SPAK (STK39) Antibody (C-term) Blocking peptide
Synthetic peptide
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
Primary Accession | Q9UEW8 |
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Clone Names | 70319128 |
Peptide ID | 70319128 |
Gene ID | 27347 |
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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 AP1448b was selected from the C-term region of human STK39. 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. |
Name | STK39 |
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Synonyms | SPAK |
Function | May act as a mediator of stress-activated signals. Mediates the inhibiton of SLC4A4, SLC26A6 as well as CFTR activities by the WNK scaffolds, probably through phosphorylation. |
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.
Background
STK39 is a serine/threonine kinase that is thought to function in the cellular stress response pathway. The kinase is activated in response to hypotonic stress, leading to phosphorylation of several cation-chloride-coupled cotransporters. The catalytically active kinase specifically activates the p38 MAP kinase pathway, and its interaction with p38 decreases upon cellular stress, suggesting that this kinase may serve as an intermediate in the response to cellular stress.
References
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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