EMBO/sd-character-level-ner huggingface dataset:
(B) SUV aggregation assay using Folch liposomes and the indicated proteins. The proteins were added after a short delay. The symbols above, below the images or next to the curves represent Atg5 (blue oval), Atg12 (red circle) and Atg16 (green Y). The overall shape of the Atg5-Atg12/Atg16 complex is according to the structural model of the complex as proposed in Fujioka et al (2010). Scale bars: 10 μm.
m, Isotopomer distribution for alpha-ketoglutarate (aKG) following steady-state tracing with uniformly carbon-13-labelled substrates (n = 3). Data are mean ± s.d.
(D) Steady-state analysis of the FFAT peptide / MSP domain of MOSPD2 interaction: equilibrium responses (Req) extracted from panel A were plotted as a function of the MSP domain of MOSPD2 concentration, and fitted with a 1:1 binding model
(c) Top: Probability of an EF sample to be classified as non-EF (>0.5). Bottom: Probability of sample belonging to 'rest' to be classified as EF (>0.5). Red dotted line signifies the 0.5 prediction probability. Y-axis: Prediction probability ranging from 0-1.
Western blot for tight junction proteins in b.End3 cells treated with unconditioned, microglia conditioned media or PLX3397.
(C) ELISA measurement of β2-transferrin in CSF of control subjects (n=65) and sporadic ALS patients (n=55), FTD-ALS patients (n=12) and behavioral variant FTD patients (bvFTD, n=16).
TIGAR regulates intracellular ROS levels in response to nutrient starvation or metabolic stress.(B) Basal, nutrient starvation-induced (5 h) or metabolic stress-induced (18 h) ROS levels in U2OS cells in the presence of either scrambled, TIGAR siRNA1 or TIGAR siRNA2, measured by flow cytometry after DCF treatment. The results are expressed as the mean intensity of cell fluorescence (and standard deviation). * represents significant difference from control conditions (P<0.05).
(J) FACS analysis of IFN-γ+ and TNF-α+ CD8+ T cells (%) post-ICS induction of T cell (spleen-derived from tumor-bearing mice) activation by RM1 parental, RM1 BD Irf- BV and RM1 BD Irf7 OE cells (n = 6 per condition/group).
(B, C) Imaging and signal quantification upon staining for cl. casp3 and DAPI in PBS and AMD treated tumors, N = 5 tumors per condition, 2 sections per tumor, 5 random fields, ** p = 0.0079, Mann-Whitney test. Mean ± SEM. Scale bar, 50µm, arrows point at cl. Casp3.
(c) Interactions of the UVRAG C-terminal truncated mutants with Vps16. At 48 h post-transfection with HA-Vps16 and Flag-UVRAG C-terminal mutants, 293T WCLs were immunoprecipitated with anti-Flag, followed by immunoblotting with anti-HA.
Sagittal section of adult mouse brain showing lacZ expression driven by EE2. HC, hippocampus.
C Primary root length of seedlings grown on FP or FP supplemented with 50 or 100 mM NaCl. *p<0.05, Student's t-test. D Lateral root number of seedlings grown on FP or FP supplemented with 50 or 100 mM NaCl. *p<0.05, Student's t-test. Data information: biological replicates: n=7-20.
I. Hypergeometric overlap of the up- and down-regulated genes (E) with gene-sets from different datasets. We calculated enrichment of the deregulated genes relative to those gene-sets and used a Fisher's exact test p value after multiple adjustments to estimate the significance of the overlap. Immune related genes based on expression quantitative loci (e-QTL) were retrieved from a previous study. RNAseq data from CKp25 mice at 2 and 6 weeks after induction were retrieved from GSE65159 and up- and downregulated genes compared to littermate controls were determined after differential expression (significant genes; adjusted p value<0.05). Up- and downregulated transcripts in human AD patients compared to control subjects were determined by analysis of the available data (GSE44770). Proteins those are over- and reduced-expressed in AD patients compared to controls were retrieved from a previous study. Overlap analysis for the up- and down-regulated genes due to over-expression of microRNAs were performed to those separately from the disease conditions. Human orthologs of the mouse deregulated genes were used to perform the overlap analysis in human datasets. Color code represents fold enrichment. *FDR<0.05, **FDR<0.01, ***FDR<0.001
F. Quantification of cell death (cleaved PARP) in H82 treated tumors in D. Tumors were analyzed 7 days after the first treatment (ie: 400mm3; n=3/group. U-test, bars indicate SD).
