Akt induces β-cell proliferation by regulating cyclin D1, cyclin D2, and p21 levels and cyclin-dependent kinase-4 activity

Diabetes

Volumn 55, Issue 2, 2006, Pages 318-325

  Fatrai, Szabolcs ^a   Elghazi, Lynda ^a   Balcazar, Norman ^a   Cras Méneur, Corentin ^a   Krits, Irina ^a   Kiyokawa, Hiroaki ^b   Bernal Mizrachi, Ernesto ^a  

^a WASHINGTON UNIVERSITY SCHOOL OF MEDICINE   (United States)

^b UNIVERSITY OF ILLINOIS   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

CYCLIN D1; CYCLIN D2; CYCLIN DEPENDENT KINASE 4; PROTEIN KINASE B; PROTEIN P21;

ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ARTICLE; CELL FUNCTION; CELL PROLIFERATION; CONTROLLED STUDY; DIABETES MELLITUS; ENZYME ACTIVITY; ENZYME REGULATION; GENE DELETION; HETEROZYGOSITY; HOMOZYGOSITY; MOLECULAR DYNAMICS; MOUSE; NONHUMAN; NUCLEOTIDE SEQUENCE; PANCREAS INSUFFICIENCY; PANCREAS ISLET BETA CELL; PRIORITY JOURNAL; PROTEIN FUNCTION; REGULATORY MECHANISM;

ANIMALS; ANIMALS, NEWBORN; CELL PROLIFERATION; CYCLIN D1; CYCLIN-DEPENDENT KINASE 4; CYCLIN-DEPENDENT KINASE INHIBITOR P21; CYCLINS; FEMALE; GENE DELETION; GENE EXPRESSION REGULATION, ENZYMOLOGIC; GLUCOSE; INSULIN-SECRETING CELLS; MALE; MICE; MICE, TRANSGENIC; PROTO-ONCOGENE PROTEINS C-AKT; SIGNAL TRANSDUCTION;

EID: 33644754585     PISSN: 00121797     EISSN: 00121797     Source Type: Journal    
DOI: 10.2337/diabetes.55.02.06.db05-0757     Document Type: Article

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