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GPD1L Antibody (N-term) Blocking peptide
Synthetic peptide
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
| Primary Accession | Q8N335 |
|---|---|
| Clone Names | 91013045 |
| Gene ID | 23171 |
|---|---|
| Other Names | Glycerol-3-phosphate dehydrogenase 1-like protein, GPD1-L, GPD1L, KIAA0089 |
| Format | Peptides are lyophilized in a solid powder format. Peptides can be reconstituted in solution using the appropriate buffer as needed. |
| 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 | GPD1L (HGNC:28956) |
|---|---|
| Synonyms | KIAA0089 |
| Function | Plays a role in regulating cardiac sodium current; decreased enzymatic activity with resulting increased levels of glycerol 3- phosphate activating the DPD1L-dependent SCN5A phosphorylation pathway, may ultimately lead to decreased sodium current; cardiac sodium current may also be reduced due to alterations of NAD(H) balance induced by DPD1L. |
| Cellular Location | Cytoplasm. Note=Localized to the region of the plasma membrane |
| Tissue Location | Most highly expressed in heart tissue, with lower levels in the skeletal muscle, kidney, lung and other organs |
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Provided below are standard protocols that you may find useful for product applications.
Background
The protein encoded by this gene catalyzes the conversionof sn-glycerol 3-phosphate to glycerone phosphate. The encodedprotein is found in the cytoplasm, associated with the plasmamembrane, where it binds the sodium channel, voltage-gated, type V,alpha subunit (SCN5A). Defects in this gene are a cause of Brugadasyndrome type 2 (BRS2) as well as sudden infant death syndrome(SIDS).
References
Rose, J.E., et al. Mol. Med. 16 (7-8), 247-253 (2010) :Liu, M., et al. Circ. Res. 105(8):737-745(2009)Valdivia, C.R., et al. Am. J. Physiol. Heart Circ. Physiol. 297 (4), H1446-H1452 (2009) :Makiyama, T., et al. Circ. J. 72(10):1705-1706(2008)London, B., et al. Circulation 116(20):2260-2268(2007)
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