Figure 1 ASO functions ASO functions Target mRNA fates depending on ASO mechanism of action that is determined by where the ASO is targeted and by ASO.

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Figure Pedigrees of the SCA42 families identified in this study
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Figure 2 Sanger sequencing, conservation, and summary of known ACO2 mutations Sanger sequencing, conservation, and summary of known ACO2 mutations (A)
Figure 1 Summary of prior diagnostic workup in neuromuscular disorder cases Summary of prior diagnostic workup in neuromuscular disorder cases Percentage.
Figure 3 Pedigree of familial idiopathic transverse myelitis
Figure 1 Box plot of the venous diameter in lesions
Figure 2 Needle biopsy of the left vastus lateralis
Figure 2 Spinal cord lesions
Figure 1 Hierarchical clustering (HCL) outcome of all tested samples with the expression profile of the case report set as unknown Hierarchical clustering.
Figure 2 Anti-LINGO-1 (Li81) does not affect cytokine production
Figure 1 Treg percentage and suppressive function increased during each round of Treg infusions Treg percentage and suppressive function increased during.
Figure 1 Spine MRI, sagittal and axial views of patients with idiopathic transverse myelitis with VPS37A mutations Spine MRI, sagittal and axial views.
Figure 1 Comparison of miR-150-5p (log scale), prednisone dose (mg), and QMG score between the thymectomy (ETTX) and prednisone groups Comparison of miR-150-5p.
Figure 2 Neurochemical profiles for each neurocognitive trajectory
Figure Pedigree of the family
Figure 4 Detection of EBER+ cells in MS and control brains by in situ hybridization Detection of EBER+ cells in MS and control brains by in situ hybridization.
Figure 3 Transcripts of the splicing mutation (c
Figure 1 Linear relationship between CSF inflammation and glucose in meningitis; analysis stratified by diagnostic category (aseptic, n = 115 and microbial,
Figure 2 Luciferase assays of transiently transfected HEK 293 cells with reporter constructs containing the 766-bp wild-type KCNJ18 or c.-542 T/A mutant.
Figure 2 Correlation between total IgG levels and anti-AQP4 IgG titer
Figure Association of hippocampal subfield volumes to cognition by neopterin level, volumes, and cognition adjusted for age, education, race, sex, and.
Figure 1 Dominant and recessive missense and nonsense variants in neurofilament light (NEFL)‏ Dominant and recessive missense and nonsense variants in.
Figure WDR45 sequence changes in patients A and B
Figure 1 ROC curve of ASFMR1-TV2
Figure 3 Temporal trends in FALS incidence
Table 4 Associations in SNP array data between the Braak stage and previously known AD risk loci (341 variants) comparing participants with Braak stage.
Figure 1 All patients with pediatric genetic movement disorders, their genetic diagnoses, and type of genetic investigations All patients with pediatric.
Figure 5 Neurite structure is not disrupted by the lack of neurofilament light (NEFL)‏ Neurite structure is not disrupted by the lack of neurofilament.
Figure 2 Linkage analysis of chromosome 19
Figure 1 White matter lesion central vein visibility in MS and absence in small vessel disease (SVD)‏ White matter lesion central vein visibility in MS.
Figure Family tree with the HLA haplotyping of 6 members of the family
Figure 1 Family pedigree and MRI
Figure 2 Functionally significant genes
Table 2 Rs number, gene, OR, 95% CI, and permutation p value for the statistical significant variants resulted from allelic association analysis association.
Figure 1 Family pedigree and DNA sequencing results
Figure 4 Voltage-clamp recordings of KCNJ18 carrying the patient's SNVs expressed in Xenopus laevis oocytes under control conditions and after application.
Figure Diagrammatic levodopa pharmacokinetics after single doses of immediate release (IR) carbidopa/levodopa (CD/LD) and 3 strengths of extended release.
Figure 1 [18F]florbetapir standardized uptake value ratio analytical method [18F]florbetapir standardized uptake value ratio analytical method Flowchart.
Figure Alluvial plot of modified Rankin Scale (mRS) scores during and at the end of hospital stay Alluvial plot of modified Rankin Scale (mRS) scores during.
Figure 3 Voltage-clamp recording of the wild-type KCNJ18 (left) and the KCNJ18 carrying the patient's SNVs (right) expressed in Xenopus laevis oocytes.
Figure 1 Responder rates of patients at 4 weeks compared with prevaccinated levels Responder rates of patients at 4 weeks compared with prevaccinated levels.
Figure 6 Cellular composition after tissue dissociation
Figure 1 Pedigree and genetic findings
Figure 1 Histamine flare in patients and controls
Figure 2 Changes in fatigue under treatment
Figure 1 Considerations for concussed athletes leading to medical care or return to sport (RTS)‏ Considerations for concussed athletes leading to medical.
Figure 2 Longitudinal relationship between CSF glucose and protein changes Longitudinal relationship between CSF glucose and protein changes Delta glucose.
Figure 2 Global tau-PET distribution in familial prion disease mirrors the distribution seen in Alzheimer disease Global tau-PET distribution in familial.
Figure 2 Kaplan-Meier survival graphs for 10-year risks of overall and post-90-day recurrent ischemic stroke (IS) and death Kaplan-Meier survival graphs.
Figure 1 Annualized percentage brain volume change
Figure 2 BVL according to on-study disability worsening
Figure 2 Repopulation of CD19+ cells in low and high BSA patients and calculation of the BSA Repopulation of CD19+ cells in low and high BSA patients and.
Figure 2 Pathogenic deletions upstream of LMNB1
Figure 2 Frequency of the proportion of total WMLs with central veins in PPMS, RRMS, and SVD Frequency of the proportion of total WMLs with central veins.
Figure 1 bvFTD PINBPA network
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Figure 2 Seizure outcomes
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Figure 2 Pedigrees of families and segregation analysis of variants c
Figure Unique second neurofibromatosis type 1 (NF1) gene mutations in multiple café-au-lait macules (CALMs) from an individual with segmental NF1 Unique.
Figure 2 LMNB1 mRNA expression
Figure 3 Within-group comparisons (before–after)‏
Figure 2 Between-group comparisons
Figure 1 Segmentation of the normal-appearing periependymal white matter Segmentation of the normal-appearing periependymal white matter The figure demonstrates.
Figure 2 Time from incident ADS event to MS diagnosis
Figure 4 Venn diagram for B-cell Sup proteins compared with proteins from exosome-enriched fractions from a human B-cell line Venn diagram for B-cell Sup.
Figure 3 A receiver operating characteristic curve of days to IVMP as a predictor of failure to regain 0.2 logMAR (20/30) vision (AUC 0.84, p < 0.001)‏
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Figure 1 ASO functions ASO functions Target mRNA fates depending on ASO mechanism of action that is determined by where the ASO is targeted and by ASO chemistry. ASO = antisense oligonucleotide; DMD = Duchenne muscular dystrophy; ESE = exonic splicing enhancer; ISS = intronic splicing silencer; LncRNA = long noncoding RNA; SMN = survival motor neuron. Daniel R. Scoles et al. Neurol Genet 2019;5:e323 Copyright © 2019 The Author(s). Published by Wolters Kluwer Health, Inc. on behalf of the American Academy of Neurology.