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2. Targeting the glycine-rich domain of TDP-43 with antibodies prevents its aggregation in vitro and reduces neurofilament levels in vivo

3. TDP-43 condensates and lipid droplets regulate the reactivity of microglia and regeneration after traumatic brain injury

13. Intrinsically disordered RNA-binding motifs cooperate to catalyze RNA folding and drive phase separation

14. Author Response: PURA Syndrome-causing mutations impair PUR-domain integrity and affect P-body association

15. PURA Syndrome-causing mutations impair PUR-domain integrity and affect P-body association

19. The new missense G376V-TDP-43 variant induces late-onset distal myopathy but not amyotrophic lateral sclerosis

22. PURA Syndrome-causing mutations impair PUR-domain integrity and affect P-body association

26. Creating overview and summary figures

28. Motor neuron intrinsic and extrinsic mechanisms contribute to the pathogenesis of FUS-associated amyotrophic lateral sclerosis

30. Monomethylated and unmethylated FUS exhibit increased binding to Transportin and distinguish FTLD-FUS from ALS-FUS

31. FET Proteins TAF15 and EWS Are Selective Markers that Distinguish FTLD with FUS Pathology from Amyotrophic Lateral Sclerosis with 'FUS' Mutations

32. Multi-omics profiling identifies a deregulated FUS-MAP1B axis in ALS/FTD–associated UBQLN2 mutants

39. Phosphorylation Regulates CIRBP Arginine Methylation, Transportin-1 Binding and Liquid-Liquid Phase Separation

42. The phase separation-dependent FUS interactome reveals nuclear and cytoplasmic function of liquid–liquid phase separation

46. Disease-linked TDP-43 hyperphosphorylation suppresses TDP-43 condensation and aggregation

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