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探討在神經退化性疾病中調控核醣核酸結合蛋白MBNL2表現之機轉

為了解決Gamma SL PTT的問題，作者王李馨 這樣論述：

中文摘要 iAbstract iiContents iiiIntroduction 1Myotonic dystrophy type 1 (DM1) 1Cerebral involvement of adult-onset DM1 2Genetic basis of DM1 4Molecular mechanism in DM1 4Mouse models of DM1 with expression of CUG repeats 6RNA-binding protein: Muscleblind-like (MBNL) family

8MBNL1 and MBNL2 knockout mice 9Calcium-dependent cysteine protease: Calpain 11Calpain-1 and -2 11Calpain-1 and -2 deficient mice 12Calpain-1 and -2 in neurodegeneration 13Alzheimer’s disease (AD) 14Disease stages of AD 14Clinical presentations of AD 15Brain atrophy of AD

15Two pathological hallmarks of AD 16The aims of the study 20Materials and methods 211. Animals 212. Primary hippocampal neuron culture, drug treatment, virus infection and transfection 213. Cell culture and transient transfection 234. Total protein extraction and sub

cellular fractionation 245. Immunoprecipitation (IP) 256. Immunoblotting analysis 257. RNA preparation, RT-PCR and splicing analysis 268. Immunofluorescence staining and immunohistochemistry 279. Quantification of fluorescent images of brain sections 2910. Quantif

ication of fluorescent images of neurons 3011. Antibodies 3012. Plasmids 3113. Statistical analysis 31Results 331. Characterize the role of MBNL2 in neuronal maturation1.1. MBNL2 is expressed postnatally and increased as neuronal maturation 331.2. MBNL2 expression

is required for promoting adult pattern of RNA processingand neuronal differentiation 342. Determine how neurodegenerative conditions reduce MBNL2 expression2.1. Glutamate-induced excitotoxicity reduces MBNL2 protein expression viaNMDAR activation 352.2. NMDAR-mediated Calpain-2 acti

vation causes MBNL2 protein degradation 362.3. Calcium-dependent nuclear translocation of CAPN2 is associated with reducedMBNL2 expression 382.4. Dysregulated calcium homeostasis reduces MBNL2 expression 392.5. Enhanced nuclear translocation of CAPN2 occurs in the EpA960/CamKII-Cre

brain 402.6. Enhanced nuclear translocation of CAPN2 in neurodegeneration recapitulates thefetal developmental pattern 413. Explore the possibility of the reduced MBNL2 expression associated re-induced fetalpattern of RNA processing as a common feature among neurodegenerative disorders3.

1. Enhanced nuclear translocation of CAPN2, reduced MBNL2 expression and associated aberrant MBNL2-regulated alternative splicing in the degenerative brains of AD 41Discussion 44Perspective 48References 49List of figuresFigure 1. MBNL2 is expressed postnatally and increased with bra

in maturation 64Figure 2. MBNL2 is expressed in the more differentiated cells during hippocampusmaturation 65Figure 3. MBNL2 is expressed ubiquitously in the adult mouse brain 66Figure 4. MBNL2 is expressed in the neurons, oligodendrocytes and astrocytes 67Figure 5. The knockdown

efficiency of MBNL2 shRNAs in cultured neurons 68Figure 6. The alternative splicing and polyadenylation of MBNL2 targets show a fetal to adult transition during neuronal differentiation 70Figure 7. MBNL2 depletion disrupts the developmental RNA processing transition in cultured neurons

71Figure 8. MBNL2 depletion impairs dendrite maturation in cultured neurons 72Figure 9. Glutamate treatment induces excitotoxicity in mature cultured neurons showing condensed nucleus 74Figure 10. Glutamate-induced excitotoxicity reduces MBNL2 protein level in mature cultured neurons 75

Figure 11. Glutamate reduces MBNL2 level via NMDAR activation in cultured neurons 77Figure 12. NMDAR-mediated MBNL2 reduction is calcium dependent 78Figure 13. The alternative splicing and polyadenylation of MBNL2 targets are disrupted in neurons treated with glutamate or NMDA 79Figure 14.

