M
Michael W. Glynn
Researcher at University of Michigan
Publications - 7
Citations - 2885
Michael W. Glynn is an academic researcher from University of Michigan. The author has contributed to research in topics: Lamin & Progeria. The author has an hindex of 6, co-authored 7 publications receiving 2675 citations. Previous affiliations of Michael W. Glynn include National Institutes of Health.
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Journal ArticleDOI
Recurrent de novo point mutations in lamin A cause Hutchinson-Gilford progeria syndrome
Maria Eriksson,W. Ted Brown,Leslie B. Gordon,Leslie B. Gordon,Michael W. Glynn,Joel Singer,Laura J. Scott,Michael R. Erdos,Christiane M. Robbins,Tracy Moses,Peter Berglund,Amalia Dutra,Evgenia Pak,Sandra G. Durkin,Antonei B. Csoka,Michael Boehnke,Thomas W. Glover,Francis S. Collins +17 more
TL;DR: Evidence of mutations in lamin A (LMNA) as the cause of Hutchinson–Gilford progeria syndrome is presented, and the discovery of the molecular basis of this disease may shed light on the general phenomenon of human ageing.
Journal ArticleDOI
Mutations in FOXC2 (MFH-1), a forkhead family transcription factor, are responsible for the hereditary lymphedema-distichiasis syndrome.
Jianming Fang,Susan L. Dagenais,Robert P. Erickson,Martin F. Arlt,Michael W. Glynn,Jerome L. Gorski,Laurie H. Seaver,Thomas W. Glover +7 more
TL;DR: FoxC2 represents the second known gene to result in hereditary lymphedema, and LD is only the second hereditary disorder known to be caused by a mutation in a forkhead-family gene, and FOXC2 haploinsufficiency results in LD.
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Incomplete processing of mutant lamin A in Hutchinson-Gilford progeria leads to nuclear abnormalities, which are reversed by farnesyltransferase inhibition
TL;DR: Exposure to a farnesyltransferase inhibitor (FTI) caused a significant improvement in the nuclear morphology of cells expressing GFP-progerin and in HGPS cells, suggesting that FTIs may represent a therapeutic option for patients with HGPS.
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Polyalanine expansion in HOXA13: three new affected families and the molecular consequences in a mouse model
Jeffrey W. Innis,Douglas P. Mortlock,Douglas P. Mortlock,Zhi Chen,Zhi Chen,Michael Ludwig,Melissa E. Williams,Thomas M. Williams,Colleen D. Doyle,Zhihong Shao,Michael W. Glynn,Davor Mikulic,Katarina Lehmann,Stefan Mundlos,Boris Utsch,Boris Utsch +15 more
TL;DR: To determine the molecular basis for impaired HOXA13 function, homologous recombination in ES cells in mice was performed to expand the size of the third largest polyalanine tract by 10 residues (HOXA 13(ALA28)).
Journal ArticleDOI
Mutation of the FOXC2 gene in familial distichiasis.
Brian P. Brooks,Brian P. Brooks,Susan L. Dagenais,Christine C. Nelson,Michael W. Glynn,Mark S Caulder,Catherine A. Downs,Thomas W. Glover +7 more
TL;DR: This finding suggests that hereditary distichiasis and LD may not be separate genetic disorders but different phenotypic expressions of the same underlying disorder.