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Publication : Ataxia and Purkinje cell degeneration in mice lacking the CAMTA1 transcription factor.

First Author  Long C Year  2014
Journal  Proc Natl Acad Sci U S A Volume  111
Issue  31 Pages  11521-6
PubMed ID  25049392 Mgi Jnum  J:212232
Mgi Id  MGI:5578376 Doi  10.1073/pnas.1411251111
Citation  Long C, et al. (2014) Ataxia and Purkinje cell degeneration in mice lacking the CAMTA1 transcription factor. Proc Natl Acad Sci U S A 111(31):11521-6
abstractText  Members of the calmodulin-binding transcription activator (CAMTA) family of proteins function as calcium-sensitive regulators of gene expression in multicellular organisms ranging from plants to humans. Here, we show that global or nervous system deletion of CAMTA1 in mice causes severe ataxia with Purkinje cell degeneration and cerebellar atrophy, partially resembling the consequences of haploinsufficiency of the human CAMTA1 locus. Gene-expression analysis identified a large collection of neuronal genes that were dysregulated in the brains of CAMTA1-mutant mice, and elucidation of a consensus sequence for binding of CAMTA proteins to DNA revealed the association of CAMTA-binding sites with many of these genes. We conclude that CAMTA1 plays an essential role in the control of Purkinje cell function and survival. CAMTA1-mutant mice provide a model to study the molecular mechanisms of neurodegenerative diseases and for screening potential therapeutic interventions for such disorders.
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