Results 51 to 60 of about 226,162 (289)

Oxidation of the cysteine-rich regions of parkin perturbs its E3 ligase activity and contributes to protein aggregation [PDF]

open access: yes, 2011
Background Accumulation of aberrant proteins to form Lewy bodies (LBs) is a hallmark of Parkinson's disease (PD). Ubiquitination-mediated degradation of aberrant, misfolded proteins is critical for maintaining normal cell function.
Ma Yuliang   +10 more
core   +2 more sources

Electron‐Induced Molecular Programming Drives Interfacial Chemistry for Ah‐Level Zinc Batteries

open access: yesAdvanced Materials, EarlyView.
We establish an electron‐driven molecular programming strategy that converts spontaneous solid electrolyte interphase formation into a bonding‐defined interfacial architecture. Coordinative integration of p‐bromoaniline with ZnF2 forms a dipole‐regulated molecular lock that reconfigures interfacial electrostatics, suppresses parasitic water reactions ...
Feifei Wang   +12 more
wiley   +1 more source

The Mitochondrial Deubiquitinase USP30 Regulates AKT/mTOR Signaling

open access: yesFrontiers in Pharmacology, 2022
Mitophagy is an intracellular mechanism to maintain mitochondrial health by removing dysfunctional mitochondria. The E3 ligase Parkin ubiquitinates the membrane proteins on targeted mitochondria to initiate mitophagy, whereas USP30 antagonizes Parkin ...
Ruohan Zhang   +7 more
doaj   +1 more source

Parkin is activated by PINK1-dependent phosphorylation of ubiquitin at Serine65 [PDF]

open access: yes, 2014
We have previously reported that the Parkinson's disease-associated kinase PINK1 (PTEN-induced putative kinase 1) is activated by mitochondrial depolarization and stimulates the Parkin E3 ligase by phosphorylating Ser(65) within its Ubl (ubiquitin-like ...
Agne Kazlauskaite   +50 more
core   +2 more sources

Parkin Blushed by PINK1 [PDF]

open access: yesNeuron, 2006
Mutations in the PTEN-induced putative kinase 1 (PINK1) are a common cause of autosomal recessive Parkinson's disease. In a recent issue of Nature, two independent reports by and show that loss of Drosophila PINK1 leads to defects in mitochondrial function resulting in male sterility, apoptotic muscle degeneration, and minor loss of dopamine neurons ...
Tan, Jeanne M.M., Dawson, Ted M.
openaire   +2 more sources

Targeting Lactate and Lactylation in Cancer Metabolism and Immunotherapy

open access: yesAdvanced Science, EarlyView.
Lactate, once deemed a metabolic waste, emerges as a central regulator of cancer progression. This review elucidates how lactate and its epigenetic derivative, protein lactylation, orchestrate tumor metabolism, immune suppression, and therapeutic resistance.
Jiajing Gong   +5 more
wiley   +1 more source

Additional feedforward mechanism of Parkin activation via binding of phospho-UBL and RING0 in trans

open access: yeseLife
Loss-of-function Parkin mutations lead to early-onset of Parkinson’s disease. Parkin is an auto-inhibited ubiquitin E3 ligase activated by dual phosphorylation of its ubiquitin-like (Ubl) domain and ubiquitin by the PINK1 kinase. Herein, we demonstrate a
Dipti Ranjan Lenka   +6 more
doaj   +1 more source

Phenotypic Discordance in Siblings with Identical Compound Heterozygous PARK2 Mutations

open access: yesBrain Sciences, 2017
PARK2 mutations are the most common cause of early-onset Parkinson’s disease. No genotype-phenotype correlation exists, and phenotypic variability is quite common.
David Isaacs   +3 more
doaj   +1 more source

Implication of alterations in Parkin gene among North Indian patients with colorectal cancer

open access: yesThe Turkish Journal of Gastroenterology, 2020
Background/Aims: Alterations in Parkin (PRKN) have been described in many cancers; however, the molecular mechanism that contributes to loss of Parkin expression in colorectal cancer (CRC) remains unclear.
Raj Ranjan Tiwari   +6 more
doaj   +1 more source

Time‐Controlled Refrigerated Stem Cell Therapy Mitigates Scleroderma Fibrosis via Modulation of Mitochondrial Autophagy and Gut Metabolism

open access: yesAdvanced Science, EarlyView.
This study established an RT‐MSCs‐based therapeutic approach for scleroderma in mice. RT‐MSCs attenuated fibrosis by regulating mitochondrial autophagy and restored gut microbiota homeostasis. Metabolomic analyses confirmed recovery of key metabolites, and RT‐MSCs demonstrated favorable lesion targeting and safety profiles.
Xue Xia   +5 more
wiley   +1 more source

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