MafA-deficient and beta cell-specific MafK-overexpressing hybrid transgenic mice develop human-like severe diabetic nephropathy

Biochemical and Biophysical Research Communications

Volumn 389, Issue 2, 2009, Pages 235-240

  Shimohata, Homare ^a,b   Yoh, Keigyou ^a   Fujita, Akiko ^a   Morito, Naoki ^a   Ojima, Masami ^a   Tanaka, Hiromi ^a   Hirayama, Kouichi ^b   Kobayashi, Masaki ^b   Kudo, Takashi ^a   Yamagata, Kunihiro ^a   Takahashi, Satoru ^a  

^a UNIVERSITY OF TSUKUBA   (Japan)

^b TOKYO MEDICAL UNIVERSITY   (Japan)

Author keywords

Diabetes mellitus; Diabetic nephropathy; MafA; MafK

Indexed keywords

CREATININE; TRANSCRIPTION FACTOR MAFA; TRANSCRIPTION FACTOR MAFK;

ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ARTICLE; CELL STRUCTURE; CONTROLLED STUDY; CREATININE BLOOD LEVEL; DIABETES MELLITUS; DIABETIC NEPHROPATHY; EMBRYO DEVELOPMENT; FEMALE; HISTOPATHOLOGY; MOUSE; NONHUMAN; PANCREAS ISLET BETA CELL; PRIORITY JOURNAL; PROTEIN EXPRESSION; PROTEINURIA; UNINEPHRECTOMY;

ANIMALS; DIABETIC NEPHROPATHIES; DISEASE MODELS, ANIMAL; FEMALE; HUMANS; ISLETS OF LANGERHANS; KIDNEY; MAF TRANSCRIPTION FACTORS, LARGE; MAFK TRANSCRIPTION FACTOR; MICE; MICE, TRANSGENIC;

MUS; MUS MUSCULUS;

EID: 70349314313     PISSN: 0006291X     EISSN: 10902104     Source Type: Journal    
DOI: 10.1016/j.bbrc.2009.08.124     Document Type: Article

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