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AB3796

Sigma-Aldrich

Anti-5′-Lipoxygenase Antibody

Chemicon®, from rabbit

Synonym(s):

Arachidonate 5-lipoxygenase, 5-LO

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About This Item

UNSPSC Code:
12352203
eCl@ss:
32160702
NACRES:
NA.41

biological source

rabbit

Quality Level

100

antibody form

purified immunoglobulin

antibody product type

primary antibodies

clone

polyclonal

species reactivity

rabbit, rat, mouse, human

manufacturer/tradename

Chemicon®

technique(s)

ELISA: suitable
immunoprecipitation (IP): suitable
western blot: suitable

NCBI accession no.

NM_000698.2

UniProt accession no.

P09917

shipped in

dry ice

target post-translational modification

unmodified

Gene Information

human ... ALOX5(240)

General description

5′-Lipoxygenase is a critical enzyme in the formation of leukotrienes from arachidonic acid. Upon activation, the enzyme translocates to either a nuclear or plasma membrane compartment.

Specificity

5′-Lipoxygenase

Immunogen

Purified human 5′-Lipoxygenase

Application

Anti-5′-Lipoxygenase Antibody detects level of 5′-Lipoxygenase & has been published & validated for use in ELISA, IP & WB.
Western blot: 1:1,000. Reacts with a 79 kDa band
Immunoprecipitation: 5 μL/mL lysate
ELISA: 1:1000 – 1:100,000
Optimal working dilutions must be determined by the end user.

Physical form

Format: Purified
Purified immunoglobulin in PBS with 50% Glycerol and 0.02% sodium azide

Analysis Note

Control
POSITIVE CONTROL: placenta, lung, and leukocytes.

Other Notes

Concentration: Please refer to the Certificate of Analysis for the lot-specific concentration.

Legal Information

CHEMICON is a registered trademark of Merck KGaA, Darmstadt, Germany

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Storage Class

10 - Combustible liquids

wgk_germany

WGK 2

Certificates of Analysis (COA)

Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.

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Daryle J DePianto et al.
JCI insight, 6(8) (2021-03-12)
Compromised regenerative capacity of lung epithelial cells can lead to cellular senescence, which may precipitate fibrosis. While increased markers of senescence have been reported in idiopathic pulmonary fibrosis (IPF), the origin and identity of these senescent cells remain unclear, and
Anna M Adamusiak et al.
International archives of allergy and immunology, 157(4), 354-362 (2011-11-30)
The pathogenesis of rhinosinusitis in aspirin-exacerbated airway disease is closely linked to the disequilibrium in arachidonic acid metabolism. Although considerable amounts of data concerning impaired eicosanoid production are available, the precise mechanism and pathogenesis of the disease are still unknown.
Fen Yin et al.
Arteriosclerosis, thrombosis, and vascular biology, 33(6), 1153-1161 (2013-04-06)
To evaluate whether exposure to air pollutants induces oxidative modifications of plasma lipoproteins, resulting in alteration of the protective capacities of high-density lipoproteins (HDLs). We exposed apolipoprotein E-deficient mice to diesel exhaust (DE) at ≈ 250 µg/m(3) for 2 weeks

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