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PITRM1 Antibody #24770

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  • WB

    Supporting Data

    REACTIVITY H M
    SENSITIVITY Endogenous
    MW (kDa) 117
    SOURCE Rabbit
    Application Key:
    • WB-Western Blotting 
    Species Cross-Reactivity Key:
    • H-Human 
    • M-Mouse 

    Product Information

    Product Usage Information

    Application Dilution
    Western Blotting 1:1000

    Storage

    Supplied in 10 mM sodium HEPES (pH 7.5), 150 mM NaCl, 100 µg/ml BSA and 50% glycerol. Store at –20°C. Do not aliquot the antibody.

    Protocol

    Specificity / Sensitivity

    PITRM1 Antibody recognizes endogenous levels of total PITRM1 protein.

    Species Reactivity:

    Human, Mouse

    Source / Purification

    Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Leu1021 of human PITRM1 protein. Antibodies are purified by protein A and peptide affinity chromatography.

    Background

    Pitrilysin metalloproteinase 1 (PITRM1 or PreP) is a mitochondria-enriched presequence peptidase that processes the mitochondrial targeting sequence (MTS) of proteins imported across the inner mitochondrial membrane (1). Mitochondria normally function to regulate many cellular processes, such as energy production and apoptosis, and its dysfunction may contribute indirectly or directly to human neurodegenerative diseases like Alzheimer’s disease (AD) (2) and Parkinson’s disease (PD) (3). Interestingly, β-amyloid peptide (Aβ), the pathological hallmark of AD, accumulates in mitochondria and inhibits Cym1, the PITRM1 yeast ortholog, leading to impaired MTS processing and accumulation of unprocessed mitochondrial proteins, suggesting an indirect role of Aβ and mitochondrial dysfunction via PITRM1 (4). In addition to biochemical association of PITRM1 with Aβ-dependent mitochondrial dysfunction, human genetics suggest a more direct link as PITRM1 genetic variants have been associated with AD (5,6). The specific mechanism is currently poorly understood but may involve impairment of PITRM1-dependent degradation of Aβ, directly resulting in pathological accumulation of Aβ in mitochondria (6).
    For Research Use Only. Not For Use In Diagnostic Procedures.
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