| 货号 | 96752S |
| 同种亚型 | Rabbit IgG |
| 反应种属 | H M R |
| 来源宿主 | Rabbit IgG |
| 应用 | W IP |
| 目标/特异性 | Atg14 (D1A1N) Rabbit mAb recognizes endogenous levels of total Atg14 protein. |
| 使用方法 | WB(1:1000) IP (1:200) |
| 供应商 | CST |
| 灵敏度 | Endogenous |
| 背景 | 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 Vsp34, including p105/Vsp15, Beclin-1, UVRAG, Atg14, and Rubicon, to determine Vsp34 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). |
| 运输条件 | 0.75 |
| 存放说明 | -20C |
| 计算分子量 | 65 |
| 参考文献 | 1 . Reggiori, F. and Klionsky, D.J. (2002) Eukaryot Cell 1, 11-21. 2 . Codogno, P. and Meijer, A.J. (2005) Cell Death Differ 12 Suppl 2, 1509-18. 3 . Levine, B. and Yuan, J. (2005) J Clin Invest 115, 2679-88. 4 . Corvera, S. (2001) Traffic 2, 859-66. 5 . Yan, Y. and Backer, J.M. (2007) Biochem Soc Trans 35, 239-41. 6 . Stack, J.H. et al. (1995) J Cell Biol 129, 321-34. 7 . Zeng, X. et al. (2006) J Cell Sci 119, 259-70. 8 . Liang, C. et al. (2006) Nat Cell Biol 8, 688-99. 9 . Itakura, E. et al. (2008) Mol Biol Cell 19, 5360-72. 10 . Sun, Q. et al. (2008) Proc Natl Acad Sci U S A 105, 19211-6. 11 . Zhong, Y. et al. (2009) Nat Cell Biol 11, 468-76. 12 . Matsunaga, K. et al. (2009) Nat Cell Biol 11, 385-96. 13 . Park, J.M. et al. (2016) Autophagy 12, 547-564. |
Western blot analysis of extracts from HCT 116 and HCT 116/Atg14 shRNA knockout cells using Atg14 (D1A1N) Rabbit mAb (upper) and β-Actin (D6A8) Rabbit mAb #84576 (lower). HCT 116/Atg14 shRNA cells were kindly provided by Dr. Do-Hyung Kim, University of Minnesota, Minneapolis, MN. | |
Immunoprecipitation of Atg14 from HCT 116 cell extracts. Lane 1 is 10% input, lane 2 is precipitated with Rabbit (DA1E) mAb IgG XP® Isotype Control #3900, and lane 3 is Atg14 (D1A1N) Rabbit mAb. Western blot was performed using Atg14 (D1A1N) Rabbit mAb. A confirmation specific secondary antibody was used to avoid reactivity with IgG. | |
Western blot analysis of extracts from various cell lines using Atg14 (D1A1N) Rabbit mAb. |
