SignalSilence® p16 INK4A siRNA I #6598
Supporting Data
| REACTIVITY | H |
Species Cross-Reactivity Key:
- H-Human
Product Information
Product Usage Information
CST recommends transfection with 100 nM p16 INK4A siRNA I 48 to 72 hours prior to cell lysis. For transfection procedure, follow protocol provided by the transfection reagent manufacturer. Please feel free to contact CST with any questions on use.
Each vial contains the equivalent of 100 transfections, which corresponds to a final siRNA concentration of 100 nM per transfection in a 24-well plate with a total volume of 300 μl per well.
Storage
Product Description
Quality Control
Oligonucleotide synthesis is monitored base by base through trityl analysis to ensure appropriate coupling efficiency. The oligo is subsequently purified by affinity-solid phase extraction. The annealed RNA duplex is further analyzed by mass spectrometry to verify the exact composition of the duplex. Each lot is compared to the previous lot by mass spectrometry to ensure maximum lot-to-lot consistency.
Background
Cyclin-dependent kinases (CDKs) are activated in part by forming complexes with cyclins. For example, CDK4 and CDK6 associate with the D-type cyclins and phosphorylate the retinoblastoma protein. This phosphorylation is a necessary event for cells to enter S-phase (1). The inhibitors of CDK4 (INK4) family include p15 INK4B, p16 INK4A, p18 INK4C and p19 INK4D. p18 has been shown to function as a haploinsufficient tumor suppressor in vivo (2). All INK4 proteins are composed of 32 amino acid ankyrin motifs and selectively inhibit CDK4/6 activity. Mutational analyses of p18 implicate the third and the amino-terminal portion of the fourth ankyrin repeat in mediating binding to CDK4/6 (3). The interaction of INK4 family members can be a binary complex with CDK4/6 or ternary complex with cyclin D-bound CDK4/6 and ultimately results in the inhibition of cell cycle progression (4,5).
p16 INK4A directly inhibits the activity of cyclin D, thereby inhibiting S-phase entry (6,7). As such, expression of p16 INK4A is commonly associated with cellular senescence, and disruption of the p16 INK4A gene is frequently observed in human cancers.
- Lukas, J. et al. (1996) Mol. Cell. Biol. 16, 6917-6925.
- Bai, F. et al. (2003) Mol. Cell. Biol. 23, 1269-1277.
- Noh, S.J. et al. (1999) Cancer Res. 59, 558-564.
- Guan, K.L. et al. (1994) Genes Dev. 8, 2939-2952.
- Hirai, H. et al. (1995) Mol. Cell. Biol. 15, 2672-2681.
- Sherr, C.J. (2001) Nat Rev Mol Cell Biol 2, 731-7.
- Lowe, S.W. and Sherr, C.J. (2003) Curr Opin Genet Dev 13, 77-83.
限制使用
除非 CST 的合法授书代表以书面形式书行明确同意，否书以下条款适用于 CST、其关书方或分书商提供的书品。 任何书充本条款或与本条款不同的客书条款和条件，除非书 CST 的合法授书代表以书面形式书独接受， 否书均被拒书，并且无效。
专品专有“专供研究使用”的专专或专似的专专声明， 且未专得美国食品和专品管理局或其他外国或国内专管机专专专任何用途的批准、准专或专可。客专不得将任何专品用于任何专断或治专目的， 或以任何不符合专专声明的方式使用专品。CST 专售或专可的专品提供专作专最专用专的客专，且专用于研专用途。将专品用于专断、专防或治专目的， 或专专售（专独或作专专成）或其他商专目的而专专专品，均需要 CST 的专独专可。客专：(a) 不得专独或与其他材料专合向任何第三方出售、专可、 出借、捐专或以其他方式专专或提供任何专品，或使用专品制造任何商专专品，(b) 不得复制、修改、逆向工程、反专专、 反专专专品或以其他方式专专专专专品的基专专专或技专，或使用专品开专任何与 CST 的专品或服专专争的专品或服专， (c) 不得更改或专除专品上的任何商专、商品名称、徽专、专利或版专声明或专专，(d) 只能根据 CST 的专品专售条款和任何适用文档使用专品， (e) 专遵守客专与专品一起使用的任何第三方专品或服专的任何专可、服专条款或专似专专