Anti-CPT2 C-terminal Rabbit Antibody [H24H13]

Catalog No.: F2414

    Application: Reactivity:

    Usage Information

    Dilution
    1:1000 - 1:10000
    1:50 - 1:100
    1:50 - 1:100
    Application
    WB, IHC, IF
    Reactivity
    Mouse, Rat, Human
    Source
    Rabbit
    Storage Buffer
    PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3
    Storage (from the date of receipt)
    -20°C (avoid freeze-thaw cycles), 2 years
    Predicted MW Observed MW
    74 kDa 74 kDa, 70 kDa, 67 kDa
    *Why do the predicted and actual molecular weights differ?
    The following reasons may explain differences between the predicted and actual protein molecular weight.
    Positive Control Human fetal kidney tissue; Mouse heart tissue; Mouse kidney tissue; Rat kidney tissue; Rat liver tissue; Human fetal liver tissue; Human fetal kidney tissue; Human liver tissue; Human skeletal muscle tissue; Human liver carcinoma tissue; Mouse kidney tissue; Rat colon tissue; HeLa cell; HAP1 cell; MCF7 cell
    Negative Control

    Datasheet & SDS

    Biological Description

    Specificity
    Anti-CPT2 C-terminal Rabbit Antibody [H24H13] detects endogenous levels of total C-terminal region of CPT2 protein.
    Clone
    H24H13
    Synonym(s)
    CPT1, CPT2, Carnitine palmitoyltransferase II, CPT II
    Background
    Carnitine palmitoyltransferase 2 (CPT2) is a mitochondrial enzyme located in the inner mitochondrial membrane that plays a crucial role in fatty acid metabolism by converting long-chain acylcarnitines to acyl-CoA, facilitating their entry into the β-oxidation pathway for energy production. CPT2 consists of two major domains: the N-terminal domain and the C-terminal domain, each featuring a six-stranded antiparallel β-sheet flanked by α-helices. The C-terminal domain is vital for substrate specificity, enzyme stability, and membrane association. It forms part of the active site where catalysis occurs and contains hydrophobic patches that mediate its interaction with the mitochondrial membrane and the carnitine-acylcarnitine translocase (CACT), enabling efficient substrate channeling. CPT2 acts as a rate-limiting enzyme in the mitochondrial fatty acid oxidation process, with its activity regulated by substrate availability and membrane interactions. Mutations or dysfunction in CPT2, particularly affecting its C-terminal domain, lead to metabolic disorders like CPT2 deficiency, characterized by impaired fatty acid breakdown, muscle weakness, and metabolic crises.
    References
    • https://pubmed.ncbi.nlm.nih.gov/16781677/
    • https://pubmed.ncbi.nlm.nih.gov/19430727/

    Tech Support

    Answers to questions you may have can be found in the inhibitor handling instructions. Topics include how to prepare stock solutions, how to store inhibitors, and issues that need special attention for cell-based assays and animal experiments.

    Handling Instructions

    Tel: +1-832-582-8158 Ext:3
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