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A unique clonal JAK2 mutation leading tocausesconstitutive signaling
These mutationscauseconstitutive signaling
A change in structural integrity of c - Kit mutant D816Vcausesconstitutive signaling
Alteration of an extracellular agonist recognition domaincausesconstitutive signaling
Increased ROS production and inhibitedmay contributeAkt signaling
by mutations of TSC1 and TSC2 and other regulatory proteins(passive) caused bymTOR signaling
of Ca2 +(passive) was composedCa2+]i signaling
Nitric oxide appearsto influenceAkt signaling
Alterations of Jak - STAT components of interferoncan contributeIFN)-mediated signaling
An excess dietary vitamin E concentrationdoes ... influenceNrf2 signaling
Glucocorticoid receptors are also believedto influencecytokine signaling
by ceramide(passive) caused byapoptotic signaling
Numerous kinasesinfluenceWnt signaling
in tumor models(passive) was discoveredWNT signaling
either reduced expression of Klf4 in Hhip(passive) may be caused byKlf4 signaling
sleep fragmentationinfluenceddopaminergic signaling
secreted lipid - modified glycoproteins(passive) is composed byWNT signaling
multiple waysto influenceWnt signaling
high affinity of MICA to NKG2D(passive) caused byNKG2D signaling
by their interaction(passive) caused byCD40 signaling
a model in whichinfluencesproinflammatory signaling
cell typescan influenceIL-15 signaling
in part(passive) is influencedMyocellular signaling
by dysfunction of Neuron 2(passive) caused byGABAergic signaling
by mutations(passive) caused byIL-7 signaling
creationinfluencesNMDA signaling
by exposure to high glucose results in the sustained activation of components of a intracellular signaling axis required for cell polarization(passive) caused bysignaling
by ligand binding to the receptor(passive) caused bysignaling
by receptor or ligand deficiency(passive) caused bysignaling
Inhibition of VEGF receptorresultedsignaling
by increased TrkB receptor levels with decreased survival(passive) caused bysignaling
by increased AR expression , gene amplification , gene transcription , and tumor growth(passive) caused bysignaling
by chronically elevated insulin and leptin levels(passive) caused bysignaling
the ability of the specific cytokine ligandto causesignaling
by ligand binding(passive) caused bysignaling
The absence of co - receptorleadssignaling
TNF receptor 1may contributesignaling
by different BRAF mutations(passive) caused bysignaling
Activation of EGFRcausessignaling
by protein phosphatase 2A ( PP2A ) , whose activity was increased by(passive) was caused bysignaling
to generating and perpetuating seizures ( Maroso et al . , 2010may contributeto generating and perpetuating seizures ( Maroso et al . , 2010
to increased transcription of CYP1A1 and CYP1B1 , which encode proteins that convert the PAHs into mutagensleadingto increased transcription of CYP1A1 and CYP1B1 , which encode proteins that convert the PAHs into mutagens
to increased transcription of CYP1A1 and CYP1B1 , which encode proteins that convert PAHs to mutagensleadingto increased transcription of CYP1A1 and CYP1B1 , which encode proteins that convert PAHs to mutagens
to inflammasome activationleadingto inflammasome activation
to an increase in the expression of PGC-1a in human skeletal muscle [ 5,6leadingto an increase in the expression of PGC-1a in human skeletal muscle [ 5,6
T cell responses in vivo and in vitroinfluencesT cell responses in vivo and in vitro
Ser-555 ULK1 phosphorylation and ULK1-mediated autophagycausesSer-555 ULK1 phosphorylation and ULK1-mediated autophagy
in amelioration of lipid metabolism in hepatocytesto resultin amelioration of lipid metabolism in hepatocytes
the production of FMRP at the synapsecan ... causethe production of FMRP at the synapse
apoptosiscausesapoptosis
deficiency of gonadotropin - releasing hormone in humans and micecausesdeficiency of gonadotropin - releasing hormone in humans and mice
to the activation of pathways that control cellular proliferation and survivalnormally leadsto the activation of pathways that control cellular proliferation and survival
to a prolonged protein kinase B ( AKT ) and extracellular signal - regulated kinase 2 activation in T cellsleadsto a prolonged protein kinase B ( AKT ) and extracellular signal - regulated kinase 2 activation in T cells
to protein /leadingto protein /
to the activation of NF - B as well as T cell responses in vivoleadingto the activation of NF - B as well as T cell responses in vivo
