https://scholar.dgist.ac.kr/handle/20.500.11750/265 2026-04-16T13:22:42Z https://scholar.dgist.ac.kr/handle/20.500.11750/60241 Title: RITA 또는 이의 유도체를 포함하는 뇌신경계 질환 예방 또는 치료용 조성물 Author(s): 정성희; 유성운 https://scholar.dgist.ac.kr/handle/20.500.11750/60221 Title: Odors modulate self face perception and frontal ERP responses Author(s): Yoon, Seongwon; Moon, Sun Ae; Kim, Kwangsu; Bae, Jisub; Lee, Jeewon; Moon, Cheil Abstract: The face is crucial for social interactions, as it conveys various personal characteristics and influences social judgments. Although previous studies have demonstrated that odors can modulate facial perception and evaluation, these investigations largely focused on others’ faces (other-face). The neural mechanisms underlying self-face perception remain less explored. This study examined how odors differing in pleasantness modulate self-face perception and associated neural responses measured via event-related potentials (ERPs). Thirty-one healthy participants (14 women, 17 men) evaluated their self-faces after exposure to a neutral odor (lavender), an unpleasant odor (isovaleric acid), or solvent control (control). Exposure to isovaleric acid, compared with air and lavender, significantly reduced self-face attractiveness and preference ratings. Beyond these behavioral effects, we observed odor-related modulation of ERP amplitude and latency across multiple time windows, and Positive potential (PP) amplitude in the 300–600 ms interval was positively associated with self-face preference and attractiveness. These neural responses correlated with subjective self-evaluations, highlighting a critical period for affective self-assessment influenced by olfactory stimuli. These results suggest that odors modulate self-face perception and frontal ERP responses. Our findings suggest that everyday olfactory environments subtly shape self-perception, underscoring the broader impact of odors on social and psychological functioning. 2025-12-31T15:00:00Z https://scholar.dgist.ac.kr/handle/20.500.11750/60207 Title: A decade of progress in understanding LRRTM and Slitrk synaptic cell-adhesion molecules Author(s): Kim, Dongwook; Kim, Byeongchan; Um, Ji Won; Ko, Jaewon Abstract: For over a decade, synaptic cell-adhesion molecules (CAMs) have been recognized as fundamental determinants of neural circuit specificity and diversity. Among the CAMs, leucine-rich repeat (LRR)-containing transmembrane proteins have been established as crucial regulators of synaptic properties across diverse cell-types and brain regions. This minireview focuses on two families of LRR-containing CAMs: leucine-rich repeat transmembrane proteins (LRRTMs) and the Slit and Trk-like family (Slitrks). We provide a comprehensive synthesis of significant findings on LRRTMs and Slitrks since their initial characterization more than 15 years ago. Furthermore, we outline key unresolved questions to stimulate future studies on their functional mechanisms in neural circuit assembly and their pathophysiological roles in various neurological disorders. 2026-02-28T15:00:00Z https://scholar.dgist.ac.kr/handle/20.500.11750/60202 Title: Cereblon (CRBN) inhibits prostate cancer metastasis by negatively regulating 6-phosphogluconate dehydrogenase (6PGD) Author(s): Guchhait, Koushik; Yoon, Hyeon-Seung; An, Hyun-Su; Shin, Seungheon; Nam, Hye Seung; Yanqui-Rivera, Francisco D.; Ona, Samara M.; Mendez, Miguel A.; Hwang, Jong Yeon; Park, Daeho; Park, Chul-Seung; Han, Jee-Young; Chung, Doo Yong; Park, Seokjae; Kim, Eun-Kyoung; Yang, Su-Geun; Cho, Steve K. Abstract: Metastasis is the primary cause of mortality in advanced prostate cancer, and the emergence of resistance to androgen receptor (AR)-targeted therapies highlights the urgent need for alternative therapeutic strategies. Metabolic reprogramming has increasingly been recognized as a key driver of metastatic progression. In this study, we uncover a novel tumor-suppressive role for cereblon (CRBN), a substrate receptor of the CRL4CRBN E3 ubiquitin ligase complex, in modulating prostate cancer metastasis through regulation of 6-phosphogluconate dehydrogenase (6PGD), a critical enzyme in the oxidative pentose phosphate pathway (oxPPP). CRBN directly binds a conserved C-terminal alpha-helix in 6PGD, promoting its polyubiquitination and proteasomal degradation independently of immunomodulatory drugs (IMiDs). Genetic or pharmacological loss of CRBN via CRISPR/Cas9, RNA interference, or PROTAC-mediated degradation stabilized 6PGD and elevated the NADPH/NADP+ ratio. Conversely, re-expression of wild-type CRBN reduced 6PGD levels, restored NADPH/NADP+ ratio, and suppressed cell migration and invasion. Transcriptomic profiling revealed CRBN-induced upregulation of CDH1 and downregulation of the EMT marker MMP1, while CRBN degradation produced the opposite pattern-both effects were reversed by 6PGD inhibition. These regulatory effects were conserved across multiple cancer cell lines and observed in CRBN-deficient mouse tissues. Functional studies using intra-splenic xenograft models further demonstrated that CRBN suppresses metastatic dissemination. Collectively, our findings identify 6PGD as a novel endogenous substrate of CRBN and establish the CRBN-6PGD axis as a critical metabolic checkpoint in prostate cancer metastasis. Therapeutic targeting of this pathway may offer promising strategies for CRBN-deficient or 6PGD-driven cancers. 2026-02-28T15:00:00Z