(C, D) Differentiating cells are identified by staining with BrdU and DCX. Brain sections were prepared 10 days after BrdU injection.
(A) Na+ density from MD simulation (m2-00-f-3), measured in mol/l. The bulk density is ~150 mM. Only one binding site is visible with this cut through the density. The membrane is omitted for clarity. (B) Top-view of the binding site; Na+ positions are shown as small spheres, drawn at 10-ns intervals. Yellow/cyan/solid gray: simulation m2-00-p-2, which started with a Na+ modelled near D244. Red/transparent red/transparent gray: simulation m2-00-f-3 during which a Na+ ion spontaneously entered the binding site and bound in almost the exact same binding pose as in the simulation where the ion was modelled. (C) Cut through the density (same view as (B)) for simulation m2-00-f-3. (D) Cut through the density (same view as (B)) for the simulation M2-00-p-2 (over the part of the trajectory with a Na+ bound). (E) Na+ coordinating residues as see in MD (from trajectory m2-00-p-2, protomer A). The side chain carboxylates of D244 and D215 interacted with the ion together with the backbone carbonyl oxygens for T214 and S240 and typically two water molecules. (F) Na+ coordinating residues (from trajectory m2-00-p-2, protomer B). Only the sidechain carboxylate of D244 contributed to binding together with the backbone carbonyl oxygens of T214 and S240 and typically two water molecules.
Confocal images (z-axis-projected stacks) of Lamin B2 stained neuronal nuclei from the CA1 pyramidal cell layer of adult Satb2flx/flx and Satb2flx/flx::CamK2a-Cre (Satb2CamkCre) mice. Scale bars: 10 μm.
C Analysis of body weight from postnatal day 14 until day 32 (P-values for Phb2fl/fl or Phb2het versus Phb2pko: *P = 0.0372 at day 27, *P = 0.0311 at day 28, *P = 0.0157 at day 29, **P = 0.008 at day 30, **P = 0.0013 at day 31, **P = 0.0035 at day 32, n = 3 for Phb2fl/fl and n = 4 for Phb2het and Phb2pko).
(A) Density plots of subunits of protein complexes (as defined in the CORUM database) encoded on all disomic chromosomes compared with non‐CORUM proteins (left panel); the same for proteins encoded on the tetrasomic chromosome 5 (right panel). The differences between CORUM and non‐CORUM populations of chromosome 5 are statistically significant (Wilcoxon rank sum test). Dashed lines indicate medians of the populations.
(D) Quantification of the number of αSMA+ β1 integrin+ cells. WT, N=3; TK, N=3 biological replicates. Unpaired t-test performed comparing WT to TK.
D, Hypomethylated CpGs were enriched at neuronal super-enhancers (p < 0.001; hypergeometric test). Depicted are methylation percentages of the 615 hypomethylated CpGs located within neuronal super-enhancers.
(J) RagA/B KO HEK293A cells (lanes 1, 2), RagA/B KO ArfGAP1 KO cells (KO-1) (lanes 3, 4), RagA/B KO ArfGAP1 KO cells with HA-tagged ArfGAP1 overexpressed for 24 hours (lanes 5, 6) were cultured under normal condition (NC) or starved of amino acids (-AA) for 30 minutes. mTORC1 activity was analyzed as in (H).
HME control (vec) and KO1-3 cells were incubated with olaparib for 30 min followed by treatment with 500 μM H2O2 for 15 min. PAR accumulation was assessed by the Western method, with anti-PAR. β-actin is shown as a loading control.
(I-L) AIN‐1::GFP aggregates are separable from PGL granules, detected by anti‐SEPA‐1, in atg‐3 mutant embryos.
(b) Ciclesonide escape mutant. Vero cells treated with ciclesonide were infected with parental MERS-CoV or ciclesonide escape mutant. Viral titer was measured as described in panel a.
