Render Target: STATIC
Render Timestamp: 2024-12-03T11:44:55.823Z
Commit: cd2fae6ca3f811b1ddb1df24ac291ed56d5d501b
XML generation date: 2024-09-30 01:57:38.933
Product last modified at: 2024-11-21T12:45:51.545Z
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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.

FUNDC1 (E2F4T) Rabbit mAb #49240

Filter:
  • WB
  • IP

    Supporting Data

    REACTIVITY H M R
    SENSITIVITY Endogenous
    MW (kDa) 17
    Source/Isotype Rabbit IgG
    Application Key:
    • WB-Western Blotting 
    • IP-Immunoprecipitation 
    Species Cross-Reactivity Key:
    • H-Human 
    • M-Mouse 
    • R-Rat 

    Product Information

    Product Usage Information

    Application Dilution
    Western Blotting 1:1000
    Immunoprecipitation 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

    FUNDC1 (E2F4T) Rabbit mAb recognizes endogenous levels of total FUNDC1 protein. Bands of unknown origin were detected at 45 and 100 kDa.

    Species Reactivity:

    Human, Mouse, Rat

    Source / Purification

    Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues near the amino terminus of human FUNDC1 protein.

    Background

    Mitophagy, a selective form of autophagy targeting damaged mitochondria, is regulated through several protein complexes, including FUNDC1, BNIP3 and BNIP3L/Nix, and PINK1/Parkin (reviewed in 1). FUNDC1 resides on the mitochondrial outer membrane protein and regulates mitochondrial dynamics and hypoxia-induced mitophagy (2-4). It contains an amino-terminal LC3-interacting region (LIR) that is responsible for associating with LC3 and recruiting mitochondria to the autophagosome. The phosphorylation state of FUNDC1 can regulate its activity by affecting its binding to LC3 (4-6). Under normal conditions, FUNDC1 is phosphorylated at Tyr18 by Src, which is inhibited during hypoxia, leading to dephosphorylation (4). FUNDC1 activity is also inhibited by phosphorylation by CK2 at Ser13, which is overcome during hypoxia by the phosphatase PGAM5 which dephosphorylates this site (5). Furthermore, the autophagy kinase ULK1 phosphorylates FUNDC1 at Ser17 which enhances binding to LC3 (6). The levels of FUNDC1 can also be tightly regulated through the ubiquitin/proteasome pathway via the E3 ligase MARCH5, which targets FUNDC1 for degradation (7).
    For Research Use Only. Not For Use In Diagnostic Procedures.
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