research use only

ME2 Antibody [B19K5]

Cat.No.: F3618

    Application: Reactivity:
    • F3618-wb
      Lane 1: Jurkat, Lane 2: K562, Lane 3: HL60, Lane 4: 293T

    Usage Information

    Dilution
    1:1000-1:10000
    1:50-1:100
    1:100
    Application
    WB, IHC, IF, FCM
    Reactivity
    Human
    Source
    Rabbit Monoclonal Antibody
    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
    65 kDa

    Datasheet & SDS

    Biological Description

    Specificity
    ME2 Antibody [B19K5] detects endogenous levels of total ME2 protein.
    Clone
    B19K5
    Synonym(s)
    NAD-ME; Malic enzyme 2; ME2
    Background
    Mitochondrial malic enzyme 2 (ME2) is a NAD(P)‑dependent dehydrogenase that belongs to the mitochondrial malic enzyme family and is expressed in tissues with high metabolic demand, such as the liver, skeletal muscle, and pancreatic islets. It localizes to the mitochondrial matrix, where it catalyzes the oxidative decarboxylation of malate to pyruvate, generating NAD(P)H and CO₂ and thereby linking the tricarboxylic acid cycle to cytosolic pathways that depend on reducing equivalents. ME2 activity is regulated by key metabolites, including activation by fumarate and inhibition by ATP, which couples its catalytic output to the energetic state of the cell and ensures that NAD(P)H production aligns with mitochondrial capacity and substrate availability. Through the malate‑aspartate shuttle and related metabolite exchanges, ME2 participates in the transfer of reducing equivalents between the cytosol and mitochondria, supporting respiration, ATP synthesis, and the maintenance of redox balance. ME2 also contributes to glucose‑induced insulin secretion by modulating the flux of carbon intermediates and redox cofactors that influence the mitochondrial ATP/ADP ratio and downstream signaling to exocytosis. ME2‑mediated NADPH generation can also impact biosynthetic pathways and redox‑sensitive processes, including aspects of lipid metabolism and stress‑response signaling, which has led to its implication in metabolic dysregulation associated with diabetes and related metabolic disorders.
    References
    • https://pubmed.ncbi.nlm.nih.gov/35435229/
    • https://pubmed.ncbi.nlm.nih.gov/19691144/

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