Zobrazeno 1 - 10
of 41
pro vyhledávání: '"Nadiezhda Cantu-Medellin"'
Autor:
Andria R. Robinson, Matthew J. Yousefzadeh, Tania A. Rozgaja, Jin Wang, Xuesen Li, Jeremy S. Tilstra, Chelsea H. Feldman, Siobhán Q. Gregg, Caroline H. Johnson, Erin M. Skoda, Marie-Céline Frantz, Harris Bell-Temin, Hannah Pope-Varsalona, Aditi U. Gurkar, Luigi A. Nasto, Renã A.S. Robinson, Heike Fuhrmann-Stroissnigg, Jolanta Czerwinska, Sara J. McGowan, Nadiezhda Cantu-Medellin, Jamie B. Harris, Salony Maniar, Mark A. Ross, Christy E. Trussoni, Nicholas F. LaRusso, Eugenia Cifuentes-Pagano, Patrick J. Pagano, Barbara Tudek, Nam V. Vo, Lora H. Rigatti, Patricia L. Opresko, Donna B. Stolz, Simon C. Watkins, Christin E. Burd, Claudette M. St. Croix, Gary Siuzdak, Nathan A. Yates, Paul D. Robbins, Yinsheng Wang, Peter Wipf, Eric E. Kelley, Laura J. Niedernhofer
Publikováno v:
Redox Biology, Vol 17, Iss , Pp 259-273 (2018)
Accumulation of senescent cells over time contributes to aging and age-related diseases. However, what drives senescence in vivo is not clear. Here we used a genetic approach to determine if spontaneous nuclear DNA damage is sufficient to initiate se
Externí odkaz:
https://doaj.org/article/d9a5a11c481f443f90c56186ddad5c93
Autor:
Jeffrey R. Koenitzer, Gustavo Bonacci, Steven R. Woodcock, Chen-Shan Chen, Nadiezhda Cantu-Medellin, Eric E. Kelley, Francisco J. Schopfer
Publikováno v:
Redox Biology, Vol 8, Iss C, Pp 1-10 (2016)
Nitro-fatty acids (NO2-FA) are metabolic and inflammatory-derived electrophiles that mediate pleiotropic signaling actions. It was hypothesized that NO2-FA would impact mitochondrial redox reactions to induce tissue-protective metabolic shifts in cel
Externí odkaz:
https://doaj.org/article/734c0fe8f5364d86a1484b0e58752578
Autor:
Rommel C. Morales, Edward S.M. Bahnson, George E. Havelka, Nadiezhda Cantu-Medellin, Eric E. Kelley, Melina R. Kibbe
Publikováno v:
Redox Biology, Vol 4, Iss C, Pp 226-233 (2015)
Background: Nitric oxide (•NO) is more effective at inhibiting neointimal hyperplasia following arterial injury in male versus female rodents, though the etiology is unclear. Given that superoxide (O2•−) regulates cellular proliferation, and
Externí odkaz:
https://doaj.org/article/b3f9873747b84e6aab06cb70d879b2ed
Publikováno v:
Redox Biology, Vol 1, Iss 1, Pp 353-358 (2013)
Nearly 30 years have passed since the discovery of xanthine oxidoreductase (XOR) as a critical source of reactive species in ischemia/reperfusion injury. Since then, numerous inflammatory disease processes have been associated with elevated XOR activ
Externí odkaz:
https://doaj.org/article/7ee0d88e00dd4772b59d15102a469d7a
Autor:
Adam C. Straub, Soma Jobbagy, Francisco J. Schopfer, Mark T. Gladwin, Mizanur Rahaman, Eric E. Kelley, Courtney Sparacino-Watkins, Anh T. Nguyen, Catherine J. Baty, Nolan T Carew, Scott A. Hahn, Megan P. Miller, Emil Martin, Nadiezhda Cantu-Medellin, Katherine C. Wood
Publikováno v:
Circulation Research. 121:137-148
Rationale: Soluble guanylate cyclase (sGC) heme iron, in its oxidized state (Fe 3+ ), is desensitized to NO and limits cGMP production needed for downstream activation of protein kinase G–dependent signaling and blood vessel dilation. Objective: Al
