https://ir.ymlib.yonsei.ac.kr/handle/22282913/168742 Sat, 11 Jul 2026 01:20:22 GMT 2026-07-11T01:20:22Z https://ir.ymlib.yonsei.ac.kr/handle/22282913/210210 Title: Impact of gut microbiota on host stem cells across the gastrointestinal tract Authors: Jeong, Haengdueng; Lee, Yura; Nam, Ki Taek; 이유라 Abstract: The gut microbiota plays a pivotal role in maintaining gastrointestinal (GI) homeostasis by influencing epithelial integrity, immunity, and metabolism. Recent studies have uncovered that gut microbiota can directly or indirectly modulate the behavior and function of adult stem cells across the GI tract, which are essential for tissue regeneration and disease prevention. Moreover, key microbial metabolites including short-chain fatty acids (SCFAs), tryptophan-derived indoles, succinate, secondary bile acids, and retinoic acid exert diverse effects on stem cell quiescence, proliferation, and differentiation. This review provides current knowledge on the interaction between gut microbiota and host stem cells in the stomach, intestine, and colon. Tue, 01 Dec 2026 00:00:00 GMT https://ir.ymlib.yonsei.ac.kr/handle/22282913/210210 2026-12-01T00:00:00Z https://ir.ymlib.yonsei.ac.kr/handle/22282913/211445 Title: Design, synthesis and biological evaluation of symmetric thiadiazole carboxamide derivative as glutaminase inhibitor Authors: Cyriac, Rajath; Lee, Eun Ji; Kwon, Yeongju; Yun, Mi Ran; Jung, Myoung Eun; Ahn, Sunjoo; Chae, Chang Hak; Choi, Gildon; Cho, Byoung Chul; Lee, Kwangho; 윤미란 Abstract: Metabolic reprogramming toward glutamine anaplerosis is a well-established vulnerability in tumors harboring co-occurring KRAS and KEAP1 mutations, creating a dependency on glutaminase (GLS)-mediated glutaminolysis for survival and growth. Although allosteric GLS inhibitors such as BPTES (Bis-2-(5-phenylacetamido-1,3,4thiadiazol-2-yl)ethyl sulfide) and later-generation analogs such as CB-839 (Telaglenastat) have pharmacologically validated this target, their clinical utility has been constrained by suboptimal drug-like properties, including poor solubility and bioavailability. To overcome these limitations, we developed TRG-192, a novel symmetric amidothiadiazole derivative engineered with a distinct chemical scaffold to enhance physicochemical and pharmacokinetic profiles. In vitro characterization revealed that TRG-192 is a potent GLS inhibitor (IC50 = 68 nM). This biochemical potency translated to a functional effect in a cellular model of glutamine dependence, as evidenced by a significant depletion of intracellular glutamate pools in LDK378-resistant (LR) cells. Furthermore, TRG-192 demonstrated a favorable preclinical safety profile in initial toxicological assessments. Collectively, these data-encompassing potent target engagement, functional on-target activity, and preliminary safety-provide a compelling rationale for the advancement of TRG-192 into in vivo efficacy studies. Wed, 01 Jul 2026 00:00:00 GMT https://ir.ymlib.yonsei.ac.kr/handle/22282913/211445 2026-07-01T00:00:00Z https://ir.ymlib.yonsei.ac.kr/handle/22282913/211938 Title: Phosphatidylserine-Rich circulating extracellular vesicles activate TAM receptor signaling to promote skin wound repair Authors: Lee, Young Joo; Choi, Ho-Ik; Hwang, Jee-hyun; Park, Miso; Choi, Munkyung; Kim, Hyun Young; Kim, Yun Seok; Nam, Ki Taek; Kim, Jin-Ki; Lim, Kyung-Min; Kang, Keon Wook Abstract: Phosphatidylserine (PS) is an anionic phospholipid that acquires signaling activity when exposed on membrane surfaces. Although small extracellular vesicles (sEVs) have been implicated in diverse biological processes, the contribution of membrane-associated PS to vesicle-mediated signaling remains incompletely understood. Here, we show that circulating small extracellular vesicles (csEVs) activate dermal fibroblasts and keratinocytes through a PS-dependent receptor signaling mechanism. Pharmacological blockade of PS using annexin V markedly attenuated csEV-induced cellular proliferation, migration, and paracrine factor expression. Mechanistically, PS-rich csEV membranes activated TAM family receptors and inhibition of TAM receptors suppressed csEV-induced cellular responses. To determine whether PS-mediated membrane signaling is sufficient to account for csEV bioactivity, we generated phosphatidylserine liposomes (PSLs) as a reductionist membrane mimetic. PSLs reproduced key csEVinduced responses in fibroblasts and keratinocytes in vitro and recapitulated csEV activity in ex vivo porcine skin explants and in vivo mouse wound models. Collectively, our data identify membrane-exposed phosphatidylserine as a key determinant of csEV bioactivity and define a PS-TAM receptor signaling axis that regulates skin cell activation. Wed, 01 Jul 2026 00:00:00 GMT https://ir.ymlib.yonsei.ac.kr/handle/22282913/211938 2026-07-01T00:00:00Z https://ir.ymlib.yonsei.ac.kr/handle/22282913/212917 Title: Mitochondria-Damaging Self-Reporting Probe for Cancer Therapy Authors: Xu, Hai; Lee, Yura; Yoon, Sanghee; Wang, Yun; Cho, Yejin; Choi, Seongyu; Lu, Lu; Zhang, Hua; Choi, Sun; Nam, Ki Taek; Yoon, Juyoung Abstract: Mitochondrial damage induced by chemotherapeutic agents through disruption of the mitochondrial membrane potential (Delta Psi m) remains a central challenge in drug development and evaluation. However, the assessment of Delta Psi m-targeting drugs using commercially available fluorescent probes is often unreliable, as these dyes can interfere with, mask, or artificially amplify drug-induced mitochondrial dysfunction, frequently resulting in misleading conclusions and translational failure. Herein, we report a class of cationic chemotherapeutic small molecules (DPPs) possessing intrinsic fluorescence migration-based self-reporting capability, which enables direct and non-invasive monitoring of drug action without the need for external probes. Among them, DPP-1 and DPP-2 disrupt mitochondrial function, trigger excessive reactive oxygen species generation, and induce highly selective apoptosis. Remarkably, both compounds exhibit concentration-dependent mitochondrial-to-nuclear translocation, enabling the real-time visualization of therapeutic progression at the subcellular level. In vivo studies further confirm their potent tumor growth inhibition and negligible systemic toxicity effects. This self-reporting mitochondria-targeted chemotherapeutic platform provides a highly promising strategy for integrated cancer diagnosis and precision therapy. Mon, 01 Jun 2026 00:00:00 GMT https://ir.ymlib.yonsei.ac.kr/handle/22282913/212917 2026-06-01T00:00:00Z