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1. CRISPR interference to evaluate modifiers of C9ORF72-mediated toxicity in FTD

2. Poly(GR) interacts with key stress granule factors promoting its assembly into cytoplasmic inclusions

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3. Plasma PolyQ-ATXN3 Levels Associate With Cerebellar Degeneration and Behavioral Abnormalities in a New AAV-Based SCA3 Mouse Model

4. HDAC6 Interacts With Poly (GA) and Modulates its Accumulation in c9FTD/ALS

5. Microglial lysosome dysfunction contributes to white matter pathology and TDP-43 proteinopathy in GRN-associated FTD

6. Enhanced phosphorylation of T153 in soluble tau is a defining biochemical feature of the A152T tau risk variant

7. Hexanucleotide Repeat Expansions in c9FTD/ALS and SCA36 Confer Selective Patterns of Neurodegeneration In Vivo

8. The pathological phenotypes of human TDP-43 transgenic mouse models are independent of downregulation of mouse Tdp-43.

9. Aging is not associated with proteasome impairment in UPS reporter mice.

10. Two FTD-ALS genes converge on the endosomal pathway to induce TDP-43 pathology and degeneration

11. Enhanced phosphorylation of T153 in soluble tau is a defining biochemical feature of the A152T tau risk variant

12. C9orf72 poly(GR) aggregation induces TDP-43 proteinopathy

13. Microglial lysosome dysfunction contributes to white matter pathology and TDP-43 proteinopathy in GRN-associated FTD

14. An acetylation–phosphorylation switch that regulates tau aggregation propensity and function

15. Hexanucleotide Repeat Expansions in c9FTD/ALS and SCA36 Confer Selective Patterns of Neurodegeneration In Vivo

16. Heterochromatin anomalies and double-stranded RNA accumulation underlie C9orf72 poly(PR) toxicity

17. Additional file 1: of Enhanced phosphorylation of T153 in soluble tau is a defining biochemical feature of the A152T tau risk variant

18. C9ORF72 poly(GA) aggregates sequester and impair HR23 and nucleocytoplasmic transport proteins

19. Heterochromatin anomalies and double-stranded RNA accumulation underlie

20. Poly(GR) impairs protein translation and stress granule dynamics in C9orf72-associated frontotemporal dementia and amyotrophic lateral sclerosis

21. Poly(GP) proteins are a useful pharmacodynamic marker for C9ORF72-associated amyotrophic lateral sclerosis

22. Severe amygdala dysfunction in a MAPT transgenic mouse model of frontotemporal dementia

23. Wild-Type Human TDP-43 Expression Causes TDP-43 Phosphorylation, Mitochondrial Aggregation, Motor Deficits, and Early Mortality in Transgenic Mice

24. Aberrant cleavage of TDP-43 enhances aggregation and cellular toxicity

25. The pathological phenotypes of human TDP-43 transgenic mouse models are independent of downregulation of mouse Tdp-43

26. P1‐185: Wild‐type human TDP‐43 induces mitochondrial abnormalities and axonal degeneration in transgenic mice

27. Aging is not associated with proteasome impairment in UPS reporter mice

28. Poly(GP) proteins are a useful pharmacodynamic marker for C9ORF72-associated amyotrophic lateral sclerosis.

29. Wild-Type Human TDP-43 Expression Causes TDP-43 Phosphorylation, Mitochondrial Aggregation, Motor Deficits, and Early Mortality in Transgenic Mice.

30. An acetylation-phosphorylation switch that regulates tau aggregation propensity and function.