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表观遗传学基础和围产医学发展 被引量:2

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摘要 遗传学的经典原理已为临床医师所熟悉并得到广泛应用;分子遗传学的核心是生命过程中所需要的各种蛋白质由基因决定,并因此决定生命体的表型。随着医学的发展,特别是遗传学和病理生理学的发展,许多临床现象和疾病机制难以用经典的遗传学原理加以解释,如源于分化的成熟体细胞的克隆动物未老先衰;具有相同DNA序列的同卵双生双胞胎在表型和疾病易感性方面表现出明显的差异;组织特异性基因在不同受体、组织的表达不同,以及复杂疾病的发生机制与遗传学理论不一致,等等。
作者 朱建幸
出处 《中华围产医学杂志》 CAS 北大核心 2012年第2期80-84,共5页 Chinese Journal of Perinatal Medicine
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  • 1Egger G, Liang G, Aparicio A, et al. Epigenetics in human disease and prospects for epigenetic therapy. Nature, 2004, 429:457-463.
  • 2Zeisel SH. Epigenetic mechanisms for nutrition determinants of later health outcomes. Am J Clin Nutr, 2009, 89.. 1488S- 1493S.
  • 3Suzuki MM, Bird A. DNA methylation landscapes.. provocative insihts from epigenomics. Nat Rev Genet,2008,9: 465 476.
  • 4Dolinoy DC, Weidman JR, Waterland RA, et al. Maternal genistein alters goat color and protects Avy mouse offspring from obesity by modifying the fetal epigenome. Environ Health Perspect,2006,114 : 567-572.
  • 5Waterland RA, Jirtle R1.. Transposable elements: targets for early nutritional effects on epigenetic gent regulation. Mol Cell Biol 2003,23: 5290-5300.
  • 6Kouzarides T. Chromatin modifications and their function. Cell, 2007,128 : 693-705.
  • 7Johnstone RW. Histone-deacetylase inhibitors:novel drugs for the treatment of eaneer. Nat Rev Drug Diseov, 2002, 1:287- 299.
  • 8Newcastle University. Epigenetics and developmental programming conference, Newcastle upon Tyne, UK, 2011. Newcastle upon Tyne, UK: Institute of Genetics, Newcastle University, 2011.

同被引文献20

  • 1Banister CE? Koestler DC,Maccani MA,et al. Infantgrowth restriction is associated with distinct patterns of DNAmethylation in human placentas. Epigenetics, 2011,6 : 920-927.
  • 2Simmons RA. Developmental origins of diabetes: the role ofepigenetic mechanisms. Curr Opin Endocrinol Diabetes Obes,2007, 14:13-16.
  • 3Oyekan A. PPARs and their effects on the cardiovascularsystem. Clin Exp Hyperten.s, 2011,33:287-293.
  • 4Rees WD, McNeil CJ,Maloney CA. The roles of PPARs inthe fetal origins of metabolic health and disease. PPAR Res,2008, 2008:459030.
  • 5Kono T,Ahn G* Moss DR, et al. PPAR-y activationrestores pancreatic islet SERCA2 levels and prevents (3-celldysfunction under conditions of hyperglycemic and cytokinestress. Mol Endocrinol, 2012,26: 257-271.
  • 6Fujiki K, Kano F,Shiota K, et al. Expression of theperoxisome proliferator activated receptor gamma gene isrepressed by DNA methylation in visceral adipose tissue ofmouse models of diabetes. BMC Biol, 2009, 7:38.
  • 7Martin-Gronert MS, Tarry-Adkins JL, Cripps RL, et al.Maternal protein restriction leads to early life alterations inthe expression of key molecules involved in the aging processin rat offspring. Am J Physiol Regul Integr Comp Physiol,2008, 294: R494-R500.
  • 8Chuang CC, Yang RS, Tsai KS, et al. Hyperglycemiaenhances adipogenic induction of lipid accumulation: involvementof extracellular signal-regulated protein kinase 1/2,phosphoinositide 3-kinase/Akt, and peroxisome proliferator-activated receptor gamma signaling. Endocrinology, 2007,148: 4267-4275.
  • 9Ling C, Del Guerra S, Lupi R,et al. Epigenetic regulation ofPPARGC1A in human type 2 diabetic islets and effect oninsulin secretion. Diabetologia, 2008,51 :615-622.
  • 10Gemma C,Sookoian S,Alvarinas J, et al. Maternalpregestational BMI is associated with methylation of thePPARGC1A promoter in newborns. Obesity (Silver Spring),2009,17: 1032-1039.

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