Product Pathways - Autophagy Signaling
Atg9A (D4O9D) Rabbit mAb #13509
|13509S||100 µl (10 western blots)||---||In Stock||---|
|13509||carrier free and custom formulation / quantity||email request|
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|W||1:1000||Human, Mouse, Rat, Monkey||Endogenous||100-110||Rabbit IgG|
Species cross-reactivity is determined by western blot.
Applications Key: W=Western Blotting, IP=Immunoprecipitation
Specificity / Sensitivity
Atg9A (D4O9D) Rabbit mAb recognizes endogenous levels of total Atg9A protein.
Source / Purification
Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Gly780 of human Atg9A protein.
Western blot analysis of extracts of various cell lines using Atg9A (D4O9D) Rabbit mAb.
Western blot analysis of extracts from RD cells, transfected with 100 nM SignalSilence® Control siRNA (Unconjugated) #6568 (-) or SignalSilence® Atg9A siRNA I #7051 (+), using Atg9A (D4O9D) Rabbit mAb (upper) or β-Actin (D6A8) Rabbit mAb #8457 (lower). The Atg9A (D4O9D) Rabbit mAb confirms silencing of Atg9A expression while the β-Actin (D6A8) Rabbit mAb is used as a loading control.
Immunoprecipitation of Atg9A from Hep G2 cell extracts using Rabbit (DA1E) mAb IgG XP® Isotype control #3900 (lane 2) or Atg9A (D4O9D) Rabbit mAb (lane 3). Lane 1 is 10% input. Western blot analysis was performed using Atg9A (D4O9D) Rabbit mAb.
Autophagy is a catabolic process for the autophagosomic-lysosomal degradation of bulk cytoplasmic contents (1,2). It is generally activated by conditions of nutrient deprivation but is also 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 is directed by a number of autophagy-related (Atg) genes (4).
Atg9, one of the Atg proteins identified in yeast, is essential for autophagosome formation (5). There are two human functional orthologues based on the yeast homolog Atg9p: Atg9A, which has also been identified as Atg9L1 and mAtg9, and Atg9L2, which was first reported as nitric-oxide synthase 3 antisense (NOS3AS) (6,7). Atg9A is an integral membrane protein that is required for both the initiation and the expansion of the autophagosome (6,7). Recruitment of Atg9A to the autophagosomal membrane is dynamic and transient as Atg9A also cycles between autophagy-related structures known as omegasomes, the trans-Golgi network (TGN), and endosomes, and at no point becomes a stable component of the autophagosomal membrane (6,8). The precise regulation of Atg9A trafficking is not fully clarified, yet it is suggested to involve p38 mitogen-activated protein kinase (MAPK)-binding protein p38IP and the Beclin-1-binding protein Bif-1 (9,10).
- 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.
- Klionsky, D.J. et al. (2003) Dev Cell 5, 539-45.
- Noda, T. et al. (2000) J Cell Biol 148, 465-80.
- Young, A.R. et al. (2006) J Cell Sci 119, 3888-900.
- Yamada, T. et al. (2005) J Biol Chem 280, 18283-90.
- Orsi, A. et al. (2012) Mol Biol Cell 23, 1860-73.
- Webber, J.L. and Tooze, S.A. (2010) EMBO J 29, 27-40.
- Takahashi, Y. et al. (2011) Autophagy 7, 61-73.
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For Research Use Only. Not For Use In Diagnostic Procedures.
XP® is a trademark of Cell Signaling Technology, Inc.
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.