Aminolevulinate Delta Synthase 1 (ALAS1) Antibody
260€ (50 µl)
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Name
Aminolevulinate Delta Synthase 1 (ALAS1) Antibody
Category
Primary Antibodies
Provider
Abbexa
Reference
abx213700
Tested Applications
ELISA, IHC
Description
ALAS1 Antibody is a Rabbit Polyclonal against ALAS1.
Documentos del producto
Instrucciones
Data sheet
Especificaciones del producto
| Category | Primary Antibodies |
| Immunogen Target | Target: Aminolevulinate Delta Synthase 1 (ALAS1) Immunogen: Fusion protein of human ALAS1. |
| Host | Rabbit |
| Reactivity | Human, Mouse, Rat |
| Recommended Dilution | ELISA: 1/1000 - 1/2000, IHC: 1/15 - 1/50. Optimal dilutions/concentrations should be determined by the end user. |
| Clonality | Polyclonal |
| Conjugation | Unconjugated |
| Isotype | IgG |
| Purification | Antigen Affinity Chromatography. |
| Size 1 | 50 µl |
| Size 2 | 100 µl |
| Form | Liquid |
| Tested Applications | ELISA, IHC |
| Buffer | PBS, pH 7.4, containing 0.05% NaN3 and 40% Glycerol. |
| Availability | Shipped within 5-10 working days. |
| Storage | Aliquot and store at -20°C. Avoid repeated freeze/thaw cycles. |
| Dry Ice | No |
| UniProt ID | P13196 |
| Gene ID | 211 |
| Alias | ALAS1,ALAS3,ALASH,Delta-ALA synthase 1 |
| Background | Antibody anti-ALAS1 |
| Status | RUO |
| Note | THIS PRODUCT IS FOR RESEARCH USE ONLY. NOT FOR USE IN DIAGNOSTIC, THERAPEUTIC OR COSMETIC PROCEDURES. NOT FOR HUMAN OR ANIMAL CONSUMPTION. |
Background
5-Aminolevulinate Synthase 1 (ALAS1) is the ubiquitously expressed, non-specific isoform of the enzyme catalyzing the first and rate-limiting step of heme biosynthesis. ALAS1 converts glycine and succinyl-CoA into 5-aminolevulinic acid (ALA) within mitochondria, a critical precursor in the heme production pathway. Its expression and activity are tightly regulated by intracellular heme levels, reflecting its central role in maintaining heme homeostasis. ALAS1 is induced in response to increased demand for cytochromes in liver cells, particularly during drug metabolism and detoxification processes mediated by cytochrome P450 enzymes. Dysregulation of ALAS1 can lead to disorders such as acute intermittent porphyria (AIP), characterized by the accumulation of toxic heme precursors, resulting in neurovisceral symptoms. Therapeutic modulation of ALAS1 activity, including heme supplementation or small-molecule inhibitors, is a key strategy in managing porphyric crises and related metabolic dysfunctions.
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