ELISA/assay

Horse Aminolevulinate Delta Dehydratase ELISA Kit

MBS034879

48-Strip-Wells

470 USD

ELISA Kit

Horse Aminolevulinate Delta Dehydratase ELISA Kit

[Aminolevulinate Delta Dehydratase]

[aminolevulinate, delta-, dehydratase, isoform CRA_a; Delta-aminolevulinic acid dehydratase; delta-aminolevulinic acid dehydratase; porphobilinogen synthase; aminolevulinate, delta-, dehydratase; aminolevulinate dehydratase; Porphobilinogen synthase]

[ALAD]

[ALAD; ALAD; PBGS; ALADH; ALADH]

HEM2_HUMAN

Horse

No significant cross-reactivity or interference between this analyte and analogues is observed.

Store all reagents at 2-8 degree C

Assay Type: Quantitative Sandwich. Detection Range: 0.625 ng/ml - 20 ng/ml. Sensitivity: 0.1 ng/ml

Intra-assay Precision: Intra-assay CV (%) is less than 15%. Inter-assay Precision: Inter-assay CV (%) is less than 15%. [CV(%) = SD/mean ×100].

Background: This Quantitative Sandwich ELISA kit is only for in vitro research use only, not for drug, household, therapeutic or diagnostic applications! This kit is intended to be used for determination the level of ALAD (hereafter termed "analyte") in undiluted original Horse body fluids, tissue homogenates, secretions or feces samples. This kit is NOT suitable for assaying non-biological sources of substances.

119607786

EAW87380.1

P13716

36,295 Da

Heme Biosynthesis Pathway (198818); Heme Biosynthesis Pathway (106326); Metabolism Pathway (477135); Metabolism Of Porphyrins Pathway (106325); Porphyrin And Chlorophyll Metabolism Pathway (83021); Porphyrin And Chlorophyll Metabolism Pathway (407); Superpathway Of Heme Biosynthesis From Glycine (545289); Tetrapyrrole Biosynthesis II (from Glycine) Pathway (142231)

The ALAD enzyme is composed of 8 identical subunits and catalyzes the condensation of 2 molecules of delta-aminolevulinate to form porphobilinogen (a precursor of heme, cytochromes and other hemoproteins). ALAD catalyzes the second step in the porphyrin and heme biosynthetic pathway; zinc is essential for enzymatic activity. ALAD enzymatic activity is inhibited by lead and a defect in the ALAD structural gene can cause increased sensitivity to lead poisoning and acute hepatic porphyria. [provided by RefSeq, Jul 2008]

ALAD: Catalyzes an early step in the biosynthesis of tetrapyrroles. Binds two molecules of 5-aminolevulinate per subunit, each at a distinct site, and catalyzes their condensation to form porphobilinogen. Defects in ALAD are the cause of acute hepatic porphyria (AHEPP). A form of porphyria. Porphyrias are inherited defects in the biosynthesis of heme, resulting in the accumulation and increased excretion of porphyrins or porphyrin precursors. They are classified as erythropoietic or hepatic, depending on whether the enzyme deficiency occurs in red blood cells or in the liver. AHP is characterized by attacks of gastrointestinal disturbances, abdominal colic, paralysis, and peripheral neuropathy. Most attacks are precipitated by drugs, alcohol, caloric deprivation, infections, or endocrine factors. Belongs to the ALADH family. 2 isoforms of the human protein are produced by alternative splicing. Protein type: Cofactor and Vitamin Metabolism - porphyrin and chlorophyll; EC 4.2.1.24; Lyase. Chromosomal Location of Human Ortholog: 9q33.1. Cellular Component: cytosol; nucleus. Molecular Function: identical protein binding; porphobilinogen synthase activity; zinc ion binding; lead ion binding; catalytic activity. Biological Process: porphyrin metabolic process; protoporphyrinogen IX biosynthetic process; protein homooligomerization; heme biosynthetic process. Disease: Porphyria, Acute Hepatic

48-Strip-Wells

470 USD

96-Strip-Wells

680

5x96-Strip-Wells

3100

10x96-Strip-Wells

6095