http://www.cnr.it/ontology/cnr/individuo/prodotto/ID20942
Genetic interactions between Drosophila melanogaster menin and Jun/Fos. (Articolo in rivista)
- Type
- Label
- Genetic interactions between Drosophila melanogaster menin and Jun/Fos. (Articolo in rivista) (literal)
- Anno
- 2006-01-01T00:00:00+01:00 (literal)
- Alternative label
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori
- Cerrato A; Parisi M; Santa Anna S; Missirlis F; Guru S; Agarwal S; Sturgill D; Talbot T; Spiegel A; Collins F; Chandrasekharappa S; Marx S; Oliver B. (literal)
- Pagina inizio
- Pagina fine
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroVolume
- Rivista
- Note
- ISI Web of Science (WOS) (literal)
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#affiliazioni
- Aniello Cerrato a,!, Michael Parisi a, Sonia Santa Anna b, Fanis Missirlis c, Siradanahalli Guru b,1,
Sunita Agarwal a, David Sturgill a, Thomas Talbot d, Allen Spiegel a, Francis Collins b,
Settara Chandrasekharappa b, Stephen Marx a, Brian Oliver a
a National Institute of Diabetes and Digestive and Kidney Diseases, Department of Health and Human Services, Bethesda, MD 20892, USA
b National Human Genome Research Institute, Department of Health and Human Services, Bethesda, MD 20892, USA
c National Institute of Child Health and Human Development, Department of Health and Human Services, Bethesda, MD 20892, USA
d Office of the Director, National Institutes of Health, Department of Health and Human Services, Bethesda, MD 20892, USA (literal)
- Titolo
- Genetic interactions between Drosophila melanogaster menin and Jun/Fos. (literal)
- Abstract
- Menin is a tumor suppressor required to prevent multiple endocrine neoplasia in humans. Mammalian menin protein is associated with
chromatin modifying complexes and has been shown to bind a number of nuclear proteins, including the transcription factor JunD. Menin shows
bidirectional effects acting positively on c-Jun and negatively on JunD. We have produced protein null alleles of Drosophila menin (mnn1) and
have over expressed the Mnn1 protein. Flies homozygous for protein-null mnn1 alleles are viable and fertile. Localized over-expression of Mnn1
causes defects in thoracic closure, a phenotype that sometimes results from insufficient Jun activity. We observed complex genetic interactions
between mnn1 and jun in different developmental settings. Our data support the idea that one function of menin is to modulate Jun activity in a
manner dependent on the cellular context. (literal)
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- Autore CNR
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