D
Dana M. Bis-Brewer
Researcher at University of Miami
Publications - 15
Citations - 286
Dana M. Bis-Brewer is an academic researcher from University of Miami. The author has contributed to research in topics: Hereditary spastic paraplegia & Gene. The author has an hindex of 7, co-authored 13 publications receiving 144 citations. Previous affiliations of Dana M. Bis-Brewer include John P. Hussman Institute for Human Genomics.
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Journal ArticleDOI
Biallelic mutations in SORD cause a common and potentially treatable hereditary neuropathy with implications for diabetes.
Andrea Cortese,Andrea Cortese,Andrea Cortese,Yi Zhu,Adriana P. Rebelo,Sara Negri,Steve Courel,Lisa Abreu,Chelsea Bacon,Yunhong Bai,Dana M. Bis-Brewer,Enrico Bugiardini,Elena Buglo,Matt C. Danzi,Shawna M. E. Feely,Alkyoni Athanasiou-Fragkouli,Nourelhoda A Haridy,Nourelhoda A Haridy,Rosario Isasi,Alaa Khan,Matilde Laura,Stefania Magri,Menelaos Pipis,Chiara Pisciotta,Eric Powell,Alexander M. Rossor,Paola Saveri,Janet E. Sowden,Stefano Tozza,Jana Vandrovcova,Julia E. Dallman,Elena Grignani,Enrico Marchioni,Steven S. Scherer,Beisha Tang,Zhiqiang Lin,Abdullah Al-Ajmi,Rebecca Schüle,Matthis Synofzik,Thierry Maisonobe,Tanya Stojkovic,Michaela Auer-Grumbach,Mohamed A. Abdelhamed,Sherifa A. Hamed,Ruxu Zhang,Fiore Manganelli,Lucio Santoro,Franco Taroni,Davide Pareyson,Henry Houlden,David N. Herrmann,Mary M. Reilly,Michael E. Shy,R. Grace Zhai,Stephan Züchner +54 more
TL;DR: Functional studies suggest that SORD deficiency may be treatable with aldose reductase inhibitors and may contribute to a better understanding of the pathophysiology of diabetes.
Journal ArticleDOI
Glutathione S-Transferase Regulates Mitochondrial Populations in Axons through Increased Glutathione Oxidation
Gaynor A. Smith,Gaynor A. Smith,Gaynor A. Smith,Tzu Huai Lin,Tzu Huai Lin,Amy E. Sheehan,Amy E. Sheehan,Wynand van der Goes van Naters,Lukas J. Neukomm,Lukas J. Neukomm,Hillary K. Graves,Dana M. Bis-Brewer,Dana M. Bis-Brewer,Stephan Züchner,Stephan Züchner,Marc R. Freeman,Marc R. Freeman +16 more
TL;DR: It is shown that the Drosophila glutathione S-transferase Gfzf prevents mitochondrial hyperfusion in axons, and demonstrates that GSTs are key in vivo regulators of axonal mitochondrial length and number.
Journal ArticleDOI
Truncating Mutations in UBAP1 Cause Hereditary Spastic Paraplegia.
Mohammad Ali Farazi Fard,Adriana P. Rebelo,Elena Buglo,Hamid Nemati,Hassan Dastsooz,Ina Gehweiler,Ina Gehweiler,Selina Reich,Selina Reich,Jennifer Reichbauer,Jennifer Reichbauer,Beatriz Quintáns,Andrés Ordóñez-Ugalde,Andrea Cortese,Steve Courel,Lisa Abreu,Eric Powell,Matt C. Danzi,Nicole B. Martuscelli,Dana M. Bis-Brewer,Feifei Tao,Fariba Zarei,Parham Habibzadeh,Majid Yavarian,Farzaneh Modarresi,Mohammad Silawi,Zahra Tabatabaei,Masoume Yousefi,Hamid Reza Farpour,Christoph Kessler,Christoph Kessler,Elisabeth Mangold,Xenia Kobeleva,Ivailo Tournev,Ivailo Tournev,Teodora Chamova,Amelie J. Mueller,Tobias B. Haack,Mark A. Tarnopolsky,Ziv Gan-Or,Ziv Gan-Or,Guy A. Rouleau,Guy A. Rouleau,Matthis Synofzik,Matthis Synofzik,María-Jesús Sobrido,Albena Jordanova,Albena Jordanova,Rebecca Schüle,Rebecca Schüle,Stephan Züchner,Mohammad Ali Faghihi +51 more
TL;DR: It is shown that mRNA in the fibroblasts of affected individuals escapes nonsense-mediated decay and thus leads to the expression of truncated proteins, and UBAP1 provides a bridge toward a more unified pathophysiology.
Journal ArticleDOI
Genetic modifiers and non-Mendelian aspects of CMT.
TL;DR: The current state and future role of alternative, non-Mendelian forms of genetics in CMT are reviewed and the newly identified modifier and risk genes may offer alternative targets for pharmacotherapy of inherited and, potentially, even acquired forms of neuropathies.
Journal ArticleDOI
Perspectives on the Genomics of HSP Beyond Mendelian Inheritance.
TL;DR: A more inclusive perspective on the potential final architecture of HSP genomics is suggested, suggesting efforts to narrow the heritability gap will ultimately lead to more precise and comprehensive genetic diagnoses, which is the starting point for emerging, highly specific gene therapies.