김태일 교수
Tae Il Kim
연세대학교 내과 · 의학
연구실 소개
김태일 교수의 연구실은 면역세포의 항원 인식 메커니즘과 신경혈관 연관 반응을 중심으로 면역학적 및 뇌혈관 영상 기반의 기초 의학 연구를 수행하고 있습니다. 특히 플라즈마세포성 수상세포에서의 DNA 인식 수용체와 TLR9 외의 MyD88 의존성 DNA 센서의 기능을 단백질 분석 및 유전자 조절 메커니즘으로 규명하고 있으며, 뇌에서의 혈류 변화와 산소 수준 반응의 정량적 분석을 위해 고해상도 MRI 기술을 응용하고 있습니다. 이와 더불어 장기염증성 질환인 장백류병의 진단 기준 개발 및 당뇨병 환자에서 메트포르민의 항암 효과에 대한 임상적 영향을 평가하는 임상역학 연구도 함께 진행하고 있습니다.
연구 현황
연구 성과 추이
표시된 성과는 수집된 데이터 기준으로 산출되며, 일부 차이가 있을 수 있습니다.
주요 논문
15Toll-like receptor 9 (TLR9) senses microbial DNA and triggers type I IFN responses in plasmacytoid dendritic cells (pDCs). Previous studies suggest the presence of myeloid differentiation primary response gene 88 (MyD88)-dependent DNA sensors other than TLR9 in pDCs. Using MS, we investigated C-phosphate-G (CpG)-binding proteins from human pDCs, pDC-cell lines, and interferon regulatory factor 7 (IRF7)-expressing B-cell lines. CpG-A selectively bound the aspartate-glutamate-any amino acid-aspart
Nine factors have been found to be associated with IPPB and polypectomy should be undertaken with caution under these conditions.
Metformin use has been associated with decreased cancer risk and mortality. However, the effects of metformin on clinical outcomes of colorectal cancer (CRC) are not defined. This study aimed to evaluate the association between metformin use and mortality of CRC in diabetic patients. We identified 595 patients who were diagnosed both CRC and diabetes mellitus. Patients were compared by two groups; 258 diabetic patients taking metformin and 337 diabetic patients not taking metformin. Patient's de
Quantifying both arterial cerebral blood volume (CBV(a)) changes and total cerebral blood volume (CBV(t)) changes during neural activation can provide critical information about vascular control mechanisms, and help to identify the origins of neurovascular responses in conventional blood oxygenation level dependent (BOLD) magnetic resonance imaging (MRI). Cerebral blood flow (CBF), CBV(a), and CBV(t) were quantified by MRI at 9.4 T in isoflurane-anesthetized rats during 15-s duration forepaw sti
OBJECTIVES: It is difficult to diagnose intestinal Behçet's disease (BD) due to various extraintestinal manifestations emerging at different time points in the disease course and a lack of reliable diagnostic criteria. We conducted this study to develop and validate novel diagnostic criteria for intestinal BD. METHODS: Experts from three universities generated the preliminary diagnostic criteria for intestinal BD, and a consensus was reached using a modified Delphi method with 13 gastroenterolog
Determination of compartment-specific cerebral blood volume (CBV) changes is important for understanding neurovascular physiology and quantifying blood oxygenation level-dependent (BOLD) functional magnetic resonance imaging (fMRI). In isoflurane-anesthetized cats, we measured the spatiotemporal responses of arterial CBV (CBV(a)) and total CBV (CBV(t)) induced by a 40-second visual stimulation, using magnetization transfer (MT)-varied BOLD and contrast-agent fMRI techniques at 9.4 T. To determin
Genotoxic stress triggers signal transduction pathways that mediate either the protection or apoptosis of affected cells. The interferon regulatory factors (IRFs) are involved in a wide range of host defense mechanisms against environmental stresses. Treatment with DNA-damaging agents, including doxorubicin and UV radiation, caused phosphorylation of the IRF3 transcription factor. Phosphorylation of IRF3 induced its interaction with the transcriptional co-activator cAMP-response element binding
Metformin has been known to suppress cancer stem cells (CSCs) in some cancers. However, the differential effects of metformin on CSCs and their mechanisms have not been reported. Herein, metformin induced pAMPK activation and pS6 suppression in metformin-sensitive (HT29) cells, but not in metformin-resistant (SW620) cells. The oxygen consumption rate was higher in HT29 cells than in SW620 cells and showed a prominent decrease after metformin treatment in HT29 cells. In glutamine-depleted medium,
Cancer stem cells (CSCs) play a pivotal role in cancer relapse or metastasis. We investigated the CSC-suppressing effect of nonsteroidal anti-inflammatory drugs (NSAIDs) and the relevant mechanisms in colorectal cancer. We measured the effect of NSAIDs on CSC populations in Caco-2 or SW620 cells using colosphere formation and flow cytometric analysis of PROM1 (CD133)(+) CD44(+) cells after indomethacin treatment with/without prostaglandin E2 (PGE2) or peroxisome proliferator-activated receptor γ
Drosophila protects itself from infection by microbial organisms by means of its pivotal defense, the so-called innate immunity system. This is its sole defense as it lacks an adaptive immunity system such as is found in mammals. The strong conservation of innate immunity systems in organisms from Drosophila to mammals, and the ease with which Drosophila can be manipulated genetically, makes this fly a good model system for investigating the mechanisms of virulence of a number of medically impor
Metformin is a well-known AMPK (AMP-activated protein kinase) activator that suppresses cancer stem cells (CSCs) in some cancers. However, the mechanisms of the CSC-suppressing effects of metformin are not yet well understood. In this study, we investigated the CSC-suppressive effect of metformin via the mevalonate (MVA) pathway in colorectal cancer (CRC). Two colorectal cancer cell lines, HT29 and DLD-1 cells, were treated with metformin, mevalonate, or a combination of the two. We measured CSC
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