## Abstract ## Background Inherited apolipoprotein (Apo) A‐I deficiency is an orphan disorder characterized by high‐density lipoprotein (HDL)‐cholesterol deficiency and premature atherosclerosis. Constitutive over‐expression of ApoA‐I might provide a means to treat this disease. The present study
✦ LIBER ✦
Marked high density lipoprotein deficiency due to apolipoprotein A-I Tomioka (codon 138 deletion)
✍ Scribed by Masamichi Wada; Tatsuya Iso; Bela F. Asztalos; Noriaki Takama; Tadashi Nakajima; Yukihiro Seta; Katsumi Kaneko; Yasuhiro Taniguchi; Hideo Kobayashi; Katsuyuki Nakajima; Ernst J. Schaefer; Masahiko Kurabayashi
- Book ID
- 118422561
- Publisher
- Elsevier Science
- Year
- 2009
- Tongue
- English
- Weight
- 439 KB
- Volume
- 207
- Category
- Article
- ISSN
- 0021-9150
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The effect of a polymorphism, guanine (G) to adenine (A) substitution in the promoter of apolipoprotein A-I gene at a position 78 bp upstream of the transcription initiation site, on the serum high-density lipoprotein (HDL)-cholesterol level was studied in 168 Japanese subjects with HDL-cholesterol