from CD14 activityresultingfrom CD14 activity
to either cell survival or cell deathleadingto either cell survival or cell death
to cellular growth , proliferation , adhesion , motility , division , survival , and migrationleadsto cellular growth , proliferation , adhesion , motility , division , survival , and migration
to inhibition of hormone secretion , proliferation , and induction of apoptosisleadingto inhibition of hormone secretion , proliferation , and induction of apoptosis
in the inactivation of NF - B activity ... and contributes to cell growth inhibition and apoptosis in pancreatic cancer cellsresultsin the inactivation of NF - B activity ... and contributes to cell growth inhibition and apoptosis in pancreatic cancer cells
to reduced cellular proliferation and cytokine production ( 3leadingto reduced cellular proliferation and cytokine production ( 3
in changes in cytokine expression or the integrin activation stateresultedin changes in cytokine expression or the integrin activation state
in activation of the downstream effector IRF3 leading to the expression of type I IFNs and IFN stimulated genes ( ISGsresultingin activation of the downstream effector IRF3 leading to the expression of type I IFNs and IFN stimulated genes ( ISGs
in sustained and exaggerated pathway activation that drives uncontrolled tumor survival and proliferationresultin sustained and exaggerated pathway activation that drives uncontrolled tumor survival and proliferation
to autoimmunity including autoantigen presentation to activate T cells and pro - inflammatory signaling by cytokines secretion and complement activationcan leadto autoimmunity including autoantigen presentation to activate T cells and pro - inflammatory signaling by cytokines secretion and complement activation
to cellular responses such as cell spreading and focal adhesion formationleadsto cellular responses such as cell spreading and focal adhesion formation
to ER phosphorylation and estrogen - independent transcriptional activation of ER - dependent genesleadingto ER phosphorylation and estrogen - independent transcriptional activation of ER - dependent genes
in ER down - regulation through phosphorylation and activation of SMAD5 nuclear signaling that can lead to endocrine resistance and tumor progressionresultsin ER down - regulation through phosphorylation and activation of SMAD5 nuclear signaling that can lead to endocrine resistance and tumor progression
to the GH - induced changes in enzymatic activity , transport function , and gene expression that ultimately culminate in changes in growth and metabolismcontributeto the GH - induced changes in enzymatic activity , transport function , and gene expression that ultimately culminate in changes in growth and metabolism
to the activation of intracellular protein kinases and the phosphorylation of STAT3leadsto the activation of intracellular protein kinases and the phosphorylation of STAT3
to widespread activation of T cells and diabetes developmentledto widespread activation of T cells and diabetes development
in the appearance of cellular effects as cell proliferation as well as survival [ 2resultsin the appearance of cellular effects as cell proliferation as well as survival [ 2
to the growth , proliferation , invasion and metastasis of the cellledto the growth , proliferation , invasion and metastasis of the cell
to inhibition of the mTOR signaling pathway ... and subsequently to reduced cell proliferation , protein synthesis , and tumor angiogenesis ( 4leadsto inhibition of the mTOR signaling pathway ... and subsequently to reduced cell proliferation , protein synthesis , and tumor angiogenesis ( 4
to cellular growth , differentiation and proliferationleadsto cellular growth , differentiation and proliferation
to the expression of disease resistance - related genesleadingto the expression of disease resistance - related genes
to the activation of intracellular protein kinases and the phosphorylation ofleadsto the activation of intracellular protein kinases and the phosphorylation of
in the activation of the transcription factor NF - B and the mitogen - activated protein kinase ( MAPK ) pathwaysresultsin the activation of the transcription factor NF - B and the mitogen - activated protein kinase ( MAPK ) pathways
to activation of T cell responseleadsto activation of T cell response
to cell division , increased motility , angiogenesis and decreased apoptosismay leadto cell division , increased motility , angiogenesis and decreased apoptosis