ReviewMolecular and cellular neurosciences2015
Pathologic and therapeutic implications for the cell biology of parkin.
Review in Molecular and cellular neurosciences, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
19 citing papers in PubMed, 34 citations in OpenAlex.
- Multifaceted Proteome Analysis at Solubility, Redox, and Expression Dimensions for Target Identification.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- The mystery of phospho-Drp1 with four adaptors in cell cycle: when mitochondrial fission couples to cell fate decisions.Cell cycle (Georgetown, Tex.) · 2023Article
- Neuroprotective Effects of Carnosic Acid: Insight into Its Mechanisms of Action.Molecules (Basel, Switzerland) · 2023Review
- Human Induced Pluripotent Stem Cell Phenotyping and Preclinical Modeling of Familial Parkinson's Disease.Genes · 2022Review
- Harnessing the Therapeutic Potential of the Nrf2/Bach1 Signaling Pathway in Parkinson's Disease.Antioxidants (Basel, Switzerland) · 2022Review
- Nanomedicine for Neurodegenerative Disorders: Focus on Alzheimer's and Parkinson's Diseases.International journal of molecular sciences · 2021Review
- Pharmacological antagonism of kainate receptor rescues dysfunction and loss of dopamine neurons in a mouse model of human parkin-induced toxicity.Cell death & disease · 2020Article
- The Role of Mitochondria in Neurodegenerative Diseases: the Lesson from Alzheimer's Disease and Parkinson's Disease.Molecular neurobiology · 2020Review
- Neuronal Mitophagy: Lessons from a Pathway Linked to Parkinson's Disease.Neurotoxicity research · 2019Review
- Parkinson's disease-linked Parkin mutations impair glutamatergic signaling in hippocampal neurons.BMC biology · 2018Article
- Alterations in the E3 ligases Parkin and CHIP result in unique metabolic signaling defects and mitochondrial quality control issues.Neurochemistry international · 2018Review
- Modulation of ARTS and XIAP by Parkin Is Associated with Carnosic Acid Protects SH-SY5Y Cells against 6-Hydroxydopamine-Induced Apoptosis.Molecular neurobiology · 2018Article
- Neuronal Proteomic Analysis of the Ubiquitinated Substrates of the Disease-Linked E3 Ligases Parkin and Ube3a.BioMed research international · 2018Review
- Trumping neurodegeneration: Targeting common pathways regulated by autosomal recessive Parkinson's disease genes.Experimental neurology · 2017Review
- Quantitative proteomic analysis of Parkin substrates in Drosophila neurons.Molecular neurodegeneration · 2017Article
- Cysteines as Redox Molecular Switches and Targets of Disease.Frontiers in molecular neuroscience · 2017Review
- Mitochondrial quality control: Cell-type-dependent responses to pathological mutant mitochondrial DNA.Autophagy · 2016Article
- Mechanism and disease association of E2-conjugating enzymes: lessons from UBE2T and UBE2L3.The Biochemical journal · 2016Review
- VPS35 pathogenic mutations confer no dominant toxicity but partial loss of function in Drosophila and genetically interact with parkin.Human molecular genetics · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Mutations in the E3 ligase parkin are the most common cause of autosomal recessive Parkinson's disease (PD), but it is believed that parkin dysfunction may also contribute to idiopathic PD. Since its discovery, parkin has been implicated in supporting multiple neuroprotective pathways, many revolving around the maintenance of mitochondrial health quality control and governance of cell survival. Recent advances across the structure, biochemistry, and cell biology of parkin have provided great insights into the etiology of parkin-linked and idiopathic PD and may ultimately generate novel therapeutic strategies to slow or halt disease progression. This review describes the various pathways in which parkin acts and the mechanisms by which parkin may be targeted for therapeutic intervention. This article is part of a Special Issue entitled 'Neuronal Protein'.
Indexed as
Identifiers
What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.