EMBO/sd-character-level-ner huggingface dataset:
B. Side view of the Elongator architectural model highlighting the cavity (red outline) spanning through the centre of the Elp456 hexamer.
(G) Intestinal crypt lysates were incubated with anti-REST antibody and protein A/G beads in 4℃ overnight. Recombinant SRCAP protein was added with different concentrations, followed by immunoblotting.
A representative super-resolution micrograph of immunostained Eph4 epithelial cell sheets with the graph showing fluorescent intensities along the line. LUZP1 co-localized better with myosin IIB than with ZO-1. a.u., arbitrary units. Scale bar, 10 μm.
The relative levels of CIB1 in WT and co-1 backgrounds over the course of 20 hours under LDs were calculated Data information: Error bars represent the standard deviation of three biological replicates of the Western blots.
ChgB immunoreactivity of zoomed area indicated in (C) (top panel). Reconstructed ChgB localizations of dSTORM imaging (middle panel). Lower panel shows overlay of dSTORM ChgB localizations and ChgB immunoreactivity (confocal, 40x). Calibration bar represents no (0) to high (255) clustering of dSTORM localizations. Scale bar: 2 µm.
(A) scRNA-seq of 2,335 control and 3,358 EML1-heKO cells (3 pooled independent batches, 3 organoids each). Cells shown in UMAP plot and colored by annotated cell type. Data information: RG1: radial glia1, RG to bRG: radial glia to basal radial glia, RG2: radial glia to young neurons, IP: intermediate progenitors, YN: young neurons, MLC: mesenchymal-like cells.
Western blot analysis of C2C12 myoblasts treated with EGF, LIF, or EGF+LIF while in differentiation media and stained with phosphor-p38, total p38, myogenin, MF20 and GAPDH. Cells were treated with EGF (50ng/ml), LIF (1000U/ml) or EGF+LIF after 48 hours in differentiation media, and every 6 hours following initial treatment, followed by cell lysis at 72 hours. R Phospho-p38 western blot signal intensity normalized to total p38 signal intensity in control, EGF-treated, LIF-treated and EGF+LIF-treated C2C12s. Signal intensity was measured by placing ROIs over western blot bands using LI-COR Image Studio. (n=3 technical replicates) Two-tailed t-test, error bars = +/- SD S Myogenin western blot signal intensity normalized to GAPDH signal intensity in control, EGF-treated, LIF-treated and EGF+LIF-treated C2C12s. Signal intensity was measured by placing ROIs over western blot bands using LI-COR Image Studio. (n=3 technical replicates) Two-tailed t-test, error bars = +/- SD T MF20 western blot signal intensity normalized to GAPDH signal intensity in control, EGF-treated, LIF-treated and EGF+LIF-treated C2C12s. Signal intensity was measured by placing ROIs over western blot bands using LI-COR Image Studio. (n=3 technical replicates) Two-tailed t-test, error bars = +/- SD
(B) Subunit rotation and head swivel observed in the S. cerevisiae eEF3-80S complex derived from the selected class from the 3D classification shown in (A). 18S rRNA structures illustrating the degree of rotation of the small subunit relative to the large subunit based alignments of the large subunit from a non-rotated structure reference (PDB ID: 6SNT) Matsuo et al., 2020(). The degree of head swiveling (right side) is illustrated based on alignments of the 18S rRNA body from a non-headed swivel reference structure (PDB ID: 6SNT) Matsuo et al., 2020().
(d-i) CftrF508del mice treated with cystamine or PBS in the presence or absence of 3-MA (e-i) (n = 7 per group). (e) Quantification of LC3 dots (per mm2 of lung tissue). Means ± s.d. Asterisk, P 0.01; ANOVA.
(E) A scatter plot comparing the peaks of cis-regulatory regions between EPCR+++ and EPCR+ HSCs in the steady state.
Violin plots of the distributions of fractions of total RPFs and mRNA reads in each reading frame for all E. coli transcripts.
