Aminolevulinate Delta Synthase 1 (ALAS1) Antibody (HRP)

Este producto es parte de ALAS -5-aminolevulinate synthase erythroid (specific) mitochondrial (erythroid)
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169€ (20 µg)

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935106861
info@markelab.com
name
Aminolevulinate Delta Synthase 1 (ALAS1) Antibody (HRP)
category
Primary Antibodies
provider
Abbexa
reference
abx334497
tested applications
ELISA

Description

ALAS1 Antibody (HRP) is a Rabbit Polyclonal against ALAS1.

Documents del producto

Instrucciones
Data sheet
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Product specifications

CategoryPrimary Antibodies
Immunogen TargetAminolevulinate Delta Synthase 1 (ALAS1)
HostRabbit
ReactivityHuman
Recommended DilutionOptimal dilutions/concentrations should be determined by the end user.
ClonalityPolyclonal
ConjugationHRP
IsotypeIgG
Purity> 95%
PurificationPurified by Protein G.
Size 120 µg
Size 250 µg
Size 3100 µg
Size 4200 µg
Size 51 mg
FormLiquid
Tested ApplicationsELISA
Buffer0.01 M PBS, pH 7.4, 0.03% Proclin-300 and 50% Glycerol.
AvailabilityShipped within 5-10 working days.
StorageAliquot and store at -20°C. Avoid exposure to light. Avoid repeated freeze/thaw cycles.
Dry IceNo
UniProt IDP13196
Gene ID211
AliasALAS1,ALAS3,ALASH,Delta-ALA synthase 1
BackgroundAntibody anti-ALAS1
StatusRUO

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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