EMBO/sd-character-level-ner huggingface dataset:
Flow cytometric analysis of mitochondrial volume (MTG) (B, n=5, technical replicates per clone), total MMP (TMRE) (C, n=5, technical replicates per clone) calculated by dividing median fluorescence intensity (MFI) for total TMRE expression by MTG in NSCs generated from control lines, WS5A and CP2A iPSCs.
Overexpression of wild-type dfmr1 (UAS-dfmr1wt) using a LNv neuron-specific driver line (Pdf-Gal4) causes reduction of branching area-"axonal collapse"-in the sLNv axonal termini. dfmr1ΔCt and dfmr1wt+NLS overexpression phenocopies overexpression of dfmr1wt, suggesting that the truncation of the C-terminus or the presence of the patient NLS alone does not impair or alter the functional efficacy of dfmr1 in this context. However, overexpression of dfmr1ΔCt+NLS fails to cause collapse of sLNv termini, indicating a significant loss or change of Dfmrp protein function. Axonal morphology is visualized by expressing CD8-GFP under the control of the same neuronal driver. Scale bar represents 10 μm.Quantification of axonal termini branching in LNv neurons overexpressing various dfmr1 alleles. Overexpression of dfmr1wt, dfmr1ΔCt, or dfmr1wt+NLS significantly reduced axonal branching area [****P < 0.0001; control 101.3 ± 29.76 SD, n = 30; UAS-dfmrwt 45.41 ± 21.69 SD, n = 29; UAS-dfmrΔCt 52.31 ± 14.67 SD, n = 32; UAS-dfmrwt+NLS 72.45 ± 21.83 SD, n = 29; UAS-dfmrΔCt+NLS 117.8 ± 36.96 SD, n = 28]. dfmr1ΔCt+NLS overexpression does not result in a significant change of axonal branching area compared to the background control [Pdf-Gal4, UAS-GFP] (P = 0.672). For quantification purposes, each branching area (n) was manually outlined, starting from the first point of defasculation of the axonal bundle. These measurements were normalized for variability in brain size across samples using LNv commissure length measurements for each brain. Two-tailed t-tests using Welch's correction were then used to compare controls with mutant phenotypes (GraphPad). Error bars represent mean values with SD. Dots visible for box plots of UAS-dfmrwt and UAS-dfmrΔCt represent samples that outlier the whiskers.
(Left panel) We define the recovery time (RT) as the time required for a population (red line) to double in response to a transient antibiotic treatment (blue shading). (Right panel) The postantibiotic effect (PAE) induced by an antibiotic treatment refers to the additional time required for a population to recover (red line) in comparison to the untreated control (black line).
Liver morphology of WT and Cideb-/- liver under chow diet and HFLF diet. H/E staining, oil red-O staining, immunohistochemistry and ultra-structure (Electron Microscope) were performed. Scale bar represented 50 µm in the upper three rows of images, and 2 µm in the bottom row of images. LD: lipid droplet, ER: endoplasmic reticulum, M: mitochondrial, N: nucleus.
A. Confocal microscopy shows that active Akt (phospho-S473Akt) is localized in the basal body of primary cilia (right side panels show higher magnification).B. INVS is localized in the proximal region of the INVS compartment in primary cilia (INVS compartment, right side panels show higher magnification).C. INVS co-localizes with γ-tubulin, a centrosome marker.D. Anti-phospho-Akt substrates stain positively at the basal region of the primary cilia (arrows), as determined by anti-acetylated tubulin (right side panels show higher magnification).
(B) Representation of the KEGG terms associated with differentially expressed RNAs and their corresponding proteins in 5 affected patients versus 6 controls showing major pathway changes in patient muscle
I) Representative images of IL-33 immunostaining on WT colon at the completion of the AOM/DSS carcinogen protocol compared with no treatment control. Arrows in the inset point to IL-33+ stromal cells and arrowheads point to lack of IL-33 nuclear stain in colonic epithelial cells (scale bar: 100 μm).
