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    <title>Repository Community: null</title>
    <link>https://scholar.dgist.ac.kr/handle/20.500.11750/265</link>
    <description />
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        <rdf:li rdf:resource="https://scholar.dgist.ac.kr/handle/20.500.11750/60414" />
        <rdf:li rdf:resource="https://scholar.dgist.ac.kr/handle/20.500.11750/60411" />
        <rdf:li rdf:resource="https://scholar.dgist.ac.kr/handle/20.500.11750/60358" />
        <rdf:li rdf:resource="https://scholar.dgist.ac.kr/handle/20.500.11750/60353" />
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    <dc:date>2026-06-16T07:32:35Z</dc:date>
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  <item rdf:about="https://scholar.dgist.ac.kr/handle/20.500.11750/60414">
    <title>Shared and Divergent Transcriptional Programs of Oligodendrocyte Differentiation Across Vertebrate Species Revealed by scRNA-seq Analysis</title>
    <link>https://scholar.dgist.ac.kr/handle/20.500.11750/60414</link>
    <description>Title: Shared and Divergent Transcriptional Programs of Oligodendrocyte Differentiation Across Vertebrate Species Revealed by scRNA-seq Analysis
Author(s): Yun, Tery; Park, Junhee; Baek, Myungin
Abstract: A myelination is essential for neural function in the vertebrate central nervous system, yet the molecular details of how the oligodendrocyte differentiation program has evolved remain poorly understood. Here, we performed a cross-species single-cell transcriptomic analysis of oligodendrocyte lineage cells in the spinal cord of five vertebrate species: fugu, mudskipper, chicken, mouse, and human. Pseudotime trajectory analysis revealed a shared oligodendrocyte progenitor cell (OPC) to committed oligodendrocyte precursor (COP) to myelin-forming oligodendrocyte (MOL) differentiation trajectory across all species, and CAME-based cross-species mapping confirmed the homology of OPC and MOL identities, while COP showed reduced mapping in teleosts compared with amniotes. Among stage-specific DEGs, highly shared genes (≥4 species) were organized into four co-expression modules encompassing cell projection organization, myelination, synapse assembly, and ribonucleoprotein biogenesis, with evolutionary core genes (all 5 species) enriched for oligodendrocyte differentiation and Wnt signaling. Strikingly, amniote-exclusive genes were enriched for synaptic vesicle transport, cell projection organization, predominantly at the OPC stage. This asymmetry indicates that amniotes have expanded the oligodendrocyte differentiation program at the progenitor stage, potentially linked to the myelination demands of terrestrial locomotor circuits. Our findings provide insights into how the oligodendrocyte differentiation program has been shaped by both deep evolutionary conservation and lineage-specific adaptation.</description>
    <dc:date>2026-04-30T15:00:00Z</dc:date>
  </item>
  <item rdf:about="https://scholar.dgist.ac.kr/handle/20.500.11750/60411">
    <title>CSDE1 Associates with TOM20 and Mitochondrial Protein-Encoding mRNAs in Sensory Neurons</title>
    <link>https://scholar.dgist.ac.kr/handle/20.500.11750/60411</link>
    <description>Title: CSDE1 Associates with TOM20 and Mitochondrial Protein-Encoding mRNAs in Sensory Neurons
Author(s): Jin, Hoyong; Jang, Eunsu; Park, Eunhye; Lee, Ju Yeon; Song, Ju Hwan; Cho, Yongcheol
Abstract: Mitochondrial proteostasis in neurons relies on the coordinated expression, targeting, and import of a predominantly nuclear-encoded proteome to meet high metabolic demands. Here, we identify the RNA-binding protein cold shock domain containing E1 (CSDE1) as a TOM20-associated factor linked to mitochondrial protein-encoding mRNAs in sensory neurons. CSDE1 immunoprecipitation followed by sequencing from na &amp; iuml;ve dorsal root ganglion tissue revealed association with nuclear-encoded mitochondrial mRNAs enriched for inner membrane/matrix and oxidative phosphorylation pathways. A subset of CSDE1 localized to mitochondria and associated with the outer mitochondrial membrane import receptor TOM20 via its N-terminal region in an RNA-independent manner. In cultured sensory neurons, CSDE1 depletion reduced the mitochondrial-fraction abundance of representative nuclear-encoded electron transport chain mRNAs and decreased the abundance of selected mitochondrial proteins in the mitochondrial fraction. CSDE1 depletion reduced TMRM-positive mitochondrial puncta density along sensory neurites, without significantly increasing MitoSOX-detectable mitochondrial superoxide signals under either basal or oxidative challenge conditions. These findings identify CSDE1 as a TOM20-associated RNA-binding protein linked to mitochondrial protein-encoding transcripts in sensory neurons and support a model in which CSDE1 contributes to mitochondria-associated post-transcriptional regulation.</description>
