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    <title>Repository Collection: null</title>
    <link>https://scholar.dgist.ac.kr/handle/20.500.11750/15990</link>
    <description />
    <pubDate>Mon, 03 Aug 2026 10:44:44 GMT</pubDate>
    <dc:date>2026-08-03T10:44:44Z</dc:date>
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      <title>Constitutive DUSP2 expression enhances lymphoid cell proliferation by activating CDK1 and promotes lymphomagenesis</title>
      <link>https://scholar.dgist.ac.kr/handle/20.500.11750/60550</link>
      <description>Title: Constitutive DUSP2 expression enhances lymphoid cell proliferation by activating CDK1 and promotes lymphomagenesis
Author(s): Qian, Yu; Panaampon, Jutatip; Chapuy, Bjoern; Zhang, Xueyan; Zhao, Xiujuan; Wang, Zhe; Zhang, Pengfei; Payungwong, Tongchai; Zhang, Aretina; Ke, Qiang; Zhong, Jing; Yuan, Ping; Zhang, Lei; Hong, Min; Choi, Il-Kyu; Guan, Jiankun; Calado, Dinis Pedro; Rodig, Scott; Pozdnyakova, Olga; Rajewsky, Klaus; Godinho, Susana A.; Jirawatnotai, Siwanon; Wu, Hao; Shipp, Margaret A.; Dougan, Stephanie K.; Zhang, Baochun
Abstract: DUSP2 is known as a nuclear dual-specificity phosphatase, highly restricted to immune cells. Its expression is induced by antigenic and mitogenic stimuli and has been implicated in immune cell differentiation and functions. However, its role in immune cell mitotic proliferation and hematologic malignancies has not been rigorously examined. Here, we show DUSP2 is highly expressed in human B-cell, T cell, and other hematologic malignancies. Ablating DUSP2 expression in lymphoma cell lines decreases growth and viability. In mice, transgenic Dusp2 expression promotes B-cell and T cell proliferation, and malignant transformation. Mechanistically, DUSP2 promotes cell cycle progression by activating CDK1 through dephosphorylation at inhibitory Tyr15 and Thr14, which is mediated not by its own phosphatase activity, but instead by a structural motif that recruits CDC25 phosphatases. This work reveals an unexpected oncogenic role for DUSP2 in lymphoid malignancies and the function of a structural motif, which represents an appealing target site for therapeutic intervention.</description>
      <pubDate>Tue, 30 Jun 2026 15:00:00 GMT</pubDate>
      <guid isPermaLink="false">https://scholar.dgist.ac.kr/handle/20.500.11750/60550</guid>
      <dc:date>2026-06-30T15:00:00Z</dc:date>
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    <item>
      <title>NKG2D-mediated cytotoxicity of CD4 cytotoxic T cells in multiple myeloma</title>
      <link>https://scholar.dgist.ac.kr/handle/20.500.11750/58692</link>
      <description>Title: NKG2D-mediated cytotoxicity of CD4 cytotoxic T cells in multiple myeloma
Author(s): Kim, Sojeong; Kwak, Jeong-Eun; Koh, June-Young; Lee, Ji Eun; Kook, Hye Won; Kim, Minchae; Chung, Haerim; Kim, Yuri; Kim, Soo Jeoong; Kim, Jin Seok; Cheong, June-Won; Lee, Min Goo; Lee, Hoyoung; Park, Su-Hyung; Shin, Eui-Cheol; Shin, Saeam; Yoon, Sun Och; Choi, Il-Kyu; Lee, Jeong Seok; Cho, Hyunsoo
Abstract: Emerging evidence indicates that CD4+ T cells contribute to antitumor immunity beyond their traditional roles as helpers or regulators. However, the specific subset of CD4+ T cells mediating beneficial outcomes in patients with multiple myeloma remains unclear. Here, we performed single-cell RNA sequencing and T-cell receptor sequencing on CD4+ T cells sorted from the bone marrow of patients across the stages of myeloma progression. We identified several distinct states of CD4+ cytotoxic T lymphocytes (CTLs) that were significantly increased and clonally expanded in patients with myeloma. CD4+ CTLs displayed transcriptional and phenotypic characteristics indicative of cytotoxicity, demonstrating their ability to directly kill myeloma cells. This cytotoxicity, however, was abrogated by NKG2D blockade. Notably, the abundance of NKG2D+CD4+ CTLs correlated with improved survival in patients with myeloma. Our findings suggest that harnessing CD4+ CTLs could lead to novel strategies for enhancing immunotherapy outcomes in multiple myeloma.</description>
