PLEK (pleckstrin; also known as p47) was originally identified as the major PKC substrate in platelets and later is found to be expressed in all cells of the hemopoietic system. Through two pleckstrin homology (PH) domains at its N and C termini, PLEK may interact with various protein and/or lipid ligands and serve as an intracellular adaptor/targeting protein. Predominantly cytosolic in unstimulated cells, PLEK would undergo transient redistribution to phagosomal membrane in response to stimuli. PLEK has been found to be hyperphosphorylated in diabetic mononuclear phagocytes and promote proinflammatory cytokine secretion in diabetes. (10477609, 17579087)
Western Blot:U-937 Cells, 1:500-1:5000; IHC: Human lung cancer Tissue, 1:20-1:200; IP:U-937 Cells, 1:500-1:5000
Type: Primary
Antigen: PLEK
Clonality: Polyclonal
Clone:
Conjugation: Unconjugated
Epitope:
Host: Rabbit
Isotype: IgG
Reactivity: Human, Mouse, Rat