MBNL2 mRNA level is unchanged in cultured neurons treated with glutamate or NMDA 81Figure 15. MBNL2 protein is stable in the neurons 82Figure 16. NMDAR signaling-mediated MBNL2 reduction requires calpain activity incultured neurons 83Figure 17. Protein expression of CAPN1 and CAPN2 are alte

red in NMDA-treatedneurons 84Figure 18. MBNL2 binds to both CAPN1 and CAPN22 in HEK293 cells 85Figure 19. Knockdown efficiency of CAPN1 or CAPN2 shRNAs in neurons 86Figure 20. NMDAR-mediated calpain-2 activation causes MBNL2 degradation inneurons 87Figure 21. Depletion of CAPN2 preserves

MBNL2-regulated alternative splicing andpolyadenylation in neurons upon NMDA treatment 88Figure 22. CAPN2 is predominantly expressed in the cytoplasm of mature neurons 90Figure 23. NMDA treatment induces the nuclear translocation of CAPN2 in neurons 91Figure 24. NMDAR-mediated MBNL2 reduct

ion requires calpain-2 expression in thenucleus and cytoplasm of neurons 92Figure 25. NMDA-induced nuclear translocation of CAPN2 requires calcium 93Figure 26. Nuclear translocation of CAPN2 involves in MBNL2 degradation 94Figure 27. Dysregulated calcium homeostasis induces the nuclear tran

slocation of CAPN2 and reduced MBNL2 expression in neurons 95Figure 28. CAPN2 depletion preserves MBNL2 expression in the neurons with dysregulated calcium homeostasis 96Figure 29. Effect of CAPN2 depletion on the RNA processing pattern of MBNL2 targets in A23187-treated neurons 97Figure 30

. CAPN2 nuclear translocation is occurred in the EpA960/CaMKII-Cre mouse brains 98Figure 31. Nuclear-to-cytoplasmic distribution of CAPN2 during neuronal differentiation 99Figure 32. Nuclear translocation of CAPN2 occurs in the APP/PS1 and THY-Tau22brains 100Figure 33. Reduced MBNL2 express

ion in the APP/PS1 and THY-Tau22 brains 101Figure 34. Aberrant MBNL2-regulated alternative splicing in the APP/PS1 and THY-Tau22 brains 102

鑑定逆境相關蛋白基因在番茄免疫途徑抗番茄黃化捲葉泰國病毒之研究

為了解決Gamma SL PTT的問題，作者蔡昀珊 這樣論述：

番茄黃化捲葉泰國病毒 (tomato yellow leaf curl Thailand virus, TYLCTHV) 對於臺灣番茄 (Solanum lycopersicum) 產業造成嚴重損害。前人研究指出雙子葉植物和單子葉植物中的逆境相關蛋白 (stress associated proteins, SAPs) 在水楊酸 (salicylic acid, SA) 所調控的抗病毒免疫途徑中扮演重要角色，為了探討番茄SAP是否具有相似的抗病毒免疫能力，本實驗目為在番茄中找出參與對抗TYLCTHV之SAPs。在模式番茄 (S. lycopersicum cv. Micro-Tom) 中進行

親緣演化樹分析，確認出七個SAP基因，即SlSAP4-LIKE、SlSAP5、SlSAP5-LIKE、SlSAP8、SlSAP8-LIKE、SlSAP11和SlSAP12；其中，水楊酸可以誘導SlSAP4-LIKE、SlSAP5、SlSAP8-LIKE和SlSAP12等基因的表現量。再者，TYLCTHV的感染則可誘導SlSAP5、SlSAP8、SlSAP8-LIKE和SlSAP12的基因表現量。此外，在番茄植株中短暫過表現番茄SAP試驗發現水楊酸調控免疫相關基因受到SlSAP4-LIKE、SlSAP5、SlSAP8-LIKE和SlSAP12所調控；茉莉酸相關基因則受SlSAP8之調控；乙烯相關

基因受到SlSAP8和SlSAP11的調控。另一方面，在TYLCYHV感染番茄系統中短暫過表現番茄SAP指出，SlSAP4-LIKE、SlSAP5、SlSAP8、SlSAP8-LIKE和SlSAP12可參與抗病毒免疫反應，其中，SlSAP5、SlSAP8和SlSAP8-LIKE對於減少TYLCTHV的積累有較佳的影響。此外，在in silico 啟動子分析顯示，在SlSAP5啟動子區域具有一個水楊酸反應相關的TGACG序列模體 (motif)，且SlSAP8和SlSAP8-LIKE啟動子區域則各發現一個與水楊酸反應相關的W-box序列模體。研究結果為利用SAP基因開發抗TYLCTHV策略奠定重

要基礎。