Monkeys ptt的問題，透過圖書和論文來找解法和答案更準確安心。 我們找到下列股價、配息、目標價等股票新聞資訊

在帕金森氏症的細胞與生物模式中探討PLA2G6及PLA2G6點突變

為了解決Monkeys ptt的問題，作者劉涵芳 這樣論述：

Table of Contents中文摘要 iAbstract iiTable of Contents iiiList of Figures vList of tables viAbbreviation viiChapter 1. Introduction - 1 -1.1 Phospholipase A2, group VI - 1 -1.2 Parkinson’s disease - 2 -1.3 PLA2G6 and young-onset dystonia-parkinsonism (Parkinson disease-14, P

ARK14) - 3 -1.4 PLA2G6 activity and lipid metabolites - 4 -1.5 Zebrafish as a Model for Neurodegenerative Disorders - 5 -Chapter 2. Materials and Methods - 7 -2.1 Animal Maintenance - 7 -2.2 mRNA preparation and microinjection - 7 -2.3 Zebrafish behavior - 8 -2.4 Histological an

alysis - 8 -2.5 Phospholipase activity assay - 11 -2.6 High performance liquid chromatography (HPLC) - 12 -2.7 Lipophilic metabolites extraction and data processing - 12 -2.8 Mouse behavior - 13 -2.9 Cell culture and Immunocytochemistry - 14 -2.10 Western blot - 15 -2.11 Quantit

ative reverse transcription PCR (qRT-PCR) - 16 -2.12 Statistical analysis - 17 -Chapter 3. Results - 18 -3.1 Characterization of PLA2G6 mutations in zebrafish - 18 -3.1.1 Overexpression of PLA2G6 mutations in zebrafish - 18 -3.1.2 PLA2G6 mutation D331Y and T572I overexpression induced

motility defects in zebrafish - 18 -3.1.3 PLA2G6 mutation D331Y and T572I overexpression caused dopamine neuron loss in zebrafish - 20 -3.2 PLA2G6 phospholipase activity and lipid metabolites - 21 -3.2.1 Zebrafish Pla2g6 is homologous to human PLA2G6 - 21 -3.2.2 PLA2G6 mutation D331Y or

T572I results in decreased phospholipase activity and disturbed lipidome - 22 -3.2.3 Dietary DHA supplementation relieved the motility defects of PLA2G6D331Y/D331Y mice at an early stage of disease onset - 23 -3.3 PLA2G6 in dopaminergic neuron development - 25 -3.3.1 Zebrafish pla2g6 expre

ssed mainly in the central nervous system - 25 -3.3.2 PLA2G6 mutation D331Y or T572I reduced neuronal precursor cells through increased apoptosis - 26 -3.4 The role of PLA2G6 in regulating cellular processes - 27 -3.4.1 Transduction of human wild type PLA2G6 improved proliferation in dopami

nergic neuron cell line - 27 -3.4.2 PLA2G6 play a protective role in dopaminergic neuron cell line under ROS stress - 28 -Chapter 4. Discussion - 29 -4.1 PLA2G6 mutations in PARK14 - 29 -4.2 PLA2G6 mutation and phospholipase activity in PARK14 - 30 -4.3 The role of DHA in PLA2G6 mutat

ion-induced PD - 31 -4.4 PLA2G6-mediated apoptosis in the dopaminergic neuron. - 33 -4.5 PLA2G6 and its metabolites in neurodevelopment. - 34 -4.6 The potential signaling regulation role of PLA2G6 - 36 -Chapter 5. Conclusion - 37 -References - 38 -Figures and Legends - 48 -Table

s - 68 -Publications - 73 -List of FiguresFigure 1. Alignment of PLA2G6 human and zebrafish homologue. - 49 -Figure 2. Schematic illustration of PLA2G6 domains and six point mutations of PARK14. - 50 -Figure 3. Injection of PLA2G6D331Y or PLA2G6T572I causes motility defects in zebrafish.

- 51 -Figure 4. Injection of PLA2G6D331Y or PLA2G6T572I decreases dopaminergic neurons and dopamine levels. - 52 -Figure 5. Injection of PLA2G6D331Y, PLA2G6T572I, or pla2g6 deletion constructs alters phospholipase activity in zebrafish. - 53 -Figure 6. Co-expression of zebrafish pla2g6 res

cues the behavioral defects induced by PLA2G6D331Y or PLA2G6T572I. - 54 -Figure 7. Lipid metabolites are disturbed in PLA2G6D331Y or PLA2G6T572I injected embryos. - 55 -Figure 8. Dietary DHA supplementation does not affect the body weight and diet consumption of PLA2G6 knock-in mice. - 56 -

Figure 9. Dietary DHA supplementation relieves the motility defects of PLA2G6D331Y/D331Y mice at an early stage of disease onset. - 58 -Figure 10. Dietary DHA supplementation does not relieve the motility defects of PLA2G6D331Y/D331Y mice at a late stage of disease onset. - 59 -Figure 11. Zebr

afish pla2g6 is expressed in the developing nervous system. - 60 -Figure 12. Injection of PLA2G6D331Y or PLA2G6T572I reduces the expression of the neuronal precursor marker and induces cell apoptosis. __ - 61 -Figure 13. Injection of PLA2G6D331Y or PLA2G6T572I does not affect the expression of

the neural progenitor marker. - 62 -Figure 14. Expression of human PLA2G6 enhances the proliferation of MN9D cells. - 63 -Figure 15. Expression of hPLA2G6 reduces cell apoptosis upon 6-OHDA treatment in MN9D cells. - 64 -Figure 16. 3D structure predictions of PLA2G6 and the effect of D331Y

or T572I mutation analyzed by PyMOL software. - 65 -Figure 17. Injection of PLA2G6 mutation PLA2G6D331Y or PLA2G6T572I, or pla2g6 deletion constructs pla2g6∆ANK or pla2g6∆Ptt affect the expression of Notch signaling downstream genes. - 66 -Figure 18. The summary of this study. - 67 -List o

f tablesTable 1. List of lipid metabolites identified in PLA2G6D331Y or PLA2G6T572I injected embryos. - 69 -Table 2. Lipid metabolites identified conditions in LC-MS and METLIN database. - 70 -Table 3. Primers used for gene cloning in this thesis. - 71 -Table 4. Primers used for qRT-PCR ana

lysis in this thesis - 72 -