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To Purchase # 11972S
|11972S||100 µl (10 western blots)||$112.00.0|
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- Additional protein information
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LC3 Control Cell Extracts #11972
Untreated LC3 Control Cell Extracts: Total cell extracts from HeLa cells serve as a negative control. Supplied in SDS sample buffer.
Chloroquine treated LC3 Control Cell Extracts: Total cell extracts from HeLa cells treated with 50 μM chloroquine overnight serve as a negative control. This lysate pair is produced as a control for western blotting of LC3A and LC3B. LC3C cannot be detected in these lysates.
Autophagy is a catabolic process for the autophagosomic-lysosomal degradation of bulk cytoplasmic contents (1,2). Autophagy is generally activated by conditions of nutrient deprivation, but it has also been associated with a number of physiological processes including development, differentiation, neurodegenerative diseases, infection, and cancer (3). Autophagy marker Light Chain 3 (LC3) was originally identified as a subunit of microtubule-associated proteins 1A and 1B (termed MAP1LC3) (4) and subsequently found to contain similarity to the yeast protein Apg8/Aut7/Cvt5 critical for autophagy (5). Three human LC3 isoforms (LC3A, LC3B, and LC3C) undergo post-translational modifications during autophagy (6-9). Cleavage of LC3 at the carboxy terminus immediately following synthesis yields the cytosolic LC3-I form. During autophagy, LC3-I is converted to LC3-II through lipidation by a ubiquitin-like system involving Atg7 and Atg3 that allows for LC3 to become associated with autophagic vesicles (6-10). The presence of LC3 in autophagosomes and the conversion of LC3 to the lower migrating form, LC3-II, have been used as indicators of autophagy (11).
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