(E) The percentage of HSV-1 latently-infected neurons or reactivating neurons at 48 hrs post treatment with LY294002 and WAY-150138 were scored for either predominantly nuclear or nuclear/cytoplasmic Gadd45b mRNA localization and displayed as mean ± SEM. Each purple dot represents a biological replicate experiment. (F) Quantification of nuclear or nuclear/cytoplasmic Gadd45b mRNA in uninfected neurons at 48 hrs post treatment with either LY294002 or in DMSO. Each light blue dot represents a biological replicate experiment. Data information: P values equal to or less than 0.05 were considered significant, asterisks denote statistical significance (*, p<0.05; ****, p<0.0001).
F. Bar chart showing percent positive cells gated for EpCAM+ population (left) or SOX1+ population (right). As predicted by scRNA-seq, more D2 EB cells express EpCAM compared to B6 and more B6 EB cells express SOX1 compared to D2 (N = 3, two-sided t-test, EpCAM p-value = 0.0012, and SOX1 p-value = 0.0048).
(C, D) Representative Western blot (C) and quantification (D) of Tim23 in homogenates from spinal cords using β-actin as normalizer. Results are expressed as mean ± SEM and relative to Non Tg at 30 days; n=6 mice (3 males and 3 females). ***p= 0.0002 (Non Tg vs. SOD1-G93A at 120 days) by paired one-way ANOVA with Tukey's correction. No other statistically significant differences were found (paired Friedman's test with Dunn's correction at 30 days and paired one-way ANOVA with Tukey's correction at 60 and 90 days). Tim23 is decreased in SOD1-G93A spinal cord relative to Non Tg at 120 days.
(b-e) Immunofluorescence for GFAP, nestin or SOX2 and DAPI in the DG (b,c) from Ctrl and FIP200GFAP cKO mice at P28. The boxed areas in c-e are shown in more detail in insets (c). Dotted lines indicate boundaries of the granular zone (GZ) and SGZ (b). Arrows mark GFAP+nestin+ and GFAP+SOX2+ NSCs with radial glial morphology (b,c), and arrowheads mark GFAP+nestin− and GFAP+SOX2− astrocytes.
(B), (C) Heat maps of differentially expressed genes between Ctcflos tr1 (ASO 1) KD and control cells (B) 24 hours after the KD (780 up- and 657 down-regulated genes) and (C) 72 hours after the KD (692 up- and 715 down-regulated genes). Row-wise centered log2 normalized counts are displayed. (
(B) Mean fluorescence intensity of H2-Kb staining on RM1 BD Irf- cells by FACS ± MS275, poly I:C or combination treatment (n = 3).
(B) Representative cases of FOXM1+/+ and FOXM1-/- NPCs clones. Scale bar, 20μm. (C) Graph shows the number of cells per clone in FOXM1+/+ and FOXM1-/- human NPCs (FOXM1+/+ n=12; FOXM1-/- n=13; at least three biological replicates. two-tailed unpaired t-test, P= 0.0014). (
a Odor discrimination. Grin2aS/S learned to discriminate between amyl acetate and ethyl butyrate in a rewarded go/no go-paradigm (250 trials for each odor stimulus, pseudo-randomized, and counterbalanced by stimulus identity across animals). Acquisition was similar for all three genotypes.
Immunoblots and quantification of p-HSL and ATGL protein in gWAT of male OXGR1REAG mice treated with AKG for 12 weeks (n = 8 per group).
Vam3 and Nyv1 were tagged with mCitrine and EGFP as shown Fig. 3A but the spacer was extended (S34) by an additional 25-amino acid sequence (SGGGGSGGGGSGGGGSGGGGAAAGG) to the previous short spacer. (A) Protein levels on isolated vacuoles from these strains were compared as in Fig. 3B.
F-G. Alveolar diameter (F) and number of alveoli (G) in BALO at days 15, 21, 30 and 40 of culture was measured from n=5 BALO in n=3 biological replicates with tdTomato+ rMC.
(D) Plot of T. thermophila MT plus-end growth rates as a function of tubulin concentration. Error bars represent the mean +/- 95% CI. For each concentration, data is obtained from at least 2 independent experiments (n=41).
B, heatmap of relative expression of markers that most differentiate the sub-communities of CD14+ monocytes by difference in mean expression levels for all samples (n = 42 patients × 2 timepoints = 84 samples). Markers are filtered to those different at a significance threshold of FDR < 0.05 (moderated paired t-test, mixed effects model) and fold change > 1.3; for a view of all differences significant at FDR < 0.05 The mean intensity of each channel across all sub-communities is shown by the adjacent purple heatmap.
