Results 81 to 90 of about 37,375 (191)

Vivid views of the PINK1 protein [PDF]

open access: yesNature, 2017
Structures of an unusual enzymatic domain in PINK1 provide insights into how this protein regulates the function of organelles called mitochondria, and how mutations in PINK1 contribute to Parkinson’s disease. Structures of an unusual enzymatic domain in PINK1 provide insights into how this protein regulates the function of organelles called ...
Salima, Daou, Frank, Sicheri
openaire   +2 more sources

PINK1 deficiency impairs osteoblast differentiation through aberrant mitochondrial homeostasis

open access: yesStem Cell Research & Therapy, 2021
Background PTEN-induced kinase 1 (PINK1) is a serine/threonine-protein kinase in mitochondria that is critical for mitochondrial quality control.
So-Young Lee   +12 more
doaj   +1 more source

Protective effects of Buyinqianzheng Formula on mitochondrial morphology by PINK1/Parkin pathway in SH-SY5Y cells induced by MPP+

open access: yesJournal of Traditional Chinese Medical Sciences, 2020
Objective: Buyinqianzheng Formula (BYQZF) is clinically employed in traditional Chinese medicine to treat Parkinson’s disease (PD) by improving mitochondrial dysfunction.
Haojie Ma   +9 more
doaj   +1 more source

Distinct Mechanisms of Pathogenic DJ-1 Mutations in Mitochondrial Quality Control [PDF]

open access: yes, 2018
The deglycase and chaperone protein DJ-1 is pivotal for cellular oxidative stress responses and mitochondrial quality control. Mutations in PARK7, encoding DJ-1, are associated with early-onset familial Parkinson’s disease and lead to pathological ...
Abeti   +66 more
core   +3 more sources

Endorepellin remodels the endothelial transcriptome toward a pro-autophagic and pro-mitophagic gene signature. [PDF]

open access: yes, 2018
Regulation of autophagy by proteolytically cleaved fragments of heparan sulfate proteoglycans is a novel and current research focus in tumor biology. Endorepellin is the C-terminal angiostatic fragment of the heparan sulfate proteoglycan perlecan and ...
Andreuzzi, Eva   +5 more
core   +1 more source

Role of mitophagy in spinal cord ischemia-reperfusion injury

open access: yesNeural Regeneration Research
Spinal cord ischemia-reperfusion injury, a severe form of spinal cord damage, can lead to sensory and motor dysfunction. This injury often occurs after traumatic events, spinal cord surgeries, or thoracoabdominal aortic surgeries.
Yanni Duan   +9 more
doaj   +1 more source

Dissecting PINK1/parkin mitophagy dynamics

open access: yes, 2022
Mitochondria homeostasis is crucial for cellular integrity. Several quality control mechanisms can revert mitochondrial damage. However, in situations of acute and irreversible mitochondrial stress, specific pathways are activated to promote the selective degradation of mitochondria: mitophagy.
openaire   +2 more sources

The role of mitophagy in periodontitis bone tissue

open access: yesKouqiang hemian waike zazhi
[Objective:] To investigate changes in mitophagy levels in bone tissue during periodontitis in mice and to explore the effects of lipopolysaccharide (LPS)-induced mitophagy on the osteogenic differentiation capacity of mouse embryonic osteoblast ...
CAI Yuyi   +4 more
doaj   +1 more source

αSynuclein control of mitochondrial homeostasis in human-derived neurons is disrupted by mutations associated with Parkinson’s disease [PDF]

open access: yes, 2017
The etiology of Parkinson’s disease (PD) converges on a common pathogenic pathway of mitochondrial defects in which α-Synuclein (αSyn) is thought to play a role.
Alloatti, Matías   +12 more
core   +1 more source

PINK1 mutants associated with recessive Parkinson’s disease are defective in inhibiting mitochondrial release of cytochrome c

open access: yesNeurobiology of Disease, 2007
Mutations in PTEN-induced kinase 1 (PINK1) gene cause recessive familial type 6 of Parkinson’s disease (PARK6). We investigated molecular mechanisms underlying PINK1 neuroprotective function and PARK6 mutation-induced loss of PINK1 function ...
Hung-Li Wang   +7 more
doaj   +1 more source

Home - About - Disclaimer - Privacy