| 货号 | 6212S |
| 描述 | SignalSilence® LC3B siRNA I from Cell Signaling Technology (CST) allows the researcher to specifically inhibit LC3B expression using RNA interference, a method whereby gene expression can be selectively silenced through the delivery of double stranded RNA molecules into the cell. LC3B siRNA I will not inhibit expression of LC3A or LC3C. 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 |
| 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, neurodegenerative diseases, infection and cancer (3). Autophagy marker Light Chain 3 (LC3) was originally identified as a subunit of microtubule-associated proteins 1A and 1B (termed MAP1LC3) (4), and subsequently found to contain similarity to the yeast protein Apg8/Aut7/Cvt5 critical for autophagy (5). Three human LC3 isoforms (LC3A, LC3B, and LC3C) undergo post-translational modifications during autophagy (6-9). Cleavage of LC3 at the carboxy terminus immediately following synthesis yields the cytosolic LC3-I form. During autophagy, LC3-I is converted to LC3-II through lipidation by a ubiquitin-like system involving Atg7 and Atg3 that allows for LC3 to become associated with autophagic vesicles (6-10). The presence of LC3 in autophagosomes and the conversion of LC3 to the lower migrating form LC3-II have been used as indicators of autophagy (11). |
| 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. Mann, S.S. and Hammarback, J.A. (1994) J. Biol. Chem. 269, 11492-97. Lang, T. et al. (1998) EMBO J. 17, 3597-607. Kabeya, Y. et al. (2000) EMBO J. 19, 5720-28. He, H. et al. (2003) J. Biol. Chem. 278, 29278-87. Tanida, I. et al. (2004) J. Biol. Chem. 279, 47704-10. Wu, J. et al. (2006) Biochem. Biophys. Res. Commun. 339, 437-42. Ichimura, Y. et al. (2000) Nature 408, 488-92. Kabeya, Y. et al. (2004) J. Cell Sci. 117, 2805-12. |
Western blot analysis of extracts from HeLa cells, transfected with 100 nM SignalSilence® Control siRNA (Unconjugated) #6568 (-), SignalSilence® LC3B siRNA I (+) or SignalSilence® LC3B siRNA II #6213 (+), using LC3B (D11) XP® Rabbit mAb #3868 and α-Tubulin (11H10) Rabbit mAb #2125. The LC3B (D11) XP® Rabbit mAb confirms silencing of LC3B expression, while the α-Tubulin (11H10) Rabbit mAb is used to control for loading and specificity of LC3B siRNA. Western blot 分析HeLa细胞的提取物，用100 nM SignalSilence® Control siRNA (Unconjugated) #6568 (-)、SignalSilence® LC3B siRNA I (+) 或 SignalSilence® LC3B siRNA II #6213 (+)转染。使用的抗体是LC3B (D11) XP® Rabbit mAb 兔单抗#3868 和 α-Tubulin (11H10) Rabbit mAb 兔单抗#2125。以 α-Tubulin (11H10) Rabbit mAb 兔单抗作为加样和特异性的LC3B siRNA对照，LC3B (D11) XP® Rabbit mAb 兔单抗证实LC3B 表达的沉默。 |
