Validated using a knockout cell line

Anti-LC3B antibody [EPR18709] - BSA and Azide free (ab221794)


  • Product name
    Anti-LC3B antibody [EPR18709] - BSA and Azide free
    See all LC3B primary antibodies
  • Description
    Rabbit monoclonal [EPR18709] to LC3B - BSA and Azide free
  • Host species
  • Tested applications
    Suitable for: ICC/IF, IP, WBmore details
  • Species reactivity
    Reacts with: Mouse, Rat, Human
  • Immunogen

    Synthetic peptide (the amino acid sequence is considered to be commercially sensitive) within Human LC3B aa 1-100. The exact sequence is proprietary.
    Database link: Q9GZQ8

  • Positive control
    • WB: BMDM, U-87 MG, C6 and RAW 264.7 whole cell lysates; Human brain, mouse heart, rat heart, mouse brain and rat brain lysates. IP: HeLa whole cell lysate.
  • General notes

    Use our conjugation kits for antibody conjugates that are ready-to-use in as little as 20 minutes with <1 minute hands-on-time and 100% antibody recovery: available for fluorescent dyes, HRP, biotin and gold.

    Our RabMAb® technology is a patented hybridoma-based technology for making rabbit monoclonal antibodies. For details on our patents, please refer to RabMab® patents

    This product is a recombinant rabbit monoclonal antibody.



Our Abpromise guarantee covers the use of ab221794 in the following tested applications.

The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.

Application Abreviews Notes
ICC/IF Use at an assay dependent concentration.
IP Use at an assay dependent concentration.
WB Use at an assay dependent concentration. Detects a band of approximately 14, 16 kDa (predicted molecular weight: 15 kDa).


  • Function
    Probably involved in formation of autophagosomal vacuoles (autophagosomes).
  • Tissue specificity
    Most abundant in heart, brain, skeletal muscle and testis. Little expression observed in liver.
  • Sequence similarities
    Belongs to the MAP1 LC3 family.
  • Post-translational
    The precursor molecule is cleaved by APG4B/ATG4B to form LC3-I. This is activated by APG7L/ATG7, transferred to ATG3 and conjugated to phospholipid to form LC3-II.
  • Cellular localization
    Cytoplasm > cytoskeleton. Endomembrane system. Cytoplasmic vesicle > autophagosome membrane. LC3-II binds to the autophagic membranes.
  • Information by UniProt
  • Database links
  • Alternative names
    • ATG8F antibody
    • Autophagy-related protein LC3 B antibody
    • Autophagy-related ubiquitin-like modifier LC3 B antibody
    • LC3B antibody
    • LC3II antibody
    • MAP1 light chain 3 like protein 2 antibody
    • MAP1 light chain 3-like protein 2 antibody
    • MAP1A/1BLC3 antibody
    • MAP1A/MAP1B LC3 B antibody
    • MAP1A/MAP1B light chain 3 B antibody
    • MAP1ALC3 antibody
    • MAP1LC3B a antibody
    • Map1lc3b antibody
    • Microtubule associated protein 1 light chain 3 beta antibody
    • Microtubule-associated protein 1 light chain 3 beta antibody
    • Microtubule-associated proteins 1A/1B light chain 3B antibody
    • MLP3B_HUMAN antibody
    see all


  • This ICC data was generated using the same anti-LC3B antibody clone, EPR18709, in a different buffer formulation (cat# ab192890).

    ab192890 staining LC3B in HAP1 cells (wildtype and MAP1LC3B knockout) +/- Chloroquine (50μM, 24 hours). The cells were fixed with 100% methanol (5 min), permeabilized with 0.1% Triton X-100 for 5 minutes and then blocked with 1% BSA/10% normal goat serum/0.3M glycine in 0.1% PBS-Tween for 1h. The cells were then incubated overnight at +4°C with ab192890 at 1μg/ml and ab195889, Mouse monoclonal to alpha Tubulin (Alexa Fluor® 594), at 1/250 dilution (shown in pseudocolor red) followed by a further incubation at room temperature for 1h with a goat secondary antibody to Rabbit IgG (Alexa Fluor® 488) (ab150081) at 2 μg/ml (shown in green). Nuclear DNA was labelled with DAPI (shown in blue).

    Image was taken with a confocal microscope (Leica-Microsystems, TCS SP8).


ab221794 has not yet been referenced specifically in any publications.

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