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PMID : 27576135 the chaperone 78-kDa glucose - regulated protein ( GRP78 ) protects the MPD against PDI - dependent disulfide - bond isomerization by binding to this domain and , therebypreventingADAM17 inhibition
resveratrol(passive) triggered byproteasome inhibition
The qnr genes encode proteins that prevent fluoroquinolones from interacting with DNA / type - II - topoisomerase complexes formed during DNA replicationthus preventingfluoroquinolone inhibition
Pubmed ] Activation of GABAB receptorscausespresynaptic inhibition
Neuroscience 20 : 1001–1009 , 1987.OpenUrlCrossRefMedlineWeb of Science Peng YY and Frank E. Activation of GABAB receptorscausespresynaptic inhibition
a assortment of inhibitors(passive) triggered bybiosynthesis inhibition
9239 - 9248 , 2017 Activation of GABAB receptorscausespresynaptic inhibition
J Neurosci 1990;10:336 - 345 https://doi.org/10.1523/JNEUROSCI.10-01-00336.1990 Peng YY , Frank E. Activation of GABAB receptorscausespresynaptic inhibition
as with most COX-2 inhibitorscan causeCOX-1 inhibition
1995 Peng , Y. Y. and Frank , E. Activation of GABAB receptorscausespresynaptic inhibition
Guangqiang Jiang and David D. Excitatory neurotransmitterscan causepresynaptic inhibition
release of an inhibitory substance onto the outsides of the presynaptic nerve fibrils before their own endings terminate on the postsynaptic neuron(passive) is caused byPresynaptic inhibition
release of an inhibitory substance onto the outsides of the presy - naptic nerve fibrils before their own endings terminate on the postsynaptic neuron(passive) is caused byPresynaptic inhibition
Raman et al . , 1996preventstubulin inhibition
1986 ; Shirayama et al . , 1993preventedmuscarinic inhibition
| Molecular Neurodegeneration | Full Text Histoneleadsdeacetylase inhibition
the extracellular Cl− concentration ( Muanprasat et al . , 2004(passive) influenced byCFTR inhibition
an inhibition of the voltage - dependent Ca2 + currents ( Kretz et al . 1986b(passive) may also be caused byPresynaptic inhibition
retrograde signal from metabotropic glutamate to cannabinoid receptors , NEURON , 31(3 ) , 2001 , pp(passive) caused byPresynaptic inhibition
Publisher Site | Google Scholar R. Gordon , E. A. Albornoz , D. C. Christie et al .preventsInflammasome inhibition
43 2000 Pertussis toxin ... Ribeiro , J. A. article openAccess 44 2008 Potential therapeutic interest of adenosine A2A receptors in psychiatric disorders Cunha , Rodrigo A. ; Ferré , Sergi ; Vaugeois , Jean - Marie ; Chen , Jiang - Fan article openAccess 45 2014preventspresynaptic inhibition
retrograde signal from metabotropic glutamate to cannabinoid receptors , Neuron 31:463 ( 2001).PubMedCrossRefGoogle Scholar R. I. Wilson , G. Kunos , and R. A. Nicoll , Presynaptic specificity of endocannabinoid signaling in the hippocampus(passive) caused byPresynaptic inhibition
Deletion of N - terminal residues 2 - 46preventedPKC inhibition
rOAT1 andpreventsrOAT3AbstractFulltextPDFCOX-2 inhibition
when injected into COS-7 cells containing wild type NgR and Nogo - A , our soluble binding domain of NgRpreventedaxonal inhibition
This vermox canadapreventsinfamously inhibition
L135 pretreatment ( 100 nM , 10 μl ) caused no effect on RS - induced reflex potentiation ( RS+L135 ) ,preventedQ110-dependent inhibition
Q110 administrationpreventedQ110-dependent inhibition
Enkephalincausespresynaptic inhibition
another drugcausespresynaptic inhibition
Thelitz , S , Oishi , P , Sanchez , LS , Bekker , JM , Ovadia , B , Johengen , MJ , Black , SM & Fineman , JR 2004preventsPhosphodiesterase-3 inhibition
basal PGE2 ... thosecausedTxB2 inhibition
insulin and growth factors(passive) caused byFoxO inhibition
the different dosing regimens(passive) caused bymTOR inhibition
