| 货号 | 6213S |
| 描述 | SignalSilence® LC3B siRNA II 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 II 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 #6212 (+) or SignalSilence® LC3B siRNA II (+), 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 #6212 (+)或SignalSilence® LC3B siRNA II (+)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。用α-Tubulin (11H10) Rabbit mAb 兔单抗作为加样，并验证特异性的LC3B siRNA对照，LC3B (D11) XP® Rabbit mAb 兔单抗证实LC3B 表达的沉默。 |
