https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/65 2026-07-24T02:53:26Z 2026-07-24T02:53:26Z Nguyen, Tuan Hoang Anh Kim, Pok-Son Kutzner, Arne Heese, Klaus https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/213261 2026-06-12T05:30:29Z 2026-12-01T00:00:00Z

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).

2026-12-01T00:00:00Z Dash Sharma, Sidharth Sensharma, Sreemoyee Kutzner, Arne Fuhrer, Erwin Pramanik, Gopal Heese, Klaus Pramanik, Subrata https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/217632 2026-06-26T05:30:40Z 2026-07-01T00:00:00Z

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.

2026-07-01T00:00:00Z 양윤모 https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/218470 2026-07-22T14:10:58Z 2026-06-24T00:00:00Z

Title: Functional characterization of the S1-like protein YabR in Bacillus subtilis Authors: 양윤모

2026-06-24T00:00:00Z 양윤모 https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/218469 2026-07-22T14:10:56Z 2026-06-24T00:00:00Z

Title: Noncanonical zinc binding in ribosomal protein paralogs of Staphylococcus aureus Authors: 양윤모

2026-06-24T00:00:00Z