Our Top Cited LC3B Antibody

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Autophagy labs swear by our LC3B antibody.

Our LC3B antibody (NB100-2220) is the gold standard to monitor autophagosome
formation and autophagy induction.

The most cited LC3B antibody

With over 500 citations, our LC3B antibody is the most widely trusted and used antibody to monitor LC3 expression.

LC3 publications

Figure 1: Total publications of Novus’s LC3B antibody (NB100-2220), as well as total publications of the second and third most published LC3B antibodies. Data from CiteAb.

A glimpse of citations from high impact journals

Our LC3B antibody has been instrumental in scientific breakthroughs and discoveries. Here is a look at a few publications featuring our LC3B antibody:

Wu X, Fleming A, Ricketts T et al. Autophagy regulates Notch degradation and modulates stem cell development and neurogenesis. Nat Commun. 2016. PMID: 26837467.

Sharifi M, Mowers E, Drake L,et al. Autophagy promotes focal adhesion disassembly and cell motility of metastatic tumor cells through the direct interaction of paxillin with LC3. Cell Reports. 2016. PMID: 27184837.

Zavodszky E, Seaman MN, Moreau K et al. Mutation in VPS35 associated with Parkinson’s disease impairs WASH complex association and inhibits autophagy. Nat Commun. 2014. PMID: 24819384.

Shoji-Kawata S, Sumpter R, Leveno M et al. Identification of a candidate therapeutic autophagy-inducing peptide. Nature. 2013 PMID: 23364696.

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Perfect 5 Star Reviews

Figure 2: Customer ratings (1-5) by application for our LC3B antibody (NB100-2220).

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Recommended by Autophagy Manuals

Our LC3B antibody is recommended by key autophagy manuals and specifically noted as “reliable”.

Read more here: Barth S, Glick D, Mac leod K et al. Autophagy: assays and artifacts. J Pathol. 2010. PMID: 20225337.

Western blot data generated with our top cited LC3 antibody

WB data generated with Novus top cited LC3 antibody

Western blot: WB analysis lysates from HeLa cells that were left untreated (blank) or were treated with 10-20 uM each of autophagy inducing peptides (Tat-D11, Tat-L11, Tat-Beclin 1) or with 10-20 uM of non-inducing control peptides (Tat-L11S). HeLa lysates were then analyzed for the expression of LC3-1/LC3-II using 2ug/ml of anti-LC3B (NB100-2220). Anti-Actin (AF4000) was used as a loading control. LC3-II expression was induced by all autophagy inducing peptides, but Tat-D11 exhibited superior induction when compared to other treatment and control groups.

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