B. IFA of the indicated trypanosome cell lines using the mAb25 (marker for the axoneme, left panels) and an anti-IFT172 antibody (marker for IFT, right panels). The top panels show the phase contrast images merged with DAPI (cyan) that stains nuclear and mitochondrial DNA. Scale bars correspond to 5 µm.
(F) Quantification of cell death in response to NMDA stimulation in the presence or absence of PRR7 and either WT c-Jun or a dominant negative c-Jun4A (4A). Overexpression of WT c-Jun caused extensive neuronal cell death (84.8±2.4%) that was reduced in neurons knocked down for PRR7 (43.8±9.2). Overexpressing 4A conferred neuroprotection to NMDA excitotoxicity (50.8±7.9%) but was not additive with PRR7 knockdown (42.3±8.1%) (n=3 independent experiments). Significance was determined using two-way ANOVA in conjugation with Tukey post-hoc test. Images are representative 10X widefield micrographs showing transduced neurons (green- GFP) and PI staining (red). Data is presented as mean±sem. All % values represent comparisons to control.
A, B Gross morphology of the TA injury at 6 months after massive muscle ablation, revealing the new artificial TA regeneration (arrow) when grafted with PF-embedded Mabs-PlGF (B) and absence of TA muscle (arrow) when treated with empty PF as a control (A).
A, PXR (luciferase) reporter assay in HEK293T cells transiently transfected with PXR plasmids (wild-type and ligand binding domain mutant C285I/C301A). RLU, relative light units are shown normalized to beta-galactosidase (β-Gal) expression. The histogram represents one experimental data (of n > 2 independent experiments each performed in quadruplicate) mean (95 %CI); n.s. not significant; * p < 0.05, two-way ANOVA.
(E) Principal component analysis of two independent experiments, for the H3K4me3 ChIP-Seq signals across the yeast genome in the three indicated strains.
D) Cells generated in (A) were treated with doxycycline for 72h. During the last 24h, recombinant type I IFN was added to upregulate endogenous MDA5 protein expression. Protein lysates were analyzed by SDD-AGE and SDS-PAGE using the indicated antibodies to determine protein oligomerization and total expression levels, respectively (n=3).
(b) Effect of methylpyruvate (MetPyr) on ATP levels in WT p53−/− HCT116 cells depleted of glucose. ATP levels were measured as in a, in the presence of glucose and 15 min after its withdrawal or replacement by MetPyr.
Growth curves of the DDX58- and IFIH1-deficient MCF7 (left) and T47D (right) cells upon HNRNPC knock-down. Each sample has 3 replicates. Error bars represent mean ± SD.
(G) Quantification and representative images of CD11c+ cells over the total number of F4/80+ cells in vehicle and glufosinate (20mg/kg) treated mice (n=6). Six images per tumor were analysed. Scale bars: 50 µm.
(E) Ratios of DED proteins quantified at the TRAIL-R2 DISC in A549, HCT116 and DU145 cells; increasing concentrations of AMG655 are indicated by colour intensity.
A,B, Staining for Isolectin B4+ blood vessels in control (A) and Gpr124ECcKO (B) forebrains. Asterisks mark the lateral ventricles.
(E) β′-COP or Rab1a/b were depleted as in D, and analyzed by indirect immunofluorescence using anti-GM130 and GFP fluorescence. In β′-COP panel, the asterisk indicates cells that did not show an accumulation of GFP-LC3-positive AVs.
D) Syntaxin 8 protein levels were quantified from the respective Western blots by densitometric analysis and normalized to those of TMEM192. Bars represent mean values of n=3 animals ± SD normalized to mean Syntaxin 8 levels of wildtype mice. Statistical significance was calculated applying an unpaired, two-sided Student's t-test. * p≤0.05. Note that Syntaxin 8 is accumulating in SPPL2c-/- mice.
C. MEFs from knockout mice did not show primary cilia when transfected with KV10.1. Cells were co-transfected with human KV10.1 and mVenus, serum starved for 48 hours and then fixed and stained for cilia (AcTub). Venus-positive cells did not show cilia. Scale bar: 25 µm.
