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Anand Swaroop

Researcher at National Institutes of Health

Publications -  528
Citations -  53580

Anand Swaroop is an academic researcher from National Institutes of Health. The author has contributed to research in topics: Retinitis pigmentosa & Retinal degeneration. The author has an hindex of 89, co-authored 508 publications receiving 43170 citations. Previous affiliations of Anand Swaroop include Vision-Sciences, Inc. & Yale University.

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Deletion of Aryl Hydrocarbon Receptor AHR in Mice Leads to Subretinal Accumulation of Microglia and RPE Atrophy

TL;DR: This study suggests that AHR has a protective role in the retina as an environmental stress sensor and its altered function may contribute to human AMD progression and provide a target for pharmacological intervention.
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Human retinopathy-associated ciliary protein retinitis pigmentosa GTPase regulator mediates cilia-dependent vertebrate development

TL;DR: It is proposed that RPGR is involved in cilia-dependent cascades during development in zebrafish and provided evidence for a heterogenic effect of the disease-causing mutations on the function of RPGR.
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Pluripotent stem cell-derived retinal organoids for disease modeling and development of therapies.

TL;DR: The current status and future potential of combining retinal organoids as human models with recent technologies to advance the development of gene, cell, and drug therapies for retinopathies are discussed.
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Next generation sequencing technology and genomewide data analysis: Perspectives for retinal research

TL;DR: The basic design of commonly used NGS-based methods, specifically whole exome sequencing, transcriptome, and epigenome profiling are illustrated, and recommendations for data analyses are provided.
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Analysis of the RPGR gene in 11 pedigrees with the retinitis pigmentosa type 3 genotype: paucity of mutations in the coding region but splice defects in two families.

TL;DR: The hypothesis that mutations in the reported RPGR gene are not a common defect in the RP3 subtype of XLRP and that a majority of causative mutations may reside either in as yet unidentified RPGR exons or in another nearby gene at Xp21.1 is supported.