免疫原
synthetic peptide corresponding to amino acids 366-380 of human FAH
应用
Anti-FAH (366-380) antibody is suitable for western blot at a dilution of 1:500-1:2,000.
Yale Center for High Throughput Cell Biology IF-tested antibodies. Each antibody is tested by immunofluorescence against HUVEC cells using the Yale HTCB IF protocol. To learn more about us and Yale Center for High Throughput Cell Biology partnership, visit sigma.com/htcb-if.
Yale Center for High Throughput Cell Biology IF-tested antibodies. Each antibody is tested by immunofluorescence against HUVEC cells using the Yale HTCB IF protocol. To learn more about us and Yale Center for High Throughput Cell Biology partnership, visit sigma.com/htcb-if.
生化/生理作用
FAH is the terminal enzyme in the tyrosine catabolism pathway. It is mainly expressed in the liver and kidney. Deficiency in FAH results Type 1 hereditary tyrosinemia (HT), an autosomal recessive disorder.
外形
Solution in 0.01 M phosphate buffered saline, pH 7.4, containing 15 mM sodium azide
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储存分类代码
12 - Non Combustible Liquids
WGK
WGK 2
闪点(°F)
Not applicable
闪点(°C)
Not applicable
个人防护装备
Eyeshields, Gloves, multi-purpose combination respirator cartridge (US)
法规信息
新产品
此项目有
Y Labelle et al.
Biochimica et biophysica acta, 1180(3), 250-256 (1993-01-22)
Fumarylacetoacetate hydrolase (FAH) is the terminal enzyme in the catabolic pathway of tyrosine. This enzyme which is mainly expressed in the liver and kidney is deficient in hereditary tyrosinemia type 1. As some affected individuals present neurologic abnormalities, we studied
Y Labelle et al.
Human molecular genetics, 2(7), 941-946 (1993-07-01)
Hereditary tyrosinemia type 1 is an autosomal recessive disease caused by a deficiency of the last enzyme in the catabolic pathway of tyrosine, fumarylacetoacetate hydrolase (FAH). To analyze the mutations involved in this disease, and as a first step towards
Faiqa Imtiaz et al.
Molecular genetics and metabolism, 104(4), 688-690 (2011-07-19)
Hereditary Tyrosinemia Type 1 (HT1) is an autosomal recessive disorder resulting from a deficiency of fumarylacetoacetase caused by mutations in the fumarylacetoacetate hydrolase (FAH) gene. We detected 11 novel and 6 previously described pathogenic mutations in a cohort of 43
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