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DNA methylationcausestranscriptional inhibition
GSK3-mediated phosphorylationscausetranscriptional inhibition
Serum withdrawalcausedinhibition of AKT
retrograde signal from metabotropic glutamate to cannabinoid receptors(passive) caused byPresynaptic inhibition
Nerve agents and other organophosphate pesticidescauseacetylcholinesterase inhibition
by increased brain gamma - aminobutyric acid ( GABA ) concentration(passive) caused byinhibition
This primary afferent depolarizationcausespresynaptic inhibition
These agents bind to gamma - aminobutyric acid ( GABA ) receptors in the central nervous system ( CNScausinginhibition
The receptor is directly coupled to a chloride ion channel and activation results in an influx of chloride ions and rapid hyperpolarisationcausinginhibition
endogenous adenosine(passive) caused bypresynaptic inhibition
specific effects of the undissociated acid on metabolic or physiological activities(passive) may have been caused byInhibition
the inhibitory effects ... the undissociated form of the acidcausesinhibition
the concentrations of these inhibitors ... shownto causeinhibition
effects of molecules that are a substrate and decrease rates of enzymes(passive) are caused byInhibition
potentiating the specific subunits of the GABA receptor , which activates the protein kinase C and causes sedation(passive) is caused byInhibition
this effect ... cAMP signaling cascadecausesinhibition of
Acetylcholine can sometimes be shown ... , and again this inhibition depends on the concentration of calciumto causeinhibition
NO binding to Cox , both in isolated mitochondria and in whole cells(passive) caused byinhibition
Damaged cell studies of the concentrationcausedinhibition
by amino acid mutations , non - protein kinases and applications(passive) caused byinhibition
BBR also suppressed the nuclear translocation of p50 / p65 NF - B proteins and their binding to COX-2 promoter , ... COX-2causinginhibition of
the concentration of [ ATP ] increasescausesinhibition
GABA binding resulting in hyperpolarization of the synaptic transmembrane potential of the affected neuron(passive) is provoked byInhibition
Activation of alpha receptors in the gastrointestinal tractcausesinhibition
AMP and ATP ... AMP bindingcausesinhibition
Binding of the B7 of to CTLA-4 of T - cellscausesinhibition
by cyclin B1 expression in HEK293 T cells(passive) caused byinhibition
Ca channel stimulation ... receptorscauseinhibition
the flow of chloride into the cell which also block the flow of calcium into the cellcausinginhibition
a decrease in GABA signaling(passive) caused byinhibition
by the binding of an inhibitor to an enzyme somewhere other than to the active site(passive) is causedinhibition
Binding of the B7 of APC to CTLA-4 of T - cellscausesinhibition
by the effective amount of inhibitor used(passive) caused byinhibition
AMP - Activated Kinase catalyzes phosphorylation of Acetyl - CoA Carboxylasecausinginhibition
Histoneleadsdeacetylase inhibition
by mutant p53 modulation of DNA(passive) caused byinhibition
by the limited levels of the gene product required for fungal proliferation(passive) caused byinhibition
by GABA A - receptors(passive) caused byinhibition
potentiating the specific subunits of the GABA receptor , which(passive) is caused byInhibition
that could bind to the GABAA receptor covalentlycausinginhibition
false negatives lcan causefalse negatives l
NPC disease - like cholesterol accumulation in SH - SY5Y cellscausesNPC disease - like cholesterol accumulation in SH - SY5Y cells
Tumor lethality(passive) caused byTumor lethality
in decreased proliferation , irreversible cell cycle arrest , increased apoptosis , reduced haemopoietic colony formation , altered gene expression pattern , reduction in self - renewal and a significant reduction in the phosphorylation of downstream target proteinsresultedin decreased proliferation , irreversible cell cycle arrest , increased apoptosis , reduced haemopoietic colony formation , altered gene expression pattern , reduction in self - renewal and a significant reduction in the phosphorylation of downstream target proteins
to increased SIRT1 andledto increased SIRT1 and
in an accumulation of SSB lesions induced by direct asbestos exposure in human mesothelial cellsresultedin an accumulation of SSB lesions induced by direct asbestos exposure in human mesothelial cells
in metabolic reprogramming , which enhanced the generation of CD8 + memory cellsresultedin metabolic reprogramming , which enhanced the generation of CD8 + memory cells
in decreased proliferation , irreversible cell cycle arrest , increased apoptosis , reduced haemopoietic colony formation , altered gene expression pattern , reduction in self - renewal and a significant reresultedin decreased proliferation , irreversible cell cycle arrest , increased apoptosis , reduced haemopoietic colony formation , altered gene expression pattern , reduction in self - renewal and a significant re
