| 货号 | 24799S |
| 同种亚型 | Rabbit IgG |
| 反应种属 | Human\Mouse\Moneky |
| 来源宿主 | Rabbit IgG |
| 应用 | WB, ChIP |
| 目标/特异性 | POLR1A (D6S6S) Rabbit mAb recognizes endogenous levels of total POLR1A protein. |
| 使用方法 | W ChIP |
| 供应商 | CST |
| 灵敏度 | Endogenous |
| 背景 | RNA polymerase I (RNAPI) is a large multi-protein complex that functions as a DNA dependent, RNA polymerase, which is primarily responsible for the transcription of ribosomal RNA (rRNA) genes. The largest subunit, Rpa194, or POLR1A, along with selectivity factor 1 (SL1), and the transactivator protein upstream binding factor (UBF) make up the core transcriptional machinery of the RNAPI complex (1-3). The RNAPI complex is recruited specifically to rDNA promoters by SL1, which contains TBP and TAF proteins, to transcribe precursors to rRNA (2). These precursors are processed into 18S, 5.8S, and 28S mature rRNAs, which make up most of the ribosomal structure (1). Similar to the RNA polymerase II complex, there are other core components that are required for transcription of target genes such as the TFIIH complex and SPT6 (4, 5). Overexpression of nascent rRNA has been shown to be associated with poor prognosis in certain cancer types, and enlarged nucleoli are a hallmark of cellular proliferation and aggressive tumors (6-8). Oncogenes such as Myc, Ras, and PI3K can drive RNAPI-mediated rRNA transcription, making POLR1A a key therapeutic target (9). Indeed, specific targeting of RNAPI activity with a small molecule inhibitor can induce autophagy selectively in tumor cells while having minimal effects in normal cells (10). Additionally, mutations in POLR1A are associated with acrofacial dysostosis, Cincinnati type, a cranioskeletal malformation syndrome. Loss of function mutations result in disrupted ribosome biogenesis and p53-mediated cell death affecting skeletal precursor cells or the neural-crest (11). |
| 存放说明 | -20C |
| 计算分子量 | 200 |
| 参考文献 | 1 . Russell, J. and Zomerdijk, J.C. (2006) Biochem Soc Symp , 203-16. 2 . Jantzen, H.M. et al. (1990) Nature 344, 830-6. 3 . Comai, L. et al. (1992) Cell 68, 965-76. 4 . Iben, S. et al. (2002) Cell 109, 297-306. 5 . Engel, K.L. et al. (2015) Mol Cell Biol 35, 2321-31. 6 . Williamson, D. et al. (2006) Genes Chromosomes Cancer 45, 839-45. 7 . Derenzini, M. et al. (2000) J Pathol 191, 181-6. 8 . Maggi, L.B. and Weber, J.D. (2005) Cancer Invest 23, 599-608. 9 . Woods, S.J. et al. (2015) Biochim Biophys Acta 1849, 821-9. 10 . Drygin, D. et al. (2011) Cancer Res 71, 1418-30. 11 . Weaver, K.N. et al. (2015) Am J Hum Genet 96, 765-74. |
Chromatin immunoprecipitations were performed with cross-linked chromatin from 4 x 106 HeLa cells and either 10 μl of POLR1A (D6S6S) Rabbit mAb or 2 μl of Normal Rabbit IgG #2729 using SimpleChIP® Enzymatic Chromatin IP Kit (Magnetic Beads) #9003. The enriched DNA was quantified by real-time PCR using SimpleChIP® Human 28S rDNA Repeat Primers #14901, SimpleChIP® Human β-Actin Promoter Primers #13653, and SimpleChIP® Human α Satellite Repeat Primers #4486. The amount of immunoprecipitated DNA in each sample is represented as signal relative to the total amount of input chromatin, which is equivalent to one. | |
Western blot analysis of extracts from various cell lines using POLR1A (D6S6S) Rabbit mAb. |
