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Qaagi - Book of Why

Causes

Effects

hepatocyte growth factor / scatter factor2(passive) triggered bya receptor tyrosine kinase

insulin receptorsresultingin receptor tyrosine kinase

0007 ] Strategiesresultin agonists of tyrosine kinase receptors

of at least three domains : an extracellular ligand binding domain , a transmembrane domain and a cytoplasmic catalytic domain that can phosphorylate tyrosine residues(passive) are composedReceptor tyrosine kinases

of an extracellular ligand binding domain , a single transmembrane helix , and an intracellular effector domain(passive) are most typically composedReceptor tyrosine kinases

of an extracellular ligand - binding domain Aloe Vera(passive) are composedReceptor tyrosine kinases

a tyr kinase receptorcausesthe tyrosine kinase receptors to dimerize

Another linkleadsfrom the receptor tyrosine kinase

commonly(passive) is ... triggeredTyrosine kinase receptor endocytosis

supportsignaling originatingfrom a receptor tyrosine kinase

KIT(passive) was ... discoveredThe receptor tyrosine kinase

To elucidate the role of receptor … ( More ) Ellen Margrethe Haugsten , Malgorzata Zakrzewska , +4 authorscan influenceJørgen Wesche Endocytosis of tyrosine kinase receptors

as a component of the fusion protein nucleophosmin(passive) was initially discoveredALK ) receptor tyrosine kinase

as an element from the fusion protein nucleophosmin(passive) was discoveredALK ) receptor tyrosine kinase

three different domains : extracellular ( ECD ) , intracellular ( ICD ) and transmembrane [ 4 , 7 , 8(passive) composed bya tyrosine kinase receptor

Activation optioncausesa tyrosine kinase receptor

ubiquitylation of the endocytic machinery(passive) is influenced byTyrosine kinase receptor internalization

three IgG - like domains and an acidic box in the extracellular space , a transmembrane domain and two intracellular tyrosine kinase domains(passive) composed bya tyrosine kinase receptor

Activation of various surface receptors including G protein‐coupled receptors ( GPCRs ) andleadsreceptor tyrosine kinases

processes such as feedback and internalizationmay influencereceptor tyrosine kinase signaling[5 , 6

an effortto discovernovel tyrosine kinase receptors

The junction at the site of the translocationcausesoverexpression of a receptor tyrosine kinase

Activation of G protein - coupled receptors ( GPCRs ) orleadstyrosine kinase receptors

gene mutations(passive) triggered byreceptor tyrosine kinases

that different antidepressants induce LPA1 activationleadingto receptor tyrosine kinase transactivation

first(passive) was ... discoveredThe receptor tyrosine kinase MERTK

Mutations in the binding site forleadsCbl tyrosine kinase receptors

The diversity in the signaling pathways activated by either G protein - coupled receptors ( GPCR ) orresultstyrosine kinase receptors

Tyrosine phosphorylation of GRP78 upon α2 M * binding Binding of growth factors to their cognate cell surface receptorscausestyrosine phosphorylation of the receptors

using drugsinfluencingthe receptors of tyrosine kinase

the downstream responses and finally stimulates cell division.[5triggersthe downstream responses and finally stimulates cell division.[5

the downstream responses and finally stimulates cell division ( 18triggersthe downstream responses and finally stimulates cell division ( 18

multiple signal transduction pathways at once Abnormal functioning of RTKscan triggermultiple signal transduction pathways at once Abnormal functioning of RTKs

multiple signal transduction pathways at once A kinase , alternatively known as a phosphotransferasecan triggermultiple signal transduction pathways at once A kinase , alternatively known as a phosphotransferase

in activation of ARresultingin activation of AR

to signaling from many receptors and participates as a signal transducer in multiple downstream pathways , including regulation of the actin cytoskeletoncontributesto signaling from many receptors and participates as a signal transducer in multiple downstream pathways , including regulation of the actin cytoskeleton

both the duration and the specificity of the signal emittedcan influenceboth the duration and the specificity of the signal emitted

to dimerization and activation by sequential autophosphorylation of specific tyrosine residuesleadsto dimerization and activation by sequential autophosphorylation of specific tyrosine residues

a variety of downstream signaling pathways , such as the RAF / RAS / MAPK cascade that results in phosphorylation of the ER and co - regulatory molecules such as AIB1 / Src-3 [ 12,13,14,15,16,17triggersa variety of downstream signaling pathways , such as the RAF / RAS / MAPK cascade that results in phosphorylation of the ER and co - regulatory molecules such as AIB1 / Src-3 [ 12,13,14,15,16,17

