|Other Names||STE20/SPS1-related proline-alanine-rich protein kinase, Ste-20-related kinase, DCHT, Serine/threonine-protein kinase 39, STK39, SPAK|
|Target/Specificity||The synthetic peptide sequence used to generate the antibody AP7968c was selected from the Center region of human SPAK . A 10 to 100 fold molar excess to antibody is recommended. Precise conditions should be optimized for a particular assay.|
|Format||The synthetic peptide was lyophilized with 100% acetonitrile and is supplied as a powder. Reconstitute with 0.1 ml deionized water for a final concentration of 1 mg/ml.|
|Storage||Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C.|
|Precautions||This product is for research use only. Not for use in diagnostic or therapeutic procedures.|
|Function||May act as a mediator of stress-activated signals.|
|Cellular Location||Cytoplasm. Nucleus. Note=Nucleus when caspase-cleaved.|
|Tissue Location||Predominantly expressed in brain and pancreas followed by heart, lung, kidney, skeletal muscle, liver, placenta and testis|
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Provided below are standard protocols that you may find useful for product applications.
SPAK is a serine/threonine kinase containing an N-terminal series of proline and alanine repeats (PAPA box), followed by a serine/threonine kinase catalytic domain, a nuclear localization signal, a consensus caspase cleavage recognition motif, and a C-terminal region. Northern blot analysis detects ubiquitous expression, most abundantly in brain and pancreas. SPAK can phosphorylate itself and an exogenous substrate in vitro. SPAK immunoprecipitates from transfected mammalian cells in a complex with another serine/threonine kinase that phosphorylates catalytically inactive SPAK. SPAK activates the p38 MAP kinase pathway in cotransfection assays. Full-length SPAK is expressed in the cytoplasm in transfected cells, while a mutant corresponding to caspase-cleaved STK39 localizes predominantly in the nucleus.
Dowd, B.F., et al., J. Biol. Chem. 278(30):27347-27353 (2003).Johnston, A.M., et al., Oncogene 19(37):4290-4297 (2000).
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