Results 121 to 130 of about 23,381 (243)

The Roles of PINK1 and Parkin in Parkinson's Disease

open access: yesPLoS Biology, 2010
​ResearchResearch into the causes of both sporadic and familial Parkinson's disease have led to the idea that a key risk factor might be mitochondrial dysfunction. The neurons of the substantia nigra, which are specifically lost in Parkinson's disease, seem to be especially vulnerable to the effects of mitochondrial damage.
openaire   +4 more sources

Neuropsychiatric‐Led Presentation of Late‐Onset Parkin‐Related Parkinson's Disease

open access: yes
Movement Disorders Clinical Practice, EarlyView.
Sarah Fullam   +4 more
wiley   +1 more source

Dental Pulp Stem Cell‐Derived Intracellular Vesicles Inhibit OSCC by Delivering PTEN to Suppress PI3K/AKT/mTOR Signalling Pathway

open access: yesCell Proliferation, EarlyView.
DPSC‐IVs suppressed PI3K/AKT/mTOR signalling pathway by delivering PTEN to tumour cells, which reduced the expression of Bcl‐2 and elevated that of Bax. Meanwhile, DPSC‐IVs activated PINK1/Parkin mediated mitophagy, which further raised ROS levels.
Yu Luo   +10 more
wiley   +1 more source

Levodopa and Melanoma: Practical Recommendations for Parkinson's Disease—International Parkinson and Movement Disorder Society Scientific Issues Committee Viewpoint

open access: yes
Movement Disorders Clinical Practice, EarlyView.
Giorgia Sciacca   +27 more
wiley   +1 more source

Itgb1‐Mediated Stabilization of Vimentin Alleviates Excessive Mechanical Stress‐Induced Nucleus Pulposus Cell Pyroptosis and Intervertebral Disc Degeneration via PINK1‐Parkin‐Dependent Mitophagy

open access: yesCell Proliferation, EarlyView.
Excessive mechanical stress induces nucleus pulposus cell pyroptosis and intervertebral disc degeneration. Itgb1 inhibits MNAT1‐mediated ubiquitination and degradation of Vimentin. Vimentin alleviates excessive mechanical stress‐induced nucleus pulposus cell pyroptosis and intervertebral disc degeneration through PINK1‐Parkin‐dependent mitophagy ...
Xuening Liu   +7 more
wiley   +1 more source

PLIN5 Protects Against Ang II‐Induced Podocyte Lipotoxicity by Interacting With FKBP8 and Preserving Lipid Droplet–Mitochondria Contact

open access: yesCell Proliferation, EarlyView.
PLIN5‐FKBP8 tethers lipid droplets to mitochondria to counteract Ang II‐induced lipotoxicity. ABSTRACT Chronic kidney disease (CKD) remains a major global health challenge. Angiotensin II (Ang II)‐induced lipotoxicity is an important contributor to podocyte injury.
Ping Wang   +7 more
wiley   +1 more source

Mitochondrial transfer in acute myeloid leukaemia and multiple myeloma: Mechanisms, consequences and potential therapeutic opportunities

open access: yesThe FEBS Journal, EarlyView.
Mitochondria can be transferred from bone marrow cells to cancer cells in acute myeloid leukaemia and multiple myeloma, boosting tumour energy production, growth, and drug resistance. This review highlights key transfer mechanisms and shows how targeting mitochondrial movement and dynamics may offer new therapeutic strategies to limit cancer ...
Ebubechukwu Nwarunma   +1 more
wiley   +1 more source

PINK1 modulates Prdx2 to reduce lipotoxicity‐induced apoptosis and attenuate cardiac dysfunction in heart failure mice with a preserved ejection fraction

open access: yesClinical and Translational Medicine
Introduction Heart failure with preserved ejection fraction (HFpEF) is a complex condition characterized by metabolic dysfunction and myocardial lipotoxicity.
Hao Zhang   +10 more
doaj   +1 more source

Ubiquitin and ubiquitin‐like modifications in the endoplasmic reticulum stress response

open access: yesThe FEBS Journal, EarlyView.
Endoplasmic reticulum (ER) stress activates various proteostasis control processes, including the unfolded protein response, ribosome‐associated quality control, and ER‐associated degradation. Ubiquitin and ubiquitin‐like modifications dynamically regulate these processes to determine cell fate, promoting adaptation or inducing cell death.
Tony Avril   +2 more
wiley   +1 more source

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