A, IgA1 and IgA2 subtypes specific for spike protein were measured in plasma and saliva at different time point (T0,T1, T2) of vaccinated naïve (plasma: n=64; saliva: n=63 (IgA1), n=55 (IgA2)) or SARS-CoV-2-Exp (plasma: n=21; saliva: n=18) subjects. Subjects received the first vaccine dose at day 0 (T0), and the 2nd dose at day 21 (T1) (indicated with an arrow). T2 corresponds to 7-10 days after the 2nd dose. For plasma samples the titers of antigen specific IgA1 and IgA2 are expressed in IU/ml and AU, respectively (see Methods). LoD is indicated by a dotted line: LoD (IgA1)=74.64; LoD (IgA2)=0.009. For saliva samples the titers of antigen specific Ig were normalized by dividing the values of SARS-CoV-2 specific Ig by total IgA concentration of each sample. The normalization was applied only to values higher than LoD. The adjusted values are expressed in AU.
E. Overexpression of VEAL2 significantly changes efflux of dextran conjugated FITC measuring permeability levels. Bar graph representing relative quantification of efflux of dextran conjugated FITC measuring permeability levels in control and VEAL2 overexpressed HUVEC cells. Data obtained from 3 different biological replicates and plotted as mean percentage fold change values ± standard deviation.
(E, F) Measurement of the intracellular ER-scission activity. U2OS cells transiently expressing EGFP-FAM134B (WT), EGFP-FAM134B (84-233) or EGFP-FAM134B (Δ84-233) at same levels, lysosomal degradation of EGFP-FAM134B was blocked by Bafilomycin A1 (Baf A1) or DMSO. GFP-positive puncta were quantified for each cell in (F). For Each group, at least 30 cells were counted. Scale bars, 10 μm. ***P<0.001, "ns" means no significance, one-way ANOVA, error bars indicate SEM.
Flow cytometric analysis of cells treated with TQS for 4 hours and stained with TO-PRO-3 (E and F). Data are means ± SEM of three independent experiments. *P<0.1, ****P<0.0001 (ANOVA).
(D) Western blot using antibodies against GFP of extracts from hac1Δ, ire1Δ, or vps4Δ pep4Δ cells expressing GFP-Atg8. Mutant cells were grown under regular conditions, UPR-inducing conditions (+DTT), or nitrogen starvation conditions (N starv).
B GC-MS-based quantification of intracellular essential amino acid levels in MeWo cells mock or si-SLC1A5-transfected for 24 hr and then treated with LDHAi for 48 hr. Data information: Statistical analysis was performed by ordinary one-way Anova for the comparison of more than two groups. Data are shown as the mean ± SD, n = 3. ns: not significant, *p ≤ 0.05, **p ≤ 0.01, ***p ≤ 0.001, ****p ≤ 0.0001
(b) Flow cytometry of cell size at various stages of P14 differentiation, assessed by forward scatter (FSC).
A. and B. Binding of ASC filaments (A) or α-synuclein PFFs (B) to multiple proteins. Serial dilutions of ASC filaments and α-synuclein PFFs were performed and bound fractions were detected using anti-ASC or anti-α-synuclein (MJFR1) antibodies. ASC filaments did not interact with any of the proteins (A). Conversely, α-synuclein PFFs strongly bound LAG3, CD4, and MTBD tau and showed moderate binding properties to PrPC, APOE3, and TDP-43. No binding between α-synuclein PFFs and nAra h 2 or BSA could be detected. Values represent means ± SD of technical duplicates.
H, I Quantitative analyses of the ALP activity (n=4) and calcium mineralization (n=5). Results are shown as mean ± SEM; *: p<0.05, **: p<0.01 and ***: p<0.001 by t test
(A) Quantification of iFRAP experiments using HeLa cells expressing SMC3-LAP in the wild-type form (wt) or with lysines 105-106 mutated to glutamines (QQ) or arginines (RR) and synchronized in G1-phase. Error bars denote s.e.m., n > 25 cells per condition.(B) Quantification of chromatin residence time of SMC3-LAP alleles in G1-phase.
