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Erlotinib ... a small oral EGFR tyrosine kinase inhibitorcausesreverse inhibition of the EGFR tyrosine kinase domain
this effect ... tyrosine residuesresultin inhibition of tyrosine phosphorylation
by the presence of EGCG(passive) caused bythe tyrosine kinase inhibition ( Figure 7B
the enzyme tyrosine kinaseresultsin inhibition of tyrosine phosphorylation
Missense mutations affecting cysteine residues within the extracellular domain of the receptorcausesconstitutive tyrosine kinase activation
tyrosine residuesresultin inhibition of tyrosine phosphorylation
by various single mutations(passive) caused bytyrosine kinase inhibitor treatment
EGFR activation with receptor dimerization andleadsreceptor tyrosine kinase phosphorylation
Ligand induced dimerization causes the formation of the EGFR ligand receptor complexcausingintracellular tyrosine kinase phosphorylation
dimerization causes the formation of the EGFR ligand receptor complexcausingintracellular tyrosine kinase phosphorylation
A newly developed molecule , STI-571 ( Gleveec ) , binds selectively to CD117resultingin inhibition of tyrosine phosphorylation
the activity of whichmay resultinhibition kinase
this activitycould resultfrom kinase inhibition
The epidermal growth factorcontributesEGF)/Src tyrosine kinase pathway
The V617F mutation in exon 14 of JAK2 kinasecausesactivation of tyrosine kinase
a standardized datasetfor kinase inhibition
that is glutathionylated during oxidative stressresultingin inhibition of the kinase
that AMPT competes with tyrosine at the tyrosine - binding sitecausinginhibition of tyrosine hydroxylase
Treatment with MET proto - oncogenecan causereceptor tyrosine kinase inhibitor
a receptorpromptstyrosine kinase sign transduction
that AMPT competes with tyrosine at the tyrosine - binding sitecausinginhibition of tyrosine
Its binding to cell surfacecausesreceptor tyrosine kinase
to block different cytokine receptor signaling pathways(passive) are designedTyrosine kinase inhibitors
by EGFR gatekeeper T790 M mutation in non - small - cell lung cancer (passive) caused bytyrosine kinase inhibitors
to blockade the downstream signaling pathways that promote tumor growth and metastasis when stimulated by angiogenic factors(passive) are designedTyrosine kinase inhibitors ( TKI
by Kyowa Kirin(passive) discovered bytyrosine kinase inhibitor ( TKI
by Kyowa Hakko Kirin(passive) discovered bytyrosine kinase inhibitor ( TKI
the BCR - ABL fusion genecausesthe overproduction of tyrosine kinase
by Eisai(passive) discovered bykinase inhibitor
of a receptor and a tyrosine kinase(passive) is composedAn EGFR tyrosine kinase
of a receptor and tyrosine kinase(passive) is composedAn EGFR tyrosine kinase
to optimize VEGF blockage while minimizing off - target toxicities(passive) was designedtyrosine kinase inhibitor ( TKI
Therapy with an epidermal growth factormay contributetyrosine kinase inhibitor
by Eisai(passive) discovered bytyrosine kinase inhibitor
Taiho Pharmaceutical(passive) discovered bytyrosine kinase inhibitor
by Taiho Pharmaceutical(passive) discovered bytyrosine kinase inhibitor
the BCR - ABL gene(passive) caused byThe tyrosine kinase
by the BCR - ABL gene(passive) caused byThe tyrosine kinase
by the [ [ BCR / ABL(passive) caused bythe [ [ tyrosine kinase
Furthermore , to illustrate an extra circumstance , insulin - associated factors have been determinedto influencetyrosine kinase
to protein kinase C - induced c - Jun N - terminal kinase activationleadsto protein kinase C - induced c - Jun N - terminal kinase activation
to protein kinase C - induced cleadsto protein kinase C - induced c
to increased extracellular adenosine concentrationsmight leadto increased extracellular adenosine concentrations
to apoptotic cell deathledto apoptotic cell death
oncogenic switch to HER2 signaling in a preclinical studycausedoncogenic switch to HER2 signaling in a preclinical study
simultaneous bone loss and excess bone formationcausessimultaneous bone loss and excess bone formation
simultaneous bone loss and excess bone formation within growing bone in ratscausessimultaneous bone loss and excess bone formation within growing bone in rats
simultaneous bone loss and excess bone formation within growing bonecausessimultaneous bone loss and excess bone formation within growing bone
