서울대학교 · 의학
다른 황 교수의 연구실은 주로 간담췌생식기계암 및 혈액계 종양의 위험 인자와 병태생리학을 규명하는 데 초점을 맞추고 있습니다. 특히 담석, 총담도절제술, 흡연 등의 생활습관 요인과 위암, 간세포암, 림프종 등 악성 종양 간의 연관성을 대규모 코hort 연구 및 임상 사례를 통해 분석하고 있습니다. 영상 진단 기법(예: PET/CT)과 생존 예후 분석을 융합한 정밀의료 기반의 연구가 특징입니다.
표시된 성과는 수집된 데이터 기준으로 산출되며, 일부 차이가 있을 수 있습니다.
Dental pulp stem cells (DPSCs), as one type of mesenchymal stem cells (MSCs), have the capability of self-renewal and multipotency to differentiate into several cell lineages, including osteogenesis, odontoblasts, chondrogenesis, neurogenesis, and adipogenesis. It has found that tumor necrosis factor-α (TNF-α) can promote osteogenic differentiation of human DPSCs in our previous studies. Other experimentation revealed that signal transducer and activator of transcription 3 (STAT3) underwent a ra
Activation of nuclear receptor estrogen receptor α (ERα) exerts cardiovascular protective effects by modulating the expression of ERα target genes. However, the underlying mechanism remains unclear. PARP1 is a ubiquitous multifunctional nuclear enzyme. In this study, we examined the interplay between PARP1 and ERα, and identified PARP1 as an important regulator of ERα-dependent transcription. We showed that PARP1 could directly bind to ERα, and ERα could be poly(ADP-ribosyl)ated by PARP1. Poly(A
PARP-1 inhibits adiponectin and AdipoR1 expression as well as PPAR gamma transactivation through poly(ADP-ribosyl)ation of PPAR gamma in cultured rat cardiac fibroblasts.
The rising prevalence of bone diseases in an aging population underscores the urgent need for innovative and clinically translatable solutions in bone tissue engineering. While significant progress has been made in refining the chemical properties of biomaterials, the structural design of scaffolds-a critical determinant of repair success-remains comparatively underexplored. Structural parameters such as porosity, pore size, and interconnectivity are not only essential for achieving mechanical s
PARP1 is indispensable for TGF-β1 induced Smad3 activation in rat VSMCs. Targeting PARP1 may be a promising therapeutic approach against vascular diseases induced by dysregulation of TGF-β/Smad3 pathway.
The transcription factor Sp1 is implicated in the activation of G0/G1 phase genes. Modulation of Sp1 transcription activities may affect G1-S checkpoint, resulting in changes in cell proliferation. In this study, our results demonstrated that activated poly(ADP-ribose) polymerase 1 (PARP-1) promoted cell proliferation by inhibiting Sp1 signaling pathway. Cell proliferation and cell cycle assays demonstrated that PARP inhibitors or PARP-1 siRNA treatment significantly inhibited proliferation of h