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GPR97對於延緩人類嗜中性白血球的凋亡之機制及訊號傳遞探討

為了解決Latrotoxin 中文的問題，作者張育綺 這樣論述：

指導教授推薦書口試委員會審定書致謝 iii中文摘要 vAbstract viTable of contents viiList of figures ixAbbreviation xChapter 1: Introduction -11.1 G protein-coupled receptors (GPCRs) -11.1.1 GPCR activation and desensitization -11.2 Adhesion G protein-coupled receptors -21.3 G protein-coupled receptor 97 -31.4 Neutrophi

ls and integrin Mac-1 -41.5 GPR97 interaction with mPR3 on neutrophils -61.6 Proteinase 3 and Proteinase-activated receptor 2 -61.7 Signaling pathways of neutrophil survival -8Chapter 2: Hypothesis and specific aims -10Chapter 3: Materials and methods -113.1 Cell culture -113.2 Transformation -11

3.3 Plasmid DNA purification -113.4 Cell transfection -113.4.1 Calcium phosphate transfection -113.4.2 Lipofectamine transfection -123.5 Protein purification by protein A beads -133.6 Cells lysates with modified RIPA buffer -143.7 Western blotting -143.8 Enzyme-linked immunosorbent assay (ELISA) -15

3.9 Human neutrophils isolation -153.10 Neutrophil ligand binding assay -163.11 Assessment of neutrophil apoptosis -163.12 Assessment of PR3 activity -173.13 Phorbol myristate acetate (PMA)-induced neutrophil apoptosis -17Chapter 4: Results -184.1 Binding of GPR97 to its ligand on human

neutrophils -184.2 Interaction between GPR97 and PR3 at various concentrations -184.3 Neutrophils morphology was modulated by GPR97-mPR3 interaction -194.4 GPR97 binding induced delayed spontaneous apoptosis in human neutrophils -194.5 GPR97-mediated neutrophil apoptosis delay is dependent

on lipid raft integrity -204.6 Induction of apoptosis in human neutrophils using blocking antibodies of integrin Mac-1 -214.7 Differential modulation of the enzymatic activity of soluble and mPR3 by GPR97 -214.8 GPR97-induced neutrophils apoptosis delay is due to the activation of mPR3 -224

.9 ERK and PI3K signaling pathway are involved in GPR97-mediated neutrophil apoptosis delay -234.10 PAR-2 activation by mPR3 is involved in GPR97-mediated apoptosis delay on human neutrophils -234.11 GPR97-mediated neutrophil apoptosis delay is mediated through SHP-2 signaling -234.12 GPR97 delays n

eutrophil spontaneous apoptosis but not PMA-induced apoptosis of human neutrophils -24Chapter 5: Discussion -25Chapter 6: References -29Chapter 7: Figures -36List of figuresFigure 1 GPR97 binds to human neutrophils with a bimodal pattern -36Figure 2 Analysis of GPR97 interaction with PR3 in vitro

by ELISA-like assays -37Figure 3 GPR97-binding induced neutrophil morphological change -38Figure 4 GPR97 binding to neutrophils delays spontaneous cell apoptosis -39Figure 5 GPR97-mediated apoptosis delay is dependent on the lipid raft microdomains -40Figure 6 Integrin Mac-1 does not involve

in GPR97-mediated apoptosis delay of human neutrophils -41Figure 7 Differential modulation of the enzymatic activity of membrane PR3 by GPR97 -42Figure 8 GPR97-induced apoptosis delay of human neutrophils is due to the activation of mPR3 -44Figure 9 GPR97-binding regulated human neutrophils survival

through the ERK and PI 3-kinase signaling pathways -45Figure 10 PAR-2 is involved in GPR97-induced apoptosis delay of human neutrophils -46Figure 11 SHP-2 inhibitor reduced GPR97-mediated neutrophil apoptosis delay -47Figure 12 GPR97 does not block PMA-induced apoptosis of human neutrophils -48Figu

re 13 Model of GPR97/mPR3/PAR-2 mediated survival of human neutrophils -49

以螢光高效能液相層析串聯質譜分析愷他命對小鼠大腦皮質組織蛋白質體之影響

為了解決Latrotoxin 中文的問題，作者謝郁琦 這樣論述：

愷他命 (ketamine) 在1970年被核准作為麻醉藥物使用，過去相關研究中發現，在麻醉劑量以下，愷他命會產生類似思覺失調症等精神病副作用，並具有快速且有效之抗憂鬱症效果，此外，其神經毒性可能造成之傷害亦逐漸受到重視，然而造成這些複雜作用之機轉目前仍尚未有明確定論。本研究即以蛋白質體分析方法，比較小鼠大腦皮質組織在給予愷他命後表現量改變之蛋白質，藉由分析這些差異蛋白質之功能了解愷他命引起精神疾病相關作用或損傷之機轉。本次研究將投予愷他命之小鼠大腦皮質均質化，並利用螢光衍生化試劑DAABD-Cl (4-[2-(Dimethylamino)ethylaminosulfonyl]-7-chlo

ro-2,1,3-benzoxadiazole)衍生化後，再以螢光高效能液相層析儀(FD-HPLC)分離及定量，螢光強度具顯著差異之蛋白質波峰則以液相層析串聯質譜儀 (LC-MS/MS) 與數據庫檢索系統進行蛋白質身分鑑定。蛋白質體分析結果共鑑定出35個表現量具顯著差異之蛋白質，其功能與能量代謝、訊息傳遞路徑、神經發育及細胞骨架等有關，其中V-type proton ATPase subunit a、HACE1及TMEPAI可能分別經由不同之機制，而導致相關受體活化及訊息傳遞路徑之調控，產生類精神病及抗憂鬱症之雙重作用，此外，本研究中發現V-type proton ATPase subunit

a、HACE1、TPI、GPR124、brevican及PI3K-C2α之表現量異常，其可能造成細胞死亡，而與愷他命之神經毒性有關。本研究有助於了解愷他命於精神疾病相關作用或損傷之機轉，以應用於損傷之評估及治療方式之開發。