 and the processing of its substrates , IL-1
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 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 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 Foxp3 transcriptionleadsto Foxp3 transcription
to IL-1Beta productionleadingto IL-1Beta production
to cleavage of pro - IL-1 andleadsto cleavage of pro - IL-1 and