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These mutationsleadto constitutive activation of the tyrosine kinase receptor
that undergo dimerization following ligand bindingresultingin activation of the receptor tyrosine kinase
Treatment of cells with ephrinB2ledto NMDA receptor tyrosine phosphorylation
EGFR activation with receptor dimerization andleadsreceptor tyrosine kinase phosphorylation
BDNF through activation ofcausestyrosine kinase B ( TrkB ) receptors
recombinant ephrinB2 was shownto causeNMDA receptor tyrosine phosphorylation
Binding of the neurotrophins to the trk receptorsleadsto receptor tyrosine phosphorylation
Mutationsresultingin constitutively active tyrosine kinase receptors
phospholipase C gamma 1contributesto receptor - mediated tyrosine kinase signal transduction
The epidermal growth factorcontributesEGF)/Src tyrosine kinase pathway
Cbl ... in turncausesdownregulation of tyrosine kinase receptors
insulincausestyrosine autophosphorylation of the receptors
the cancerresultsfrom an aberrant tyrosine kinase receptor
Treatment with MET proto - oncogenecan causereceptor tyrosine kinase inhibitor
a receptorpromptstyrosine kinase sign transduction
as a proto - oncogene(passive) was ... discoveredtransfection ) receptor tyrosine kinase
Its binding to cell surfacecausesreceptor tyrosine kinase
Binding of growth factors , such as IGF - Ileadsto their tyrosine kinase receptors
KIT(passive) was ... discoveredThe receptor tyrosine kinase
to block different cytokine receptor signaling pathways(passive) are designedTyrosine kinase inhibitors
as a proto - oncogene(passive) was ... discoveredreceptor tyrosine kinase
of three major domains(passive) are composedAll receptor tyrosine kinase
to blockade the downstream signaling pathways that promote tumor growth and metastasis when stimulated by angiogenic factors(passive) are designedTyrosine kinase inhibitors ( TKI
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 Taiho Pharmaceutical(passive) discovered bytyrosine kinase inhibitor
Taiho Pharmaceutical(passive) discovered bytyrosine kinase inhibitor
first(passive) was ... discoveredAbl tyrosine kinase
the BCR - ABL gene(passive) caused byThe tyrosine kinase
by gain - of - function mutations(passive) caused bytyrosine kinase
Furthermore , to illustrate an extra circumstance , insulin - associated factors have been determinedto influencetyrosine kinase
diseases and cancerscan also causediseases and cancers
to recruitment of enzymes and adapter proteins that activate intracellularleadingto recruitment of enzymes and adapter proteins that activate intracellular
to the inhibition of cell proliferation in gefitinib - resistant and -delicate non - small cell lung malignancy ( NSCLC ) cellsleadingto the inhibition of cell proliferation in gefitinib - resistant and -delicate non - small cell lung malignancy ( NSCLC ) cells
to the activation of the Map kinase ( Mapkleadingto the activation of the Map kinase ( Mapk
cell death within human cardiac progenitor cellsare causingcell death within human cardiac progenitor cells
to RAS activation which subsequently result in GTP substitution of GDPleadsto RAS activation which subsequently result in GTP substitution of GDP
the dNA-influencethe dNA-
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
to increased susceptibilityleadsto increased susceptibility
simultaneous bone loss and excess bone formation within growing bonecausessimultaneous bone loss and excess bone formation within growing bone
candidate genes(passive) influenced bycandidate genes
dysfunction in adult rat cardiac fibroblasts in vitrocausedysfunction in adult rat cardiac fibroblasts in vitro
in increased accumulation ofresultin increased accumulation of
to transformationleadsto transformation
to tumor growth , progression , and metastasisleadsto tumor growth , progression , and metastasis
in constitutive tyrosine kinase activity and elevated downstream signalingresultingin constitutive tyrosine kinase activity and elevated downstream signaling
to activation of MAP kinasesleadsto activation of MAP kinases
of an extracellular alpha - chain disulfide - bonded to a membrane spanning beta - chain ( 18 , 28composedof an extracellular alpha - chain disulfide - bonded to a membrane spanning beta - chain ( 18 , 28
in oncogenesisresultsin oncogenesis
in cell deathmay resultin cell death
of two and twocomposedof two and two
to dimerization and activationleadsto dimerization and activation
in the [ [ polymerization ] ] ofresultingin the [ [ polymerization ] ] of
to receptor autophosphorylation and consequent activation of both PI3 K and Rasleadsto receptor autophosphorylation and consequent activation of both PI3 K and Ras
in the polymerization of actin filamentsresultingin the polymerization of actin filaments
to their dimerization and activation of their kinase activityleadsto their dimerization and activation of their kinase activity
to invasive tumour growth in rhabdomyosarcomascontributesto invasive tumour growth in rhabdomyosarcomas
in endothelial cell proliferation , migration , and angiogenesis 20resultingin endothelial cell proliferation , migration , and angiogenesis 20
in the [ [ polymerization ] ] of [ [ actin ] ] filaments , which cross - linkedresultingin the [ [ polymerization ] ] of [ [ actin ] ] filaments , which cross - linked
to the activation of a number of intracellular signaling pathwaysleadingto the activation of a number of intracellular signaling pathways
to an activation of signal transducer and activator of transcription 3leadingto an activation of signal transducer and activator of transcription 3
to intracellular signalingleadingto intracellular signaling
to angiogenesiscontributesto angiogenesis
to intracellularleadingto intracellular
the cascade(passive) prompted bythe cascade
to survivalcontributeto survival
in a loss of apoptosis and uncontrolled proliferation of the tumorresultingin a loss of apoptosis and uncontrolled proliferation of the tumor
in endothelial cell proliferation , migration , and angiogenesis 20resultingin endothelial cell proliferation , migration , and angiogenesis 20
changes in growth and differentiationcausingchanges in growth and differentiation