F Relative Ucp1 expression in BAT of mice that received AAV GFP (control) or PLTP at 10 weeks of HFD. n=4 for GFP, n=5 for PLTP and n=4 for PLTPM159E. Tbp was used as an internal control. *P<0.05, **P<0.01 by ANOVA one-way followed by Tukey's test.
B-F: TEM images o MOSPD2 (D: siMOSPD2 -silenced HeLa cells. An interpretation scheme representing contacts between organelles is shown on the right; the ER, endosomes and ILV are in dark, light and medium gray, respectively. Mitochondria and Golgi are in pink and light green, respectively. Scale bars: 500 µm
C) Evaluation of three independent experiments of B (n=3, mean +SEM, Student's t-test, * p=0.012, t = 3.4803, df = 4).
(D) Upper, mapping β-catenin regions binding to ESM1. Schematic diagram of full-length β-catenin and deletion mutants. Lower, mapping ESM1 regions binding to β-catenin. Schematic diagram of full-length ESM1 and deletion mutants.
B) Analysis of LC3-II and P-mTOR by western-blot in the lumbar spinal cord of control and treated animals. Proteins were detected by Western blotting using β-tubulin for calibration of sample loading. The protein bands were quantified by Image Multigauge v3.0 software. Immunoblots are representative of one of three experiments with similar results. These results were quantitated in arbitrary units and were represented in the accompanying graphs as mean ± SEM. *, *** Indicate differences of p-value <0.05 <0.001 with the control group, respectively. ## Indicate differences of p-value <0.01 with the group of animals treated with L-BMAA.
Oscillations in acetyl-CoA m+2 when feeding [U-13C]-glutamine, representing reductive glutamine metabolism (i). For measurements of metabolite concentrations (a-b), red marks represent mean and s.d. of n=5. For measurements of fractional isotopic labeling (c-i), red marks represent mean and s.d. of n=3.
AGS cells were infected with H. pylori or treated with 20 ng/ml LTα1β2 for the indicated times. Total cell lysates were analyzed by immunoblotting using the indicated antibodies.
(C) The upregulation of NOD2 gene expression was assessed by quantitative PCR. The results are depicted as the mean fold change in NOD2 gene expression relative to unstimulated cells (n = 11).
Select 2D class averages of the particles that were used to calculate the 2019-nCoV S reconstruction (left). Side and top views of the prefusion structure of the 2019-nCoV S protein with a single RBD in the "up" conformation (right). The two RBD "down" protomers are shown as cryo-EM density in either white or gray and the RBD "up" protomer is shown in ribbons, colored corresponding to the schematic in Fig 1A.
(H) Schematic diagram of intra-embryonic nasal injection in wild-type E11.5 embryos and collection of embryos at E14.5.
(C-E)Mice were analyzed for total fecal IgA by ELISA. Mann-Whitney test. Error bars are SD. C57BL/6 n=14; Vα14 n=11; Jα18-/- n=13.
(I) Fasting plasma glucose (N=8 per group; P=0.007) and (J) insulin (N=7 per group; P=0.0024) after 3 weeks of treatment in CTRL and BAM15 treated animals.
C The SPRY domain and two coiled-coil domains of RNF123 are both required for interaction with RIG-I CARD. HEK293T cells (1×106) were transfected with HA-RIG-I CARD together with F-RNF123 or its mutants (8 μg each). Cell lysates were immunoprecipitated (IP) with anti-Flag (α-F). The immunoprecipitates were analyzed by western blotting (immunoblotting [IB]) with anti-HA (α-HA) or anti-Flag (α-F). Whole-cell lysates (WCL) were analyzed by western blotting with anti-HA and anti-Flag antibodies.
(D) FEZ1 interacts with SCOC in vitro. GST‐pulldown assays using in vitro translated 35S‐labelled Myc-FEZ1 (right) or 35S‐labelled Myc‐control (left) and GST or GST-SCOC (asterisk in bottom panel). Bound proteins were detected by autoradiography following SDS-PAGE (top), protein loading by coomassie blue (bottom).
