Julie A. Coventry

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The most well-described example of an inherited speech and language disorder is that observed in the multigenerational KE family, caused by a heterozygous missense mutation in the FOXP2 gene. Affected individuals are characterized by deficits in the learning and production of complex orofacial motor sequences underlying fluent speech and display impaired(More)
Mutations in the FOXP2 gene cause a severe communication disorder involving speech deficits (developmental verbal dyspraxia), accompanied by wide-ranging impairments in expressive and receptive language. The protein encoded by FOXP2 belongs to a divergent subgroup of forkhead-box transcription factors, with a distinctive DNA-binding domain and motifs that(More)
The Menkes disease gene encodes a P-type transmembrane ATPase (ATP7A) that translocates cytosolic copper ions across intracellular membranes of compartments along the secretory pathway. ATP7A moves from the trans-Golgi network (TGN) to the cell surface in response to exogenously added copper ions and recycles back to the TGN upon copper removal. The protein(More)
The Menkes disease ATPase (MNK) is a copper transporter that localizes to the mammalian trans-Golgi network (TGN) and shows substantial co-localization wih a ubiquitous TGN resident protein and marker, TGN46. We tested our hypothesis that these two TGN residents and integral membrane proteins are localized to biochemically distinct TGN sub-compartments(More)
ATP7A (MNK) regulates copper homeostasis by translocating from a compartment localized within the trans-Golgi network to the plasma membrane (PM) in response to increased copper load. The mechanisms that regulate the biogenesis of the MNK compartment and the trafficking of MNK are unclear. Here we show that the architecture of the MNK compartment is linked(More)
Holloway ZG, Grabski R, Szul T, Styers ML, Coventry JA, Monaco AP, Sztul E. Activation of ADP-ribosylation factor regulates biogenesis of the ATP7A-containing trans-Golgi network compartment and its Cu-induced trafficking. Am J Physiol Cell Physiol 293: C1753–C1767, 2007. First published October 3, 2007; doi:10.1152/ajpcell.00253.2007.—ATP7A (MNK) regulates(More)
Animals Generation of Foxp2 Mutant Mice We used a gene-driven ENU-based screening approach to generate an allelic series for murine Foxp2. R552H and N549K mice were derived from a large scale ENU mutagenesis project at Medical Research Council Harwell laboratories (Oxfordshire), United Kingdom [S1]. ENU was injected in founder mice of a BALB/c genetic(More)
Mutations in the FOXP2 gene cause a severe communication disorder involving speech deficits (developmental verbal dyspraxia), accompanied by wide-ranging impairments in expressive and receptive language. The protein encoded by FOXP2 belongs to a divergent subgroup of forkhead-box transcription factors, with a distinctive DNA-binding domain and motifs that(More)
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