Peter M.J. Quinn
@PeterMJQuinn
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Assistant Professor of Ophthalmology and Principal Investigator of the PrimeSight Lab at the University of Pennsylvania. #CRB1 #PRPH2. Tweets are my own.
Joined December 2015
New Publication Alert from the PrimeSight Laboratory! Thrilled to share our latest article: “Prime Editing for the Investigation of Aberrant Splicing Defect Associated with a Pathogenic PRPH2 Variant” is accepted in @MolTherapy Nucleic Acids. #PRPH2 #PrimeEditing #RP #IRDs
Prime Editing for the Investigation of Aberrant Splicing Defect Associated with a Pathogenic PRPH2 Variant https://t.co/Va6xW9MUlo
#MTNA
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Thanks to all those that supported this research in some part including private donations, @CureCRB1, @FightBlindness, and @NatEyeInstitute
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Our findings highlight the potential of prime editing as a precise and safe method for installing and correcting pathogenic PRPH2 mutations in hiPSCs, paving the way for future genotype-phenotype studies and therapy development for PRPH2-mediated IRDs.
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Jose Ronaldo Lima de Carvalho, MD, a Research Associate working with faculty member @PeterMJQuinn, has received a prestigious research grant from the Knights Templar Eye Foundation! https://t.co/fPXF4WOOgc
#ophthalmology #scheieeye #upenn #pennmedicine #research #visionscience
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It was my pleasure to discuss therapeutic editing on International World CRISPR Day with the PRPH2 Grass Roots Community. Please listen to me discussing CRISPR technology on the Eye on the Cure podcast earlier this year. #CRISPR #CRB1 #PRPH2 #IRDs
https://t.co/rIV92JaROE
fightingblindness.org
Peter Quinn, PhD, a principal investigator and associate research scientist at Columbia University, talks to host Ben Shaberman about the promise of emerging CRISPR/Cas9 gene editing therapies,...
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Job opportunity Quinn Lab: Postdoctoral Scientist Position in Gene Therapy and Disease Modeling. See link for details l. https://t.co/sMG50x8rT5
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Our data further highlights the impact of compensatory regulation between miR clusters with implications for the development of miR-based therapeutics.
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We elucidated the underlying mechanisms associated with the therapeutic modulation of miR-181a/b in retinitis pigmentosa, providing insights into the metabolic processes linked to its RPE-specific downregulation.
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Congratulations to Bruna and the Tsang Lab for their new publication in @BioMedCentral Cell & Bioscience. This is another manuscript I helped with during my time in the Tsang lab. https://t.co/biFynToPSA
cellandbioscience.biomedcentral.com
Background Retinitis pigmentosa (RP) is a genetically heterogeneous group of degenerative disorders causing progressive vision loss due to photoreceptor death. RP affects other retinal cells,...
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Our data further highlights the impact of compensatory regulation between miR clusters with implications for the development of miR-based therapeutics.
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We elucidated the underlying mechanisms associated with the therapeutic modulation of miR-181a/b in retinitis pigmentosa, providing insights into the metabolic processes linked to its RPE-specific downregulation.
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This study describes novel interactors of the retinal Crumbs complex and reveals homo- and heterotypic interactions of CRB1 and CRB2 that are not significantly affected by patient-associated mutations https://t.co/O3MwzXC0Fb
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Thanks to @LSAjournal for the great publishing experince!
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Fourth, various patient-described missense mutations in CRB1 or CRB2 did not or only mildly altered the CRB1–CRB2 interaction in vitro, hinting toward a strong CRB1–CRB2 interaction.
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The identified retinal protein interactions linked the crumbs complex to signaling, ciliary homeostasis, actin and microtubule cytoskeleton, lipid metabolism, cell adhesion, and ion transport.
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Third, the CRB2 retinal protein–protein interaction network included CRB1 and the core CRB complex members MPP5 and EPB41L5, corroborating this interaction in a retinal context.
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Second, we showed by co-IP that canonical CRB1 and CRB2 interact homo- and heterotypically but not with CRB3, indicating the necessity of the extracellular domain for this interaction.
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First, we confirmed that canonical CRB1 and CRB2 co-localize at the OLM in human iPSC–derived retinal organoids and adult human retina.
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Happy to share a new manuscript in collaboration with the lab of Marius Ueffing. In this study, we investigated the interaction of canonical CRB1 and CRB2 in the retina.
life-science-alliance.org
Crumbs homolog 1 ( CRB1 ) is one of the key genes linked to retinitis pigmentosa and Leber congenital amaurosis, which are characterized by a high clinical heterogeneity. The Crumbs family member...
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Recent conference abstracts from the lab: https://t.co/CexZE3pJJ1
https://t.co/CFkjgQZKOT
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