LC3B (Microtubule-associated protein 1A/1B-light chain 3B) is a ubiquitin-like protein central to autophagy, a cellular recycling process critical for maintaining homeostasis. LC3B antibodies are indispensable tools for detecting LC3B-I (cytosolic form) and LC3B-II (lipidated, autophagosome-bound form), enabling researchers to study autophagic flux and its dysregulation in diseases such as cancer, neurodegeneration, and metabolic disorders . These antibodies are validated across applications including Western blot (WB), immunofluorescence (IF), immunohistochemistry (IHC), and flow cytometry .
LC3B antibodies are pivotal for:
Autophagosome Tracking: LC3B-II accumulation (e.g., under chloroquine treatment) indicates blocked autophagosome-lysosome fusion .
Disease Mechanisms: Dysregulated LC3B correlates with tumor progression , neurodegenerative aggregates , and HCV infection .
Structural Studies: LC3B interacts with autophagy receptors (e.g., p62/SQSTM1) and ribosomes .
LC3B antibodies are rigorously validated using knockout (KO) cell lines (e.g., HeLa LC3B KO) . For example:
CAB7198: Detects 14–16 kDa bands in chloroquine-treated 293T cells, absent in KO lysates .
GTX127375: Binds LC3B in autophagosomes of HepG2 cells under thapsigargin stress .
ab48394: Distinguishes LC3B-II upregulation in wild-type vs. KO HeLa cells .
Cross-reactivity: Most antibodies (e.g., MAB85581, ab51520) show no cross-reactivity with LC3A or LC3C due to isoform-specific epitopes .
RNA Binding: LC3B binds AAUAAA motifs in mRNA 3'UTRs, promoting CCR4-NOT-mediated degradation (e.g., PRMT1 mRNA) .
Oxidative Stress: ROS-induced LC3B enhances apoptosis and reduces tumor growth independent of autophagy .
Cancer: LC3B knockdown reduces annexin V+ apoptosis in ovarian cancer cells .
Neurodegeneration: LC3B co-localizes with α-synuclein aggregates in Parkinson’s models .
KEGG: sce:YJL134W
STRING: 4932.YJL134W