WB, IF-IC, FC-FP
H M R
Endogenous
65
Rabbit IgG
#Q6ZNE5
22863
Product Information
Product Usage Information
| Application | Dilution |
|---|---|
| Western Blotting | 1:1000 |
| Immunofluorescence (Immunocytochemistry) | 1:400 - 1:800 |
| Flow Cytometry (Fixed/Permeabilized) | 1:400 - 1:1600 |
Storage
Specificity / Sensitivity
Species Reactivity:
Human, Mouse, Rat
Source / Purification
Monoclonal antibody is produced by immunizing animals with a synthetic phospho-peptide corresponding to residues surrounding Ser29 of human Atg14 protein.
Background
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 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. These proteins are involved in the formation of autophagosomes, cytoplasmic vacuoles that are delivered to lysosomes for degradation. The class III type phosphoinositide 3-kinase (PI3K) Vps34 regulates vacuolar trafficking and autophagy (4,5). Multiple proteins associate with Vps34, including p105/Vps15, Beclin-1, UVRAG, Atg14, and Rubicon, to determine Vps34 function (6-12). Atg14 and Rubicon were identified based on their ability to bind to Beclin-1 and participate in unique complexes with opposing functions (9-12). Rubicon, which localizes to the endosome and lysosome, inhibits Vps34 lipid kinase activity; knockdown of Rubicon enhances autophagy and endocytic trafficking (11,12). In contrast, Atg14 localizes to autophagosomes, isolation membranes and ER, and can enhance Vps34 activity. Knockdown of Atg14 inhibits starvation-induced autophagy (11,12).
The serine/threonine kinase ULK1 phosphorylates Atg14 at Ser29 to promote autophagsome formation (13).
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- 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.
- Corvera, S. (2001) Traffic 2, 859-66.
- Yan, Y. and Backer, J.M. (2007) Biochem Soc Trans 35, 239-41.
- Stack, J.H. et al. (1995) J Cell Biol 129, 321-34.
- Zeng, X. et al. (2006) J Cell Sci 119, 259-70.
- Liang, C. et al. (2006) Nat Cell Biol 8, 688-99.
- Itakura, E. et al. (2008) Mol Biol Cell 19, 5360-72.
- Sun, Q. et al. (2008) Proc Natl Acad Sci U S A 105, 19211-6.
- Zhong, Y. et al. (2009) Nat Cell Biol 11, 468-76.
- Matsunaga, K. et al. (2009) Nat Cell Biol 11, 385-96.
- Park, J.M. et al. (2016) Autophagy 12, 547-64.
Species Reactivity
Species reactivity is determined by testing in at least one approved application (e.g., western blot).
Western Blot Buffer
IMPORTANT: For western blots, incubate membrane with diluted primary antibody in 5% w/v BSA, 1X TBS, 0.1% Tween® 20 at 4°C with gentle shaking, overnight.
Applications Key
WB: Western Blotting IF-IC: Immunofluorescence (Immunocytochemistry) FC-FP: Flow Cytometry (Fixed/Permeabilized)
Cross-Reactivity Key
H: human M: mouse R: rat Hm: hamster Mk: monkey Vir: virus Mi: mink C: chicken Dm: D. melanogaster X: Xenopus Z: zebrafish B: bovine Dg: dog Pg: pig Sc: S. cerevisiae Ce: C. elegans Hr: horse GP: Guinea Pig Rab: rabbit All: all species expected
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