Figure 2 M1 and M23 AQP4 isoforms compared by freeze-fracture electron microscopic and Western blot analyses M1 and M23 AQP4 isoforms compared by freeze-fracture.

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Date of download: 6/1/2016 Copyright © 2016 American Medical Association. All rights reserved. From: Aquaporin 4 Expression and Tissue Susceptibility to.
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RASSF2DSARAH-GF (b) MST1-F (a) M F G 70 kD a 55 kD b 36 kD
1&3: hGH-sc(Fc)2 2&4: hGH-Fc anti-Fc anti-hGH
Figure 2 ALSFRS-R changes (A) Amyotrophic Lateral Sclerosis Functional Rating Scale-Revised (ALSFRS-R) slope after 6 months of treatment without (left)
Figure 1 Box plot of the venous diameter in lesions
Figure 2 GlyR antibody binding
Cloning, expression, and functional characterization of the von Willebrand factor–cleaving protease (ADAMTS13)‏ by Barbara Plaimauer, Klaus Zimmermann,
Figure 1 Immunofluorescence pattern of patient septin-5-immunoglobulin G binding to mouse tissues Immunofluorescence pattern of patient septin-5-immunoglobulin.
Figure 1 Stiff-person syndrome spectrum patient serum bound to membranes of live GlyRα1-transfected HEK293 cells Stiff-person syndrome spectrum patient.
Figure 3 Antibodies to MOG using different secondary antibodies: Anti-human IgG (H + L), IgG1, or IgM(A) Comparison of binding to full-length myelin oligodendrocyte.
Figure 2 Serums of patients with stiff-person syndrome spectrum disorders containing GlyRα1-Binding IgG specifically induces internalization of GlyRα1.
Complex I Complex III Complex IV Complex II Supplemental Figure 3
Figure 1 Percent positivity by clinical feature Overall, 6
Suppl.Figure 1 Transfected HEK293 cells -130kDa -100KDa Blot: -V5
Figure 2 Anti-LINGO-1 (Li81) does not affect cytokine production
Figure 2 Expression of GABAA receptor and LGI1 by patient's thymomaTissue sections of the patient's thymoma incubated with biotinylated immunoglobulin.
Figure DPPX antibodies as detected by fluorescence-based immunohistochemistry and a cell-based assayImmunohistochemistry displayed binding of the patient's.
Figure 1 Reactivity of the patients' antibodies with rat brain and HEK cell-based assays Rat hippocampal dentate gyrus neuropils were stained with patient.
Cellular localization of the chimeric Iff5-Iff1C, Iff5-Iff2C, Iff5-Iff4C, Iff5-Iff7C, and Iff5-Iff10C proteins. Cellular localization of the chimeric Iff5-Iff1C,
Figure 1 Flow diagram of the assays and the samples that were evaluatedA total of 1,109 samples were initially screened at a serum dilution of 1:20 for.
Model of Aquaporin-4 Supramolecular Assembly in Orthogonal Arrays Based on Heterotetrameric Association of M1-M23 Isoforms  Byung-Ju Jin, Andrea Rossi,
Figure 2 Brain biopsy Brain biopsy (A) Double staining with anti-aquaporin-4 (AQP4) antibody (dark green) and Luxol fast blue (blue) is shown. Loss of.
Figure 3 Gene expression in CSF cell pellets
Figure 2 Correlation between total IgG levels and anti-AQP4 IgG titer
WDR11 forms a tertiary complex with EMX1 and GLI3
Figure 2 Overview of the patient's history and immunofluorescence pattern of patient CSF IgG Overview of the patient's history and immunofluorescence pattern.
Figure 4 Glatiramer acetate treatment negatively regulates IFN-β production by targeting components of the IFN-β enhanceosome (A) Wild-type (WT) monocytes.
Fig. 4. Identification of GRP78 as the target antigen of NMO-rAbs ON and ON Identification of GRP78 as the target antigen of NMO-rAbs.
A, Western blot analysis of fetuin-A in AGA (lanes 1–5 and 10–13) and IUGR (lanes 6–9, 14, and 15) UC plasma samples. A, Western blot analysis of fetuin-A.
Figure 1 Schematic overview of flow cytometry Schematic overview on the analysis of peripheral immune cells by flow cytometry. Schematic overview of flow.
Figure 1 Evolution of blood cell counts during 18-month treatment and follow-up (A) Mean white blood cell count, (B) mean lymphocyte count, (C) mean eosinophil.
Cellular localization of the Iff2, Iff3 (or -9), Iff5, Iff6, and Iff8 proteins. Cellular localization of the Iff2, Iff3 (or -9), Iff5, Iff6, and Iff8 proteins.
Figure 4 Aquaporin-4 immunoglobulin G (AQP4-IgG) index in time-matched paired serum-CSF specimens: 3 attack/preattack pairs and 7 bridge/remission pairs.
Figure 5 Pairwise correlations between selected patient-reported outcomes and performance tests in patients with MS (A) The number of pairwise correlations.
Figure 3 Longitudinal performance of 2 MS–cohabitant participant pairs on Ishihara color testing Both response speed and response accuracy are provided.
Localization of the Iff8 extended protein.
Figure 4 Confirmatory cohorts to assess MOG-IgG1 assay(A) All 81 aquaporin-4 (AQP4)- seropositive patients (blue) from the Oxford National neuromyelitis.
Figure 3 Detection of synapsin Ia, Ib, and IIa in cell-based assays, colocalization of patient IgA and commercial synapsin antibodies in hippocampus sections.