Effect of CEP55 knockdown on cell proliferation in MDA-MB-231 cells assessed using the IncuCyte ZOOM® live cell imager (phase-only processing module). The percentage of cell confluence was determined using an IncuCyte mask analyzer. Graph represents the mean±SEM of three independent experiments.
(B) Expression of LIMT was determined in a panel of 44 cancer and non-cancer cell lines using real-time qPCR. Expression levels were normalized to the GAPDH transcript and presented in arbitrary units. N, non-cancer cell line.
Simulated levels of FT and ATHB2 mRNA (as calculated by taking the area under the curve) across multiple photoperiods.
C Western blot analysis of SDS-PAGE of total lysates from 143B cells overexpressing tagged APOPT1 (as indicated) and exposed to 100 µM H2O2, as illustrated by the scheme (H2O2 treatment), for the indicated times. The graphs represent the densitometric quantification of the tagged APOPT1 signal at each time point. The graph inset shows that the increase of APOPT1 occurs in the first minutes after the exposure to H2O2
(E) Left panel: the response of mitochondrial matrix-localized roGFP2-Prx1 and roGFP2 probes expressed in wild-type cells to exogenous H2O2 at the indicated concentrations. Cells were grown in SGal (-Leu) medium and harvested at early exponential phase. Right panel: model illustrating that hyperoxidation of the Prx1 moiety in the roGFP2-Prx1 sensor leads to a roGFP2-like behavior.
(E) Mean ± SEM number of Calbindin positive cells in the posterior zone (lobules IX-X) of the Cb from the different mouse groups (n= 7 mice per group Two-way Anova, Bonferroni post hoc).
(F) Flow cytometric analysis of p-STAT5 levels in pro-B cells (B220+CD19+Kit+IgM-) and leukemic B220low B cells of Pax5Jak2/+ mice (black) as well as in control pro-B cells of Pax5+/+ (WT) mice (grey) at the age of 4-5 weeks. A representative flow cytometric analysis of the bone marrow of a Pax5Jak2/+ mouse (left) and representative intracellular p-STAT5 stainings (middle) are shown. The p-STAT5 levels in pro-B and leukemic B220low B cells (right) are quantified as MFI values relative to that of Pax5+/+ pro-B cells. Statistical data are presented as mean values with SEM and were analyzed by the two-tailed unpaired Student's t-test: *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001. Each dot corresponds to one mouse.
Immunoblot of endogenous LKB1, USP28 and ∆Np63 in KPL and KPLU tumours. (VINCULIN as loading control). Western blot shown are representative of three independent experiments (n=3). Representative immunoblot of endogenous NOTCH1, c-MYC and c-JUN in KPL and KPLU (ACTIN as a control). n=3
A Immunoblotting of subcellular fractions from serum-starved rat cardiomyoblasts (H9c2 cells). Input: homogenate before fractionation; Cyto: cytosol; ER: endoplasmic reticulum; Crude M: crude mitochondrial fraction, also containing MAM; Pure Mito: mitochondria; MAM: mitochondria associated-ER membranes. Cytochrome c (Cyt c) was used as a mitochondrial marker, VDAC as an outer mitochondrial membrane marker, calnexin as an ER marker, Sigma1R and FACL4 as MAM markers, and tubulin as a cytosolic marker. B Immunoblotting of subcellular fractions from rat heart. C Immunoblotting of subcellular fractions from rat kidney.
(C) (left) Venn diagrams represent the number of identified peptides significantly enriched in Fam134b-/- and Canx-/- MEFs. (right). List of peptides upregulated in both Fam134b-/- and Canx-/- MEFs.
C. B56 binding site mutant APC/C (1-L557A/V560A) is less active in ubiquitylation assay than WT APC/C. The purified recombinant WT APC/C or B56 binding motif mutant APC/C (1-L557A/V560A) was incubated with ∆APC anaphase extract. The recovered APC/C-Cdc20 complex was subjected to ubiquitylation assay using 35S-labelled cyclin B as a substrate. Samples were taken at indicated time points and analysed by SDS-PAGE and autoradiography. D. Quantification of C. Error bars, s.e.m. from three independent experiments.
(I, J) Ketone body concentration in cell culture medium of MCEC treated with 2 mM D-β-hydroxybutyrate (β-OHB) or 2 mM acetoacetate (AcAc) after 24 hours. Data are presented as mean ± SD. n=3; *, p<0.05; ***, p<0.001 unpaired Student's t-test.
