Render Target: SSR
Render Timestamp: 2024-11-14T23:07:12.865Z
Commit: 3c1f305a63297e594ac8d7bb5424007d592d68be
XML generation date: 2024-09-30 01:59:20.892
Product last modified at: 2024-09-30T08:01:28.947Z
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PDP - Template Name: Monoclonal Antibody
PDP - Template ID: *******c5e4b77
R Recombinant
Recombinant: Superior lot-to-lot consistency, continuous supply, and animal-free manufacturing.

TIM23 (E1Q7L) Rabbit mAb #34822

Filter:
  • WB
  • IF

    Supporting Data

    REACTIVITY H M R
    SENSITIVITY Endogenous
    MW (kDa) 22
    Source/Isotype Rabbit IgG
    Application Key:
    • WB-Western Blotting 
    • IF-Immunofluorescence 
    Species Cross-Reactivity Key:
    • H-Human 
    • M-Mouse 
    • R-Rat 

    Product Information

    Product Usage Information

    Application Dilution
    Western Blotting 1:1000
    Immunofluorescence (Immunocytochemistry) 1:400 - 1:800

    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

    TIM23 (E1Q7L) Rabbit mAb recognizes endogenous levels of total TIM23 protein.

    Species Reactivity:

    Human, Mouse, Rat

    Source / Purification

    Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Ala29 of human TIM23 protein.

    Background

    TIM23 is a subunit of the mitochondrial import inner membrane translocase complex. This complex mediates translocation of presequence-containing proteins into the mitochondrial matrix and inner membrane. Besides TIM23, there are multiple subunits in the complex, including TIM17A, TIM17B, and TIM50 (1,2). Studies show that mutant huntingtin (mHTT), the protein causing neurodegenerative Huntington’s disease, binds to TIM23 subunit. There are less soluble matrix mitochondrial proteins imported by the TIM23 complex in cells expressing mHTT and in the brain tissues of Huntington’s disease patients when compared with controls (2). In addition, asbestos causes translocation of NOX4 to the mitochondrial matrix through direct interaction with TIM23 in lung macrophages. TIM23 increases NOX4-induced reactive oxygen species (ROS) in mitochondria and metabolic reprogramming to oxidative phosphorylation (3).
    For Research Use Only. Not For Use In Diagnostic Procedures.
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