Molecular regulation of Fas expression in β-cells

Diabetes

Volumn 50, Issue SUPPL. 1, 2001, Pages

  Darville, Martine I ^a   Liu, Dongbo ^a   Chen, Meng Chi ^a   Eizirik, Décio L ^a  

^a DIABETES RESEARCH CENTER   (Belgium)

Author keywords

[No Author keywords available]

Indexed keywords

CCAAT ENHANCER BINDING PROTEIN; CYTOKINE; FAS ANTIGEN; GAMMA INTERFERON; INTERLEUKIN 1BETA; N(G) METHYLARGININE; NITRIC OXIDE; NITRIC OXIDE SYNTHASE; TRANSCRIPTION FACTOR; TUMOR NECROSIS FACTOR ALPHA;

APOPTOSIS; AUTOIMMUNITY; BINDING SITE; CELL DEATH; CONFERENCE PAPER; FLUORESCENCE ACTIVATED CELL SORTER; GENE EXPRESSION REGULATION; GENETIC TRANSFECTION; INSULIN DEPENDENT DIABETES MELLITUS; KNOCKOUT MOUSE; PANCREAS ISLET BETA CELL; PRIORITY JOURNAL; PROMOTER REGION; REGULATORY MECHANISM; REVERSE TRANSCRIPTION POLYMERASE CHAIN REACTION;

EID: 0035124875     PISSN: 00121797     EISSN: None     Source Type: Journal    
DOI: 10.2337/diabetes.50.2007.s83     Document Type: Conference Paper

References (5)

1. Fas and Fas ligand expression in inflamed islets in pancreas sections of patients with recent-onset type I diabetes mellitus
2. Mouse islet cell lysis mediated by IL-1-induced Fas
3. Nitric oxide production and Fas surface expression mediate two independent pathways of cytokine-induced murine β-cell damage
4. Nitric oxide primes pancreatic beta cells for Fas-mediated destruction in insulin-dependent diabetes mellitus
5. -1-)