ArticleThe EMBO journal2000
The level of DLDB/CHIP controls the activity of the LIM homeodomain protein apterous: evidence for a functional tetramer complex in vivo.
Article in The EMBO journal, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed.
- Crystal structure of human LDB1 in complex with SSBP2.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Holdase activity of secreted Hsp70 masks amyloid-β42 neurotoxicity in Drosophila.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Chi and dLMO function antagonistically on Notch signaling through directly regulation of fng transcription.Scientific reports · 2016Article
- Anti-Aβ single-chain variable fragment antibodies exert synergistic neuroprotective activities in Drosophila models of Alzheimer's disease.Human molecular genetics · 2015Article
- Silk gland factor-2, involved in fibroin gene transcription, consists of LIM homeodomain, LIM-interacting, and single-stranded DNA-binding proteins.The Journal of biological chemistry · 2013Article
- p∆TubHA4C, a new versatile vector for constitutive expression in Drosophila.Molecular biology reports · 2013Article
- Molecular analysis of sex chromosome-linked mutants in the silkworm Bombyx mori.Journal of genetics · 2010Review
- Regulation of LIM-domain-binding 1 protein expression by ubiquitination of Lys134.The Biochemical journal · 2010Article
- Transcription intermediary factor 1gamma decreases protein expression of the transcriptional cofactor, LIM-domain-binding 1.Biochemical and biophysical research communications · 2010Article
- The transcriptional co-factor Chip acts with LIM-homeodomain proteins to set the boundary of the eye field in Drosophila.Development (Cambridge, England) · 2010Article
- The Ldb1 and Ldb2 transcriptional cofactors interact with the Ste20-like kinase SLK and regulate cell migration.Molecular biology of the cell · 2009Article
- Regulation of estrogen-dependent transcription by the LIM cofactors CLIM and RLIM in breast cancer.Cancer research · 2009Article
- Single-stranded DNA-binding proteins regulate the abundance and function of the LIM-homeodomain transcription factor LHX2 in pituitary cells.Biochemical and biophysical research communications · 2008Article
- Drosophila LIM-only is a positive regulator of transcription during thoracic bristle development.Genetics · 2008Article
- GATA4/FOG2 transcriptional complex regulates Lhx9 gene expression in murine heart development.BMC developmental biology · 2008Article
- Single-stranded DNA-binding proteins regulate the abundance of LIM domain and LIM domain-binding proteins.Genes & development · 2007Article
- SCL assembles a multifactorial complex that determines glycophorin A expression.Molecular and cellular biology · 2004Article
- LIM-domain-binding protein 1: a multifunctional cofactor that interacts with diverse proteins.EMBO reports · 2003Review
- Identification of a TAL1 target gene reveals a positive role for the LIM domain-binding protein Ldb1 in erythroid gene expression and differentiation.Molecular and cellular biology · 2003Article
- Ssdp proteins interact with the LIM-domain-binding protein Ldb1 to regulate development.Proceedings of the National Academy of Sciences of the United States of America · 2002Article
Corrections and comments
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Authors and funding
4 authors.
Funding
Abstract
The LIM homeodomain (LIM-HD) protein Apterous (Ap) and its cofactor DLDB/CHIP control dorso- ventral (D/V) patterning and growth of Drosophila wing. To investigate the molecular mechanisms of Ap/CHIP function we altered their relative levels of expression and generated mutants in the LIM1, LIM2 and HD domains of Ap, as well as in the LIM-interacting and self-association domains of CHIP. Using in vitro and in vivo assays we found that: (i) the levels of CHIP relative to Ap control D/V patterning; (ii) the LIM1 and LIM2 domains differ in their contributions to Ap function; (iii) Ap HD mutations cause weak dominant negative effects; (iv) overexpression of ChipDeltaSAD mutants mimics Ap lack-of-function, and this dominant negative phenotype is caused by titration of Ap because it can be rescued by adding extra Ap; and (v) overexpression of ChipDeltaLID mutants also causes an Ap lack-of-function phenotype, but it cannot be rescued by extra Ap. These results support the model that the Ap-CHIP active complex in vivo is a tetramer.
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