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The hypothesis that the NF - Y protein complex was binding directly to one or more of these sites andthereby influencingtranscriptional activation
Methylation of CpG sites can turn a gene offcan causetranscriptional activation
transcription factors to bind more easily to regulatory sites on DNAcausingtranscriptional activation
histone marks previously associated with active genesdo ... causetranscriptional activation
critical interactions between transcription factors and their regulators ... the same regionscausetranscriptional activation
complexes with genesmay causetranscriptional activation
binds the kappaB response elementcausingtranscriptional activation
a general adaptor protein and chromatin modifiercausingtranscriptional activation
this finding ... are knownto causetranscriptional activation
the nucleuscausingtranscriptional activation
DNA demethylationcausestranscriptional activation
their ligandscausetranscriptional activation
the ability of Rho ... , as well asto influencetranscriptional activation
abilityto causetranscriptional activation
by the nuclear translocation of NFE2L2(passive) caused bytranscriptional activation
the ability of Rhoto influencetranscriptional activation
by DNA - binding activators(passive) caused bytranscriptional activation
E1A is knownto influencetranscriptional activation
little abilityto causetranscriptional activation
Constructscausetranscriptional activation
the ability of Rho ... , as well as affect cell cycle progressionto influencetranscriptional activation
by natural steroid hormones(passive) normally caused bytranscriptional activation
H2A and H4causingtranscriptional activation
G - proteins and G - protein combined receptors involved with myometrial contraction G - protein combined receptorcan leadGPCR ) activation
the mitochondriacausedinflammasome activation
NLRP3contributesinflammasome activation
the potentialto influencesaccade activation
reactive oxygen species ( ROS ) productioncausinginflammasome - activation
Mutations of -catenincausingWnt activation
DNA binding activators , such as FTZ - F1 and GCN4(passive) caused bytranscriptional activation
signaling cascadecausesNLRP3 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
the drug of abuse(passive) caused bydopaminergic activation
The binding of an agonistcausesGPCR activation
both extracellular glutamate and intracellular glutathione(passive) can be influenced byMicroglial activation
dietary factors(passive) are influenced bymicroglial activation
cytokinescould causeosteoclast activation
LPS - induced anhedonia(passive) is influenced byLPS - induced anhedonia
to the production and secretion of IL-1leadsto the production and secretion of IL-1
to the production and secretion ofleadsto the production and secretion of
in cAMP production and PKA activation ( 57classically resultsin cAMP production and PKA activation ( 57
to increasedleadsto increased
in expression of a reporter gene that allows detection of the interactionresultingin expression of a reporter gene that allows detection of the interaction
to production of typeleadsto production of type
to the phosphorylation of very specific proteins inside the cellfrequently leadsto the phosphorylation of very specific proteins inside the cell
to paralysisleadsto paralysis
to PHcontributesto PH
in less IL-6 production in cells undergoing productive infection compared to controlsresultedin less IL-6 production in cells undergoing productive infection compared to controls
to cell differentiationleadingto cell differentiation
to the exchange of GDP for GTP by a G proteinleadsto the exchange of GDP for GTP by a G protein
in phosphorylation ofresultedin phosphorylation of
to the production of IFN- ? and pro - inflammatory cytokinesleadsto the production of IFN- ? and pro - inflammatory cytokines
from estradiol - ER binding to estrogen responsive cells ( MCF7resultingfrom estradiol - ER binding to estrogen responsive cells ( MCF7
particular behaviors requires modulating the activity of specific neuronscausesparticular behaviors requires modulating the activity of specific neurons
to cleavage of cytoskeletal proteinsleadingto cleavage of cytoskeletal proteins
to cell death in certain cell types including thymocytes , monocytes , cardiomyocytes , and neuronal cellsmay contributeto cell death in certain cell types including thymocytes , monocytes , cardiomyocytes , and neuronal cells
to Ca2+mobilizationleadsto Ca2+mobilization
to inhibition of wild - type CaV2.1 currentsleadsto inhibition of wild - type CaV2.1 currents
downstream signaling , including activation of the Akt and mitogen - activated kinase pathwayscausesdownstream signaling , including activation of the Akt and mitogen - activated kinase pathways
to an increase of T34 phosphorylation and a decrease of T75 phosphorylationleadsto an increase of T34 phosphorylation and a decrease of T75 phosphorylation
to formation of a membrane - less compartment in cells and secretion of molecules called cytokines that promote inflammationleadsto formation of a membrane - less compartment in cells and secretion of molecules called cytokines that promote inflammation
to an increase in cyclic adenosine monophosphate ( cAMP ) , phosphorylation of protein kinase A ( PKA ) , and activation of target cytosolic and nuclear proteinsleadsto an increase in cyclic adenosine monophosphate ( cAMP ) , phosphorylation of protein kinase A ( PKA ) , and activation of target cytosolic and nuclear proteins
to activation of also HSF1leadsto activation of also HSF1
to dendritic remodelingcontributesto dendritic remodeling
in constriction of pain producing intracranial blood vessels and inhibition of neuropeptide release that leads to decreased inflammation in sensitive tissues and reduced central trigeminal pain signal transmissionovernight of these 5-HT1B and 5-HT1D receptors may resultin constriction of pain producing intracranial blood vessels and inhibition of neuropeptide release that leads to decreased inflammation in sensitive tissues and reduced central trigeminal pain signal transmission
to the EMTcontributesto the EMT
inhibition of expression regulated antiapoptotic metastatic gene products enhancement apoptosis myeloid leukemia cellscausinginhibition of expression regulated antiapoptotic metastatic gene products enhancement apoptosis myeloid leukemia cells
increase proliferation of the receptor and intracellular signalingcausesincrease proliferation of the receptor and intracellular signaling
to the activation of various downstream signaling pathway that are involved in regulating endothelial cell migration , proliferation , and survivalleadsto the activation of various downstream signaling pathway that are involved in regulating endothelial cell migration , proliferation , and survival
in the activation of mitogen - activated protein kinases and Src kinasealso resultsin the activation of mitogen - activated protein kinases and Src kinase
in changes in gene expression , production and/or secretion of molecules ( e.g. , cytokines , inflammatory mediatorscan resultin changes in gene expression , production and/or secretion of molecules ( e.g. , cytokines , inflammatory mediators
in the activation of mitogen - activated protein kinases and Src kinase.[29also resultsin the activation of mitogen - activated protein kinases and Src kinase.[29
in the activation of mitogen - activated protein kinases and Src kinase.[33also resultsin the activation of mitogen - activated protein kinases and Src kinase.[33
in the activation of mitogen - activated protein kinases and Src kinase.[42also resultsin the activation of mitogen - activated protein kinases and Src kinase.[42
in clinically detectable cognitive decreaseresultingin clinically detectable cognitive decrease
insulin resistance by transcriptional activation of several inflammatory genesmay causeinsulin resistance by transcriptional activation of several inflammatory genes
in the activation of mitogen - activated protein kinases and Src kinase.[45also resultsin the activation of mitogen - activated protein kinases and Src kinase.[45