    <dc:date>2026-04-30T15:00:00Z</dc:date>
  </item>
  <item rdf:about="https://scholar.dgist.ac.kr/handle/20.500.11750/60358">
    <title>Juvenile-to-adult refinement of thalamic reticular circuits via LRRTM3 enables high-resolution sensory encoding</title>
    <link>https://scholar.dgist.ac.kr/handle/20.500.11750/60358</link>
    <description>Title: Juvenile-to-adult refinement of thalamic reticular circuits via LRRTM3 enables high-resolution sensory encoding
Author(s): Lee, Dongsu; Han, Kyung Ah; Jeong, Hyeonyeong; Ha, Go Eun; Lee, Hyeongjin; Kim, Beom Soo; Park, Chanmi; Piao, Yao; Lee, Haeun; Kim, Joon; Yoon, Taek Han; Kim, Seungjoon; Kim, Byeongchan; Shin, Jungsu; Cho, Yujin; Kang, Sunghyun; Park, Han-Eol; Um, Ji Won; Sohn, Chang Ho; Huguenard, John R.; Ko, Jaewon; Cheong, Eunji
Abstract: Sensory processing enables adaptive behavior by accurately encoding dynamic environmental stimuli. Within thalamocortical (TC) circuits, the thalamic reticular nucleus (TRN) functions as a key inhibitory gate that regulates cortical access to sensory input. While classical models posit that sensory circuits stabilize after early critical periods, we uncover a previously unrecognized phase of synaptic refinement in TRN circuitry extending from the juvenile period into adulthood. This late-stage remodeling is driven by a progressive reduction in corticothalamic (CT) excitatory input and is essential for enhancing sensory gain, response linearity, and stimulus discriminability. We identify LRRTM3, a TRN-enriched synaptic adhesion molecule, as a molecular gatekeeper of this process. TRN-specific deletion of LRRTM3 disrupts CT–TRN refinement, elevates TRN-mediated inhibition, and impairs fine tactile discrimination. These findings revise canonical views of sensory circuit maturation, revealing that LRRTM3-mediated juvenile-to-adult TRN plasticity is essential for the emergence of high-resolution sensory encoding in the adult brain.</description>
    <dc:date>2026-03-31T15:00:00Z</dc:date>
  </item>
  <item rdf:about="https://scholar.dgist.ac.kr/handle/20.500.11750/60353">
    <title>MLPH-mediated activation of dermal papilla IGF-1 signaling drives human hair shaft elongation and anagen induction</title>
    <link>https://scholar.dgist.ac.kr/handle/20.500.11750/60353</link>
    <description>Title: MLPH-mediated activation of dermal papilla IGF-1 signaling drives human hair shaft elongation and anagen induction
Author(s): Kwack, Mi Hee; Kang, Eunho; Kim, Jewoo; Ji, Youngheum; Ju, Hyeonchang; Lee, Chang-Hun; Sung, Young Kwan; Kim, So Yeon; Moon, Cheil
Abstract: Introduction Hair loss (alopecia) is a multifactorial disorder that often causes distress. Approved therapies such as minoxidil and finasteride act indirectly and do not specifically target hair follicle (HF) cells. Erythropoietin (EPO), however, has been shown to activate dermal papilla (DP) cells via the erythropoietin receptor (EPOR), suggesting a potential role in hair follicle regeneration and hair growth. Objectives This study aimed to develop and validate Helix C-1–based EPO-derived peptides that activate DP cells and increase IGF-1 expression, while not inducing overt systemic erythropoietic effects (e.g., increases in red blood cell counts, reticulocytes, hemoglobin, or hematocrit) under the tested experimental conditions. Methods Peptides derived from the Helix C-1 region of EPO were synthesized and characterized by EPOR-binding affinity, CD spectroscopy, and ERK/AKT activation. In vitro, DP-cell metabolic activity, proliferation, and IGF-1 secretion were assessed. Ex vivo efficacy was evaluated by hair shaft elongation in hair follicle organ culture, and in vivo efficacy was tested in a murine depilation-induced anagen model with concurrent hematologic assessment to exclude erythropoiesis-related effects. Results The peptides increased DP-cell metabolic activity and proliferation, reduced oxidative stress, and enhanced IGF-1 production via EPOR-mediated ERK/AKT activation. They promoted hair shaft elongation ex vivo and promoted anagen entry in mice without significant changes in standard hematologic parameters under the tested dosing regimen. Conclusion These findings support the conclusion that MLPH promotes hair growth via an EPOR-linked, IGF-1–dependent mechanism in DP cells. Future pharmacokinetic and disease-model studies are warranted to evaluate its translational potential. © 2026 The Authors.</description>
    <dc:date>2026-02-28T15:00:00Z</dc:date>
  </item>
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