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    <title>ScholarWorks Collection:</title>
    <link>https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/66</link>
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        <rdf:li rdf:resource="https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/213261" />
        <rdf:li rdf:resource="https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/217632" />
        <rdf:li rdf:resource="https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/212901" />
        <rdf:li rdf:resource="https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/212331" />
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    <dc:date>2026-07-03T23:17:29Z</dc:date>
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  <item rdf:about="https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/213261">
    <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>
    <dc:date>2026-12-01T00:00:00Z</dc:date>
  </item>
  <item rdf:about="https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/217632">
    <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>
    <dc:date>2026-07-01T00:00:00Z</dc:date>
  </item>
  <item rdf:about="https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/212901">
    <title>A deep dive into functional ribosome specialization</title>
    <link>https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/212901</link>
    <description>Title: A deep dive into functional ribosome specialization
Authors: Park, Seohyun; Fitzgerald, Fiona; Yang, Yoon-Mo; Karbstein, Katrin
Abstract: Ribosome specialization, whereby ribosomes of distinct composition translate different sets of mRNAs, is a concept that has garnered both wide-spread excitement and skepticism from the translation field. The controversy is rooted in experimental challenges, which make rigorous controls difficult and not obvious to the nonexpert. In addition, considerations of translation mechanisms and ribosome homeostasis also suggest heterogeneity to be limited, fueling doubt. Lastly, the mechanisms by which heterogeneity can lead to specialization are often challenging to imagine and not spelled out. In this perspective, we define ribosome heterogeneity and specialization, use examples to examine both the technical challenges and potential solutions. We then consider the mechanism-based challenges with the goal of proposing biologically relevant circumstances where ribosome specialization might exist and how it might affect translation in an mRNA-specific manner. It is hoped that this article will help resolve the controversy around the subject, in addition to providing a guide for scientists entering the field, so they can concentrate their efforts fruitfully and rigorously.</description>
    <dc:date>2026-05-01T00:00:00Z</dc:date>
  </item>
  <item rdf:about="https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/212331">
    <title>Advancements in CRISPR–Cas Systems for Genome Editing towards Eradication of Human Microbial Pathogens</title>
    <link>https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/212331</link>
    <description>Title: Advancements in CRISPR–Cas Systems for Genome Editing towards Eradication of Human Microbial Pathogens
Authors: Bhattacharjee, Gargi; Gohil, Nisarg; Khambhati, Khushal; Murjani, Karan; Chu, Dinh Toi; Bui, Nhat Le; Thi, Hue Vu; Mani, Indra; Bansal, Abhisheka; Shamili, Sasanala; Satish, Lakkakula; Ramakrishna, Suresh; Alzahrani, Khalid J.; Singh, Vijai
Abstract: CRISPR–Cas systems have been explored for targeted genome editing of several organisms. It is rapid, cost-effective, specific, and versatile technology. It requires expression of multidomain single Cas9 protein and single guide RNA (sgRNA) that targets desired nucleic acids in the presence of a protospacer adjacent motif (PAM). This generates a double-stranded break that is repaired by either non-homologous end joining or a homology-directed repair pathway. Currently, several Cas protein variants have been discovered and being used for several biotechnological applications. This review highlights the recent progress of CRISPR–Cas systems for genome editing of mainly human pathogenic microorganisms for their controlling infections.</description>
    <dc:date>2026-04-01T00:00:00Z</dc:date>
  </item>
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