Autophagy Related 5 Recombinant Protein | ATG5 recombinant protein
Recombinant Human Autophagy Related 5
Sterile Filtered clear solution.
Introduction: ATG5 is a member of the autophagy-related (ATG) genes family. Autophagy is a catabolic process for the autophagosomic-lysosomal degradation of bulk cytoplasmic contents. ATG5 protein is essential for autophagy. It conjugates to ATG12 and associates with isolation membrane to form autophagosomes. In addition ATG5 takes a vital part in the apoptotic process and it is expressed relatively late in the apoptotic process, downstream of caspase activity.
NCBI and Uniprot Product Information
Uniprot Description
ATG5: Required for autophagy. Conjugates to ATG12 and associates with isolation membrane to form cup-shaped isolation membrane and autophagosome. The conjugate detaches from the membrane immediately before or after autophagosome formation is completed. The ATG5-ATG12 conjugate forms a complex with several units of ATG16. Interacts with TECPR1; the interaction is direct and does not take place when ATG16 is associated with the ATG5- ATG12 conjugate. By apoptotic stimuli. Ubiquitous. The mRNA is present at similar levels in viable and apoptotic cells, whereas the protein is dramatically highly expressed in apoptotic cells. Belongs to the ATG5 family. 2 isoforms of the human protein are produced by alternative splicing.
Protein type: Autophagy; Apoptosis; Ubiquitin conjugating system
Chromosomal Location of Human Ortholog: 6q21
Cellular Component: membrane; cytoplasm; pre-autophagosomal structure membrane; autophagic vacuole; axoneme
Molecular Function: protein binding; APG8 conjugating enzyme activity
Biological Process: response to drug; response to fungus; apoptosis; ventricular cardiac muscle cell development; C-terminal protein lipidation; post-translational protein modification; vasodilation; regulation of release of sequestered calcium ion into cytosol; cellular response to nitrogen starvation; heart contraction; regulation of cytokine secretion during immune response; mitochondrion degradation; autophagy; innate immune response; negative regulation of protein ubiquitination; blood vessel remodeling; negative regulation of interferon type I production; otolith development; negative regulation of apoptosis; autophagic vacuole formation