Results 41 to 50 of about 16,238 (247)

Proteasome Inhibitors Decrease the Viability of Pulmonary Arterial Smooth Muscle Cells by Restoring Mitofusin-2 Expression under Hypoxic Conditions

open access: yesBiomedicines, 2022
Pulmonary hypertension (PH) is a severe progressive disease, and the uncontrolled proliferation of pulmonary artery smooth muscle cells (PASMCs) is one of the main causes.
I-Chen Chen   +9 more
doaj   +1 more source

Comparative Untargeted Metabolomic Profiling of Induced Mitochondrial Fusion in Pancreatic Cancer

open access: yesMetabolites, 2021
Mitochondria are dynamic organelles that constantly alter their shape through the recruitment of specialized proteins, like mitofusin-2 (Mfn2) and dynamin-related protein 1 (Drp1).
Nicholas D. Nguyen   +8 more
doaj   +1 more source

HCT116 colorectal liver metastases exacerbate muscle wasting in a mouse model for the study of colorectal cancer cachexia [PDF]

open access: yes, 2020
Colorectal cancer (CRC) is often accompanied by formation of liver metastases (LM) and skeletal muscle wasting, i.e. cachexia. Despite affecting the majority of CRC patients, cachexia remains underserved, understudied and uncured.
Bonetto, Andrea   +3 more
core   +1 more source

Regulating a uniter: control of mitofusin 2 expression [PDF]

open access: yesCardiovascular Research, 2012
This editorial refers to ‘The promoter activity of human Mfn2 depends on Sp1 in vascular smooth muscle cells’ by E. Sorianello et al. , pp. 38–47, this issue. Sorianello et al. 1 provide important new information on the regulation on mitofusin (Mfn)2 expression.
Anne A, Knowlton, Le, Chen
openaire   +2 more sources

Loss of Mitofusin 2 Promotes Endoplasmic Reticulum Stress [PDF]

open access: yesJournal of Biological Chemistry, 2012
The outer mitochondrial membrane GTPase mitofusin 2 (Mfn2) is known to regulate endoplasmic reticulum (ER) shape in addition to its mitochondrial fusion effects. However, its role in ER stress is unknown. We report here that induction of ER stress with either thapsigargin or tunicamycin in mouse embryonic fibroblasts leads to up-regulation of Mfn2 mRNA
Gladys A, Ngoh   +2 more
openaire   +2 more sources

Mitofusin 2 Builds a Bridge between ER and Mitochondria [PDF]

open access: yesCell, 2008
Mutations in mitofusin 2 (MFN2), a dynamin-like GTPase required for mitochondrial fusion, cause the peripheral neuropathy Charcot-Marie-Tooth type 2A. In a recent report in Nature, de Brito and Scorrano (2008) demonstrate a new function of MFN2-tethering the endoplasmic reticulum and mitochondria to control the efficiency of mitochondrial uptake of Ca2+
Merkwirth, C., Langer, T.
openaire   +3 more sources

Mitofusin 2 Exerts a Protective Role in Ischemia Reperfusion Injury Through Increasing Autophagy

open access: yesCellular Physiology and Biochemistry, 2018
Background/Aims: Autophagy is essential for maintaining cellular homeostasis and the survival of terminally differentiated cells as neurons. In this study, we aim to investigate whether mitofusin 2, a mitochondrial fusion protein, mediates autophagy in ...
Cheng Peng   +12 more
doaj   +1 more source

Complementation between mouse Mfn1 and Mfn2 protects mitochondrial fusion defects caused by CMT2A disease mutations [PDF]

open access: yes, 2007
Mfn2, an oligomeric mitochondrial protein important for mitochondrial fusion, is mutated in Charcot-Marie-Tooth disease (CMT) type 2A, a peripheral neuropathy characterized by axonal degeneration.
Chan, David C., Detmer, Scott A.
core   +2 more sources

A new target for an old DUB: UCH-L1 regulates mitofusin-2 levels, altering mitochondrial morphology, function and calcium uptake

open access: yesRedox Biology, 2020
UCH-L1 is a deubiquitinating enzyme (DUB), highly abundant in neurons, with a sub-cellular localization dependent on its farnesylation state. Despite UCH-L1′s association with familial Parkinson's Disease (PD), the effects on mitochondrial bioenergetics ...
Fernanda M. Cerqueira   +9 more
doaj   +1 more source

Mitochondrial dynamics–fusion, fission, movement, and mitophagy–in neurodegenerative diseases [PDF]

open access: yes, 2009
Neurons are metabolically active cells with high energy demands at locations distant from the cell body. As a result, these cells are particularly dependent on mitochondrial function, as reflected by the observation that diseases of mitochondrial ...
Alexander   +42 more
core   +3 more sources

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