TRIM21 induced the degradation of SAMHD1, and MG132 rescued the TRIM21-mediated degradation of SAMHD1. HEK293T cells were cotransfected with SAMHD1 and VR1012 or TRIM21 expression plasmids with or without MG132 treatment for 12 h prior to harvest, and then subjected to IB with tubulin as a loading control.
Co-immunoprecipitation assays using HEK293T cells show that INVS preferentially binds to WT-Akt (second panel, lane1) or phospho-mimetic Akt (T308D/S473D, lane2), but fails to interact with phosphorylation-defective forms of Akt (T308A/S473A, lane 3).PDGF-AA stimulation of HEK293T cells results in augmented interaction of endogenous INVS with Akt (top panel, comparison between lane 1 and lane 2, untreated and PDGF-AA-stimulated conditions, respectively).
Cumulative distribution functions (CDF) of recorded waiting times for formation of vesicle (filled circles: simulations; lines: Single Poisson process with additional lag time).
E Effect of shKPC2 plasmids on endogenous KPC2. RT-PCR was performed with the indicated primers after HEK293T cells were infected with six lentiviruses encoding an shRNA control (GFPsh) and five shRNAs targeting kpc2 (Kpc2 #1-#5).
E. Correlation between expression of Ezh2 and Dot1L as depicted by TPM in different mature B-cell subsets; B1: B1 cells, MZB: marginal Zone B, FOB: follicular B, GCB: germinal Center B, SPLPB: spleen plasma blast, SPLPC: spleen plasma cells) and Bone Marrow (BMPC: Bone marrow plasma cells) A20: Germinal Center like cell lymphoma cell line. Correlation shown by scatter plot.
(C) Representative traces of spontaneous firing in GnRH neurons from control (left, black) and mutant (right, red) animals at week 2 (upper panels) and week 4 (lower panels); lower traces show an enlargement of the upper trace.
F. Model of ANGPTL2 activity in the intestinal stem cell niche. ISEMF-derived ANGPTL2 inhibits BMP signaling in an autocrine manner through the integrin α5β1-NF-κB pathway to maintain ISC stemness by regulating β-catenin and Smad 1/5 signaling.
(B) Dot plot indicating fraction of tf-Reporters delivered to the lysosome by ATG7-independent mechanisms. The median red:green ratio of each population was used to calculate fractional delivery according to the following formula: (ratiosgATG7-ratiosgATG9A)/(ratioNegativeCtl1-ratiosgATG9A), with the assumption that sgATG9A yields a true autophagy-null phenotype. Mean values for each reporter are indicated by a black bar. n=3 for each reporter.
E Transduction rates of AAV9-PHP.B at 8, 16, and 32kHz regions based on GFP fluorescence. A total of 162 IHC and 841 OHC were analyzed from 3 injected mice and 1 control littermate.
(a) Bif-1+/+ and Bif-1−/− MEFs were transfected with Flag-PI(3) KC3, then incubated in complete medium or EBSS for 2 h and subjected to an in vitro PI(3) KC3 kinase assay. The expression of Flag-PI(3) KC3 was confirmed by immunoblot analysis (left panel). A representative autoradiograph is shown (middle). The results were quantified by phosphoimaging with a Typhoon scanner and shown as fold activation (right). The data are presented as means ± s.d. of five independent experiments.
G: Relative fluorescence intensity of intracellular filipin signals in endosomes of HeLa/Ctrl, HeLa/STARD3, HeLa/STARD3 S209A, HeLa/STARD3 S209D/P210A and HeLa/STARD3 Conv-FFAT cells. Data are displayed as a Superplot (Lord et al, 2020) showing the relative filipin fluorescence intensity in endosomes of individual cells (small circles) from 6 independent experiments (mean of each experiment shown as a large circle). Independent experiments are color-coded. Means and error bars (SD) are shown as black bars. Kruskal-Wallis with Dunn's multiple comparison test (*P < 0.05; **P < 0.01; n=6 independent experiments).
Correlation between the transcription measured by EU incorporation and measured by fibrillarin and nucleolin colocalization is depicted with Pearson correlation coefficient (R) and p-value (p) (G). The same parameters are shown for the correlation between transcription measured by EU incorporation and translation measured with AHA incorporation
(I) ELISA analysis for IFN-β secreted by BMMs treated with EVs plus liposomes containing M.tb RNA. Data shown are the mean ± SD (n = 3 per group) and all data shown are representative of three independent experiments.
