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by the extract of Drymis Winteri(passive) caused byoedema inhibition
by the extract of Drymis winteri (passive) caused byoedema inhibition
retrograde signal from metabotropic glutamate to cannabinoid receptors(passive) caused byPresynaptic inhibition
Activation of GABAB receptorscausespresynaptic inhibition
malayamycin treatment(passive) caused bysporulation inhibition
by BTZ treatment(passive) caused byproteasome inhibition
by rapamycin(passive) caused bymTOR inhibition
by sodium selenate(passive) caused byAKT inhibition
MG132 treatment increased levels of high molecular weight polyubiquitinated proteins after 4 and 16 h(passive) caused byproteasome inhibition
the CLAVATA1 receptorultimately causingWUSCHEL inhibition
that has previously been shownto causepresynaptic inhibition
MG132(passive) caused byproteasome inhibition
Crcausedinhibition of U46619
by retrograde signal(passive) caused byPresynaptic inhibition
NAD+ depletion(passive) caused bySIRT1 inhibition
Nutrient insufficiency ... in whichcausesmTOR inhibition
This primary afferent depolarizationcausespresynaptic inhibition
endogenous adenosine(passive) caused bypresynaptic inhibition
by noradrenaline(passive) caused bypresynaptic inhibition
Enkephalincausespresynaptic inhibition
evidencecan influenceGABAergic inhibition
Histoneleadsdeacetylase inhibition
a sudden shockcausingvagal inhibition
an increase in the length of alkyl chainscausedseverer inhibition
> High dosescan causeCox-1 inhibition
High dosescan causeCox-1 inhibition
poisoning(passive) caused bythepetitive inhibition
By selectively exciting A - beta nerve fibres in the skin with TENS , the amount of painful stimulation being transmitted by smaller diameter A - delta and C - fibres can be reducedcausingsegmental inhibition
Indications Leptophos , as well as every other organophosphatecausesacetylcholinesterase inhibition
the mechanism of the P450-catalyzed conversion of NMH ... a nitrosomethane intermediatecausesP450 inhibition
classes of tannins & polyphenol oxidase - generated o - quinones(passive) caused byproteolytic inhibition
Robert D. McIntosh , Antimo Buonocorecan causeSaccadic inhibition
to liposomal C8-induced actions in HCC cellscontributesto liposomal C8-induced actions in HCC cells
to stabilization of actinleadsto stabilization of actin
in reduced bone lesionsresultedin reduced bone lesions
rounding in the affected epithelial cellscausesrounding in the affected epithelial cells
to an increase in Foxo3a levelsleadsto an increase in Foxo3a levels
to decreased cell proliferation and blood sugar uptakeleadsto decreased cell proliferation and blood sugar uptake
to a paradoxical increase in Akt activation ... via a release of negative feedback on upstream signaling through insulin - like growth factor-1 receptor ( IGF1R ) , or direct activation by the rapamycin - insensitive mTOR - rictor complexcan leadto a paradoxical increase in Akt activation ... via a release of negative feedback on upstream signaling through insulin - like growth factor-1 receptor ( IGF1R ) , or direct activation by the rapamycin - insensitive mTOR - rictor complex
to increased lifespanleadsto increased lifespan
cellular DDR activationcausedcellular DDR activation
to autophagic activationleadsto autophagic activation
to reduction of inflammatory cytokinesleadsto reduction of inflammatory cytokines
a reversible G2 arrest in cancer cellscausesa reversible G2 arrest in cancer cells
in efficacyresultsin efficacy
in more cellsresultedin more cells
to a reduction in cellular migrationcontributeto a reduction in cellular migration
cell growth arrest and often immunosuppressioncausescell growth arrest and often immunosuppression
to RCC cell line and xenograft tumor growth inhibitionleadsto RCC cell line and xenograft tumor growth inhibition
to protectionsurprisingly leadsto protection
to the blockage of numerous downstream targetsleadsto the blockage of numerous downstream targets
no additional enhancementcausedno additional enhancement
alsoresultedalso
to a nearly three - fold increase in reporter activityledto a nearly three - fold increase in reporter activity
to eukaryotic elongation factorleadingto eukaryotic elongation factor
in the dephosphorylation and inactivation of heat shock factor 1 ( HSF1 ) ( 39 , 40resultsin the dephosphorylation and inactivation of heat shock factor 1 ( HSF1 ) ( 39 , 40
to down - regulation of both autophagy and mitophagy and clearing of accumulated mitochondrialeadingto down - regulation of both autophagy and mitophagy and clearing of accumulated mitochondria
early metabolic alterations detected by nuclear magnetic resonance spectroscopycausesearly metabolic alterations detected by nuclear magnetic resonance spectroscopy
in a block of 4E - binding protein-1 phosphorylation , sequestration of eukaryotic initiation factor-4 subunit E , and failure to form the complex required for translationresultsin a block of 4E - binding protein-1 phosphorylation , sequestration of eukaryotic initiation factor-4 subunit E , and failure to form the complex required for translation
to loss of the prosurvival protein survivin and that depletion of survivin selectively kills cells that overexpress MYCleadsto loss of the prosurvival protein survivin and that depletion of survivin selectively kills cells that overexpress MYC
to depletion of pools of activated B cells and newly formed plasma cells ... while sparing naive B cell pools and long - lived plasma cellswould leadto depletion of pools of activated B cells and newly formed plasma cells ... while sparing naive B cell pools and long - lived plasma cells
in myeloid maturation and subsequent AML cell deathresultedin myeloid maturation and subsequent AML cell death
in a synthetic lethality in mouse lymphoma and hepatoblastoma with MYC hyper - activationresultedin a synthetic lethality in mouse lymphoma and hepatoblastoma with MYC hyper - activation
the relaxation process(passive) caused bythe relaxation process
in a functional impairment in vascular relaxationresultedin a functional impairment in vascular relaxation
elevated expression levels of the Apaf-1 apoptotic pathway proteins caspase-3 ... andcausedelevated expression levels of the Apaf-1 apoptotic pathway proteins caspase-3 ... and
a marked reduction of both invasion ( 40 % ) and cell adhesion to collagen ( 84 % ) , accompanied by an increase in TNF - induced apoptosis ( 72 %causeda marked reduction of both invasion ( 40 % ) and cell adhesion to collagen ( 84 % ) , accompanied by an increase in TNF - induced apoptosis ( 72 %
immunosuppression and was only beneficial in SOD1 G93A mice when lymphocytes were depleted [ 27 , 32causesimmunosuppression and was only beneficial in SOD1 G93A mice when lymphocytes were depleted [ 27 , 32
morphological reversion of ras - transformed cellscausesmorphological reversion of ras - transformed cells
to a decrease in the capacity of the reticulocyteleadsto a decrease in the capacity of the reticulocyte
to the downregulation of Axin2 , a constitutive Wnt targetledto the downregulation of Axin2 , a constitutive Wnt target
to the downregulation of Axin2 , a constitutive Wnt target ... in the cytoplasmledto the downregulation of Axin2 , a constitutive Wnt target ... in the cytoplasm