ArticleProceedings of the National Academy of Sciences of the United States of America2018
Genome-wide CRISPR screen for PARKIN regulators reveals transcriptional repression as a determinant of mitophagy.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 55 papers.
What it found
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Who cites it
55 citing papers in PubMed, 98 citations in OpenAlex.
- Human pluripotent stem cell engineering with CRISPR-Cas9 for Parkinson's disease.Experimental & molecular medicine · 2026Review
- Association of mitochondrial genetic background with pS65-Ub in Lewy body disease.Acta neuropathologica · 2026Article
- CRISPR-based functional genomic screening in neurodegeneration: mechanistic insights into AD, PD, and ALS.Frontiers in aging neuroscience · 2026Review
- Autophagy and mitophagy at the synapse and beyond: implications for learning, memory and neurological disorders.Autophagy · 2026Review
- Activation of endogenous PRKN by structural derepression is linked to increased turnover of the E3 ubiquitin ligase.Autophagy · 2025Article
- dFLASH; dual FLuorescent transcription factor activity sensor for histone integrated live-cell reporting and high-content screening.Nature communications · 2025Article
- Genome-wide association analysis identifies APOE as a mitophagy modifier in Lewy body disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Unlocking Disease-Modifying Treatments for TDP-43-Mediated Neurodegeneration.BioEssays : news and reviews in molecular, cellular and developmental biology · 2025Review
- CRISPR-based genetic screens in human pluripotent stem cells derived neurons and brain organoids.Cell and tissue research · 2025Review
- Synergizing CRISPR-Cas9 with Advanced Artificial Intelligence and Machine Learning for Precision Drug Delivery: Technological Nexus and Regulatory Insights.Current gene therapy · 2025Review
- Development and characterization of phospho-ubiquitin antibodies to monitor PINK1-PRKN signaling in cells and tissue.Autophagy · 2024Article
- PRKN-linked familial Parkinson's disease: cellular and molecular mechanisms of disease-linked variants.Cellular and molecular life sciences : CMLS · 2024Review
- A mutational atlas for Parkin proteostasis.Nature communications · 2024Article
- Development and characterization of phospho-ubiquitin antibodies to monitor PINK1-PRKN signaling in cells and tissue.bioRxiv : the preprint server for biology · 2024Article
- Parkin Promotes Airway Inflammatory Response to Interferon Gamma.Biomedicines · 2023Article
- A genome-wide CRISPR screen maps endogenous regulators of PPARG gene expression in bladder cancer.iScience · 2023Article
- CRISPR/Cas9 assisted stem cell therapy in Parkinson's disease.Biomaterials research · 2023Review
- Gene Modulation with CRISPR-based Tools in Human iPSC-Cardiomyocytes.Stem cell reviews and reports · 2023Review
- Understanding neural development and diseases using CRISPR screens in human pluripotent stem cell-derived cultures.Frontiers in cell and developmental biology · 2023Review
- CRISPR Libraries and Whole-Genome Screening to Identify Essential Factors for Viral Infections.Advances in experimental medicine and biology · 2023Article
Corrections and comments
- Erratum issued
Authors and funding
19 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
PARKIN, an E3 ligase mutated in familial Parkinson's disease, promotes mitophagy by ubiquitinating mitochondrial proteins for efficient engagement of the autophagy machinery. Specifically, PARKIN-synthesized ubiquitin chains represent targets for the PINK1 kinase generating phosphoS65-ubiquitin (pUb), which constitutes the mitophagy signal. Physiological regulation of PARKIN abundance, however, and the impact on pUb accumulation are poorly understood. Using cells designed to discover physiological regulators of PARKIN abundance, we performed a pooled genome-wide CRISPR/Cas9 knockout screen. Testing identified genes individually resulted in a list of 53 positive and negative regulators. A transcriptional repressor network including THAP11 was identified and negatively regulates endogenous PARKIN abundance. RNAseq analysis revealed the PARKIN-encoding locus as a prime THAP11 target, and
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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 OpenQuestion graph.