SRP5092
TIE2 (771-end), active, GST tagged human
PRECISIO® Kinase, recombinant, expressed in baculovirus infected Sf9 cells, ≥70% (SDS-PAGE), buffered aqueous glycerol solution
Synonym(e):
CD202B, TEK, VMCM, VMCM1
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Alle Fotos(2)
About This Item
UNSPSC-Code:
12352200
NACRES:
NA.32
Allgemeine Beschreibung
TIE 2 or TEK is a receptor tyrosine kinase that is expressed principally on vascular endothelium. Disrupting TIE 2 function in mice results in embryonic lethality with defects in embryonic vasculature, suggesting a role in blood vessel maturation and maintenance. Angiopoietin-1 is a secreted growth factor that binds to and activates the TIE 2 receptor tyrosine kinase. SHP2 and GRB2 are recruited to the activated TIE 2 kinase domain and are part of the cellular responses that mediate TIE 2 function. TIE 2 expression is upregulated in the endothelium of vascular "hot spots" in human breast cancer specimens. However, TIE 2 is also overexpressed in areas of active angiogenesis in normal tissues.
Physikalische Form
Supplied in 50mM Tris-HCl, pH 7.5, 150mM NaCl, 10mM glutathione, 0.1mM EDTA, 0.25mM DTT, 0.1mM PMSF, 25% glycerol.
Angaben zur Herstellung
after opening, aliquot into smaller quantities and store at -70 °C. Avoid repeating handling and multiple freeze/thaw cycles
Rechtliche Hinweise
PRECISIO is a registered trademark of Merck KGaA, Darmstadt, Germany
Lagerklassenschlüssel
10 - Combustible liquids
WGK
WGK 1
Analysenzertifikate (COA)
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A S Woolf et al.
Pediatric nephrology (Berlin, Germany), 16(2), 177-184 (2001-03-23)
Angiopoietin-1 (Ang-1) is a secreted growth factor which binds to and activates the Tie-2 receptor tyrosine kinase. The factor enhances endothelial cell survival and capillary morphogenesis, and also limits capillary permeability. Ang-2 binds the same receptor but fails to activate
Kevin G Peters et al.
Recent progress in hormone research, 59, 51-71 (2004-01-30)
Abundant data now demonstrate that the growth of new blood vessels, termed angiogenesis, plays both pathological and beneficial roles in human disease. Based on these data, a tremendous effort has been undertaken to understand the molecular mechanisms that drive blood
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