the downstream responses and finally stimulates cell division7triggersthe downstream responses and finally stimulates cell division7

in receptor dimerization / activationresultingin receptor dimerization / activation

different signaling pathways(passive) triggered bydifferent signaling pathways

multiple signal transduction pathways at once Copyright © 2008 Pearson Education , Inc. ... publishing as Pearson Benjamin Cummings Step 1 – signal molecules bind to receptors and a dimer is formedcan triggermultiple signal transduction pathways at once Copyright © 2008 Pearson Education , Inc. ... publishing as Pearson Benjamin Cummings Step 1 – signal molecules bind to receptors and a dimer is formed

in endothelial cell proliferation , migration , and angiogenesis 20resultingin endothelial cell proliferation , migration , and angiogenesis 20

to both survival advantageleadingto both survival advantage

in uncontrolled GIST cell proliferation , invasion , neoangiogenesis , and survivalresultingin uncontrolled GIST cell proliferation , invasion , neoangiogenesis , and survival

to activation of signaling pathways associated with cell growth and survivalleadsto activation of signaling pathways associated with cell growth and survival

to the regulation of cell proliferation , migration , and invasioncontributingto the regulation of cell proliferation , migration , and invasion

to the activation of a number of intracellular signaling pathwaysleadingto the activation of a number of intracellular signaling pathways

the cascade of biochemical events(passive) triggered bythe cascade of biochemical events

to regulate cell proliferation , invasion , migration , angio-discoveredto regulate cell proliferation , invasion , migration , angio-

conformational changes resulting in the endothelial cell proliferationcausingconformational changes resulting in the endothelial cell proliferation

using the Company 's proprietary Humaneered ® technologycreatedusing the Company 's proprietary Humaneered ® technology

to phosphorylation in kinase siteleadingto phosphorylation in kinase site

to its auto‐phosphorylation and activation of multiple downstream signaling networks that can drive cell proliferation , transformation , angiogenesis , invasion and metastasisleadsto its auto‐phosphorylation and activation of multiple downstream signaling networks that can drive cell proliferation , transformation , angiogenesis , invasion and metastasis

to recruitment of enzymes and adapter proteins that activate intracellular signaling pathways that control cell proliferation , differentiation , and numerous other biological processesleadingto recruitment of enzymes and adapter proteins that activate intracellular signaling pathways that control cell proliferation , differentiation , and numerous other biological processes

to downstream activation of PI3 kinase ( PI3 K ) , AKT , and ultimately mTORleadingto downstream activation of PI3 kinase ( PI3 K ) , AKT , and ultimately mTOR

to the phosphorylation of phosphatidylinositol 3-kinaseleadsto the phosphorylation of phosphatidylinositol 3-kinase

to phosphorylation and activation of Smad2/3leadingto phosphorylation and activation of Smad2/3

in increased phosphorylation on tyrosine residuesresultingin increased phosphorylation on tyrosine residues

the downstream activation of many kinases through various second messenger systems ( Ullrich and Schlessinger , 1990may triggerthe downstream activation of many kinases through various second messenger systems ( Ullrich and Schlessinger , 1990

toward blood vessel formation during angiogenesiscontributetoward blood vessel formation during angiogenesis

cellular proliferation , survival , invasion , and metastasisinfluencescellular proliferation , survival , invasion , and metastasis

to phosphorylation of IRS one and subsequent acti vationleadingto phosphorylation of IRS one and subsequent acti vation

to phosphorylation steps upon binding of its activator VEGFleadingto phosphorylation steps upon binding of its activator VEGF

to angiogenesis , the buildup of new blood vessels around a tumorcontributesto angiogenesis , the buildup of new blood vessels around a tumor

in the auto - phosphorylation of intracellular localized tyrosine residues of the EGFRresultingin the auto - phosphorylation of intracellular localized tyrosine residues of the EGFR

to phosphorylation of downstream molecules when activated through ligand binding [ 8leadingto phosphorylation of downstream molecules when activated through ligand binding [ 8

a complex cascade of events that ends with the cell passing the restriction pointtriggersa complex cascade of events that ends with the cell passing the restriction point

to phosphorylation at residues 239 , 240 ... and 317 within the collagen homologyleadsto phosphorylation at residues 239 , 240 ... and 317 within the collagen homology

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