TY - JOUR
T1 - Generation of transgenic mice producing a human transthyretin variant
T2 - A possible mouse model for familial amyloidotic polyneuropathy
AU - Sasaki, Hiroyuki
AU - Toné, Shigenobu
AU - Nakazato, Masamitsu
AU - Yoshioka, Katsuji
AU - Matsuo, Hisayuki
AU - Kato, Yoshihiro
AU - Sakaki, Yoshiyuki
N1 - Funding Information:
We thank Dr. R. M. Evans at The Salk Institute for providing the plasmid pMGH, and Dr. Y. Takagi at Fujita-Gakuen Medical College for encouragement. Ms H. Hamada typed this manuscript with great care. The work is supported by grants from the Ministry of Education, Science and Culture of Japan to H.S. and Y.S.
PY - 1986/9/16
Y1 - 1986/9/16
N2 - Type I familial amyloidotic polyneuropathy(FAP) results from the systemic deposition of a plasma transthyretin(TTR) variant with a Val ▶ Met change at position 30. In an attempt to establish a model of this disease, we generated transgenic mice producing the variant TIR. A DNA fragment containing the mouse metallothionein-I promoter fused to the structural gene coding for the human TTR variant was microinjected into fertilized mouse eggs. Among 72 mice that developed from these eggs, ten carried the fusion gene and three of these showed significant concentrations of the variant TTR in their serum. These mice may be useful in elucidating the pathogenesis of FAP and in establishing a therapy for this intractable disorder.
AB - Type I familial amyloidotic polyneuropathy(FAP) results from the systemic deposition of a plasma transthyretin(TTR) variant with a Val ▶ Met change at position 30. In an attempt to establish a model of this disease, we generated transgenic mice producing the variant TIR. A DNA fragment containing the mouse metallothionein-I promoter fused to the structural gene coding for the human TTR variant was microinjected into fertilized mouse eggs. Among 72 mice that developed from these eggs, ten carried the fusion gene and three of these showed significant concentrations of the variant TTR in their serum. These mice may be useful in elucidating the pathogenesis of FAP and in establishing a therapy for this intractable disorder.
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U2 - 10.1016/S0006-291X(86)80060-2
DO - 10.1016/S0006-291X(86)80060-2
M3 - Article
C2 - 3021142
AN - SCOPUS:0022513804
SN - 0006-291X
VL - 139
SP - 794
EP - 799
JO - Biochemical and Biophysical Research Communications
JF - Biochemical and Biophysical Research Communications
IS - 2
ER -
