Pbx1 inactivation disrupts pancreas development and in Ipf1-deficient mice promotes diabetes mellitus

Nature Genetics

Volumn 30, Issue 4, 2002, Pages 430-435

  Kim, Seung K ^a   Selleri, Licia ^b,c   Lee, Joon S ^a   Zhang, Andrew Y ^a   Gu, Xueying ^a   Jacobs, Yakop ^b   Cleary, Michael L ^b  

^a STANFORD UNIVERSITY   (United States)

^b STANFORD UNIVERSITY SCHOOL OF MEDICINE   (United States)

^c MEMORIAL SLOAN KETTERING CANCER CENTER   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

AMYLASE; HOMEODOMAIN PROTEIN; INSULIN; PANCREAS ENZYME; TRANSCRIPTION FACTOR; TRANSCRIPTION FACTOR PBX1; UNCLASSIFIED DRUG;

ANIMAL MODEL; ANIMAL TISSUE; ARTICLE; DIABETES MELLITUS; EMBRYO; EMBRYO DEVELOPMENT; GENE EXPRESSION; GENE MUTATION; GENOTYPE; HISTOLOGY; INSULIN RELEASE; MOUSE; NONHUMAN; PANCREAS; PRIORITY JOURNAL;

ANIMALS; BROMODEOXYURIDINE; CELL DIFFERENTIATION; DIABETES MELLITUS; DNA-BINDING PROTEINS; GENETIC PREDISPOSITION TO DISEASE; GENOTYPE; HOMEODOMAIN PROTEINS; IMMUNOHISTOCHEMISTRY; ISLETS OF LANGERHANS; MICE; MICE, TRANSGENIC; MICROSCOPY, CONFOCAL; PANCREAS; PROTEIN BINDING; PROTEIN STRUCTURE, TERTIARY; PROTO-ONCOGENE PROTEINS; RECOMBINATION, GENETIC; TIME FACTORS; TRANS-ACTIVATORS;

ANIMALIA;

EID: 0036544854     PISSN: 10614036     EISSN: None     Source Type: Journal    
DOI: 10.1038/ng860     Document Type: Article

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