Aldehyde Dehydrogenase 1 Family Member A2 (ALDH1A2) Antibody
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Description
ALDH1A2 Antibody is a Rabbit Polyclonal against ALDH1A2.
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Product specifications
| Category | Primary Antibodies |
| Immunogen Target | Aldehyde Dehydrogenase 1 Family Member A2 (ALDH1A2) |
| Host | Rabbit |
| Reactivity | Human, Mouse, Rat |
| Recommended Dilution | WB: 1/500 - 1/2000, IHC: 1/50 - 1/200. Optimal dilutions/concentrations should be determined by the end user. |
| Clonality | Polyclonal |
| Conjugation | Unconjugated |
| Isotype | IgG |
| Purity | ≥ 95% (SDS-PAGE) |
| Purification | Purified by immunogen affinity chromatography. |
| Size 1 | 100 µg |
| Form | Liquid |
| Tested Applications | ELISA, WB, IHC |
| Buffer | PBS, pH 7.3, with 0.02% sodium azide and 50% glycerol. |
| Availability | Shipped within 5-12 working days. |
| Storage | Aliquot and store at -20°C. Avoid repeated freeze/thaw cycles. |
| Dry Ice | No |
| UniProt ID | O94788 |
| Alias | RALDH 2,RalDH2,Retinaldehyde specific dehydrogenase type 2 |
| Background | Antibody anti-ALDH1A2 |
| Status | RUO |
| Note | Concentration: 2 mg/ml - Validity: 12 months. |
ALDH1A2, like ALDH1A1, catalyzes the conversion of retinaldehyde to retinoic acid, a critical molecule for regulating gene expression during embryonic development and organogenesis. ALDH1A2 is highly expressed during early development, particularly in tissues forming the heart, lungs, and nervous system, where it regulates retinoic acid signaling pathways essential for proper patterning and differentiation. Loss-of-function mutations in ALDH1A2 lead to congenital disorders, including congenital diaphragmatic hernia, cardiac anomalies, and craniofacial defects, due to disrupted retinoic acid gradients during development. In adults, ALDH1A2 plays a role in maintaining tissue homeostasis and regulating inflammatory responses. Its dysregulation has been linked to metabolic disorders, such as obesity and insulin resistance, as well as fibrotic diseases. ALDH1A2 is also studied in cancer biology for its role in tumor growth suppression through retinoic acid-mediated differentiation and cell cycle control.
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