A Pre-treatment of Smaducin-6 reduces LPS-induced interleukin-6 (Il6) gene expression in a dose-dependent manner in RAW264.7 cells. Il6 gene expression was analyzed by qRT-PCR.
B Three conserved lysine residues are located in the most C-terminal region of p73. Amino acid sequences of p73 of the indicated species and human p53 and p63 are aligned. *, conserved and acetylated lysine residues, black frame, highly conserved residues, gray frame, conserved residues.
). The LMF1 protein sequence from multiple species was aligned using Clustal Omega (Sievers et al., 2011)
(C) Apoptosis in U2OS cells cotransfected with scrambled or TIGAR siRNAs, and scrambled, ATG5 siRNA or ATG10 siRNA, as measured by cells with a sub-G1 DNA content. After 48 h, cells were left untreated, exposed to nutrient starvation for 6 h or to metabolic stress for 24 h. Data are shown as the mean and standard deviation from three independent experiments. In each case, the increase in apoptosis after knockdown of ATG5 or ATG10, compared with the matched control, was statistically significant; * represents significant difference from control conditions (P<0.05); # represents a lack of significant difference from control conditions (P>0.05).
C3H/HeN germfree pregnant mice were treated with the LTβR‐Fc fusion protein on day 16 and 18 of gestation to prevent the development of PP in their offspring. Pups were also treated in the neonatal period to prevent the development of ILF. Mice were colonized at 8 weeks of age with SFB or E. coli and were sacrificed on d20 or on d60 postcolonization; percentage of mice with at least one ANA. E denotes gestational day.
(K) qPCR analysis of DLL4 expression in Ago2 RIPs as a percentage of input. TREx Cells were transfected with either a scrambled control or a miR-30c antagomiR. (n=3) Data information: data are presented as mean ± SD. *P<0.05, **P<0.01, ***P<0.001 (Unpaired Student's t-test). All repeats are biological.
A, B Core histones were prepared from NSPCs treated with various concentrations of crotonate (A) and 1 μM MS-275 (B) for 24 h and subjected to western blotting analysis using anti-Kcr antibody, and the experiments were repeated three times.
A. KV10.1 localizes to pericentrin-positive structures during ciliary resorption. After short (4h) reintroduction of FCS in serum starved hTERT RPE1 cells, the signal of anti-KV10.1 antibody co-localized with pericentrin. Scale bar: 25µm.
I-L, Spheroid formation experiments with HCT116 cells upon transfection with siUSP42 (I-K) or electroporation with eSpCas9 empty plasmid (non-edited) or eSpCas9-USP42 gRNAs (L). Scale bar = 500 μm. Where indicated, cells were treated with 5 μM IWP-2 or 20 μM LGK-974 (PORCN inhibitors). The median size was quantified for n ≥ 13 spheroids from a representative experiment repeated independently n ≥ 3 is shown.
A. Relative expression of MurRF1 and MAFbx mRNAs in proximal hind limbmuscle of 12 wk mice (n = 5-6/genotype). *p<0.05 by ANOVA, n. s. = not significant.
Glucose tolerance test (GTT) and area under the curve (AUC) data for GTT in WT and DKO mice (n=8 for DKO, n=10 for WT).
A. qRT-PCR analysis showing average TBP-normalized fold expression of SOX10, MITF and GATA6 in 501mel treated with either siCTL or siSOX10 for 48h. Data information: , data are presented as mean values + SD for six replicates (n=6). The p-value (Student's t-test) is indicated, *<0.05.
(A) Representative photopic ERG flicker series at 1, 5 and 10 Hz with 3 cd.s/m2 illumination at 10 WPI. Arrowheads indicate light stimulus.
E. Expression of Ldb2 in the amygdala. LA; lateral amygdala, BLA; basolateral amygdala, Ce; central nucleus of amygdala.
C, D, Western blot analysis of (C), Fxr2 (Veh n=8, TTX n=8) and (D), Fmrp (Veh n=10, TTX n=12) during upscaling, Student's T-test *p<0.05.
C) TCID50 data, mean and SD, for one representative experiment from B with 6 technical replicates.
