K
Kanneboyina Nagaraju
Researcher at Binghamton University
Publications - 189
Citations - 9970
Kanneboyina Nagaraju is an academic researcher from Binghamton University. The author has contributed to research in topics: Duchenne muscular dystrophy & Skeletal muscle. The author has an hindex of 52, co-authored 181 publications receiving 8793 citations. Previous affiliations of Kanneboyina Nagaraju include Children's National Medical Center & Johns Hopkins University.
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Journal ArticleDOI
Sexual dimorphism in immune response genes as a function of puberty
Rebecca L. Lamason,Po Zhao,Rashmi Rawat,Adrian Davis,John C. Hall,Jae Jin Chae,Rajeev K. Agarwal,Phillip Cohen,Antony Rosen,Eric P. Hoffman,Kanneboyina Nagaraju +10 more
TL;DR: These results demonstrate that sexual dimorphism in innate and adaptive immune genes is dependent on puberty, and reveal that estrogen influences immunoglobulin levels in post-pubertal female mice via the Fas-FasL pathway.
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Deconstructing Pompe Disease by Analyzing Single Muscle Fibers: “To See a World in a Grain of Sand…”
Nina Raben,Shoichi Takikita,Maria Gabriela Pittis,Bruno Bembi,Suely K N Marie,Ashley Roberts,Laura Page,Priya S. Kishnani,Benedikt Schoser,Yin-Hsiu Chien,Evelyn Ralston,Kanneboyina Nagaraju,Paul H. Plotz +12 more
TL;DR: Analysis of vesicles of the lysosomal-degradative pathway in isolated single muscle fibers from Pompe patients showed abundant autophagosome formation and areas of autophagic buildup of a wide range of sizes, suggesting clearing or preventing autophagy buildup seems a necessary target of Pompe disease therapy.
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Muscular dystrophy in the mdx mouse is a severe myopathy compounded by hypotrophy, hypertrophy and hyperplasia
William Duddy,Stephanie Duguez,Helen Johnston,Tatiana V. Cohen,Tatiana V. Cohen,Aditi Phadke,Heather Gordish-Dressman,Kanneboyina Nagaraju,Viola F. Gnocchi,SiewHui Low,Terence A. Partridge +10 more
TL;DR: The best-known consequence of lack of dystrophin that is common to DMD and the mdx mouse is the conspicuous necrosis and regeneration of muscle fibres, and protocols for measuring this are presented, in terms both of loss of muscle nuclei previously labelled with BrdU and of the intensity of myonuclear labelling withBrdU administered during the regeneration period.
Journal ArticleDOI
Risk factors and disease mechanisms in myositis.
TL;DR: Novel approaches, better-defined phenotypes, and international, multidisciplinary consensus have contributed to progress, and it is hoped that these methods will eventually enable therapeutic intervention before the onset or major progression of disease.
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Mitochondria mediate cell membrane repair and contribute to Duchenne muscular dystrophy
Maria Candida Vila,Maria Candida Vila,Sree Rayavarapu,Marshall W. Hogarth,Jack H. Van der Meulen,Adam Horn,Adam Horn,Aurelia Defour,Shin'ichi Takeda,Kristy J. Brown,Kristy J. Brown,Yetrib Hathout,Yetrib Hathout,Kanneboyina Nagaraju,Kanneboyina Nagaraju,Jyoti K. Jaiswal,Jyoti K. Jaiswal +16 more
TL;DR: It is identified that mitochondrial deficit in muscular dystrophy compromises the repair of injured myofibers and it is shown that this repair mechanism is distinct from and complimentary to the dysferlin-mediated repair of damaged myofiber cells.