Number to send5102050100200Start from citationCreate File Select itemprevents236902291.Calpain inhibition
2 Cpreventspresynaptic inhibition
higher MMPi plasma levels at week 4(passive) caused byMMP-1 inhibition
Both Y1 and Y2 agonistscausepresynaptic inhibition
Cramer , Z , Sadek , J , Vazquez , GG , Di Marco , S , Pause , A , Pelletier , J & Gallouzi , I 2018preventsEIF4A inhibition
Mammalian target of rapamycincan leadmTOR ) inhibition
to the shrinkage or stabilization of renal AML , LAM , facial angiofibroma and subependymal giant cell astrocytoma [ 22leadsto the shrinkage or stabilization of renal AML , LAM , facial angiofibroma and subependymal giant cell astrocytoma [ 22
the onset of cytokine - induced muscle wasting by blocking the STAT3 and iNOS pathways Article Snippetpreventsthe onset of cytokine - induced muscle wasting by blocking the STAT3 and iNOS pathways Article Snippet
in increased HIF1-α translation , resulting in a regulatory loop [ 32can resultin increased HIF1-α translation , resulting in a regulatory loop [ 32
a reduction in the S - phase fraction of KRAS mutant cells ... an effect also characterised by modulation of Rb , a master control of the G1 / S checkpointcauseda reduction in the S - phase fraction of KRAS mutant cells ... an effect also characterised by modulation of Rb , a master control of the G1 / S checkpoint
to autophagy induction ( Ravikumar et al . , 2010cshould leadto autophagy induction ( Ravikumar et al . , 2010c
neuronal cell deathpreventedneuronal cell death
to cell death [ 102leadingto cell death [ 102
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
Expression of membrane - targeted Gα13 rescues spine enlargement(passive) caused byExpression of membrane - targeted Gα13 rescues spine enlargement
morphological reversion of Ras - transformed cells by a complex mechanism that involves regulation of the actin cytoskeleton Mol Cell Biol 14:4193–4202causesmorphological reversion of Ras - transformed cells by a complex mechanism that involves regulation of the actin cytoskeleton Mol Cell Biol 14:4193–4202
both suppress spine enlargement(passive) caused byboth suppress spine enlargement
elevation of microRNA-34a ( miR-34a ) , and anti - miR-34a not only restored the expression of MYCN but also increased cell survival of neuroblastoma cells treated with CDK1 inhibitorcausedelevation of microRNA-34a ( miR-34a ) , and anti - miR-34a not only restored the expression of MYCN but also increased cell survival of neuroblastoma cells treated with CDK1 inhibitor
rapid - onset of carcinogen - induced malignancies in a novel inducible HPV-16preventsrapid - onset of carcinogen - induced malignancies in a novel inducible HPV-16
ATP generation and cell cycle arrest(passive) caused byATP generation and cell cycle arrest
that ibrutinib enhances NAD+ and ATP depletion(passive) triggered bythat ibrutinib enhances NAD+ and ATP depletion
to increases in caspase - dependent cell deathledto increases in caspase - dependent cell death
the fusion of monocytes - macrophages to become multi nucleated osteoclasts [ 37preventsthe fusion of monocytes - macrophages to become multi nucleated osteoclasts [ 37
the action potential prolongation(passive) caused bythe action potential prolongation
metabolic disruption in muscle cells with smoke exposure and may explain whole body insulin resistance and mitochondrial dysfunction in vivopreventsmetabolic disruption in muscle cells with smoke exposure and may explain whole body insulin resistance and mitochondrial dysfunction in vivo
to feedback activation of the PI3 K pathway including Akt by reversing a feedback inhibition apparently mediated throughleadsto feedback activation of the PI3 K pathway including Akt by reversing a feedback inhibition apparently mediated through
in myeloid maturation and subsequent AML cell deathresultedin myeloid maturation and subsequent AML cell death
