Results 111 to 120 of about 1,007,169 (424)

Inhibition of acyl‐CoA synthetase long‐chain isozymes decreases multiple myeloma cell proliferation and causes mitochondrial dysfunction

Molecular Oncology, EarlyView.
Triacsin C inhibition of the acyl‐CoA synthetase long chain (ACSL) family decreases multiple myeloma cell survival, proliferation, mitochondrial respiration, and membrane potential. Made with Biorender.com. Multiple myeloma (MM) is an incurable cancer of plasma cells with a 5‐year survival rate of 59%.
Connor S. Murphy, Heather Fairfield, Victoria E. DeMambro, Samaa Fadel, Carlos A. Gartner, Michelle Karam, Christian Potts, Princess Rodriguez, Ya‐Wei Qiang, Habib Hamidi, Xiangnan Guan, Calvin P. H. Vary, Michaela R. Reagan   +12 more
wiley   +1 more source

Development and assessment of novel machine learning models to predict the probability of postoperative nausea and vomiting for patient-controlled analgesia

Scientific Reports, 2023
Postoperative nausea and vomiting (PONV) can lead to various postoperative complications. The risk assessment model of PONV is helpful in guiding treatment and reducing the incidence of PONV, whereas the published models of PONV do not have a high ...
Min Xie, Yan Deng, Zuofeng Wang, Yanxia He, Xingwei Wu, Meng Zhang, Yao He, Yu Liang, Tao Li   +8 more
doaj   +1 more source

Mitochondria Clumping vs. Mitochondria Fusion in CMT2A Diseases

Life, 2022
Phenotypic variations in Charcot-Marie-Tooth disease type 2A (CMT2A) result from the many mutations in the mitochondrial fusion protein, mitofusin 2 (MFN2).
Antonietta Franco, Caroline E. Walton, Xiawei Dang   +2 more
doaj   +1 more source

Humanin G (HNG) protects age-related macular degeneration (AMD) transmitochondrial ARPE-19 cybrids from mitochondrial and cellular damage. [PDF]

, 2017
Age-related macular degeneration (AMD) ranks third among the leading causes of visual impairment with a blindness prevalence rate of 8.7%. Despite several treatment regimens, such as anti-angiogenic drugs, laser therapy, and vitamin supplementation ...
Chwa, Marilyn, Cohen, Pinchas, Kenney, M Cristina, Kuppermann, Baruch D, Lu, Stephanie, Nashine, Sonali, Nesburn, Anthony B   +6 more
core   +1 more source

Etoposide‐induced cancer cell death: roles of mitochondrial VDAC1 and calpain, and resistance mechanisms

Molecular Oncology, EarlyView.
The complex mode of action of the topoisomerase II inhibitor etoposide in triggering apoptosis involves several mechanisms: overexpression of the mitochondrial protein VDAC1, leading to its oligomerization and formation of a large channel that mediates the release of pro‐apoptotic protein; and overexpression of the apoptosis regulators p53, Bax, and ...
Aditya Karunanithi Nivedita, Varda Shoshan‐Barmatz   +1 more
wiley   +1 more source

Microtubule-Mediated Misregulation of Junctophilin-2 Underlies T-Tubule Disruptions and Calcium Mishandling in mdx Mice

JACC: Basic to Translational Science, 2016
Cardiac myocytes from the mdx mouse, the mouse model of Duchenne muscular dystrophy, exhibit t-tubule disarray and increased calcium sparks, but a unifying molecular mechanism has not been elucidated.
Kurt W. Prins, MD, PhD, Michelle L. Asp, PhD, Huiliang Zhang, PhD, Wang Wang, MD, PhD, Joseph M. Metzger, PhD   +4 more
doaj   +1 more source

Encounter networks from collective mitochondrial dynamics support the emergence of effective mtDNA genomes in plant cells [PDF]

arXiv, 2021
Mitochondria in plant cells form strikingly dynamic populations of largely individual organelles. Each mitochondrion contains on average less than a full copy of the mitochondrial DNA (mtDNA) genome. Here, we asked whether mitochondrial dynamics may allow individual mitochondria to `collect' a full copy of the mtDNA genome over time, by facilitating ...
arxiv  

Familial ALS-superoxide dismutases associate with mitochondria and shift their redox potentials [PDF]

, 2006
Recent studies suggest that the toxicity of familial amyotrophic lateral sclerosis mutant Cu, Zn superoxide dismutase (SOD1) arises from its selective recruitment to mitochondria. Here we demonstrate that each of 12 different familial ALS-mutant SOD1s
Butler Gralla, Edith, Carrì, Maria Teresa, Casciati, Arianna, Cozzolino, Mauro, Crosio, Claudia, Ferri, Alberto, Nencini, Monica, Rotilio, Giuseppe, Valentine, Joan Selverstone   +8 more
core   +2 more sources

Respiratory complex I‐mediated NAD+ regeneration regulates cancer cell proliferation through the transcriptional and translational control of p21Cip1 expression by SIRT3 and SIRT7

Molecular Oncology, EarlyView.
NAD+ regeneration by mitochondrial complex I NADH dehydrogenase is important for cancer cell proliferation. Specifically, NAD+ is necessary for the activities of NAD+‐dependent deacetylases SIRT3 and SIRT7, which suppress the expression of p21Cip1 cyclin‐dependent kinase inhibitor, an antiproliferative molecule, at the translational and transcriptional
Masato Higurashi, Kazunori Mori, Hidetsugu Nakagawa, Momoko Uchida, Fumihiro Ishikawa, Motoko Shibanuma   +5 more
wiley   +1 more source

TOMM20 as a driver of cancer aggressiveness via oxidative phosphorylation, maintenance of a reduced state, and resistance to apoptosis

Molecular Oncology, EarlyView.
TOMM20 increases cancer aggressiveness by maintaining a reduced state with increased NADH and NADPH levels, oxidative phosphorylation (OXPHOS), and apoptosis resistance while reducing reactive oxygen species (ROS) levels. Conversely, CRISPR‐Cas9 knockdown of TOMM20 alters these cancer‐aggressive traits.
Ranakul Islam, Megan E. Roche, Zhao Lin, Diana Whitaker‐Menezes, Victor Diaz‐Barros, Eurico Serrano, Maria Paula Martinez Cantarin, Nancy J. Philp, Atrayee Basu Mallick, Ubaldo Martinez‐Outschoorn   +9 more
wiley   +1 more source