Rat Aminolevulinate Delta Synthase 1 (ALAS1) Protein

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Description
Rat Aminolevulinate Delta Synthase 1 (ALAS1) Protein is a Recombinant Rat protein expressed in E. coli.
Documents del producto
Product specifications
Category | Proteins and Peptides |
Immunogen Target | Aminolevulinate Delta Synthase 1 (ALAS1) |
Host | E. coli |
Origin | Rat |
Conjugation | Unconjugated |
Observed MW | Molecular Weight: Calculated MW: 62 kDa Observed MW (SDS-PAGE): 62 kDa Concentration: Prior to lyophilization: 200 µg/ml Sequence Fragment: Lys355-Ala642 Tag: N-terminal His tag and GST tag |
Expression | Recombinant |
Purity | > 90% |
Size 1 | 1 mg |
Size 2 | 5 mg |
Form | Lyophilized To keep the original salt concentration, we recommend reconstituting to the original concentration prior to lyophilization (see Concentration) in ddH2O. If a lower concentration is required, dilute in PBS, pH 7.4. If a higher concentration is required, the product can be reconstituted directly in PBS, pH 7.4, though please note that this will change the overall salt concentration. The stock concentration should be between 0.1-1.0 mg/ml. Do not vortex. |
Tested Applications | WB, SDS-PAGE |
Buffer | Prior to lyophilization: PBS, pH 7.4, containing 0.01% Sarcosyl, 1 mM DTT, 5% Trehalose and Proclin-300. |
Availability | Shipped within 1-2 months. |
Storage | Store at 2-8 °C for up to one month. Store at -80 °C for up to one year. Avoid repeated freeze/thaw cycles. |
Dry Ice | No |
Alias | ALAS1,ALAS3,ALASH,Delta-ALA synthase 1 |
Background | Protein ALAS1 |
Status | RUO |
Note | This product is for research use only. Not for human consumption, cosmetic, therapeutic or diagnostic use. |
Descripción
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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