Product Pathways - Autophagy Signaling
Atg13 (E1Y9V) Rabbit mAb #13468
|13468S||100 µl (10 western blots)||---||In Stock||---|
|13468||carrier free and custom formulation / quantity||email request|
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Species cross-reactivity is determined by western blot.
Applications Key: W=Western Blotting, IP=Immunoprecipitation, IF-IC=Immunofluorescence (Immunocytochemistry)
Specificity / Sensitivity
Atg13 (E1Y9V) Rabbit mAb recognizes endogenous levels of total Atg13 protein.
Source / Purification
Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Asn230 of human Atg13 protein.
Western blot analysis of extracts from various cell lines using Atg13 (E1Y9V) Rabbit mAb.
Western blot analysis of extracts from 293T cells, mock transfected (-) or transfected with a construct expressing Myc/DDK-tagged full-length human Atg13 (hAtg13-Myc/DDK; +), using Atg13 (E1Y9V) Rabbit mAb (upper) or Myc-Tag (71D10) Rabbit mAb #2278 (lower).
Western blot analysis of extracts from HeLa cells, transfected with 100 nM SignalSilence® Control siRNA (Unconjugated) #6568 (-) or SignalSilence® Atg13 siRNA I #12043 (+), using Atg13 (E1Y9V) Rabbit mAb (upper) or β-Actin (D6A8) Rabbit mAb #8457 (lower). The Atg13 (E1Y9V) Rabbit mAb confirms silencing of Atg13 expression, while the β-Actin (D6A8) Rabbit mAb is used as a loading control.
Immunoprecipitation of Atg13 from MCF7 cell extracts using Rabbit (DA1E) mAb IgG XP® Isotype control #3900 (lane 2) or Atg13 (E1Y9V) Rabbit mAb (lane 3). Lane 1 is 10% input. Western blot analysis was performed using Atg13 (E1Y9V) Rabbit mAb.
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 has also been associated with a number of physiological processes including development, differentiation, neurodegeneration, infection, and cancer (3). The molecular machinery of autophagy was largely discovered in yeast and referred to as autophagy-related (Atg) genes.
Atg13/Apg13 was originally identified in yeast as a constitutively expressed protein that was genetically linked to Atg1/Apg1, a protein kinase required for autophagy (4). Over-expression of Atg1 suppresses the defects in autophagy observed in Atg13 mutants (4). Autophagy requires a direct association between Atg1 and Atg13, and is inhibited by TOR-dependent phosphorylation of Atg13 under high nutrient conditions (5). Similarly, mammalian Atg13 forms a complex with the Atg1 homologues ULK1/2, along with FIP200, which localizes to autophagic isolation membranes, and regulates autophagosome biogenesis (6-8). mTOR phosphorylates both Atg13 and ULK1, suppressing ULK1 kinase activity and autophagy (7-9). ULK1 can directly phosphorylate Atg13 at a yet unidentified site, presumably to promote autophagy (7,8). Additional studies suggest that Atg13 and FIP200 can function independently of ULK1 and ULK2 to induce autophagy through an unknown mechanism (10).
- Reggiori, F. and Klionsky, D.J. (2002) Eukaryot Cell 1, 11-21.
- Codogno, P. and Meijer, A.J. (2005) Cell Death Differ 12 Suppl 2, 1509-18.
- Levine, B. and Yuan, J. (2005) J Clin Invest 115, 2679-88.
- Funakoshi, T. et al. (1997) Gene 192, 207-13.
- Kamada, Y. et al. (2000) J Cell Biol 150, 1507-13.
- Ganley, I.G. et al. (2009) J Biol Chem 284, 12297-305.
- Hosokawa, N. et al. (2009) Mol Biol Cell 20, 1981-91.
- Jung, C.H. et al. (2009) Mol Biol Cell 20, 1992-2003.
- Kim, J. et al. (2011) Nat Cell Biol 13, 132-41.
- Alers, S. et al. (2011) Autophagy 7, 1423-33.
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For Research Use Only. Not For Use In Diagnostic Procedures.
XP® is a trademark of Cell Signaling Technology, Inc.
DRAQ5® is a registered trademark of Biostatus Limited.
Tween® is a registered trademark of ICI Americas, Inc.
SignalSilence® is a trademark of Cell Signaling Technology, Inc.
Cell Signaling Technology® is a trademark of Cell Signaling Technology, Inc.