HMGCR anticorps (AA 268-842) (Fluoro647)
Aperçu rapide pour HMGCR anticorps (AA 268-842) (Fluoro647) (ABIN7964865)
Antigène
Voir toutes HMGCR AnticorpsReactivité
Hôte
Clonalité
Conjugué
Application
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Épitope
- AA 268-842
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Fonction
- Anti-HMGCR Antibody Fluoro647 Conjugated
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Réactivité croisée (Details)
- No cross-reactivity with other proteins.
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Purification
- Immunogen affinity purified.
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Immunogène
- E.coli-derived human HMGCR recombinant protein (Position: H268-V842).
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Isotype
- IgG
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Indications d'application
- Flow Cytometry, Optimal dilutions should be determined by end users.
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Restrictions
- For Research Use only
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Format
- Liquid
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Buffer
- Each vial contains 50 % glycerol, 0.9 % NaCl, 0.2 % Na2HPO4, 0.02 % Sodium azide.
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Agent conservateur
- Sodium azide
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Précaution d'utilisation
- This product contains Sodium azide: a POISONOUS AND HAZARDOUS SUBSTANCE which should be handled by trained staff only.
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Stock
- -20 °C
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Stockage commentaire
- At -20°C for one year from date of receipt. Avoid repeated freezing and thawing. Protect from light.
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Date de péremption
- 12 months
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- HMGCR (3-Hydroxy-3-Methylglutaryl-CoA Reductase (HMGCR))
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Autre désignation
- HMGCR
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Sujet
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Background: HMG-CoA reductase is the rate-limiting enzyme for cholesterol synthesis and is regulated via a negative feedback mechanism mediated by sterols and non-sterol metabolites derived from mevalonate, the product of the reaction catalyzed by reductase. Normally in mammalian cells this enzyme is suppressed by cholesterol derived from the internalization and degradation of low density lipoprotein (LDL) via the LDL receptor. Competitive inhibitors of the reductase induce the expression of LDL receptors in the liver, which in turn increases the catabolism of plasma LDL and lowers the plasma concentration of cholesterol, an important determinant of atherosclerosis. Alternatively spliced transcript variants encoding different isoforms have been found for this gene.
Gene Full Name: 3-hydroxy-3-methylglutaryl-CoA reductase
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ID gène
- 3156
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UniProt
- P04035
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Pathways
- AMPK Signaling, Negative Regulation of Hormone Secretion, Regulation of Lipid Metabolism by PPARalpha
Antigène
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