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1. LSD1/PRMT6-targeting gene therapy to attenuate androgen receptor toxic gain-of-function ameliorates spinobulbar muscular atrophy phenotypes in flies and mice

2. Defective excitation-contraction coupling and mitochondrial respiration precede mitochondrial Ca2+ accumulation in spinobulbar muscular atrophy skeletal muscle

3. Spinocerebellar ataxia 38: structure–function analysis shows ELOVL5 G230V is proteotoxic, conformationally altered and a mutational hotspot

6. Striatal Mutant Huntingtin Protein Levels Decline with Age in Homozygous Huntington’s Disease Knock-In Mouse Models

8. Small molecule inhibitors of hnRNPA2B1-RNA interactions reveal a predictable sorting of RNA subsets into extracellular vesicles

9. Decoding distinctive features of plasma extracellular vesicles in amyotrophic lateral sclerosis

10. Hydroxamic Acid-Based Histone Deacetylase (HDAC) Inhibitors Can Mediate Neuroprotection Independent of HDAC Inhibition

11. Mithramycin Is a Gene-Selective Sp1 Inhibitor That Identifies a Biological Intersection between Cancer and Neurodegeneration

13. Inhibition of transglutaminase 2 mitigates transcriptional dysregulation in models of Huntington disease

17. International Society for Extracellular Vesicles workshop. QuantitatEVs: Multiscale analyses, from bulk to single extracellular vesicle.

19. Spinocerebellar ataxia 38: structure-function analysis shows ELOVL5 G230V is proteotoxic, conformationally altered and a mutational hotspot

20. Antagonistic effect of cyclin-dependent kinases and a calcium-dependent phosphatase on polyglutamine-expanded androgen receptor toxic gain of function

23. Nitration of Hsp90 induces cell death

24. Mutations in TGM6 induce the unfolded protein response in SCA35

25. 271st ENMC international workshop: Towards a unifying effort to fight Kennedy's disease. 20-22 October 2023, Hoofddorp, Netherlands

26. Defective excitation-contraction coupling and mitochondrial respiration precede mitochondrial Ca2+ accumulation in spinobulbar muscular atrophy skeletal muscle

27. Defective cyclophilin A induces TDP-43 proteinopathy: implications for amyotrophic lateral sclerosis and frontotemporal dementia

28. Supplementary File: Neither a Novel Tau Proteinopathy nor an Expansion of a Phenotype: Reappraising Clinicopathology-Based Nosology

29. Correction: Clinical, neuropathological, and genetic characterization of STUB1 variants in cerebellar ataxias: a frequent cause of predominant cognitive impairment

31. A11 Huntingtin-mediated axonal transport requires arginine methylation by PRMT6

34. Neither a Novel Tau Proteinopathy nor an Expansion of a Phenotype: Reappraising Clinicopathology-Based Nosology

35. Additional file 1 of Decoding distinctive features of plasma extracellular vesicles in amyotrophic lateral sclerosis

36. Huntingtin-mediated axonal transport requires arginine methylation by PRMT6

37. Huntingtin-mediated axonal transport requires arginine methylation by PRMT6

38. Additional file 2 of A case report of late-onset cerebellar ataxia associated with a rare p.R342W TGM6 (SCA35) mutation

39. Additional file 3 of A case report of late-onset cerebellar ataxia associated with a rare p.R342W TGM6 (SCA35) mutation

40. Polyglutamine-Expanded Androgen Receptor Alteration of Skeletal Muscle Homeostasis and Myonuclear Aggregation Are Affected by Sex, Age and Muscle Metabolism

44. Clinical, neuropathological, and genetic characterization of STUB1 variants in cerebellar ataxias: a frequent cause of predominant cognitive impairment

46. Decoding distinctive features of plasma extracellular vesicles in amyotrophic lateral sclerosis

47. Increased transcription of transglutaminase 1 mediates neuronal death in in vitro models of neuronal stress and Aβ1–42-mediated toxicity

48. Focus on the heterogeneity of amyotrophic lateral sclerosis

49. Defective cyclophilin A induces TDP-43 proteinopathy: implications for amyotrophic lateral sclerosis and frontotemporal dementia

50. Polyglutamine-Expanded Androgen Receptor Alteration of Skeletal Muscle Homeostasis and Myonuclear Aggregation Are Affected by Sex, Age and Muscle Metabolism

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