효모에서 D-Erythroascorbic Acid의 기능

Thesis (doctoral)--서울대학교 대학원 :미생물학과,1998.Docto

Search for demarcation criteria between science and pseudoscience

학위논문 (석사)-- 서울대학교 대학원 : 협동과정 과학사및과학철학전공, 2011.2. 조인래.Maste

A Revisionary Defense of Strong Explanatory Evidence Theory

학위논문 (박사)-- 서울대학교 대학원 : 자연과학대학 협동과정 과학사및과학철학전공, 2018. 8. 조인래.이 논문에서 나는 과학자가 사용하는 실제 증거 개념을 잘 해명할 수 있는 적절한 과학적 증거 이론을 찾는다. 이를 위해 2-4장에서 기존 증거 이론(가설-연역적 증거 이론, 베이즈주의 증거 이론, 최선 설명으로의 추론(IBE))의 강점과 약점을 살핀 후, 해당 이론들이 실제 증거 개념을 해명하기에 부족하다는 점을 보인다. 다음으로 5장에서 기존 증거 이론의 문제를 정리하고 왜 이러한 문제가 발생하는지 살핀다. 여기서 나는 증거는 가설의 참을 가리키는 표지가 되어야 하는데, 기존의 증거 개념은 표지 기능을 수행하기에 미흡하기 때문에 다양한 문제들이 발생한다고 주장한다. 6장에서 나는 표지 개념에 잘 들어맞는 애친슈타인의 증거 이론(강한 설명적 증거 이론)을 소개하고 옹호한다. 이 강한 설명적 증거 이론의 핵심 축은 다음과 같다. 하나는 증거는 가설의 높은 확률을 보장해야 한다는 것이고, (p(h1장 들어가며 1 2장 가설-연역적 증거 이론 8 2.1. 입증의 예측 기준과 나타나는 문제점들 8 2.2. 가설-연역적 증거 이론의 수정안과 한계 11 2.3. 연역 논리의 근본적 한계 17 3장 긍정적 유관성 기준: 베이즈주의 증거 이론 19 3.1. 긍정적 유관성 기준과 그 위력 19 3.2. 오래된 증거의 문제 26 3.3. 긍정적 유관성 기준의 또 다른 문제 33 4장 설명과 증거: 최선 설명으로의 추론 39 4.1. 설명적 고려 39 4.2. IBE가 제공하는 것 45 4.3. IBE의 한계 49 5장 왜 기존 증거 이론은 실패하는가 55 5.1. 기존 이론의 문제 다시 살펴보기 55 5.2. 증거와 표지 59 6장 애친슈타인의 증거 이론: 강한 설명적 증거 68 6.1. 가설의 높은 확률 조건과 설명적 연결 조건 69 6.2. 옳은 설명 76 6.3. 최종 정의와 새로운 증거 개념의 장점 80 6.4. 강한 설명적 증거 개념에 대한 비판과 방어 87 6.5. 보론: 선택 절차 95 7장 수정된 강한 설명적 증거 이론 97 7.1. 선언 가설의 증거 97 7.2. 제거적 증거의 문제 106 7.3. 수정된 조건과 흥미로운 귀결 113 7.4. 강한 증거와 좋은 증거 123 8장 오래된 질문들에 대한 새로운 해답 131 8.1. 사이비 입증의 문제 131 8.2. 유사한 증거보다 다양한 증거 140 8.3. 까마귀 가설의 증거 157 9장 K-T 멸종과 소행성 충돌 가설 177 9.1. 충돌 가설로 가는 길 178 9.2. 기존 증거 이론의 문제 187 9.3. 충돌 가설의 보완: 다양한 증거 및 멸종 메커니즘 191 10장 나오며 197 참고문헌 201 Abstract 208 감사의 글 210Docto

Rad52 phosphorylation by Ipl1 and Mps1 contributes to Mps1 kinetochore localization and spindle assembly checkpoint regulation

Rad52 is well known as a key factor in homologous recombination. Here, we report that Rad52 has functions unrelated to homologous recombination in Saccharomyces cerevisiae; it plays a role in the recruitment of Mps1 to the kinetochores and the maintenance of spindle assembly checkpoint (SAC) activity. Deletion of RAD52 causes various phenotypes related to the dysregulation of chromosome biorientation. Rad52 directly affects efficient operation of the SAC and accurate chromosome segregation. Remarkably, by using an in vitro kinase assay, we found that Rad52 is a substrate of IpM/Aurora and Mps1 in yeast and humans. Ipl1-dependent phosphorylation of Rad52 facilitates the kinetochore accumulation of Mps1, and Mps1-dependent phosphorylation of Rad52 is important for the accurate regulation of the SAC under spindle damage conditions. Taken together, our data provide detailed insights into the regulatory mechanism of chromosome biorientation by mitotic kinases.OAIID:RECH_ACHV_DSTSH_NO:T201717380RECH_ACHV_FG:RR00200001ADJUST_YN:EMP_ID:A076388CITE_RATE:9.504DEPT_NM:생명과학부EMAIL:[email protected]_YN:YY