BAG6 knockdown induced the abnormal distribution of Golgi apparatus markers. Images of the cis-Golgi membrane protein GS28 and the cis-Golgi matrix protein GM130 in BAG6-suppressed CHO cells with another Chinese hamster-specific siRNA (cBAG6 siRNA#5). GS28 (green) and GM130 (red) are indicated by arrowheads. Scale bar: 10 μm. (B). Fluorescent signals were detected using a laser scanning confocal microscopy system. Nuclei were stained by Hoechst (blue).
A cartoon depicting four possible states of a microtubule nucleation site considered in the mathematical model, namely unbound, bound, nucleating and microtubule growing, as well as the transition between them. The transition rates depend on the dimer concentration c. An unbound nucleation site transitions to a bound state when a tubulin dimer binds to it with rate kmcp. A bound nucleation site starts nucleation with rate kncn and adds tubulin dimer sequentially with rate kmc to grow the microtubule. Here p and n (where p+n=12 being the size of the critical nucleus, see Methods) represents the cooperativity of tubulin dimer binding to a free and a bound nucleation site, respectively.
Endothelial cells (CD31+ quadrant) and NEM (CD11b+ quadrant) were sorted by FACS from muscles 1 week after injection with the same myoblast clones.
(b) MAPPIT screen identified RAL-interacting proteins. A MAPPIT array covering close to 8,500 preys was screened with RALA-G23V as bait. Data are shown in a volcano plot of the log ratio of normalized MAPPIT luciferase activity versus P value Source data can be found in Supplementary Table S1.
Representative immunoblots of individual KrasWT and KrasG12D lung lysates with the indicated antibodies. Semi-quantitative densitometry of pp38 and pERK1/2 MAPK protein levels in KrasWT and KrasG12D lung lysates (n = 6 per genotype).
(E) ATG16L1 knock-out HEK293A cells transfected with the indicated HA GST ATG16L1 plasmids were infected with Salmonella for 1 hour. Xenophagy rates were examined through CFU assays. Quantification of infection rates by immunofluorescence is demonstrated in the right panel. Data information: Unless otherwise indicated experiments were performed three times. Data are represented as mean ± standard deviation and p values were determined by Student's T-Test.
(E - F) APP (green) distribution within enlarged Rab5QL-GFP endosomes (magenta) in cell bodies of siCD2AP- (f) or siControl- (e) treated neurons expressing APP-RFP, upon DAPT treatment, analysed by spinning-disk confocal microscopy. APP (green) and Rab5QL (magenta) line intensity profiles along the endosome (see inset line) are shown on the right. Scale bars, 1 µm.(G) Quantification of the amount of APP fluorescence at the limiting endosomal membrane normalized to total APP fluorescence per endosome (n=3, NsiControl=32 endosomes (11 cells), NsiCD2AP=39 endosomes (15 cells); ****P<0.0001, t-test, mean ± SEM).
F HeLa cells were transfected with control or TIAR siRNAs for 72 hours before measuring expression levels of p(S22)-Lamin A by Western blot analysis (mean ± SE, n = 3). Data information statistical significance was determined by unpaired Student's t-test. ; *, p < 0.05; ***, p < 0.001.
250 µg of yeast protein extract was processed by R2-P2 using either Fe3+-IMAC, Ti4+-IMAC, Zr4+-IMAC or TiO2 magnetic beads and followed by peptide analysis with DDA-MS. Phosphopeptide enrichment was performed in triplicate.   Average number of unique phosphopeptides identified by the different enrichments (n=3).   Phosphopeptide enrichment efficiency shown as the fraction of phosphorylated peptides over total peptides (n=3).   Fraction of phosphopeptides with 1, 2 or 3 phosphorylation sites (n=3).
C. Uniform Manifold Approximation and Projection (UMAP) (Left, color-coded) and RNA velocity (Right, black arrows show streaming directions from unspliced to spliced RNA) of amnion cells where 6 unsupervised clusters were identified.
