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PHLDA2 Antibody (monoclonal) (M01)
Mouse monoclonal antibody raised against a partial recombinant PHLDA2.
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
Application 
| WB, E |
|---|---|
| Primary Accession | Q53GA4 |
| Other Accession | NM_003311 |
| Reactivity | Human |
| Host | mouse |
| Clonality | Monoclonal |
| Isotype | IgG2a Kappa |
| Clone Names | 5E4 |
| Calculated MW | 17092 Da |
| Gene ID | 7262 |
|---|---|
| Other Names | Pleckstrin homology-like domain family A member 2, Beckwith-Wiedemann syndrome chromosomal region 1 candidate gene C protein, Imprinted in placenta and liver protein, Tumor-suppressing STF cDNA 3 protein, Tumor-suppressing subchromosomal transferable fragment candidate gene 3 protein, p17-Beckwith-Wiedemann region 1 C, p17-BWR1C, PHLDA2, BWR1C, HLDA2, IPL, TSSC3 |
| Target/Specificity | PHLDA2 (NP_003302, 1 a.a. ~ 110 a.a) partial recombinant protein with GST tag. MW of the GST tag alone is 26 KDa. |
| Dilution | WB~~1:500~1000 |
| Format | Clear, colorless solution in phosphate buffered saline, pH 7.2 . |
| Storage | Store at -20°C or lower. Aliquot to avoid repeated freezing and thawing. |
| Precautions | PHLDA2 Antibody (monoclonal) (M01) is for research use only and not for use in diagnostic or therapeutic procedures. |
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Provided below are standard protocols that you may find useful for product applications.
Background
This gene is one of several genes in the imprinted gene domain of 11p15.5 which is considered to be an important tumor suppressor gene region. Alterations in this region may be associated with the Beckwith-Wiedemann syndrome, Wilms tumor, rhabdomyosarcoma, adrenocortical carcinoma, and lung, ovarian, and breast cancer. Studies of the mouse gene, however, which is also located in an imprinted gene domain, have shown that the product of this gene regulates placental growth.
References
1.Characterisation of marsupial PHLDA2 reveals eutherian specific acquisition of imprinting.Suzuki S, Shaw G, Kaneko-Ishino T, Ishino F, Renfree MB.BMC Evol Biol. 2011 Aug 19;11:244.
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