Genome-Wide Studies of Rho5-Interacting Proteins That Are Involved in Oxidant-Induced Cell Death in Budding Yeast

Rho GTPases play critical roles in cell proliferation and cell death in many species. As in animal cells, cells of the budding yeast Saccharomyces cerevisiae undergo regulated cell death under various physiological conditions and upon exposure to external stress. The Rho5 GTPase is necessary for oxidant-induced cell death, and cells expressing a constitutively active GTP-locked Rho5 are hypersensitive to oxidants. Yet how Rho5 regulates yeast cell death has been poorly understood. To identify genes that are involved in the Rho5-mediated cell death program, we performed two complementary genome-wide screens: one screen for oxidant-resistant deletion mutants and another screen for Rho5-associated proteins. Functional enrichment and interaction network analysis revealed enrichment for genes in pathways related to metabolism, transport, and plasma membrane organization. In particular, we find that ATG21, which is known to be involved in the CVT (Cytoplasm-to-Vacuole Targeting) pathway and mitophagy, is necessary for cell death induced by oxidants. Cells lacking Atg21 exhibit little cell death upon exposure to oxidants even when the GTP-locked Rho5 is expressed. Moreover, Atg21 interacts with Rho5 preferentially in its GTP-bound state, suggesting that Atg21 is a downstream target of Rho5 in oxidant-induced cell death. Given the high degree of conservation of Rho GTPases and autophagy from yeast to human, this study may provide insight into regulated cell death in eukaryotes in general

Genome-Wide Studies of Rho5-Interacting Proteins That Are Involved in Oxidant-Induced Cell Death in Budding Yeast

Rho GTPases play critical roles in cell proliferation and cell death in many species. As in animal cells, cells of the budding yeast Saccharomyces cerevisiae undergo regulated cell death under various physiological conditions and upon exposure to external stress. The GTPase is necessary for oxidant-induced cell death, and cells expressing a constitutively active GTP-locked are hypersensitive to oxidants. Yet how regulates yeast cell death has been poorly understood. To identify genes that are involved in the -mediated cell death program, we performed two complementary genome-wide screens: one screen for oxidant-resistant deletion mutants and another screen for -associated proteins. Functional enrichment and interaction network analysis revealed enrichment for genes in pathways related to metabolism, transport, and plasma membrane organization. In particular, we find that , which is known to be involved in the CVT (Cytoplasm-to-Vacuole Targeting) pathway and mitophagy, is necessary for cell death induced by oxidants. Cells lacking exhibit little cell death upon exposure to oxidants even when the GTP-locked is expressed. Moreover, interacts with preferentially in its GTP-bound state, suggesting that is a downstream target of in oxidant-induced cell death. Given the high degree of conservation of Rho GTPases and autophagy from yeast to human, this study may provide insight into regulated cell death in eukaryotes in general.OAIID:RECH_ACHV_DSTSH_NO:T201906737RECH_ACHV_FG:RR00200001ADJUST_YN:EMP_ID:A076388CITE_RATE:2.742DEPT_NM:생명과학부EMAIL:[email protected]_YN:YY

G2a protects mice against sepsis by modulating Kupffer cell activation: Cooperativity with adenosine receptor 2B

G2A is a GPCR abundantly expressed in immune cells. G2A(-/-) mice showed higher lethality, higher plasma cytokines, and an impaired bacterial clearance in response to a murine model of sepsis (cecal ligation and puncture), which were blocked by GdCl3, an inhibitor of Kupffer cells. Anti-IL-10 Ab reversed the impaired bacterial clearance in G2A(-/-) mice. Indomethacin effectively blocked both the increased i.p. IL-10 levels and the impaired bacterial clearance, indicating that disturbed PG system is the proximal cause of these phenomena. Stimulation with LPS/C5a induced an increase in Escherichia coli phagocytosis and intracellular cAMP levels in G2A(+/+) peritoneal macrophages but not G2A(-/-) cells, which showed more PGE(2)/nitrite release and intracellular reactive oxygen species levels. Heterologous coexpression of G2A and adenosine receptor type 2b (A2bAR) induced a synergistic increase in cAMP signaling in a ligand-independent manner, with the evidence of physical interaction of G2A with A2bAR. BAY 60-6583, a specific agonist for A2bAR, increased intracellular cAMP levels in Kupffer cells from G2A(+/+) but not from G2A(-/-) mice. Both G2A and A2bAR were required for antiseptic action of lysophosphatidylcholine. These results show inappropriate activation of G2A(-/-) Kupffer cells to septic insults due to an impaired cAMP signaling possibly by lack of interaction with A2bAR.OAIID:RECH_ACHV_DSTSH_NO:T201817125RECH_ACHV_FG:RR00200001ADJUST_YN:EMP_ID:A076388CITE_RATE:4.539DEPT_NM:생명과학부EMAIL:[email protected]_YN:YY