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  1. Products /
  2. Primary Antibodies /
  3. PITRM1 (F2Y2T) Rabbit mAb
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Recombinant: Superior lot-to-lot consistency, continuous supply, and animal-free manufacturing.

PITRM1 (F2Y2T) Rabbit mAb #89774

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  • WB
  • IF

    Supporting Data

    REACTIVITY H
    SENSITIVITY Endogenous
    MW (kDa) 117
    Source/Isotype Rabbit IgG
    Application Key:
    • WB-Western Blotting 
    • IF-Immunofluorescence 
    Species Cross-Reactivity Key:
    • H-Human 

    Product Information

    Product Usage Information

    Application Dilution
    Western Blotting 1:1000
    Immunofluorescence (Immunocytochemistry) 1:50 - 1:200

    Storage

    Supplied in 10 mM sodium HEPES (pH 7.5), 150 mM NaCl, 100 µg/mL BSA, 50% glycerol, and less than 0.02% sodium azide. Store at –20°C. Do not aliquot the antibody.

    Protocol

    Specificity / Sensitivity

    PITRM1 (F2Y2T) Rabbit mAb recognizes endogenous levels of total PITRM1 protein.

    Species Reactivity:

    Human

    Source / Purification

    Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues near the carboxy terminus of human PITRM1 protein.

    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).

    Database Links

    UniProt ID: Q5JRX3


    Entrez-Gene Id: 10531


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    For Research Use Only. Not For Use In Diagnostic Procedures.
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