Cet anticorps anti-HMOX1 Monoclonal Souris (Clone 1F12-A6) (ABIN453936) détecte spécifiquement HMOX1 dans WB, IP, IF, IHC (fro) et EIA.
L’anticorps est réactif avec des échantillons de Humain, Souris et Boeuf (Vache).
HMOX1
Reactivité: Humain
WB, IHC, IP, ELISA, ICC, IF
Hôte: Souris
Monoclonal
1F12-A6
PE
Indications d'application
Western blot: 1: 500 - 1000. Immunohistochemistry on frozen sections. Immunoprecipitation.
Restrictions
For Research Use only
Concentration
1.0 mg/mL
Buffer
PBS pH 7.4, 0.09 % Sodium Azide, 50 % Glycerol
Agent conservateur
Sodium azide
Précaution d'utilisation
This product contains sodium azide: a POISONOUS AND HAZARDOUS SUBSTANCE which should be handled by trained staff only.
Stock
4 °C/-20 °C
Stockage commentaire
Store at 2 - 8 °C for up to one month or (in aliquots) at -20 °C. Avoid repeated freezing andthawing. Shelf life: one year from despatch.
Date de péremption
12 months
Antigène
HMOX1
(Heme Oxygenase (Decycling) 1 (HMOX1))
Autre désignation
Heme Oxygenase 1 / HMOX1
Sujet
Heme-oxygenase is a ubiquitous enzyme that catalyzes the initial and rate-limiting steps in heme catabolism yielding equimolar amounts of biliverdin, iron and carbon monoxide. Biliverdin is subsequently converted to bilirubin and the free iron is sequestered to ferritin (1). These products have important physiological effects as carbon monoxide is a potent vasodilator, biliverdin and bilirubin are potent antioxidants, and the free iron increases oxidative stress and regulates the expression of many mRNAs (2). There are three isoforms of heme-oxygenase, HO-1, HO-2 and HO-3, however HO-1 and HO-2 are the major isoforms as they both have been identified in mammals (3). HO-1, also known as heat shock protein 32, is an inducible isoform activated by most oxidative stress inducers, cytokines, inflammatory agents and heat shock. HO-2 is a constitutive isoform which is expressed under homeostatic conditions. HO-1 is also considered to be a cytoprotective factor in that free heme is highly reactive and cytotoxic, and secondly, carbon monoxide is a mediator inhibiting the inflammatory process and bilirubin is a scavenger for reactive oxygen, both of which are the end products of heme catalyzation (4). It has also been shown that HO-1 deficiency may cause reduced stress defense, a pro-inflammatory tendency (5), susceptibility to atherosclerotic lesion formation (6), endothelial cell injury, and growth retardation (7). Upregulation of HO-1 is therefore said to be one of the major defense mechanisms of oxidative stress (4).Synonyms: HO, HO-1, HO1