the expression of adhesion moleculesinfluencesthe expression of adhesion molecules
increased proliferation and activation of the ERK pathway and promotes malignant cell growth of human glioblastoma cells ( 21causesincreased proliferation and activation of the ERK pathway and promotes malignant cell growth of human glioblastoma cells ( 21
cell toxicity in cancer cells through caspase - mediated apoptosiscausescell toxicity in cancer cells through caspase - mediated apoptosis
to revert cisplatin resistance in some preclinical models of NSCLCmay contributeto revert cisplatin resistance in some preclinical models of NSCLC
from decreased gene transcription , reduction in specific mRNA stabilitymay resultfrom decreased gene transcription , reduction in specific mRNA stability
to activation of AKT , which is the downstream signaling protein of PI3 K pathwayledto activation of AKT , which is the downstream signaling protein of PI3 K pathway
in up - regulation of E - cadherinresultedin up - regulation of E - cadherin
not only in the pronounced reduction of cell proliferation but also in an impaired tumor angiogenesisresultsnot only in the pronounced reduction of cell proliferation but also in an impaired tumor angiogenesis
to tumor regression of human tumors with high Myc levelsleadsto tumor regression of human tumors with high Myc levels
a higher increase in CDK activity compared to Chk1 inhibitioncauseda higher increase in CDK activity compared to Chk1 inhibition
in synergistic inhibition of AR - dependent and gene - specific HIF - dependent expression and prostate cancer cell growthresultedin synergistic inhibition of AR - dependent and gene - specific HIF - dependent expression and prostate cancer cell growth
a dose - dependent accumulation of cells in the G0 / G1 phase of the cell cyclecausesa dose - dependent accumulation of cells in the G0 / G1 phase of the cell cycle
in a dose - dependent accumulation of cells in the G0 / G1 phase of the cell cycleresultedin a dose - dependent accumulation of cells in the G0 / G1 phase of the cell cycle
to apoptosis in cells with constitutive ERK activationleadsto apoptosis in cells with constitutive ERK activation
to the suppression of proteins involved in proliferation ( cyclin D1 and c - mycledto the suppression of proteins involved in proliferation ( cyclin D1 and c - myc
to inhibition of cell viability and induction of apoptosis in colorectal cancer cell lines and in vivo xenograftscan leadto inhibition of cell viability and induction of apoptosis in colorectal cancer cell lines and in vivo xenografts
to the accumulation of misfolded proteins in cells resulting in endoplasmic reticulum stress ( 23leadsto the accumulation of misfolded proteins in cells resulting in endoplasmic reticulum stress ( 23
growth suppression of the cellscausesgrowth suppression of the cells
to repression of pharmacodynamic proliferation markers and to reduced lung cancer formation in vivo ( Fig . 6ledto repression of pharmacodynamic proliferation markers and to reduced lung cancer formation in vivo ( Fig . 6
in reduced embryonic growth , arrested development and increased lethalityresultedin reduced embryonic growth , arrested development and increased lethality
to increased tumor developmentcontributesto increased tumor development
to : increase in cGMP levels causing smooth muscle relaxation andleadsto : increase in cGMP levels causing smooth muscle relaxation and
in a concentration - dependent increase in nuclear area and multinucleated cellsresultsin a concentration - dependent increase in nuclear area and multinucleated cells
to growth suppression and apoptosisleadsto growth suppression and apoptosis
to apoptosis and autophagy activationleadingto apoptosis and autophagy activation
from the effect of antibody binding on intracellular protein transportcould also resultfrom the effect of antibody binding on intracellular protein transport
to reduced tumor vascularization and cancer cell deathleadsto reduced tumor vascularization and cancer cell death
to reduced tumor vascularization and cancer cell deathleadsto reduced tumor vascularization and cancer cell death
to degradation of the TYK2 kinase and apoptotic cell death in T - cell acute lymphoblastic leukemialeadsto degradation of the TYK2 kinase and apoptotic cell death in T - cell acute lymphoblastic leukemia
to off - target activity or interference with normal cellular functionsleadingto off - target activity or interference with normal cellular functions
to gene expression and splicing changes ultimately resulting in the induction of p53 in lymphoma cell linesleadsto gene expression and splicing changes ultimately resulting in the induction of p53 in lymphoma cell lines
in increased parent drug concentrations or altered metabolite formationmay resultin increased parent drug concentrations or altered metabolite formation