Anti Ubiquitin-Like Modifier-Activating Enzyme ATG7 mAb (Clone ATG7-2)

Antibodies/Primary Antibodies/Ubiquitin-SUMO-Proteasome related; Antibodies/Ubiquitin-SUMO-Proteasome related/Primary Antibodies; Research Area/Cell Biology/Apoptosis/Primary Antibodies; Research Area/Cell Biology/Autophagy/Primary Antibodies; Research Area/Cell Biology/Cell Cycle/Primary Antibodies; Research Area/Cell Biology/Hypoxic Metabolic & ER Stress/Primary Antibodies; Research Area/Cell Biology/Ubiquitin-SUMO-Proteasome related/Primary Antibodies; Research Area/Neurobiology/Axons/Primary Antibodies; Research Area/Development/Adipogenesis/Primary Antibodies; Research Area/Development/Hematopoiesis/Primary Antibodies; Research Area/Organelles & Subcellular Structures/Mitochondria/Primary Antibodies; Research Area/Cell Types/Stem Cells/Primary Antibodies

Autophagy is an evolutionaly conserved process, in which autophagosomes fuse with lysosomes and degrade bulk cytoplasmic contents (1). Autophagy is involved in many physiological processes, including development, infection, cancer, and neurodegenerative diseases (2). ATG (autophagy-related) genes were identified by genetic screening in yeast (3). Atg7 acts as an E1-like enzyme in both Atg12 and Atg8 ubiquitin-like conjugation systems. Atg7 transfers Atg12 to an E2-like enzyme Atg10, and conjugates Atg12 to Atg5. Atg7 also transfers Atg8 to another E2-like enzyme Atg3, and conjugates Atg8 to phosphatidylethanolamine (4). Many of these ATG genes are conserved in mammals. Atg7 deficient neonates die soon after birth from perineonatal starvation (5). Conditional deletion of Atg7 in the nervous system results in neurodegeneration with ubiquitin containing aggregates (6).
Source: Dr. Shigeomi Shimizu, Pathology and Cell Biology, Research Institute for Intractable Diseases, Tokyo Medical and Dental University
References:
1) Klionsky and Emr, 2000, Science, 290, 1717-21.
2) Mizushima et al., 2008, Nature, 451, 1069-75.
3) Tsukada and Ohsumi, 1993, FEBS Lett, 333, 169-74.
4) Mizushima et al., 1998, Nature, 395, 395-8.
5) Komatsu et al., 2005, J Cell Biol, 169, 425-34.
6) Komatsu et al., 2006, Nature, 441, 880-4.

Monoclonal