Vergleich

Anti-CPT1B Rabbit mAb

ArtNr PTM-7069
Hersteller PTM Biolabs
Menge 100 ul
Format Lyophilized powder
Applikationen WB, IHC-P
Clon JRMR-10677-25
Specific against Human (Homo sapiens)
Host Rabbit
Isotype IgG
Konjugat/Tag Unconjugated
Alias CPT1-M, KIAA1670, CPT I
Versandbedingung Raumtemperatur
Lieferbar
Manufacturer - Type
Primary Antibodies
Manufacturer - Category
Uncategorized
Manufacturer - Targets
CPT1B
Shipping Temperature
Ambient temperature
Storage Conditions
Store at -20°C. Avoid freeze/thaw cycles.
Manufacturer - Research Area
Signal Transduction, Cardiovascular Biology, Cancer, Metabolism
Product description
Carnitine palmitoyltransferase-1 (CPT1), localized to the mitochondrial outer membrane, translocates fatty acids across the mitochondrial membranes and catalyzes the rate-limiting step of β-oxidation. There are three isoforms of this enzyme: CPT1A (liver), CPT1B (muscle), and CPT1C (brain). Deficiency of CPT1A results in an autosomal recessive mitochondrial fatty acid oxidation disorder. Studies have shown that physiological high blood glucose and insulin levels inhibit CPT1B activity in human muscle and therefore divert long-chain fatty acids toward storage in human muscle as triglycerides. Furthermore, mice deficient in CPT1C show less food intake and reduced body weight. These findings suggest that CPT1 may play a role in metabolic syndromes.
Purification Method
Protein A purified
Constituents
PBS, Glycerol, BSA
PTM
Unmodified
Clonality
Recombinant Monoclonal
Stability
Stable for 12 months from date of receipt/reconstitution.
Background
Carnitine palmitoyltransferase-1 (CPT1), localized to the mitochondrial outer membrane, translocates fatty acids across the mitochondrial membranes and catalyzes the rate-limiting step of β-oxidation. There are three isoforms of this enzyme: CPT1A (liver), CPT1B (muscle), and CPT1C (brain). Deficiency of CPT1A results in an autosomal recessive mitochondrial fatty acid oxidation disorder. Studies have shown that physiological high blood glucose and insulin levels inhibit CPT1B activity in human muscle and therefore divert long-chain fatty acids toward storage in human muscle as triglycerides. Furthermore, mice deficient in CPT1C show less food intake and reduced body weight. These findings suggest that CPT1 may play a role in metabolic syndromes.
Cellular Localization
Mitochondrion outer membrane

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Alle Produkte sind nur für Forschungszwecke bestimmt. Nicht für den menschlichen, tierärztlichen oder therapeutischen Gebrauch.

Menge: 100 ul
Lieferbar: In stock
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