Figure 1 Distribution of MOG IgG antibody in pediatric demyelinating diseases Distribution of MOG IgG antibody in pediatric demyelinating diseases (A)
Figure 1 Annual trend in specimen type submitted as first sample for aquaporin-4 immunoglobulin G testing (serum only vs CSF only vs both) from 101,065.
Figure 1 Reibergram (CSF/serum quotient diagram) of all included patients Increasing albumin quotients reflect increasing blood-brain barrier dysfunction.
Figure 1 Anti-LINGO-1 (Li81) has no effect on activated T-cell proliferation Anti-LINGO-1 (Li81) has no effect on activated T-cell proliferation (A) Western.
Figure 1 Examples illustrating gating strategy for fluorescence-activated cell sorting (FACS)‏ Examples illustrating gating strategy for fluorescence-activated.
Figure 2 In vitro refolded human leukocyte antigen (HLA)–A2:peptide complexes activate TZR 2D1 In vitro refolded human leukocyte antigen (HLA)–A2:peptide.
Figure 2 Longitudinal relationship between CSF glucose and protein changes Longitudinal relationship between CSF glucose and protein changes Delta glucose.
Figure Avidity of IgG specific for influenza A and B following flu vaccinationAvidity of immunoglobulin (Ig) G specific for influenza A and B before and.
Figure 2 Glatiramer acetate treatment induced M2 differentiation through a MyD88-independent pathway (A) As described previously,3 M2 monocytes were treated.
Figure 1 Peripheral blood lymphocyte counts during dose titrationB-lymphocyte (CD19+; A) and total lymphocyte (CD45+; B) counts (cells/µL) in peripheral.
Characterisation of eSRS21 protein using an anti-eSRS21 antibody.
Figure Spinal cord imaging (A, B) Sagittal and axial T2-weighted cervical spine MRI demonstrating hyperintensities in the central gray matter of patient.
Figure 2 C5B3 prevented AQP4-IgG–mediated CDC without affecting AQP4-IgG binding to AQP4 C5B3 prevented AQP4-IgG–mediated CDC without affecting AQP4-IgG.
Figure 4 DNM1 mutations affect protein levels and self-dimerization (A) HeLa cells were transfected with green fluorescent protein (GFP)-tagged mutant.
Figure 3 Fluorescence-activated cell sorting (FACS) employing cells singly transfected with M1-AQP4 or M23-AQP4 or cotransfected with both AQP4 isoforms.
Figure 1 Classical pathway and lectin pathway activity in patients with multifocal motor neuropathy and controls Classical pathway (CP) activity (A) and.
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Figure 6 Multiple target epitopes exist in the N-terminal domains of Caspr2 (A) Multidomain deletion constructs of Caspr2 were generated to determine which.
Figure 2 Cell-based assay demonstrating differential binding of AChR antibodies to the adult and fetal receptorsThe fetal (gamma subunit specific) and.
Gitanjali Das et al. Neurol Neuroimmunol Neuroinflamm 2018;5:e453
V-2A-GFP/V-2A-coexpressing Mycobacterium tuberculosis antigens and GFP
Figure 2 Immunoblotting of erythrocyte membranes, lymphoblastoid cells, and co-immunoprecipitants Immunoblotting of erythrocyte membranes, lymphoblastoid.
4E-BP is present in an 80 kDa complex in unfertilized eggs.
Figure 3 C5B3 blocked MAC formation
Figure 2 Antibodies to MOG detected with anti-human IgG (H + L) as the secondary antibody(A) Schematic of the human MOG proteins tested. Antibodies to.
Western blotting for GluR1.
Effect of other nucleoside analogues on p38 MAPK phosphorylation levels. Effect of other nucleoside analogues on p38 MAPK phosphorylation levels. A, MM.1S.
Figure 1 Numbers/seropositivity rates of IVIg-naive and IVIg-exposed STRATIFY-2 enrollees* = % of enrollment samples, ** = date of IVIg and/or concentration.
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 2. Histoimmunoprecipitation and antigen identification
T-cell expression of second-generation CARs
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Figure 2 M1 and M23 AQP4 isoforms compared by freeze-fracture electron microscopic and Western blot analyses M1 and M23 AQP4 isoforms compared by freeze-fracture electron microscopic and Western blot analyses (A) Plasma membranes of HEK293 cells expressing recombinant M1-AQP4 or M23-AQP4 viewed by freeze-fracture electron microscopy. (B) Western blot analysis of the proportion of recombinant AQP4 expressed in higher-order arrays or as tetramers in HEK293 cells transfected with plasmids encoding M23 alone (lane 1), M1 alone (lane 5), or different ratios of each (lanes 2–4). Intramembranous particles in M1-AQP4 cells are predominantly singlet (A, left). Compare the large lattices of orthogonal array-like assemblies in M23-AQP4 cells (A, right). M1-AQP4 coexpression inhibits high-order array formation by M23-AQP4 (B). The y-axis indicates molecular weight (kDa) of AQP4 structures. Solubilized proteins, separated by Blue Native gel electrophoresis and transferred to PDF membrane, were probed with monoclonal AQP4-specific IgG. AQP4 immunoreactivity in largest-sized arrays (lane 1) diminishes with increasing M1:M23 ratio, and the proportion in tetrameric form increases (lane 5). AQP4 = aquaporin-4; Ig = immunoglobulin; HEK = human embryonic kidney. J.P. Fryer et al. Neurol Neuroimmunol Neuroinflamm 2014;1:e11 © 2014 American Academy of Neurology