      <pubDate>Mon, 30 Jun 2025 15:00:00 GMT</pubDate>
      <guid isPermaLink="false">https://scholar.dgist.ac.kr/handle/20.500.11750/58692</guid>
      <dc:date>2025-06-30T15:00:00Z</dc:date>
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    <item>
      <title>Recent advances in single-cell metabolomics using mass spectrometry: emerging challenges and future perspectives</title>
      <link>https://scholar.dgist.ac.kr/handle/20.500.11750/58275</link>
      <description>Title: Recent advances in single-cell metabolomics using mass spectrometry: emerging challenges and future perspectives
Author(s): Alam, Rafiqul; Lee, Jung-Hyun; Shin, Doyun; Choi, Il-Kyu; Kim, Sunghwan; Lim, Heejin; Kim, Min-Sik
Abstract: Cellular heterogeneity plays a pivotal role in organismal physiology, influencing developmental processes, disease progression, and therapeutic responses. Single-cell metabolomics (SCM) emerges as a powerful tool to interrogate the metabolic diversity of individual cells, offering insights into cellular phenotypes beyond genomics, or transcriptomics. Recent advancements in microfluidics, automation, and image analysis have enabled minimally invasive single-cell isolation, while development of innovative mass spectrometry (MS)-based techniques has transformed metabolite detection with their high sensitivity, broad detection range, and molecular specificity. Despite challenges such as the non-amplifiable nature of metabolites and their dynamic concentration ranges like proteins, significant progress has been made in MS platforms, ionization methods, and data analysis strategies. This review highlights the latest innovations in SCM, including nano-electrospray ionization, laser desorption/ionization, and other MS techniques, alongside applications in diverse cell types such as cancer cells, plant cells, neurons, stem cells, and immune cells. Integrating SCM with orthogonal single-cell omics holds promise for systems-level understanding, with potential applications in translational and clinical research. Addressing current limitations in throughput, sensitivity, and data processing will be essential to fully unlock the potential of SCM in answering fundamental and applied biological questions.</description>
      <pubDate>Fri, 31 Oct 2025 15:00:00 GMT</pubDate>
      <guid isPermaLink="false">https://scholar.dgist.ac.kr/handle/20.500.11750/58275</guid>
      <dc:date>2025-10-31T15:00:00Z</dc:date>
    </item>
    <item>
      <title>IL2-mediated modulation of small extracellular vesicles secretion and PD-L1 expression: a novel perspective for neutralizing immune suppression within cancer cells</title>
      <link>https://scholar.dgist.ac.kr/handle/20.500.11750/57322</link>
      <description>Title: IL2-mediated modulation of small extracellular vesicles secretion and PD-L1 expression: a novel perspective for neutralizing immune suppression within cancer cells
Author(s): Noh, Soojeong; Ryu, Suyeon; Jung, Dokyung; Shin, Sanghee; Jung, Inseong; Kang, Sung-Min; Kim, Christine S.; Choi, Sung-Jin; Cho, Hanchae; Schwämmle, Melanie; Jeong, Youngtae; Bucher, Felicitas; Choi, Il-Kyu; Lee, Shin Yup; Im, Sin-Hyeog; Yea, Kyungmoo; Baek, Moon-Chang
Abstract: [No Abstract Available]</description>
      <pubDate>Sat, 30 Nov 2024 15:00:00 GMT</pubDate>
      <guid isPermaLink="false">https://scholar.dgist.ac.kr/handle/20.500.11750/57322</guid>
      <dc:date>2024-11-30T15:00:00Z</dc:date>
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