Autor:
Patrick J. Pagano, Bhupesh Singla, Huiping Lin, Simon C. Watkins, Eric E. Kelley, Pushpankur Ghoshal, Douglas M. Feck, Nadiezhda Cantu-Medellin, Shanmugam Nagarajan, Lukasz Mateuszuk, Daniel N. Meijles, Gabor Csanyi, Jeffrey S. Isenberg, Imad Al Ghouleh
Publikováno v:
Antioxidants & Redox Signaling. 26:886-901
AIMS: Macropinocytosis has been implicated in cardiovascular and other disorders, yet physiological factors that initiate fluid-phase internalization and the signaling mechanisms involved remain poorly identified. The present study was designed to ex
Autor:
Nadiezhda Cantu-Medellin, Bhupesh Singla, Douglas M. Feck, Pushpankur Ghoshal, Gabor Csanyi, Huiping Lin, David Fulton, Stephen Haigh, Eric E. Kelley
Publikováno v:
Antioxidants & Redox Signaling. 26:902-916
Internalization of extracellular fluid and its solute by macropinocytosis requires dynamic reorganization of actin cytoskeleton, membrane ruffling, and formation of large endocytic vacuolar compartments, called macropinosomes, inside the cell. Althou
Autor:
Christin E. Burd, Christy E. Trussoni, Lora H. Rigatti, Jin Wang, Matthew J. Yousefzadeh, Jolanta Czerwińska, Luigi Aurelio Nasto, Erin M. Skoda, Jamie B. Harris, Tania A. Rozgaja, Caroline H. Johnson, Heike Fuhrmann-Stroissnigg, Paul D. Robbins, Renã A. S. Robinson, Nathan A. Yates, Donna B. Stolz, Aditi U. Gurkar, Eric E. Kelley, Simon C. Watkins, Jeremy S. Tilstra, Gary Siuzdak, Marie-Céline Frantz, Harris Bell-Temin, Nam Vo, Patrick J. Pagano, Peter Wipf, Hannah Pope-Varsalona, Siobhán Q. Gregg, Xuesen Li, Sara J. McGowan, Patricia L. Opresko, Nicholas F. LaRusso, Eugenia Cifuentes-Pagano, Claudette M. St. Croix, Nadiezhda Cantu-Medellin, Chelsea H. Feldman, Andria Rasile Robinson, Yinsheng Wang, Laura J. Niedernhofer, Salony Maniar, Mark A. Ross, Barbara Tudek
Publikováno v:
Redox Biology, Vol 17, Iss, Pp 259-273 (2018)
Accumulation of senescent cells over time contributes to aging and age-related diseases. However, what drives senescence in vivo is not clear. Here we used a genetic approach to determine if spontaneous nuclear DNA damage is sufficient to initiate se
Autor:
George E. Havelka, Melina R. Kibbe, Nadiezhda Cantu-Medellin, Eric E. Kelley, Rommel Morales, Edward Moreira Bahnson
Publikováno v:
Redox Biology, Vol 4, Iss C, Pp 226-233 (2015)
Redox Biology
Redox Biology
Background Nitric oxide (•NO) is more effective at inhibiting neointimal hyperplasia following arterial injury in male versus female rodents, though the etiology is unclear. Given that superoxide (O2•−) regulates cellular proliferation, and •
Autor:
Eric E. Kelley, Qun Jiang, Edward Moreira Bahnson, Melina R. Kibbe, Janet M. Vercammen, Nathaniel C. Koo, George E. Havelka, Nadiezhda Cantu-Medellin, Aaron Tsui
Publikováno v:
Nitric Oxide. 44:8-17
Superoxide (O2(•-)) promotes neointimal hyperplasia following arterial injury. Conversely, nitric oxide ((•)NO) inhibits neointimal hyperplasia through various cell-specific mechanisms, including redox regulation. What remains unclear is whether