(A) The indicated recombinant fragments of GST-Beclin1 were incubated with recombinant CHK2 in the presence of 32P-labeled ATP for in vitro kinase assays. MBP was used as a positive control. Ponceau staining indicates the expression of GST-Beclin 1 fragments for in vitro kinase assays. The asterisks in the blot indicate the domain of phosphorylated Beclin 1.
Mutation of genes encoding RpoE (HI0628) and MclA (HI0629) has similar effects on biofilm formation and antibiotic tolerance in H. influenzaeBiofilms of different H. influenzae strains were developed after 24 h in μ-well chambers in sBHI medium and were then treated with the antibiotic azithromycin as specified.(i) H. influenzae wild-type; (ii) rpoE (HI0628); (iii) mclA (HI0629); (iv) H. influenzae wild-type treated with 150 μg/ml azithromycin; (v) rpoE (HI0628) treated with 150 μg/ml azithromycin; (vi) mclA (HI0629) treated with 150 μg/ml azithromycin. For these experiments, H. influenzae was visualized with SYTO9 (green strain), as described in Materials and Methods. Scale bars = 20 μm. Images shown are representative of 12 images from five independent experiments.The biofilm biomass after treatments was quantified using COMSTAT. Data are presented as the average of five replicates, with error bars representing the standard deviation of the data. Statistical significance by two-tailed Student's t-test is indicated: **P < 0.01.
Schematic of the xenograft mouse model for MB treatment. C57BL/6J mice were inoculated with EG7-L1 cells (2 × 106 cells, s.c.) on the right flank on day 1, followed by injection (2 × 106 cells, i.v.) of CD45.1+ CTL on day 3 and day 6 respectively. The mice were randomized into 3 groups (n = 5) and treated with vehicle, MB (20 mg/kg/day, i.g.), aPD1 (10 mg/kg, every other day, i.p.) served as positive control. Tumor size was measured through calipering every other day. EG7-L1: EG7 overexpressing PD-L1.   Tumor growth curve for (A) was shown as mean ±s.e.m.   Representative image of the tumor on day 10 mentioned in (A).   Tumor weight on day 10 (n=5) mentioned in (A).   Data information: Data are representative of three independent experiments, and were analyzed by unpaired t-test. Error bars denote s.e.m. *P < 0.05; **P < 0.01; ***P < 0.001; ****P < 0.0001.
AP2-O3 protein expression from female gametocyte, female gamete, zygote, to retort stage of the ap2-o3::6HA strain. The activated gametocytes were collected at 30, 60, and 120 min and co-stained with HA and P28 antibodies. Pie charts indicate the percentage of AP2-O3+ and AP2-O3- cells. "n" is the number of cells analyzed at each time point.
A. TCs were assembled on DNA-RNA scaffolds (DNA was biotinylated and attached to streptavidin coated magnetic beads); TCs were then divided into three tubes and challenged with buffer ("-", mock treatment) or RNase J1 of Xrn1. Dissociation of RNAP from DNA was monitored by detecting RNAP with anti-β antibody in two fractions: B - beads (RNAP still bound to DNA), R - released (free in buffer). The gel strip shows representative primary data (Western blot). The graph shows averages (the bars) of two experiments (biological replicates) and the error bars show the range. The combined signal for B+R for each treatment was set as 100 %.
B-B2 Largely non‐overlapping distribution of AVP+, oxytocin+ and secretagogin+ (sgcn+) neurons in the magnocellular PVN. The mousesupraoptic nucleus (SON) harbored vasopressin+ and oxytocin+ but not secretagogin+neurons. Open arrowheads pinpoint single‐labeled neurons. Solid arrowhead denotes AVP/secretagogin dual‐labeling. lv, lateral ventricle; PVNm, magnocellular part of the paraventricular nucleus; scgn, secretagogin.B3, B4 Secretagogin+neurons had smaller somatic diameters than AVP+ or oxytocin+neurons yet without a difference in their diameter quotient, a measure of ovoid profiles (*P 0.05, Student's t‐test).
A transgenic dll4 reporter line showed no indication of different dll4 expression at the sites of kugeln (white arrowheads pointing to kugeln; n=122 kugeln from 23 3dpf embryos; 2 experimental repeats).
