Zobrazeno 1 - 10
of 10
pro vyhledávání: '"Ryan J. Russo"'
Autor:
Benjamin Greene, Ryan J Russo, Shannon Dwyer, Katie Malley, Errin Roberts, Joseph Serrielo, Peter Piepenhagen, Sheila Cummings, Susan Ryan, Christine Zarazinski, Sasidhar Uppuganti, Nikolai Bukanov, Jeffry S Nyman, Megan K Cox, Shiguang Liu, Oxana Ibraghimov‐Beskrovnaya, Yves Sabbagh
Publikováno v:
JBMR Plus, Vol 5, Iss 9, Pp n/a-n/a (2021)
ABSTRACT Osteogenesis imperfecta (OI), is a genetic disorder of bone fragility caused by mutations in collagen I or proteins involved in collagen processing. Previous studies in mice and human OI bones have shown that excessive activation of TGF‐β
Externí odkaz:
https://doaj.org/article/e9260be1938a4cbb897d1633289d0ae3
Autor:
Bing Wang, Mandy M. Smith, Stefano Zanotti, Stephen L. Madden, Hervé Husson, Vijay Modur, Laurie A. Smith, Nikolay O. Bukanov, Thomas A. Natoli, Sarah Moreno, Tyler Picariello, Katherine W. Klinger, Brenda Richards, Hyejung Park, Cheng Zhu, Oxana Ibraghimov-Beskrovnaya, Ryan J. Russo
Publikováno v:
Human Molecular Genetics
Bardet–Biedl syndrome (BBS) is a pleiotropic autosomal recessive ciliopathy affecting multiple organs. The development of potential disease-modifying therapy for BBS will require concurrent targeting of multi-systemic manifestations. Here, we show
Autor:
Katie Malley, Yves Sabbagh, Joseph Serrielo, Christine Zarazinski, Oxana Ibraghimov-Beskrovnaya, Megan K. Cox, Sasidhar Uppuganti, Nikolai Bukanov, Jeffry S. Nyman, Errin Roberts, Benjamin Greene, Ryan J. Russo, Shiguang Liu, Peter A. Piepenhagen, Sheila Cummings, Susan Ryan, Shannon Dwyer
Publikováno v:
JBMR Plus
JBMR Plus, Vol 5, Iss 9, Pp n/a-n/a (2021)
JBMR Plus, Vol 5, Iss 9, Pp n/a-n/a (2021)
Osteogenesis imperfecta (OI), is a genetic disorder of bone fragility caused by mutations in collagen I or proteins involved in collagen processing. Previous studies in mice and human OI bones have shown that excessive activation of TGF‐β signalin
Autor:
null Benjamin Greene, null Ryan J Russo, null Shannon Dwyer, null Katie Malley, null Errin Roberts, null Joseph Serrielo, null Peter Piepenhagen, null Sheila Cummings, null Susan Ryan, null Christine Zarazinski, null Sasidhar Uppuganti, null Nikolai Bukanov, null Jeffry S. Nyman, null Megan K. Cox, null Shiguang Liu, null Oxana Ibraghimov‐Beskrovnaya, null Yves Sabbagh
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::1bf23b65b1a3b634cb6529f2f8a76c36
https://doi.org/10.1002/jbm4.10530/v2/response1
https://doi.org/10.1002/jbm4.10530/v2/response1
Autor:
Olivier Duclos, Christina Bracken, Ryan J. Russo, Kelly A. Rogers, Philip Janiak, Steven R. Ledbetter, Thomas A. Natoli, Nikolay O. Bukanov, Oxana Ibraghimov-Beskrovnaya, Philippe Beauverger, Hervé Husson
Publikováno v:
American Journal of Physiology-Renal Physiology. 310:F1414-F1422
Polycystic kidney diseases (PKDs) are genetic diseases characterized by renal cyst formation with increased cell proliferation, apoptosis, and transition to a secretory phenotype at the expense of terminal differentiation. Despite recent progress in
Autor:
Katy Billot, Mandy M. Smith, Rose Pitstick, Jagesh V. Shah, Kate Zhang, George A. Carlson, Laurent Meijer, Hervé Husson, Laurie A. Smith, Oxana Ibraghimov-Beskrovnaya, Monica Lane, Nikolay O. Bukanov, Steven R. Ledbetter, Ryan J. Russo, Sarah Moreno, David R. Beier, Mikhail Sergeev
Publikováno v:
Human Molecular Genetics
Polycystic kidney diseases (PKDs) comprise a subgroup of ciliopathies characterized by the formation of fluid-filled kidney cysts and progression to end-stage renal disease. A mechanistic understanding of cystogenesis is crucial for the development o
Autor:
Katherine W. Klinger, Viatcheslav R. Akmaev, Brian P. Cook, Dongyu Liu, Oxana Ibraghimov-Beskrovnaya, Xiaohong Cao, Clarence J. Wang, Gregory M. Landes, Douglas M. Jefferson, Brenda Richards, Hervé Husson, Bruce L. Roberts, Dana Barberio, Partha Manavalan, Ryan J. Russo, Shelley A. Grubman
Publikováno v:
Genomics. 84:497-510
Autosomal dominant polycystic kidney disease (ADPKD) is caused by mutations in the PKD1 or PKD2 gene, but cellular mechanisms of cystogenesis remain unclear. In an attempt to display the array of cyst-specific molecules and to elucidate the disease p
Autor:
William R. Dackowski, Hervé Husson, Laurie A. Smith, Steven R. Ledbetter, Thomas A. Natoli, Alexei Belenky, James A. Shayman, Bing Wang, Ryan J. Russo, Kelly A. Rogers, John P. Leonard, Nikolay O. Bukanov, Oxana Ibraghimov-Beskrovnaya, Svetlana Komarnitsky, Yeva Budman
Publikováno v:
Nature medicine. 16(7)
Polycystic kidney disease (PKD) represents a family of genetic disorders characterized by renal cystic growth and progression to kidney failure. No treatment is currently available for people with PKD, although possible therapeutic interventions are
Autor:
Natacha Patey, Dominique Joly, Hervé Husson, Nikolay O. Bukanov, Bertrand Knebelmann, Oxana Ibraghimov-Beskrovnaya, Ryan J. Russo
Publikováno v:
Histochemistry and cell biology. 124(6)
Mutations in polycystin-1 (PC-1) are responsible for autosomal dominant polycystic kidney disease (ADPKD), characterized by formation of fluid-filled tubular cysts. The PC-1 is a multifunctional protein essential for tubular differentiation and matur
Autor:
Hilary F. Luderer, Katherine W. Klinger, Oxana Ibraghimov-Beskrovnaya, Ryan J. Russo, Nikolay O. Bukanov, Bruce L. Roberts, Partha Manavalan, William R. Dackowski
Publikováno v:
Genomics. 80(1)
Most cases of autosomal dominant polycystic kidney disease are caused by mutations in the gene PKD1 , encoding polycystin-1. To gain insight into the role of polycystin-1 in tubulogenesis and cystogenesis using the well-characterized canine kidney ep