Research Topics
| Laxman GangwaniSummaryAffiliation: University of Massachusetts Medical School Country: USA Publications
| Collaborators
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Detail Information
Publications
Deficiency of the zinc finger protein ZPR1 causes defects in transcription and cell cycle progressionLaxman Gangwani
Program in Molecular Medicine, University of Massachusetts Medical School, Worcester, Massachusetts 01605, USA
J Biol Chem 281:40330-40. 2006..These changes in subnuclear architecture and cell cycle progression may be caused by transcriptional defects in ZPR1-deficient cells, including decreased histone gene expression...
Deficiency of the zinc finger protein ZPR1 causes neurodegenerationBeth Doran
Program in Molecular Medicine, Department of Cell Biology, and Howard Hughes Medical Institute, University of Massachusetts Medical School, Worcester, MA 01605, USA
Proc Natl Acad Sci U S A 103:7471-5. 2006..We report that ZPR1-deficient mice exhibit axonal pathology and neurodegeneration. These data identify ZPR1 deficiency as a contributing factor in neurodegenerative disorders...
ZPR1 is essential for survival and is required for localization of the survival motor neurons (SMN) protein to Cajal bodiesLaxman Gangwani
Program in Molecular Medicine, Howard Hughes Medical Institute, University of Massachusetts Medical School, 373 Plantation St, Worcester, MA 01605, USA
Mol Cell Biol 25:2744-56. 2005..Together, these data indicate that ZPR1 contributes to the regulation of SMN complexes and that it is essential for cell survival...
Structural insights into the interaction of the evolutionarily conserved ZPR1 domain tandem with eukaryotic EF1A, receptors, and SMN complexesAshwini K Mishra
Program in Molecular Medicine and Department of Biochemistry and Molecular Pharmacology, University of Massachusetts Medical School, Worcester, MA 01655, USA
Proc Natl Acad Sci U S A 104:13930-5. 2007..Structural differences between the ZPR1 domains contribute to the observed functional divergence and provide evidence for distinct modalities of interaction with eEF1A and survival motor neuron complexes...