D. Yb Y23A and F129A mutants failed to produce flam-piRNAs. miR-310 was used as a loading control.
Representative trajectories of wild-type sperm in the absence of a fluid flow. The starting point of each trajectory was centered to the origin of a coordinate system, represented by the intersection of the dotted lines in the center of the circle. Each color represents one trajectory. Spider-web plot of the mean (± SD) angular frequencies (binning: 315°-45°, 45°-135°, 135°-225°, and 225°-315°; 127 sperm; 3 experiments) in the absence of a fluid flow. Representative trajectories of wild-type sperm in the presence of a fluid flow. Spider-web plot of the mean (± SD) angular frequencies (175 sperm; 3 experiments) of wild-type sperm in the presence of a fluid flow. The red arrow indicates the flow direction. Representative trajectories of Catsper1-/- sperm in the absence of a fluid flow. The starting point of each trajectory was centered to the origin of a coordinate system, represented by the intersection of the dotted lines in the center of the circle. Trajectories are magnified by a factor of 2.05 with respect to the plots C and E to compensate for the reduced swimming speed of the Catsper1-/- sperm. Spider-web plot of the mean (± SD) angular frequencies of Catsper1-/- sperm (297 sperm; 4 experiments) in the absence of a fluid flow. Representative trajectories of Catsper1-/- sperm in the presence of a fluid flow; Trajectories are magnified by a factor of 2.05 with respect to the plots C and E to compensate for the reduced swimming speed of the Catsper1-/- sperm, two trajectories were truncated (indicated by two parallel lines). Spider-web plot of the mean (± SD) angular frequencies (261 sperm; 4 experiments) of Catsper1-/- sperm in the presence of a fluid flow. The red arrow indicates the flow direction.
(e) Western blot analysis comparing the levels of DICER in MDA-231, T47D and MDA-435 cells.
Degradation of N-terminally V5-tagged wild-type (WT) or modified (P259A) FdoH in S. sonneiΔrhom7 with wild-type (+) or inactive (S201A, SAHA) GlpG expressed chromosomally (native) or from pUC19 (plasmid) without FdoI , +/- exposure to 400 µM CuCl2 for 30 min. : Rhomboid substrates that are uncleaved, cleaved by GlpG, are marked by black, red, arrows, respectively. Degradation products post rhomboid cleavage are marked by green arrows.
(G) Western blot analysis of total (L) and nuclear (N) lysates from immortalized (imm.) keratinocytes of CTRL and K5-R1/R2 mice for IRF1, IRF7, IRF9, Lamin A/C (nuclear marker, loading control) and GAPDH (cytosolic marker, loading control).
B) Representative images showing full length control and selected Miro1 lysine mutants (Miro15R, Miro1allR and Miro1R572K) expressing in MiroDKO MEF cells. All constructs (myc-tag, green) localise to mitochondria (Tom20, red).
D Analysis of the relationship between total counts of recipient CD3+ cells gated within CD45.2+ cells at day 3, 4 and engrafted donor CD45.1+ T cells at 18\24 days. This relationship was modeled with an asymptotic NLME model (Appendix Supplementary Statistical Methods), accounting for the different groups and multiple experiments. From the estimated model, a lower value of recipient CD3+ T cells corresponds to a higher value of engrafted donor CD4+ T cells (p=0.0006).
F The results of NPI- and AOL-adjusted analysis showing the association between CDK12 expression and the risk of metastatic relapse (MR) in breast cancer datasets generated using bc-GenExMiner 4.0 (http://bcgenex.centregauducheau.fr).
(A) Acetylated cohesinHalo488 was loaded onto DNA in the presence of Scc2-Scc4 and washed in high-salt buffer. DNA-bound cohesin was further incubated with Wapl-Pds5 plus Sororin, and then treated with buffer, Plk1, or Plk1 plus BI4834. CohesinHalo488 particles were observed in the presence of ATP and 100 mM KCl. MSD versus time is shown. D indicates the diffusion coefficient (n = 45, mean ± s.e.m.).
(A) Representative H&E stained liver, adipose tissue, and skeletal muscle sections from CTRL and BAM15 treated animals. Scale bars (black) = 100 μm.
(F) AURKB-promoter luciferase activity was measured in HEK293 cells transfected with control or WT1 overexpressing (OE) vector. ****P < 0.00005, one-way-ANOVA, (n=6).