Mouse Gene Set: IGLESIAS_E2F_TARGETS_UP

For the Human gene set with the same name, see IGLESIAS_E2F_TARGETS_UP

Standard name IGLESIAS_E2F_TARGETS_UP
Systematic name MM1010
Brief description Genes up-regulated in pancreatic cells from mice with double knockout of E2F1 [GeneID=1869] and E2F2 [GeneID=1870] compared to wild type.
Full description or abstract E2F transcription factors are thought to be key regulators of cell growth control. Here we use mutant mouse strains to investigate the function of E2F1 and E2F2 in vivo. E2F1/E2F2 compound-mutant mice develop nonautoimmune insulin-deficient diabetes and exocrine pancreatic dysfunction characterized by endocrine and exocrine cell dysplasia, a reduction in the number and size of acini and islets, and their replacement by ductal structures and adipose tissue. Mutant pancreatic cells exhibit increased rates of DNA replication but also of apoptosis, resulting in severe pancreatic atrophy. The expression of genes involved in DNA replication and cell cycle control was upregulated in the E2F1/E2F2 compound-mutant pancreas, suggesting that their expression is repressed by E2F1/E2F2 activities and that the inappropriate cell cycle found in the mutant pancreas is likely the result of the deregulated expression of these genes. Interestingly, the expression of ductal cell and adipocyte differentiation marker genes was also upregulated, whereas expression of pancreatic cell marker genes were downregulated. These results suggest that E2F1/E2F2 activity negatively controls growth of mature pancreatic cells and is necessary for the maintenance of differentiated pancreatic phenotypes in the adult.
Collection M2: Curated
      CGP: Chemical and Genetic Perturbations
Source publication Pubmed 15146237   Authors: Iglesias A,Murga M,Laresgoiti U,Skoudy A,Bernales I,Fullaondo A,Moreno B,Lloreta J,Field SJ,Real FX,Zubiaga AM
Exact source Table 1S
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Source species Mus musculus
Contributed by Kevin Vogelsang (MSigDB Team)
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identifier namespace		 MOUSE_SEQ_ACCESSION
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Version history 2022.1.Mm: First Introduced.

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