(B) Roles of Spns1, p53 and Beclin 1 in senescence equilibrium. Loss of Spns1 leads to an imbalance in homeostasis and increased senescence. This effect can be ameliorated by concurrent knockdown of Beclin 1. p53 has a comparatively less dramatic impact on Spns1-loss-induced embryonic senescence. When in the "basal" state, p53 helps retain equilibrium. When p53 is "activated" by UV irradiation, a modest increase in senescence is observed. The higher level of senescence is seen during loss of Spns1 in the absence of basal p53 or in the presence of activated p53. During loss/knockdown of all three genes (spns1, p53 and beclin 1), a state of moderate senescence is observed. An increase in senescence is accompanied by a p53-dependent decrease in cellular proliferation.
A. Transmitted light micrographs of MDGI-silenced (shMDGI1 and shMDGI2) and control (Scr) patient-derived BT12 and BT13 spheroids 11 days after gene silencing. Representative images of at least 3 independent experiments are shown. Scale bar: 200 μm.
(E) Quantification of capillary density as capillary/cardiomyocyte (CM) ratio in mice treated as described in (A). *p=0.0365, **p=0.0031.
(J) Up-regulated GO (biological processes) terms in ALSC9orf72 MN treated with either K+ channel blockers (Fisher enrichment test).
Strongly decreased levels of tyrosine-phosphorylated PTPδ protein in whole-brain lysates of Ptprd-meA-/- mice (P21-27), as shown by the immunoprecipitation of IL1RAPL1 protein from whole-brain lysates followed by immunoblotting for total and tyrosine-phosphorylated PTPδ protein.
G. AMPK deletion increases SIRT7 R388 methylation. Flag-tagged SIRT7 was stably expressed in Ampk wildtype (WT) and Ampk α1/α2 double-knockout (DKO) MEF cells and 293A cells. SIRT7 protein was immunopurified with Flag-beads, R388 methylation was determined by western blot
(C) Top panel: Representative images show PS labeling in the WT dLGN at P6 and P13. RGC inputs were labeled with CTB488. Bottom panel: Enlarged images of the boxed region in top panels. Circles indicate PS+ RGC inputs. Arrows point to the enlarged PS+ RGC inputs in the insets. (D) Quantification of the percentage of PS+ RGC inputs in total RGC inputs at P6 and P13.
Rate of oxygen consumption in P493-6 (-Tet) cells ectopically expressing miR-15a or control-miRNA vector, under basal conditions and in response to 10 μM DNP or 10 μM oligomycin where indicated (mean ± st. dev., n=8 biological replicates).
Representative confocal image and zoom of a single isolated hippocampal neuron (DIV14) immunostained for the endogenous DCV marker ChgB (green), axonal marker SMI312 (red) and dendritic marker MAP2 (blue). Areas of zoom (C) is indicated in (B). Scale bars: 20 µm (B), 5 µm (C).
(b) Representation of an Stokeslet pair, at the limits of a perpendicular section of a planar hydrodynamic active cortex (red shadow), pointing in opposite directions (white arrows) and their associated flow lines (black) and mechanical pressure fields (color-coded).
B, Topological structure of WT MC subpopulations. C, Vector field of RNA velocity projected onto the Topologizer structure for MCs collected from uninjured WT hearts or WT hearts at 2, 7, and 14 dpi. Arrows indicate the direction and ''speed'' of the velocity at each node.
A. LORE interacts with HopAO1 by MBP pull-down assays. The recombinant GST-HopAO1 and the MBP-LORE-CD were subjected to MBP pull-down analysis. MBP and GST proteins served as the negative controls. The interacting proteins were revealed by anti-GST immunoblotting. The experiment was repeated three times with similar results.
E, Quantification of mitochondria morphology (based on TOM20 immunostaining as shown in D) from HeLa cells transfected with siRNA targeting mitoNEET (siCISD1), NAF1 (siCISD2) or MiNT (siCISD3). Quantification is expressed as ratio of tubular and fragmented mitochondria. Errors bars show the standard error of the mean (SEM). (n =125-130 cells).
