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pro vyhledávání: '"Dylan J. Mittauer"'
Autor:
Olha M. Koval, Emily K. Nguyen, Dylan J. Mittauer, Karima Ait-Aissa, William C. Chinchankar, Isabella M. Grumbach
Publikováno v:
International Journal of Molecular Sciences, Vol 24, Iss 16, p 12897 (2023)
Type 2 diabetes (T2D) is associated with increased risk of atherosclerotic vascular disease due to excessive vascular smooth muscle cell (VSMC) proliferation. Here, we investigated the role of mitochondrial dysfunction and Ca2+ levels in VSMC prolife
Externí odkaz:
https://doaj.org/article/029ee44280c94cdbb8a60648414928d8
Autor:
Olha M. Koval, Emily K. Nguyen, Dylan J. Mittauer, Karima Ait-Aissa, William Chinchankar, Lan Qian, Muniswamy Madesh, Dao-Fu Dai, Isabella M. Grumbach
Publikováno v:
bioRxiv
BackgroundType 2 diabetes (T2D) is associated with a strongly increased risk for restenosis after angioplasty driven by proliferation of vascular smooth muscle cells (VSMCs). Here, we sought to determine whether and how mitochondrial dysfunction in T
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::0a1ca2a903f50fda58ba4c42cf8d2419
https://europepmc.org/articles/PMC9948984/
https://europepmc.org/articles/PMC9948984/
Autor:
Olha M, Koval, Emily K, Nguyen, Velarchana, Santhana, Trevor P, Fidler, Sara C, Sebag, Tyler P, Rasmussen, Dylan J, Mittauer, Stefan, Strack, Prabhat C, Goswami, E Dale, Abel, Isabella M, Grumbach
Publikováno v:
Science signaling. 12(579)
The role of the mitochondrial Ca(2+) uniporter (MCU) in physiologic cell proliferation remains to be defined. Here, we demonstrated that the MCU was required to match mitochondrial function to metabolic demands during cell cycling. During the G1/S tr
Autor:
Prabhat C. Goswami, Emily K. Nguyen, Isabella M. Grumbach, Olha M. Koval, Velarchana Santhana, Stefan Strack, Trevor P. Fidler, Tyler P. Rasmussen, E. Dale Abel, Dylan J. Mittauer, Sara C. Sebag
Publikováno v:
Science Signaling. 12
The role of the mitochondrial Ca2+ uniporter (MCU) in physiologic cell proliferation remains to be defined. Here, we demonstrated that the MCU was required to match mitochondrial function to metabolic demands during the cell cycle. During the G1-S tr