Human 5-aminolevulinate synthase, nonspecific, mitochondrial (ALAS1) ELISA Kit

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Description
Human 5-aminolevulinate synthase, nonspecific, mitochondrial (ALAS1) ELISA Kit is an ELISA Kit for the in vitro quantitative measurement of Human 5-aminolevulinate synthase, nonspecific, mitochondrial (ALAS1) concentrations in tissue homogenates, cell lysates and other biological fluids.
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Product specifications
Category | ELISA Kits |
Immunogen Target | 5-aminolevulinate synthase, nonspecific, mitochondrial (ALAS1) |
Reactivity | Human |
Detection Method | Colorimetric |
Assay Data | Quantitative |
Test Range | 0.156 ng/ml - 10 ng/ml |
Recommended Dilution | Optimal dilutions/concentrations should be determined by the end user. |
Size 1 | 96 tests |
Form | Lyophilized |
Tested Applications | ELISA |
Sample Type | Tissue homogenates, cell lysates and other biological fluids. |
Availability | Shipped within 5-15 working days. The validity for this kit is 6 months. |
Storage | Shipped at 4 °C. Upon receipt, store the kit according to the storage instruction in the kit's manual. |
Dry Ice | No |
UniProt ID | P13196 |
Gene ID | 211 |
OMIM | 125290 |
Alias | ALAS1,ALAS3,ALASH,Delta-ALA synthase 1 |
Background | Elisa kits for ALAS1 |
Status | RUO |
Note | Validity: The validity for this kit is 6 months. This product is for research use only. The range and sensitivity is subject to change. Please contact us for the latest product information. For accurate results, sample concentrations must be diluted to mid-range of the kit. If you require a specific range, please contact us in advance or write your request in your order comments. Please note that our ELISA and CLIA kits are optimised for detection of native samples, rather than recombinant proteins. We are unable to guarantee detection of recombinant proteins, as they may have different sequences or tertiary structures to the native protein. |
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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