Render Target: STATIC
Render Timestamp: 2024-12-05T12:21:35.002Z
Commit: 224419269841c11382c4555dbee545259bf6c379
XML generation date: 2024-09-20 06:19:47.555
Product last modified at: 2024-11-14T23:45:07.529Z
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PDP - Template Name: Cell Extracts
PDP - Template ID: *******b5396df

LC3 Control Cell Extracts #11972

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    Product Information

    Product Usage Information

    Boil for 3 minutes prior to use. Load 10 µl of untreated and chloroquine treated LC3 Control Cell Extracts per lane.

    Storage

    Supplied in SDS Sample Buffer: 62.5 mM Tris- HCl (pH 6.8 at 25°C), 2% w/v SDS, 10% glycerol, 50 mM DTT, 0.01% w/v bromophenol blue or phenol red.
    Store at –20°C, or at –80°C for long-term storage.

    Product Description

    LC3 Control Cell Extracts (HeLa Untreated): Total cell extracts from HeLa cells serve as a negative control. Supplied in SDS sample buffer.

    LC3 Control Cell Extracts (HeLa +Chloroquine): Total cell extracts from HeLa cells treated with 50 μM chloroquine overnight serve as a positive control.

    This lysate pair is produced as a control for western blotting of LC3A and LC3B. LC3C cannot be detected in these lysates.

    Background

    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 posttranslational 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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