to DNA damage response at telomeresleadsto DNA damage response at telomeres
local and systemic bone loss without inhibiting systemic markers and mediators of inflammation in both AIA and CIA rats ... while inhibition of IL-1 or TNFα would suppress systemic levels of proinflammatory cytokines in these two arthritis modelswould preventlocal and systemic bone loss without inhibiting systemic markers and mediators of inflammation in both AIA and CIA rats ... while inhibition of IL-1 or TNFα would suppress systemic levels of proinflammatory cytokines in these two arthritis models
to eIF2α phosphorylation and whether this potential relationship affects the induction of autophagycontributesto eIF2α phosphorylation and whether this potential relationship affects the induction of autophagy
in an unremitting proinflammatory response , persistent high proinflammatory and effector CD4 responseresultedin an unremitting proinflammatory response , persistent high proinflammatory and effector CD4 response
glioma induced M2 polarization of microglial cells and increase their cytotoxic potential , possibly resulting in antitumor actionsmay preventglioma induced M2 polarization of microglial cells and increase their cytotoxic potential , possibly resulting in antitumor actions
glioma growth by inhibiting M2 polarization of microglial cells ... thereby increasing their anti - tumor cytotoxic potential ( Lisi et al . , 2014preventedglioma growth by inhibiting M2 polarization of microglial cells ... thereby increasing their anti - tumor cytotoxic potential ( Lisi et al . , 2014
to an increase in FOXP3 expressing cells and a reduced IFNγ producing potential ... whereas PI3 K inhibition hardly affected the IL17A and IFNγ producing potentialledto an increase in FOXP3 expressing cells and a reduced IFNγ producing potential ... whereas PI3 K inhibition hardly affected the IL17A and IFNγ producing potential
IL-7–mediated viability and proliferation of T - ALL cells18 ( and data not shown ) , and ruxolitinib , a clinical - stage JAK1/2 pharmacological inhibitor , displays activity against IL7R mutant T - ALL patient - derived samples.20,22preventsIL-7–mediated viability and proliferation of T - ALL cells18 ( and data not shown ) , and ruxolitinib , a clinical - stage JAK1/2 pharmacological inhibitor , displays activity against IL7R mutant T - ALL patient - derived samples.20,22
NF - κB activation [ 163preventsNF - κB activation [ 163
missing self - induced NK cell - mediated rejection in vivopreventsmissing self - induced NK cell - mediated rejection in vivo
monocrotaline - induced pulmonary hypertension in ratspreventsmonocrotaline - induced pulmonary hypertension in rats
renal damage observed in hypertensive ratspreventedrenal damage observed in hypertensive rats
in increased calcium - channel blocker concentrationsresultingin increased calcium - channel blocker concentrations
in a significantly increased G2 index ( 41.6 % , P < 0.01resultedin a significantly increased G2 index ( 41.6 % , P < 0.01
in the repression of basal Nf - κb and IκBα and normalized palmitate - mediated increases in Il-6 , and Tlr4resultedin the repression of basal Nf - κb and IκBα and normalized palmitate - mediated increases in Il-6 , and Tlr4
to a marked decrease in its colocalization withleadsto a marked decrease in its colocalization with
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 %
to rapid upregulation of ErbB3 and IGF-1R expression , which results in MAPK - ERK pathway activation ... thereby limiting the efficacy of IKBKE inhibitorsleadsto rapid upregulation of ErbB3 and IGF-1R expression , which results in MAPK - ERK pathway activation ... thereby limiting the efficacy of IKBKE inhibitors
in a tip cell defect , which inhibited sprout formationresultedin a tip cell defect , which inhibited sprout formation