GPD1L Antibody (N-term)
Affinity Purified Rabbit Polyclonal Antibody (Pab)
- SPECIFICATION
- CITATIONS: 1
- PROTOCOLS
- BACKGROUND
Application ![]()
| WB, IHC-P, FC, E |
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Primary Accession | Q8N335 |
Other Accession | Q3ULJ0, NP_055956.1 |
Reactivity | Human, Mouse |
Host | Rabbit |
Clonality | Polyclonal |
Isotype | Rabbit IgG |
Calculated MW | 38419 Da |
Antigen Region | 44-73 aa |
Gene ID | 23171 |
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Other Names | Glycerol-3-phosphate dehydrogenase 1-like protein, GPD1-L, GPD1L, KIAA0089 |
Target/Specificity | This GPD1L antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 44-73 amino acids from the N-terminal region of human GPD1L. |
Dilution | WB~~1:2000 IHC-P~~1:50~100 FC~~1:10~50 |
Format | Purified polyclonal antibody supplied in PBS with 0.09% (W/V) sodium azide. This antibody is purified through a protein A column, followed by peptide affinity purification. |
Storage | Maintain refrigerated at 2-8°C for up to 2 weeks. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles. |
Precautions | GPD1L Antibody (N-term) is for research use only and not for use in diagnostic or therapeutic procedures. |
Name | GPD1L (HGNC:28956) |
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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 |

Provided below are standard protocols that you may find useful for product applications.
Background
The protein encoded by this gene catalyzes the conversion of sn-glycerol 3-phosphate to glycerone phosphate. The encoded protein is found in the cytoplasm, associated with the plasma membrane, where it binds the sodium channel, voltage-gated, type V, alpha subunit (SCN5A). Defects in this gene are a cause of Brugada syndrome 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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