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Mitofilin/IMMT (F5L3S) Rabbit Monoclonal Antibody #30671

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  • WB
  • IP
  • IHC
  • IF

    Product Specifications

    REACTIVITY H
    SENSITIVITY Endogenous
    MW (kDa) 85
    Source/Isotype Rabbit IgG
    Application Key:
    • WB-Western Blotting 
    • IP-Immunoprecipitation 
    • IHC-Immunohistochemistry 
    • IF-Immunofluorescence 
    Species Cross-Reactivity Key:
    • H-Human 

    Product Information

    Product Usage Information

    Application Dilution
    Western Blotting 1:1000
    Immunoprecipitation 1:100
    Immunohistochemistry (Paraffin) 1:100 - 1:400
    Immunofluorescence (Immunocytochemistry) 1:800 - 1:3200

    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

    Mitofilin/IMMT (F5L3S) Rabbit mAb recognizes endogenous levels of total mitofilin/IMMT protein. Diffuse staining of uncertain specificity was observed in normal human liver hepatocytes by immunohistochemistry.

    Species Reactivity:

    Human

    Source / Purification

    Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Pro174 of human mitofilin/IMMT protein.

    Background

    Mitofilin (gene name: IMMT), also known as heart muscle protein (HMP), mitochondrial contact site and cristae organizing system (MICOS) complex subunit MIC60, and MINOS2, is a key component of the MICOS complex, a large protein complex of the mitochondrial inner membrane (reviewed in 1). The MICOS complex, also known as the mitochondrial inner membrane organizing system (MINOS) and mitochondria organizing structure (MitOS), is critical in regulating mitochondria inner membrane and cristae structure and as well as interacting with the mitochondrial outer membrane to regulate protein import. Mitofilin expression regulates mitochondrial respiration, protein import, fusion/fission, and apoptosis (2,3). It was originally identified as a protein preferentially expressed in heart (4,5), but has since been identified in other tissues, where it may influence disease progression, including cancer and neurodegeneration. Expression and function of mitofilin can be regulated by various conditions, such as oxidative stress (6). Aberrant mitofilin expression in cancer leads to metabolic rewiring and gene signature changes associated with cancer progression (7). Mitofilin has also been associated with Parkinson’s disease (PD) (8). Phosphorylation of mitofilin by the mitochondrial kinase PINK1 may help stabilize mitofilin (9). Loss of PINK1 in PD thereby may result in loss of mitofilin and disruption of mitochondria structure and function.

    Alternate Names

    Cell proliferation-inducing gene 4/52 protein; cell proliferation-inducing protein 52; DKFZp779P1653; heart muscle protein; HMP; IMMT; inner membrane mitochondrial protein; inner membrane protein, mitochondrial (mitofilin); MGC111146; MIC60; MICOS complex subunit MIC60; MICOS60; MINOS2; mitochondrial contact site and cristae organizing system subunit 60; mitochondrial inner membrane organizing system 2; Mitochondrial inner membrane protein; Mitofilin; motor protein; P87; p87/89; P89; PIG4; PIG52; proliferation-inducing gene 4

    For Research Use Only. Not for Use in Diagnostic Procedures.
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