PhosphoPlus®Atg14 (Ser29) Antibody Duet#69501,Cell Signaling Technology (CST),69501

Reactivity

0

Platform ID

BAB651932653

Cell Signaling Technology (CST)

Headquarters

3 Trask Lane Danvers, MA 01923

Contact

Tel: 877-616-2355,978-867-2388
Fax: 877-616-2355

Product Specifications
Scientific Background

Specifications

NamePhosphoPlus®Atg14 (Ser29) Antibody Duet#69501
Cat. No.69501
Accession NumberQ6ZNE5
Gene ID (Entrez)22863
Reactivity0
Regulatory StatusResearch Use Only

Scientific 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 autophagosome formation (13).Reggiori, F. and Klionsky, D.J. (2002)Eukaryot Cell1, 11-21.Codogno, P. and Meijer, A.J. (2005)Cell Death Differ12 Suppl 2, 1509-18.Levine, B. and Yuan, J. (2005)J Clin Invest115, 2679-88.Corvera, S. (2001)Traffic2, 859-66.Yan, Y. and Backer, J.M. (2007)Biochem Soc Trans35, 239-41.Stack, J.H. et al. (1995)J Cell Biol129, 321-34.Zeng, X. et al. (2006)J Cell Sci119, 259-70.Liang, C. et al. (2006)Nat Cell Biol8, 688-99.Itakura, E. et al. (2008)Mol Biol Cell19, 5360-72.Sun, Q. et al. (2008)Proc Natl Acad Sci U S A105, 19211-6.Zhong, Y. et al. (2009)Nat Cell Biol11, 468-76.Matsunaga, K. et al. (2009)Nat Cell Biol11, 385-96.Park, J.M. et al. (2016)Autophagy12, 547-64.

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