Results 31 to 40 of about 23,381 (243)
Background: The mitophagy/NLRP3 inflammasome pathway is a promising therapeutic target for cerebral ischemia-reperfusion (I/R). Panax notoginseng (Burkill) F.H.
Qian Xiao +3 more
doaj +1 more source
Phosphorylation of Parkin at serine 65 is essential for its activation in vivo [PDF]
Mutations in PINK1 and Parkin result in autosomal recessive Parkinson's disease (PD). Cell culture and in vitro studies have elaborated the PINK1-dependent regulation of Parkin and defined how this dyad orchestrates the elimination of damaged ...
Thomas G. McWilliams +30 more
doaj +1 more source
Mitochondrial dysfunction plays a significant role in the pathogenesis of Parkinson’s disease (PD). Consistent with this concept, loss of function mutations in the serine/threonine kinase- PINK1 (PTEN-induced putative kinase-1) causes autosomal recessive
Smijin K. Soman, Ruben K. Dagda
doaj +1 more source
PINK1, cancer and neurodegeneration
Cancer and neurodegeneration are two age-related diseases that arise from aberrant signaling in similar cellular systems, those that balance survival and death. Thus, deregulated molecular processes such as DNA damage repair, intracellular energy balance, and key signal transduction systems, including the PI3-kinase/Akt axis can promote tumorigenesis ...
Ciara H, O'Flanagan +2 more
openaire +2 more sources
Mechanism of parkin activation by PINK1 [PDF]
Mutations in the E3 ubiquitin ligase parkin (PARK2, also known as PRKN) and the protein kinase PINK1 (also known as PARK6) are linked to autosomal-recessive juvenile parkinsonism (AR-JP)1,2; at the cellular level, these mutations cause defects in mitophagy, the process that organizes the destruction of damaged mitochondria3,4.
Gladkova, Christina +3 more
openaire +2 more sources
Adaptive mitochondrial mechanisms allow mitochondrial resilience and prevent the worsening of fibrosis, while deregulation of these mechanisms promotes the progression from no/minimal‐mild (F0‐F2) fibrosis to advanced fibrosis and cirrhosis (F3‐F4). Abstract Background and Aims Hepatitis B virus (HBV) infection causes oxidative stress (OS) and alters ...
Dimitri Loureiro +17 more
wiley +1 more source
PINK1 points Parkin to mitochondria [PDF]
For decades, it has been presumed that mitochondrial dysfunction, in the form of impaired complex I activity, may contribute to the cause of Parkinson disease (PD). ( 1) The discovery that several gene mutations cause familial forms of PD ( 1) has led to a renewed enthusiasm for the mitochondrial hypothesis of PD, but this time from a quite distinct ...
Cristofol, Vives-Bauza +1 more
openaire +2 more sources
Interaction of PINK1 with nucleotides and kinetin
The ubiquitin kinase PINK1 accumulates on damaged mitochondria to trigger mitophagy, and PINK1 loss-of-function mutations cause early onset Parkinson’s disease. Nucleotide analogs such as kinetin triphosphate (KTP) were reported to enhance PINK1 activity and may represent a therapeutic strategy for the treatment of Parkinson’s ...
Zhong Yan Gan +7 more
openaire +3 more sources
The effect of 4 weeks of continuous aerobic training with different volumes and starvation on the expression of some genes involved in liver mitophagy in healthy male Wistar rats [PDF]
Introduction and Purpose: An increase in the number of defective mitochondria and their persistence can lead to apoptosis and necrosis of cells. Regular physical exercise along with time-restricted eating (TRE) can play an important role in improving ...
Hamzeh Bayani +3 more
doaj +1 more source
PINK1/PARKIN signalling in neurodegeneration and neuroinflammation [PDF]
Abstract Mutations in the PTEN-induced kinase 1 (PINK1) and Parkin RBR E3 ubiquitin-protein ligase (PARKIN) genes are associated with familial forms of Parkinson’s disease (PD). PINK1, a protein kinase, and PARKIN, an E3 ubiquitin ligase, control the specific elimination of dysfunctional or superfluous mitochondria, thus fine-tuning ...
Peter M. J. Quinn +3 more
openaire +5 more sources

