Mouse TIE-2 Fc Chimera (TIE-2 Fc) Protein

Este producto es parte de TEK - TEK receptor tyrosine kinase
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234€ (2 µg)

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935106861
info@markelab.com
name
Mouse TIE-2 Fc Chimera (TIE-2 Fc) Protein
category
Proteins and Peptides
provider
Abbexa
reference
abx073610
tested applications
SDS-PAGE

Description

TIE-2 Fc Chimera Protein is a recombinant protein kinases.

Documents del producto

Instrucciones
Data sheet
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Product specifications

CategoryProteins and Peptides
Immunogen TargetTIE-2 Fc Chimera (TIE-2 Fc)
HostHamster
Recommended DilutionOptimal dilutions/concentrations should be determined by the end user.
OriginMouse
ExpressionRecombinant
Purity> 90% (SDS-PAGE)
Size 12 µg
Size 210 µg
Size 31 mg
FormLyophilized
Tested ApplicationsSDS-PAGE
AvailabilityShipped within 5-10 working days.
Dry IceNo
UniProt IDQ02858
AliasAngiopoietin-1 receptor,Endothelial tyrosine kinase,TIE2,VMCM,GLC3E,TIE-2,VMCM1,CD202B,Tyrosine-protein kinase receptor TEK,Tunica interna endothelial cell kinase
BackgroundProtein TEK
StatusRUO
NoteThis product is for research use only. Not for human consumption, cosmetic, therapeutic or diagnostic use.

Descripción

TEK, also known as TEK receptor tyrosine kinase (also termed Tie2 in some literature), is a receptor tyrosine kinase (RTK) with significant roles in vascular development, maintenance, and angiogenesis. Receptor tyrosine kinases are a class of cell surface receptors that, upon ligand binding, activate intracellular signaling cascades through phosphorylation. Specifically, the TEK/Tie2 receptor is primarily expressed in endothelial cells, which line blood vessels, as well as in certain subsets of hematopoietic cells. Its ligand, angiopoietin, specifically angiopoietins-1 and -2 (ANGPT1 and ANGPT2), modulates TEK signaling and plays essential roles in vessel stabilization, endothelial survival, and inflammatory responses. TEK signaling plays an essential role in regulating vascular quiescence and homeostasis. In developing and mature vasculature, TEK helps balance angiogenesis, where new blood vessels form from existing ones, with vascular stability and permeability. This function makes TEK a crucial player in several physiological and pathological processes, from wound healing to cancer and other angiogenesis-dependent diseases. Dysfunctional TEK signaling has been implicated in a range of vascular and inflammatory diseases, including tumor angiogenesis, diabetic retinopathy, and sepsis.

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