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[1] Helgadottir A, Thorleifsson G, Manolescu A, et al. A common variant on chromosome 9p21 affects the risk of myocardial infarction[J]. Science, 2007, 316:1491-1493. doi: 10.1126/science.1142842 [2] Saxena R, Voight BF, Lyssenko V, et al. Genome-wide association study of 14000 cases of seven common diseases and 3, 000 shared controls[J]. Nature, 2007, 447:661-678. doi: 10.1038/nature05911 [3] McPherson R, Pertsemlidis A, Kavaslar N, et al. A common allele on chromosome 9 associated with coronary heart disease[J]. Science, 2007, 316:1488-1491. doi: 10.1126/science.1142447 [4] Pasmant E, Sabbagh A, Vidaud M, et al. ANRIL, a long, noncoding RNA, is an unexpected major hotspot in GWAS[J]. FASEB J, 2011, 25:444-448. doi: 10.1096/fj.10-172452 [5] Pasmant E, Laurendeau I, Heron D, et al. Characterization of a germ-line deletion, including the entire INK4/ARF locus, in a melanoma-neural system tumor family:identification of ANRIL, an antisense noncoding RNA whose expression coclusters with ARF[J]. Cancer Res, 2007, 67:3963-3969. doi: 10.1158/0008-5472.CAN-06-2004 [6] Canepa ET, Scassa ME, Ceruti JM, et al. INK4 proteins, a family of mammalian CDK inhibitors with novel biological functions[J]. IUBMB Life, 2007, 59:419-426. doi: 10.1080/15216540701488358 [7] Matheu A, Maraver A, Collado M, et al. Anti-aging activity of the Ink4/Arf locus[J]. Aging Cell, 2009, 8:152-161. doi: 10.1111/j.1474-9726.2009.00458.x [8] Yap KL, Li S, Munoz-Cabello AM, et al. Molecular interplay of the noncoding RNA ANRIL and methylated histone H3 lysine 27 by polycomb CBX7 in transcriptional silencing of INK4a[J]. Mol Cell, 2010, 38:662-674. doi: 10.1016/j.molcel.2010.03.021 [9] El Messaoudi-Aubert S, Nicholls J, Maertens GN, et al. Role for the MOV10 RNA helicase in polycomb-mediated repression of the INK4a tumor suppressor[J]. Nat Struct Mol Biol, 2010, 17:862-868. doi: 10.1038/nsmb.1824 [10] Popov N, Gil J. Epigenetic regulation of the INK4b-ARF-INK4a locus:in sickness and in health[J]. Epigenetics, 2010, 5:685-690. doi: 10.4161/epi.5.8.12996 [11] Yu W, Gius D, Onyango P, et al. Epigenetic silencing of tumour suppressor gene p15 by its antisense RNA[J]. Nature, 2008, 451:202-206. doi: 10.1038/nature06468 [12] Kotake Y, Nakagawa T, Kitagawa K, et al. Long non-coding RNA ANRIL is required for the PRC2 recruitment to and silencing of p15(INK4B) tumor suppressor gene[J]. Oncogene, 2011, 30:1956-1962. doi: 10.1038/onc.2010.568 [13] Sato K, Nakagawa H, Tajima A, et al. ANRIL is implicated in the regulation of nucleus and potential transcriptional target of E2F1[J]. Oncol Rep, 2010, 24:701-707. http://www.wanfangdata.com.cn/details/detail.do?_type=perio&id=5a2b776e9167506cf20119555fa8c798 [14] Johnson AD, Hwang SJ, Voorman A, et al. Resequencing and clinical associations of the 9p21.3 Region:A comprehensive investigation in the Framingham Heart Study[J]. Circulation, 2013, 127:799-810. doi: 10.1161/CIRCULATIONAHA.112.111559 [15] Jarinova O, Stewart AF, Roberts R, et al. Functional analysis of the chromosome 9p21.3 coronary artery disease risk locus[J]. Arterioscler Thromb Vasc Biol, 2009, 29:1671-1677. doi: 10.1161/ATVBAHA.109.189522 [16] Holdt LM, Beutner F, Scholz M, et al. ANRIL expression is associated with atherosclerosis risk at chromosome 9p21[J]. Arterioscler Thromb Vasc Biol, 2010, 30:620-627. doi: 10.1161/ATVBAHA.109.196832 [17] Gizard F, Amant C, Barbier O, et al. PPAR alpha inhibits vascular smooth muscle cell proliferation underlying intimal hyperplasia by inducing the tumor suppressor p16INK4a[J]. J Clin Invest, 2005, 115:3228-3238. doi: 10.1172/JCI22756 [18] Visel A, Zhu Y, May D, et al. Targeted deletion of the 9p21 non-coding coronary artery disease risk interval in mice[J]. Nature, 2010, 464:409-412. doi: 10.1038/nature08801 [19] Saxena R, Voight BF, Lyssenko V, et al. Genome-wide association analysis identifies loci for type 2 diabetes and triglyceride levels[J]. Science, 2007, 316:1331-1336. doi: 10.1126/science.1142358 [20] Zeggini E, Weedon MN, Lindgren CM, et al. Replication of genome-wide association signals in UK samples reveals risk loci for type 2 diabetes[J]. Science, 2007, 316:1336-1341. doi: 10.1126/science.1142364 [21] Scott LJ, Mohlke KL, Bonnycastle LL, et al. A genome-wide association study of type 2 diabetes in Finns detects multiple susceptibility variants[J]. Science, 2007, 316:1341-1345. doi: 10.1126/science.1142382 [22] Peng F, Hu D, Gu C, et al. The relationship between five widely-evaluated variants in CDKN2A/B and CDKAL1 genes and the risk of type 2 diabetes:a meta-analysis[J]. Gene, 2013, 531:435-443. doi: 10.1016/j.gene.2013.08.075 [23] Al-Sinani S, Woodhouse N, Al-Mamari A, et al. Association of gene variants with susceptibility to type 2 diabetes among Omanis[J]. World J Diabetes, 2015, 6:358-366. doi: 10.4239/wjd.v6.i2.358 [24] Krishnamurthy J, Torrice C, Ramsey MR, et al. Ink4a/Arf expression is a biomarker of aging[J]. J Clin Invest, 2004, 114:1299-1307. doi: 10.1172/JCI22475 [25] Fajas L, Blanchet E, Annicotte JS. CDK4, pRB and E2F1:connected to insulin[J]. Cell Div, 2010, 5:6. doi: 10.1186/1747-1028-5-6 [26] Dagenais M, Skeldon A, Saleh M. The inflammasome:in memory of Dr. Jurg Tschopp[J]. Cell Death Differ, 2012, 19:5-12. doi: 10.1038/cdd.2011.159 [27] Bantubungi K, Hannou SA, Caron-Houde S, et al. Cdkn2a/p16Ink4a regulates fasting-induced hepatic gluconeogenesis through the PKA-CREB-PGC1alpha pathway[J]. Diabetes, 2014, 63:3199-3209. doi: 10.2337/db13-1921 [28] Ahmed W, Ali IS, Riaz M, et al. Association of ANRIL polymorphism (rs1333049:C>G) with myocardial infarction and its pharmacogenomic role in hypercholesterolemia[J]. Gene, 2013, 515:416-420. doi: 10.1016/j.gene.2012.12.044 [29] Hrdlickova B, de Almeida RC, Borek Z, et al. Genetic variation in the non-coding genome:Involvement of micro-RNAs and long non-coding RNAs in disease[J]. Biochim Biophys Acta, 2014, 1842:1910-1922. doi: 10.1016/j.bbadis.2014.03.011
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