Expression of dominant-negative STAT5 inhibits growth hormone- and prolactin-induced proliferation of insulin-producing cells

Diabetes

Volumn 50, Issue SUPPL. 1, 2001, Pages

  Galsgaard, Elisabeth Douglas ^a,b   Friedrichsen, Birgitte Nissen ^a   Nielsen, Jens Høiriis ^a   Møldrup, Annette ^a  

^a HAGEDORN RESEARCH INSTITUTE   (Denmark)

^b UNIVERSITY OF COPENHAGEN   (Denmark)

Author keywords

[No Author keywords available]

Indexed keywords

GROWTH HORMONE; INSULIN; PROLACTIN; STAT5 PROTEIN;

ANIMAL CELL; CELL PROLIFERATION; CONFERENCE PAPER; CONTROLLED STUDY; GROWTH HORMONE RELEASE; GROWTH REGULATION; INSULIN SYNTHESIS; NONHUMAN; PANCREAS ISLET BETA CELL; PRIORITY JOURNAL; PROLACTIN RELEASE; PROTEIN EXPRESSION; RAT;

EID: 0035125344     PISSN: 00121797     EISSN: None     Source Type: Journal    
DOI: 10.2337/diabetes.50.2007.s40     Document Type: Conference Paper

References (6)

1. Regulation of β-cell mass by hormones and growth factors
2. Molecular mechanism of growth hormone action
3. Identification of a growth hormone-responsive STAT5-binding element in the rat insulin 1 gene
4. Regulation of prolactin receptor (PRLR) gene expression in insulin-producing cells: Prolactin and growth hormone activate one of the rat PRLR gene promoters via STAT5a and STAT5b
5. Prolactin regulation of islet-derived INS-1 cells: Characteristics and immunocytochemical analysis of STAT5 translocation
6. Modulation of glucose responsiveness of insulinoma β-cells by graded overexpression of glucokinase