ApoA-I deficiency in mice is associated with redistribution of apoA-II and aggravated AApoAII amyloidosis[S] - Wang, Yaoyong; Sawashita, Jinko; Qian, Jinze; Zhang, Beiru; Fu, Xiaoying; Tian, Geng; Chen, Lei; Mori, Masayuki; Higuchi, Keiichi (Journal of lipid research, 2011)
Keywords: age; Aging; Amyloid - biosynthesis; amyloid heart disease; Amyloidosis - metabolism; Amyloidosis - pathology; Amyloidosis - physiopathology; Animals; Apolipoprotein A-I - deficiency; Apolipoprotein A-I - genetics; Apolipoprotein A-II - blood; Apolipoprotein A-II - genetics; apolipoproteins; cholesterol; Cholesterol, HDL - blood; distribution; Female; Gene Deletion; lipids; Liver - chemistry; Liver - metabolism; Mice; Mice, Inbred C57BL; Mice, Knockout; Myocardium - chemistry; Myocardium - metabolism; Particle Size; RNA, Messenger - analysis; RNA, Messenger - biosynthesis; Triglycerides - blood; cholesterol; apolipoproteins; lipids; amyloid heart disease; distribution; age