ArticleDevelopmental biology2006
Genetic interactions between Drosophila melanogaster menin and Jun/Fos.
Article in Developmental biology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
9 citing papers in PubMed, 26 citations in OpenAlex.
- Article
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- Nuclear elongation during spermiogenesis depends on physical linkage of nuclear pore complexes to bundled microtubules by Drosophila Mst27D.PLoS genetics · 2023Article
- Modulation of Global Gene Expression by Aneuploidy and CNV of Dosage Sensitive Regulatory Genes.Genes · 2021Article
- Multiple endocrine neoplasia type 1.Frontiers of hormone research · 2013Review
- Deficiency of the cytoskeletal protein SPECC1L leads to oblique facial clefting.American journal of human genetics · 2011Article
- The histone acetyltransferase Elp3 plays in active role in the control of synaptic bouton expansion and sleep in Drosophila.Journal of neurochemistry · 2010Article
- A new genetic model of activity-induced Ras signaling dependent pre-synaptic plasticity in Drosophila.Brain research · 2010Article
- Article
Corrections and comments
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Authors and funding
13 authors at 3 institutions in 1 country.
Funding
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.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.