TEK antibody (C-Term)

Catalog No. ABIN6242223

The Rabbit Polyclonal anti-TEK antibody has been validated for WB. It is suitable to detect TEK in samples from Mouse.

Quick Overview for TEK antibody (C-Term) (ABIN6242223)

Target: TEK (TEK Tyrosine Kinase, Endothelial (TEK))

Reactivity: Mouse

Host: Rabbit

Clonality: Polyclonal

Conjugate: This TEK antibody is un-conjugated

Application: Western Blotting (WB)

Clone: RB50277

Product Details anti-TEK Antibody

Binding Specificity: AA 782-815, C-Term

Purification: This antibody is purified through a protein A column, followed by peptide affinity purification.

Immunogen: This Mouse Tek antibody is generated from a rabbit immunized with a KLH conjugated synthetic peptide between782-815 amino acids from the C-terminal region of Mouse Tek.

Isotype: Ig Fraction

Application Details

Application Notes: WB: 1:2000

Restrictions: For Research Use only

Handling

Format: Liquid

Buffer: Purified polyclonal antibody supplied in PBS with 0.09 % (W/V) sodium azide.

Preservative: Sodium azide

Precaution of Use: This product contains Sodium azide: a POISONOUS AND HAZARDOUS SUBSTANCE which should be handled by trained staff only.

Storage: 4 °C,-20 °C

Expiry Date: 6 months

Target Details for TEK

Target: TEK (TEK Tyrosine Kinase, Endothelial (TEK))

Alternative Name: Tek

Background: Tyrosine-protein kinase that acts as cell-surface receptor for ANGPT1, ANGPT2 and ANGPT4 and regulates angiogenesis, endothelial cell survival, proliferation, migration, adhesion and cell spreading, reorganization of the actin cytoskeleton, but also maintenance of vascular quiescence. Has anti-inflammatory effects by preventing the leakage of proinflammatory plasma proteins and leukocytes from blood vessels. Required for normal angiogenesis and heart development during embryogenesis. Required for post- natal hematopoiesis. After birth, activates or inhibits angiogenesis, depending on the context. Inhibits angiogenesis and promotes vascular stability in quiescent vessels, where endothelial cells have tight contacts. In quiescent vessels, ANGPT1 oligomers recruit TEK to cell-cell contacts, forming complexes with TEK molecules from adjoining cells, and this leads to preferential activation of phosphatidylinositol 3-kinase and the AKT1 signaling cascades. In migrating endothelial cells that lack cell-cell adhesions, ANGT1 recruits TEK to contacts with the extracellular matrix, leading to the formation of focal adhesion complexes, activation of PTK2/FAK and of the downstream kinases MAPK1/ERK2 and MAPK3/ERK1, and ultimately to the stimulation of sprouting angiogenesis. ANGPT1 signaling triggers receptor dimerization and autophosphorylation at specific tyrosine residues that then serve as binding sites for scaffold proteins and effectors. Signaling is modulated by ANGPT2 that has lower affinity for TEK, can promote TEK autophosphorylation in the absence of ANGPT1, but inhibits ANGPT1-mediated signaling by competing for the same binding site. Signaling is also modulated by formation of heterodimers with TIE1, and by proteolytic processing that gives rise to a soluble TEK extracellular domain. The soluble extracellular domain modulates signaling by functioning as decoy receptor for angiopoietins. TEK phosphorylates DOK2, GRB7, GRB14, PIK3R1, SHC1 and TIE1.

Molecular Weight: 125701

UniProt: Q02858

Pathways: RTK Signaling, Growth Factor Binding