RNA-seq experiment of GRWT and GRDim mice which received normal drinking water or drinking water containing 25mM ZnSO4 for 1 week. Ileum was sampled and RNA-seq performed (N=5-6 per group). Genes downregulated by zinc compared to water control animals (LFC<0.8 and p<0.05) were considered. (A) HOMER transcription factor motif analysis of genes downregulated by zinc in GRWT (left panel) and in GRDim mice (right panel).
C Cell cycle distribution of TC1-4 epithelial tumor cells, as inferred from single cell transcriptomes.
(C) At 48h post-infection, the viability of cells infected with MHV-A59 in the presence of intracellular or extracellular antiserum was determined by ATP luminescence assay. Increasing doses of antiserum results in increased cell survival. Data information: Data was analysed using a Students t-test. Error bars depict the mean +/- SEM. All data represents at least two independent replicates.
One thousand ESCs of the indicated genotypes were placed into hanging-drop cultures to form EBs. After 3 days (referred to as day-0), differentiation was induced by plating EBs onto gelatin coated tissue culture dishes in differentiation-inducing medium. (A) Principal Component Analysis (PCA) of the proteome profiles of Tnfaip2-/- (KO) versus WT ESCs and EBs on day-0 to day-3 after differentiation induction (n=5 biological replicates per group, enlarged symbol denotes the mean).
Cells were stimulated with EGF (20 ng/ml; 10 min) as in (A), acid-washed and incubated at 37°C for the indicated intervals. Thereafter, cells were detached, fixed and analyzed using imaging flow cytometry (ImageStreamX). Shown are means ± SD from three experiments.
Human IL-1Ra expression was quantified in the plasma of mice at 6 months of age (4 months post-transplant) (n=10 mice per group). Data are expressed as mean ± STDEV and were tested by one-way ANOVA with Tukey's post-test; WT vs. LV.IL1RN P<0.0001; MPSIIIA vs. LV.IL1RN P<0.0001. Symbols above bars are versus WT.
Northern blots probing for the 5' NGD-IM in mutant cells expressing the R(CGN)12 reporter. (B) Northern blot as in (A) except uS10-WTski2∆ or uS10-K6/8Rski2∆ mutant cells with or without a deletion of Not4 (not4∆) were used. Note that the shorter 5'-NGD intermediates are also reduced in ski2∆not4∆uS10-K6/8R cells.
Quantification and representative images of F4/80+ CD11c+ cells in the lung metastasis (F), F4/80+ CD206+ (G) cells infiltration in tumors of vehicle and glufosinate-treated mice (n=6).
The bioluminescence measurements of transplanted mice treated with ruxolitinib (black) or vehicle (grey) at the indicated days after cell transfer are shown as mean radiance values with SEM (E). n, number of mice analyzed. Statistical data are shown as mean value with SEM and were analyzed by the mixed-effect model REML with Geisser-Greenhouse's correction and Tukey's multiple comparison test: *P < 0.05, ***P < 0.001.
(D-G) Tissue lysates from (D, F) spleen and (E, G) liver from 6- to 9-day old indicated mice were immunoblotted to determine pro-IL-1β cleavage to IL-1β (D-E) or GSDMD cleavage to its p30 and p20 fragments (F-G). Each lane represents a lysate from a different mouse. Positive control lanes (+) are BMDMs stimulated with LPS/ATP; negative control lanes (-) are respective organ homogenates from (D-E) caspase-1-/- or (F-G) Gsdmd-/- mice.
(I) Representative confocal images of Hela cells, TRIM16KO cells, and TRIM16KO cells complemented with Myc-NRF2 which were treated with MG132 (20 µM, 2h) and subjected to IF with Ub and p62 antibodies.
Spearman's Correlation values of the gene list '' Squamous cancer markers'' and TP63, c-JUN, c-MYC or NOTCH1 in Lung (n=1011), Cervix (n=301), Oesophagus (n=185), HNSC (n=522) and PAAD (n=178) tumours. Intense blue: Low correlation; Intense red: Strong correlation. Gepia software.
