Genomic regions identified for BMD in a large sample including epistatic interactions and gender-specific effectsu

被引:46
作者
Xiao, Peng
Shen, Hui
Guo, Yan-Fang
Xiong, Dong-Hai
Liu, Yao-Zhong
Liu, Yong-Jun
Zhao, Lan-Juan
Long, Ji-Rong
Guo, Yan
Recker, Robert R.
Deng, Hong-Wen
机构
[1] Univ Missouri, Sch Med, Dept Orthoped Surg, Kansas City, MO 64108 USA
[2] Univ Missouri, Sch Med, Dept Basic Med Sci, Kansas City, MO 64108 USA
[3] Creighton Univ, Sch Med, Dept Biomed Sci, Omaha, NE 68178 USA
[4] Creighton Univ, Sch Med, Osteoporosis Res Ctr, Omaha, NE 68178 USA
[5] Xi An Jiao Tong Univ, Sch Life Sci & Technol, Key Lab Biomed Informat Engn, Minist Educ, Xian 710049, Shanxi, Peoples R China
[6] Xi An Jiao Tong Univ, Sch Life Sci & Technol, Inst Mol Genet, Xian 710049, Shanxi, Peoples R China
[7] Hunan Normal Univ, Coll Life Sci, Lab Mol & Stat Genet, Changsha, Hunan, Peoples R China
关键词
BMD; whole genome linkage; quantitative trait loci; epistatic interaction; gender-specific;
D O I
10.1359/JBMR.060717
中图分类号
R5 [内科学];
学科分类号
1002 [临床医学]; 100201 [内科学];
摘要
A genome-wide linkage scan was conducted using a large white sample to identify QTLs for BMD. We found QTLs in the total sample and the gender-specific subgroups, as well as significant epistatic interactions underlying BMD variations.
引用
收藏
页码:1536 / 1544
页数:9
相关论文
共 59 条
[1]
Merlin-rapid analysis of dense genetic maps using sparse gene flow trees [J].
Abecasis, GR ;
Cherny, SS ;
Cookson, WO ;
Cardon, LR .
NATURE GENETICS, 2002, 30 (01) :97-101
[2]
PPARγ insufficiency enhances osteogenesis through osteoblast formation from bone marrow progenitors [J].
Akune, T ;
Ohba, S ;
Kamekura, S ;
Yamaguchi, M ;
Chung, UI ;
Kubota, N ;
Terauchi, Y ;
Harada, Y ;
Azuma, Y ;
Nakamura, K ;
Kadowaki, T ;
Kawaguchi, H .
JOURNAL OF CLINICAL INVESTIGATION, 2004, 113 (06) :846-855
[3]
Rosiglitazone causes bone loss in mice by suppressing osteoblast differentiation and bone formation [J].
Ali, AA ;
Weinstein, RS ;
Stewart, SA ;
Parfitt, AM ;
Manolagas, SC ;
Jilka, RL .
ENDOCRINOLOGY, 2005, 146 (03) :1226-1235
[4]
Multipoint quantitative-trait linkage analysis in general pedigrees [J].
Almasy, L ;
Blangero, J .
AMERICAN JOURNAL OF HUMAN GENETICS, 1998, 62 (05) :1198-1211
[5]
AMOS CI, 1994, AM J HUM GENET, V54, P535
[6]
Assessing genetic linkage and association with robust components of variance approaches [J].
Amos, CI ;
Zhu, DK ;
Boerwinkle, E .
ANNALS OF HUMAN GENETICS, 1996, 60 :143-160
[7]
BLACK DM, 1992, J BONE MINER RES, V7, P633
[8]
A whole-genome linkage scan suggests several genomic regions potentially containing quantitative trait loci for osteoporosis [J].
Deng, HW ;
Xu, FH ;
Huang, QY ;
Shen, H ;
Deng, HY ;
Conway, T ;
Liu, YJ ;
Liu, YZ ;
Li, JL ;
Zhang, HT ;
Davies, KM ;
Recker, RR .
JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, 2002, 87 (11) :5151-5159
[9]
A genomewide linkage scan for quantitative-trait loci for obesity phenotypes [J].
Deng, HW ;
Deng, HY ;
Liu, YJ ;
Liu, YZ ;
Xu, FH ;
Shen, H ;
Conway, T ;
Li, JL ;
Huang, QY ;
Davies, KM ;
Recker, RR .
AMERICAN JOURNAL OF HUMAN GENETICS, 2002, 70 (05) :1138-1151
[10]
Relevance of the genes for bone mass variation to susceptibility to osteoporotic fractures and its implications to gene search for complex human diseases [J].
Deng, HW ;
Mahaney, MC ;
Willams, JT ;
Li, J ;
Conway, T ;
Davies, KM ;
Li, JL ;
Deng, HY ;
Recker, RR .
GENETIC EPIDEMIOLOGY, 2002, 22 (01) :12-25