Polyclonal Anti-ALOX5

Rabbit IgG polyclonal antibody for Arachidonate 5-lipoxygenase (ALOX5) detection. Tested with WB, IHC-P in Human. \n\n

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SPECIFICATIONS

Price

200.00 USD

Catalog Number

PA1644

Size

100ug/vial

Applications

IHC, WB

Reactivities

Hum

Form

Lyophilized

Format

Each vial contains 5mg BSA, 0.9mg NaCl, 0.2mg Na2HPO4, 0.05mg Thimerosal, 0.05mg NaN3.

Gene Id

ALOX5

References

1. Aliberti, J., Serhan, C., Sher, A. Parasite-induced lipoxin A4 is an endogenous regulator of IL-12 production and immunopathology in Toxoplasma gondii infection. J. Exp. Med. 196: 1253-1262, 2002.\n2. Bafica, A., Scanga, C. A., Serhan, C., Machado, F., White, S., Sher, A., Aliberti, J. Host control of Mycobacterium tuberculosis is regulated by 5-lipoxygenase-dependent lipoxin production. J. Clin. Invest. 115: 1601-1606, 2005.\n3. Funk CD, Hoshiko S, Matsumoto T, Rdmark O, Samuelsson B (April 1989). \"Characterization of the human 5-lipoxygenase gene\". Proc. Natl. Acad. Sci. U.S.A. 86 (8): 2587

Swiss Prot

P09917

Storage Temp

At -20 degree C for one year. After reconstitution, at 4 degree C for one month. It can also be aliquotted and stored frozen at -20 degree C for a longer time.Avoid repeated freezing and thawing.

Additional Info

A synthetic peptide corresponding to a sequence at the C-terminal of human ALOX5, different from the related rat and mouse sequences by two amino acids.

Scientific Background

ALOX5(ARACHIDONATE 5-LIPOXYGENASE), also known as LOG5 or 5-LO(5-LIPOXYGENASE), is an enzyme that in humans is encoded by the ALOX5 gene. ALOX5 is a member of the lipoxygenase family of enzymes which also transforms EFAs into leukotrienes and is a current target for pharmaceutical intervention in a number of diseases. The enzyme 5-lipoxygenase catalyzes 2 reactions in the formation of leukotrienes. The ALOX5 gene is mapped to chromosome 10q11.21 based on an alignment of the ALOX5 sequence with the genomic sequence. Human 5-LO contains 3 nuclear localization sequences (NLSs) and a phosphorylation site involved in nuclear localization. Compared with age-matched 5-LO competent mice, the 5-LO knockout mice developed less right heart hypertrophy. Pharmacologic inhibition or ALOX5 gene disruption resulted in a significant decrease of beta-amyloid production and gamma-secretase levels. ALOX5 activity is short-lived, apparently in part because of an intrinsic instability of the enzyme.