Product Name	ALAD
Chinese Name	δ氨基乙酰丙酸脱水酶抗体
Alias	ALAD; ALADH; ALADR; Aminolevulinate dehydratase; Aminolevulinate, delta, dehydratase; Delta aminolevulinic acid dehydratase; Delta-aminolevulinic acid dehydratase; HEM2_HUMAN; Lv; PBGS; Porphobilinogen synthase.
Research Area	Cardiovascular  Cell biology
Immunogen Species	Rabbit
Clonality	Polyclonal
React Species	Mouse,  (predicted: Human, Rat, Dog, Cow, Horse, Rabbit, Sheep, )
Applications	WB=1:500-2000 ELISA=1:5000-10000 IHC-P=1:100-500 IHC-F=1:100-500 IF=1:100-500 （Paraffin sections need antigen repair） not yet tested in other applications. optimal dilutions/concentrations should be determined by the end user.
Theoretical molecular weight	36kDa
Cellular localization	The nucleus cytoplasmic Extracellular matrix Secretory protein
Form	Liquid
Concentration	1mg/ml
immunogen	KLH conjugated synthetic peptide derived from human ALAD: 151-240/330
Lsotype	IgG
Purification	affinity purified by Protein A
Buffer Solution	0.01M TBS(pH7.4) with 1% BSA, 0.03% Proclin300 and 50% Glycerol.
Storage	Shipped at 4℃. Store at -20 °C for one year. Avoid repeated freeze/thaw cycles.
Attention	This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications.
PubMed	PubMed
Product Detail	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. Involvement in disease:Defects in ALAD are the cause of acute hepatic porphyria (AHP). AHP is 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. Function: 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. Subunit: Homooctamer; active form. Homohexamer; low activity form. DISEASE: Defects in ALAD are the cause of acute hepatic porphyria (AHEPP) [MIM:612740]. 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. Similarity: Belongs to the ALADH family. SWISS: P13716 Gene ID: 210 Database links: Entrez Gene: 210 Human Entrez Gene: 17025 Mouse Omim: 125270 Human SwissProt: P13716 Human SwissProt: P10518 Mouse Unigene: 1227 Human Unigene: 6988 Mouse
Product Picture	Sample: Liver (Mouse) Lysate at 40 ug Primary: Anti-ALAD (SL7954R) at 1/1000 dilution Secondary: IRDye800CW Goat Anti-Rabbit IgG at 1/20000 dilution Predicted band size: 36 kD Observed band size: 36 kD

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