U. Bar graph represents the colocalization rate (%) of VEAL2 with PRKCB and CAMKIID proteins in HUVECs. Data from three different experiments plotted as individual values with mean percentage values ± standard deviation.
(E, F) Plots of density of nuclei (number of nuclei per 1E4 μm2) on the AT (E) and endothelial (F) faces of infected LoCs both with and without macrophages for characterization of the cellular layer integrity. The bars represent the mean value, the solid line represents the median and the error bars represent the standard deviation from at least 4 fields of view each from two independent LoCs for each timepoint. Data from uninfected controls corresponding to the 3 dpi timepoint are labelled '3C'. Data information: P-values are calculated using a one-way Kruskal-Wallis ANOVA test, * represents p≤0.05, ** represents p≤0.01, ** represents p≤0.001.
A. Schematic diagram of the full-length CENP-C protein, indicating parts involved in interactions with other proteins or homo-dimerization. Constructs used in this study are depicted below the diagram.
B Proliferation of inducible (Tet-On) sh-LDHA expression vector harboring A375 cells (n=3) treated with Dox (0.5 μg
Charts show OC cell viability after 72 h treatment with 0-20 μM cisplatin and 10 μM BI-D1870
F-G) Quantification precision assessed by calculating the intra-plate (F) and inter-plate (G) coefficients of variation (CVs) for the Columbia and LCC cohorts. Proteins with a CV below 20% and 50% in both cohorts are highlighted in light and dark red, respectively and the fractions of proteins above and below these CV thresholds are shown. A total of 2,051 proteins were consistently quantified in both cohorts.
G. Wnt inhibition induces senescence, which is further enhanced by co-treatment with olaparib. (G) The percentage of SA-β-galactosidase positively stained area (blue) in the representative images from each of the groups is shown. Multiple areas were imaged from three tumor samples per group (indicated as mouse 1, 2 and 3). The horizontal lines represent mean of replicates. p-values were calculated by Mann-Whitney U test.
IsolectinB4 (IsoB4; white), ERG (red), EdU (green) and double-positive cells (yellow). Lower panel shows ERG/EdU merged staining alone with EdU signal masked by ERG signal. Scale bar, 50 µm; error bars: SD; unpaired T test, *p < 0.05. n=5-8 retinas, one retina/mouse.
(a) Single-sample GSEA Normalised Enrichment Scores (NES) of IFN and DC BTMs of individuals with blood-culture confirmed enteric fever in Nepal and Oxford.
(A) A diagram showing Gpr56 WT, null and S4 transcripts. Solid boxes indicating exons that are transcribed. Arrowheads indicate the translation start sites.
A Confocal microscopy of U2OS cells ectopically expressing TERT-WT or TERT-K626A. Total dsRNA is stained green, and nuclei are stained blue (DAPI). Scale bar = 20 µm.
E Quantification of D. where bound DENND2B is normalized to the SM. Mean +/- SD. Welch's t-test *p=0.040. n=5 for both treatment groups from 3 independent experiments
(a) Illustration of experimental protocol outlining DSS induced colitis in Krt19BAC-CreERT2;ROSA26tdTomato mice.
B-C . MC3T3E1 cells were treated with indicated concentrations of KY-02327 for 2 days. β-Catenin and α-tubulin were detected by immunoblot (B) or immunofluorescence (C) analyses. Nuclei were counterstained with DAPI (C, blue).
(C) Pathway analysis of all under-represented gene sets in EVL-/- endothelial cells.
Mitotic duration in the indicated conditions expressing Mad1-Bub1 (Mad1 485-718 fused to Bub1 1-553ΔCD1) fusion protein. The time from NEBD to exit is indicated. Red circles represent cells still arrested in mitosis when the filming stopped.
(b) Density gradient fractions of NRK cells starved for 8 h were analysed by transmission electron microscopy (upper panel) and immunoblotted for LC3 or LAMP1 (lower panel). Proteins in fraction 1 were identified by mass spectrometry analysis. Three replicates were carried out from three independent purifications. Scale bar, 2 μm.