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APG7 Antibody
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
Application 
| WB, IF, ICC, E |
|---|---|
| Primary Accession | O95352 |
| Other Accession | NP_006386, 5453668 |
| Reactivity | Human, Mouse |
| Host | Rabbit |
| Clonality | Polyclonal |
| Isotype | IgG |
| Calculated MW | Predicted: 77 kDa Observed: 77 kDa |
| Application Notes | APG7 antibody can be used for the detection of APG7 by Western blot at 1 - 4 µg/mL. Antibody can also be used for immunocytochemistry starting at 10 µg/mL. For immunofluorescence start at 10 µg/mL. |
| Gene ID | 10533 |
|---|---|
| Other Names | APG7 Antibody: GSA7, APG7L, APG7-LIKE, Ubiquitin-like modifier-activating enzyme ATG7, ATG12-activating enzyme E1 ATG7, APG7-like, ATG7 autophagy related 7 homolog (S. cerevisiae) |
| Target/Specificity | ATG7; |
| Reconstitution & Storage | APG7 antibody can be stored at 4℃ for three months and -20℃, stable for up to one year. As with all antibodies care should be taken to avoid repeated freeze thaw cycles. Antibodies should not be exposed to prolonged high temperatures. |
| Precautions | APG7 Antibody is for research use only and not for use in diagnostic or therapeutic procedures. |
| Name | ATG7 (HGNC:16935) |
|---|---|
| Synonyms | APG7L |
| Function | E1-like activating enzyme involved in the 2 ubiquitin-like systems required for cytoplasm to vacuole transport (Cvt) and autophagy. Activates ATG12 for its conjugation with ATG5 as well as the ATG8 family proteins for their conjugation with phosphatidylethanolamine. Both systems are needed for the ATG8 association to Cvt vesicles and autophagosomes membranes. Required for autophagic death induced by caspase-8 inhibition. Facilitates LC3-I lipidation with phosphatidylethanolamine to form LC3-II which is found on autophagosomal membranes (PubMed:34161705). Required for mitophagy which contributes to regulate mitochondrial quantity and quality by eliminating the mitochondria to a basal level to fulfill cellular energy requirements and preventing excess ROS production. Modulates p53/TP53 activity to regulate cell cycle and survival during metabolic stress. Also plays a key role in the maintenance of axonal homeostasis, the prevention of axonal degeneration, the maintenance of hematopoietic stem cells, the formation of Paneth cell granules, as well as in adipose differentiation. Plays a role in regulating the liver clock and glucose metabolism by mediating the autophagic degradation of CRY1 (clock repressor) in a time-dependent manner (By similarity). |
| Cellular Location | Cytoplasm. Preautophagosomal structure. Note=Localizes also to discrete punctae along the ciliary axoneme and to the base of the ciliary axoneme |
| Tissue Location | Widely expressed, especially in kidney, liver, lymph nodes and bone marrow. |
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Provided below are standard protocols that you may find useful for product applications.
Background
APG7 Antibody: Autophagy, the process of bulk degradation of cellular proteins through an autophagosomic-lysosomal pathway is important for normal growth control and may be defective in tumor cells. It is involved in the preservation of cellular nutrients under starvation conditions as well as the normal turnover of cytosolic components. This process is negatively regulated by TOR (Target of rapamycin) through phosphorylation of autophagy protein APG1. Another member of the autophagy family of proteins is APG7 which was identified in yeast as a ubiquitin-E1-like enzyme; this function is conserved in the mammalian homolog. In mammalian cells, APG7 is essential for autophagy conjugation systems, autophagosome formation, starvation-induced bulk degradation of proteins and organelles. It has been suggested that caspase-8 may alter APG7 levels and thus the APG7 program of autophagic cell death.
References
Gozuacik D and Kimchi A. Autophagy as a cell death and tumor suppressor mechanism. Oncogene. 2004; 23:2891-906.
Kisen GO, Tessitore L, Costelli P, et al. Reduced autophagic activity in primary rat hepatocellular carcinoma and ascites hepatoma cells. Carcinogenesis 1993; 14:2501-5.
Kamada Y, Funakoshi T, Shintani T, et al. Tor-mediated induction of autophagy via Apg1 protein kinase complex. J. Cell. Biol. 2000; 150:1507-13.
Mizushima N, Noda T, Yoshimori T, et al. A protein conjugation system essential for autophagy. Nature 1998; 395:395-8.
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