to inhibit both EGFR sensitizing and EGFR T790 M resistance mutations , with clinical activity against central nervous system ( CNS ) metastasesdesignedto inhibit both EGFR sensitizing and EGFR T790 M resistance mutations , with clinical activity against central nervous system ( CNS ) metastases
inhibition of cell viabilitycausesinhibition of cell viability
feedback - dependent biphasic regulation of AKT signalingcausesfeedback - dependent biphasic regulation of AKT signaling
to tumor shrinkage for ALK - positive patientshas ledto tumor shrinkage for ALK - positive patients
to tumor shrinkagehas ledto tumor shrinkage
feedback - dependent biphasiccausesfeedback - dependent biphasic
to dephosphorylation of its two major downstream signaling components , p70 S6 kinaseleadsto dephosphorylation of its two major downstream signaling components , p70 S6 kinase
to reduced phosphorylation of STAT1 at S727can leadto reduced phosphorylation of STAT1 at S727
cell growth inhibition in vitro and reduces lung metastases in vivocausescell growth inhibition in vitro and reduces lung metastases in vivo
in suppression of this responseresultedin suppression of this response
feedback - dependent biphasic regulation of AKT signalingcausesfeedback - dependent biphasic regulation of AKT signaling
resistance(passive) caused byresistance
growth inhibition of tumors and enhancement of the activity of a number of cytotoxic drugscausegrowth inhibition of tumors and enhancement of the activity of a number of cytotoxic drugs
in significant neuroprotection in a majority of these modelsresultedin significant neuroprotection in a majority of these models
to responses in most patients with ALK - positive non - small - cell lung cancerleadsto responses in most patients with ALK - positive non - small - cell lung cancer
dephosphorylation ( Figure 4Acausesdephosphorylation ( Figure 4A
G1 arrestcauseG1 arrest
thrombotic microangiopathy , proteinuria or interstitial diseasecan causethrombotic microangiopathy , proteinuria or interstitial disease
a disease(passive) is influenced bya disease
to reduced phosphorylation of STAT1 at S727 in a number of cancers cells , and phosphorylation of STAT1-S727 could serve as a biomarker of 127373 - 66 - 4 IC50 CDK8 kinase activity in vitro and in vivocan leadto reduced phosphorylation of STAT1 at S727 in a number of cancers cells , and phosphorylation of STAT1-S727 could serve as a biomarker of 127373 - 66 - 4 IC50 CDK8 kinase activity in vitro and in vivo
to treating the cancerleadingto treating the cancer
negativelyinfluencednegatively
to reduced phosphorylation of STAT1 at S727 in a number of cancers cells , and phosphorylation of STAT1-S727 could serve as a biomarker of 127373 - 66 - 4 IC50 CDK8 kinase activity in vitro and in vivo [ 75,76,77can leadto reduced phosphorylation of STAT1 at S727 in a number of cancers cells , and phosphorylation of STAT1-S727 could serve as a biomarker of 127373 - 66 - 4 IC50 CDK8 kinase activity in vitro and in vivo [ 75,76,77
to long term durable responsesactually can leadto long term durable responses
to target multiple RTKsdesignedto target multiple RTKs
hepatotoxicity(passive) caused byhepatotoxicity
in dramatic cell death and paradoxical enrichment of cells with CSC - like propertiesresultedin dramatic cell death and paradoxical enrichment of cells with CSC - like properties
the acne - form rash(passive) caused bythe acne - form rash
hypothyroidism in a patient on levothyroxinecausinghypothyroidism in a patient on levothyroxine
transient or permanent testicular dysfunctionmay causetransient or permanent testicular dysfunction
to the improved prognosis of cancer patients and are essential for genome - based precision medicinehave contributedto the improved prognosis of cancer patients and are essential for genome - based precision medicine
specifically for the bcr - abl fusion protein that is characteristic for Philadelphia chromosome - positive leukemias ( chronic myelogenous leukemia and occasionally acute lymphocytic leukemiadesignedspecifically for the bcr - abl fusion protein that is characteristic for Philadelphia chromosome - positive leukemias ( chronic myelogenous leukemia and occasionally acute lymphocytic leukemia