| 货号 | 12043S |
| 描述 | SignalSilence® Atg13 siRNA I from Cell Signaling Technology (CST) allows the researcher to specifically inhibit Atg13 expression using RNA interference, a method whereby gene expression can be selectively silenced through the delivery of double stranded RNA molecules into the cell. All SignalSilence® siRNA products from CST are rigorously tested in-house and have been shown to reduce target protein expression by western analysis. |
| 反应种属 | Human |
| 应用 | TFN |
| 目标/特异性 | SignalSilence® Atg13 siRNA I inhibits human, mouse, and monkey Atg13 expression. |
| 供应商 | CST |
| 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 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, 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). |
| 存放说明 | -20C |
| 参考文献 | 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. |
Western blot analysis of extracts from RD cells, transfected with 100 nM SignalSilence® Control siRNA (Unconjugated) #6568 (-), or SignalSilence® Atg13 siRNA I (+), using Atg13 Antibody #6940 (upper) or β-Actin (D6A8) Rabbit mAb #8457 (lower). The Atg13 Antibody confirms silencing of Atg13 expression, while the β-Actin (D6A8) Rabbit mAb is used as a loading control. Western blot 分析RD细胞的细胞提取物，使用100 nM SignalSilence® Control siRNA (Unconjugated) #6568（-）或SignalSilence® Atg13 siRNA I (+)转染，使用抗体是Atg13 Antibody #6940 (上图)或β-Actin (D6A8) Rabbit mAb 兔单抗#8457 (下图)。Atg13 Antibody 确认Atg13表达的沉默，β-Actin (D6A8) Rabbit mAb 兔单抗主要用于检测内参。 |