Micrographs of young (top row of images) and older (bottom row of images) wild-type (WT) cells expressing Vph1-EGFP (green vacuole) and stained with CF640R WGA (magenta bud scars). Scale bar: 5 µm.
E, Resolution of the transplant-induced retinal detachment in C57BL/6J recipient retinas (n=11), as measured by the maximum detachment length (mm) over time. Fundoscopy (images on the left) was used to locate the region of cell delivery for OCT imaging (green line) shown in the images on the right. Red lines correspond to the callipers used to determine the maximum length of the detachment at each time point. Before injection (B.I.) (n=11), immediately post-injection (I.P.I.) (n=10), 5 days post-injection (5 D.P.I.) (n=11), 9 days post-injection (9 D.P.I.) (n=11), 21 days post-injection (21 D.P.I.) (n=6),
(a) Dvl2 underwent autophagy-mediated degradation. E-cadherin was used as a loading control for membrane fraction, and tubulin as a loading control for cytosolic proteins. The asterisk indicates the phosphorylated form of Dvl2.
G and H) Luciferase reporter gene assays in stimulated Jurkat T cells transfected with the pXPG plasmid containing the CSF2 (G) or IL3 (H) promoter alone or in combination with the indicated pDHS and enhancer DNA regions as defined in (D). The IL3 -4.1/1.5 construct contains a contiguous region spanning the IL3 promoter from -4.3 kb to +50 bp.
Northern blot (top 2 panels) and western blot (bottom 3 panels) analysis of ARS immunoprecipitation samples (RIP). RIP was performed using EPRS, QARS and GARS antibodies.
(D) Model of Aub function in GSCs. Aub is required intrinsically in GSCs for their self-renewal and differentiation. Aub function in self-renewal depends on translational repression of Cbl mRNA in GSCs through the recruitment of the CCR4-NOT complex. In cystoblasts, this translational repression is decreased, likely through the implication of at least another factor (X). As is the case for other translational controls in the GSC lineage, Aub/CCR4-NOT acts in fine-tuning Cbl levels. Aub function in GSC differentiation depends on activation of the Chk2 DNA damage checkpoint, consistent with a role in transposable element (TE) repression to maintain genome integrity; Ago3 has the same role in GSC differentiation.
Boxplot comparison of viral loads between severe-survival patients (yellow, n=8) and severe-fatal patients (purple, n=5). Line graph represents the temporal changes in viral load in time (days) after hospital admission of the patients. The cluster heatmap represents expression patterns of 1,541 proteins that exhibited temporal changes across time points in severe-survival (left) and severe-fatal (right) patients. The line plots indicate the expression trends of 1,541 selected proteins. VL, viral loads; FOT, the fraction of total. Differences between groups were estimated using Mann-Whitney-Wilcoxon test. The horizontal box lines in the boxplots represent the first quartile, the median, and the third quartile. Whiskers denote the range of points within the first quartile − 1.5× the interquartile range and the third quartile + 1.5× the interquartile range.
A. Schematic showing wild type C-terminal calreticulin protein sequence and neoepitope sequences for 52 bp deletion or 5 bp insertion and peptide sequence used for immunization.
Human red blood cells (RBCs) were incubated with 400 nM pigment or control ΔcylE extract, and kinetics of K+ and Hb release was monitored. Data shown are the average and SEM of six independent experiments. The time to 50% K+ and 50% Hb release with pigment was 4.8 min and 8.4 min, respectively; n = 6, P < 0.0001, extra sum-of-squares F test.
G Statistical quantification of (F) showing relative apoptosis of T387 GSCs expressing shUSP33 or shNT in normoxia or hypoxia. Disruption of USP33 increased the apoptosis of GSCs in normoxia, which was further elevated in hypoxia. Data represent three independent experiments. *, p < 0.05 (mean ± s.e.m.; two tailed unpaired t-test).
(F) Endogenous UVRAG partially colocalises with endogenous FEZ1 in HEK293 cells. Arrows show colocalisation. Scale bar=10 μm.
Western blot detection of PAX6 isoforms in cells during forebrain and retina differentiation from hESCs. D10 indicates day 10 of differentiation. The green arrow indicates the PAX6A&B isoforms. The red arrow indicates the PAX6D isoform.