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    <title>ScholarWorks Community:</title>
    <link>https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/238</link>
    <description />
    <pubDate>Sat, 04 Jul 2026 11:19:30 GMT</pubDate>
    <dc:date>2026-07-04T11:19:30Z</dc:date>
    <item>
      <title>Cell cycle-regulated expression of Fam72a from the |Srgap2-Fam72a| master gene leads to Mis18a downregulation</title>
      <link>https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/213261</link>
      <description>Title: Cell cycle-regulated expression of Fam72a from the |Srgap2-Fam72a| master gene leads to Mis18a downregulation
Authors: Nguyen, Tuan Hoang Anh; Kim, Pok-Son; Kutzner, Arne; Heese, Klaus
Abstract: The novel |Srgap2–Fam72a| master gene, comprising SLIT-ROBO Rho GTPase-activating protein 2 (Srgap2) and family with sequence similarity 72 member A (Fam72a), has attracted attention for its potential role in regulating brain plasticity and supporting advanced cognitive functions in humans. Moreover, recent studies have identified Fam72a as a new cell cycle-regulated gene. In this study, we investigated the activity of the intergenic region (IGR) between the native Srgap2 and Fam72a gene pair and the signaling pathways of Fam72a upon mitogen epidermal growth factor (Egf) stimulation. We found that, under mitogen Egf stimulation, the IGR functions as a divergent promoter, simultaneously driving the transcription of Srgap2 and Fam72a in opposite directions. Furthermore, Fam72a downregulates MIS18 kinetochore protein A (Mis18a), a tightly cell cycle-regulated gene, and interferes with the RAC-alpha serine/threonine-protein kinase (Akt1) signaling pathway by downregulating phosphorylated Akt1 at Serine 473, thereby favoring the more direct mitogen activated protein kinase 1 (Mapk1) route to promote cellular proliferation. These findings provide insight into the role of Fam72a during the cell cycle and suggest that it may contribute to the proliferation of neural stem cells (NSCs).</description>
      <pubDate>Tue, 01 Dec 2026 00:00:00 GMT</pubDate>
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      <dc:date>2026-12-01T00:00:00Z</dc:date>
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    <item>
      <title>Aberrant activation of FAM168B via chimeric PLEKHB2::FAM168B mRNA promotes breast invasive cancer progression</title>
      <link>https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/217632</link>
      <description>Title: Aberrant activation of FAM168B via chimeric PLEKHB2::FAM168B mRNA promotes breast invasive cancer progression
Authors: Dash Sharma, Sidharth; Sensharma, Sreemoyee; Kutzner, Arne; Fuhrer, Erwin; Pramanik, Gopal; Heese, Klaus; Pramanik, Subrata
Abstract: Fusion genes have emerged as pivotal oncogenic drivers across diverse cancer types. The predominant mechanisms underlying fusion gene formation include chromosomal aberrations and intergenic mRNA trans-splicing. With advances in cancer genomics and transcriptomics, the identification, prevalence, and functional characterization of fusion genes have become major areas of investigation. In this study, we performed a comprehensive analysis of fusion events involving the family with sequence similarity 168B (FAM168B) and pleckstrin homology domain–containing B2 (PLEKHB2) in breast invasive carcinoma (BRCA). Integrated DNA and RNA sequencing analyses revealed that the chimeric PLEKHB2::FAM168B mRNA transcript is generated through an intergenic mRNA trans-splicing mechanism. This chimeric transcript leads to elevated FAM168B protein expression via long intergenic non-coding RNA 02228 (LINC02228)–mediated activation of DEAD-box helicase 3 X-linked (DDX3X). This, in turn, activates the DAZ-associated protein 2 (DAZAP2)/homeodomain-interacting protein kinase 2 (HIPK2)/tumor protein 53 (TP53) signaling cascade, resulting in enhanced cell cycle progression and increased BRCA cell proliferation. In summary, our findings suggest that chimeric PLEKHB2::FAM168B mRNA may serve as a potential biomarker in BRCA.</description>
      <pubDate>Wed, 01 Jul 2026 00:00:00 GMT</pubDate>
      <guid isPermaLink="false">https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/217632</guid>
      <dc:date>2026-07-01T00:00:00Z</dc:date>
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    <item>
      <title>Designing educational chatbots in resource-constrained environments: A design science approach</title>
      <link>https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/213263</link>
      <description>Title: Designing educational chatbots in resource-constrained environments: A design science approach
Authors: Lee, Sun-Hyoung; Roh, Taewoo; Kim, Eunchan; Yoon, Sang-Hyeak
Abstract: Generative AI is expanding the role of educational chatbots in higher education, but many institutions still face financial, computational, and organizational constraints that limit the deployment of advanced systems. To address this challenge, this study uses a design science approach to develop and validate a constrained-environment educational chatbot design and operations framework for introductory human resource development (HRD) courses. The framework combines a resource-efficient small language model (SLM) with fine-tuning, retrieval-augmented generation, and prompt engineering, and is theoretically grounded in the process logics of Factory Physics, Lean, Agile, and Six Sigma to stabilize the learning flow, manage variation, and improve instructional responsiveness. The framework is instantiated through EduHRDBot and evaluated in an authentic university classroom setting for performance, efficiency, and learner experience. The findings show how design science can generate transferable design knowledge for building cost-efficient, pedagogically aligned educational chatbots in resource-constrained environments. Beyond a single-course implementation, the proposed framework offers a modular basis for broader human–AI co-learning ecosystems in higher education.</description>
      <pubDate>Mon, 01 Jun 2026 00:00:00 GMT</pubDate>
      <guid isPermaLink="false">https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/213263</guid>
      <dc:date>2026-06-01T00:00:00Z</dc:date>
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    <item>
      <title>CT Digital Twin Lung-based Regional Functional Defects Explain Airflow Obstruction in COPD</title>
      <link>https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/217845</link>
      <description>Title: CT Digital Twin Lung-based Regional Functional Defects Explain Airflow Obstruction in COPD
Authors: 김은찬</description>
      <pubDate>Mon, 18 May 2026 00:00:00 GMT</pubDate>
      <guid isPermaLink="false">https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/217845</guid>
      <dc:date>2026-05-18T00:00:00Z</dc:date>
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