https://arvinfomedia.com/myjournals/index.php/GIJAB/issue/feed 2026-05-20T05:03:46+00:00 Open Journal Systems <p><strong>Global Impact Journal: Advances in Biochemistry</strong> is a peer-reviewed journal dedicated to publishing high-quality original research articles, comprehensive reviews, and selected high-impact reprints in the areas of molecular biology, cell biology, structural biology, nucleic acid biology, chemical biology, synthetic biology, disease biology, biophysics, and theoretical biochemistry. The primary aim of the journal is to encourage researchers to report their experimental and theoretical findings in full detail, fostering transparency, reproducibility, and methodological rigor while advancing both fundamental knowledge and applied research in biochemical sciences.</p> <p>Published tri-annually, the journal is available in both print and electronic formats, ensuring wide accessibility to the research community.</p> https://arvinfomedia.com/myjournals/index.php/GIJAB/article/view/307 2026-05-20T05:03:46+00:00 Sujoy Bhattacharya sujoy.bhattacharya@vumc.org Caitlin Ang cma2240@barnard.edu Megan Soucy mes2350@cumc.columbia.edu Stephen H. Tsang sht2@cumc.columbia.edu Edward Chaum echaum@gmail.com

<p><em>Prominin-1</em> (<em>Prom1</em>/CD133) has long been recognized as a structural determinant of photoreceptor outer segment (OS) morphogenesis, yet rapidly accumulating evidence extends its role to retinal pigment epithelium (RPE) homeostasis, encompassing autophagy–lysosomal flux, outer segment phagocytosis, mitochondrial function, and regulation of inflammatory stress. This review synthesizes mechanistic and transcriptomic insights that position PROM1 as a central regulator of photoreceptor and RPE integrity, reframing <em>Prom1</em> disease as a multi-compartment retinal disorder relevant to both inherited retinal dystrophies (IRDs) and atrophic age-related macular degeneration (aAMD). We develop a dual-axis conceptual model in which Prom1 dysfunction can initiate pathology in either the photoreceptors (OS morphogenesis failure) or the RPE, including impaired autophagic flux, lysosomal activity, defective phagocytosis, and Epithelial-Mesenchymal Transition (EMT)-like de-differentiation, with secondary cross-compartmental degeneration. Clinically, autosomal-dominant missense variants associate with macular or cone-rod dystrophy, whereas biallelic truncating/splice-site mutations drive early-onset rod–cone disease and panretinal/RPE atrophy, illustrating genotype–phenotype diversity. By integrating recent high-resolution transcriptomic data from Prom1-deficient RPE cells with long-standing insights into photoreceptor biology, we highlight converging pathways of degeneration that challenge a photoreceptor-centric view and unify disparate phenotypes within a single molecular framework. These insights broaden the therapeutic landscape, advancing gene augmentation and pathway-targeted strategies to preserve RPE integrity, sustain photoreceptor function, and modify disease course in <em>PROM1</em> -associated IRDs and atrophic AMD.</p>

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