EMBO/sd-character-level-ner huggingface dataset:
C Distribution of GFP expression produced by treatment with compounds from the CCBN, LCGC and DIVERSet libraries (black), or untreated cells (grey). Results are presented as percent GFP expression relative to a positive control reference sample treated with PMA (green) and determined from three biological replicates (n=3).
The following experiments were performed in glial shNf-1/shTp53 glial cells serum starved 4 hr before assaying. Cells were expressing either Cas9 alone (control) or Cas9 and sgRNA targeting Atg7 (sgAtg7 #1 or #2). D: Quantification of total EEA1 vesicles that colocalise with Flag-S-ATG16L1 Data information: Statistical analyses were performed on at least 3 independent experiments, where error bars represent SEM and p values represent a two-tailed Student's t test: * p<0.05, ** p<0.01, *** p<0.001.
Fraction of phase-separated GPMVs at the indicated temperatures. Colors of the lines indicate the treatment conditions of MDCK cells prior to generation of GPMVs. Dashed vertical lines indicate the miscibility temperature of the indicated populations of GPMVs. Values shown represent mean±SEM. Lines were generated by fitting the data to sigmoidal functions.
Neurons expressing M18Y473D are not impaired at SV docking. Autaptic munc18-1 null hippocampal neurons expressing M18Y473D or M18WT as controls were analysed with electron microscopy on chemically fixed samples (E) There is no change in the number of docked SVs per AZ length (M18WT: 14.0 ± 0.6 docked SVs/pm AZ; M18Y473D: 14.1 ± 0.9 docked SVs/pm AZ, multilevel analysis, p = 0.934). (B-E) M18WT : N=6 autaptic neurons, n=137 synapses; M18Y473D: N=8 autaptic neurons, n=116 synapses.
B. hTR and hTERT expression, normalized to ACTB mRNA and to SW39/TEL+. Data information: Data are presented as mean ± SD. Statistical analyses were performed with Student's two-tailed unpaired t-test with Welch's correction for normality of distribution unless specified otherwise. PTM, post-translational modification.
B Concentration-dependent avoidance of saponin in control, Gr28bMi and Gr28b Df/ Gr28bMi (n ≥ 4).
(d) Phase maps corresponding to DMSO (left panel) and DBZ (right panel) detrended Venus::HES5 data shown in (b).
E Quantification of BrdU+ bulge cells of Ctr and Bcl-2EOE mice. (n=4 biological replicates; mean ± standard deviation (SD); ns=not significant, two-tailed unpaired Student's t-test).
A) Immunofluorescence staining for OCT4, ZSCAN4 and 2C::tbGFP in control and acetate treated ESC cultures. Green arrows indicate 2-cell-like cells, and inlets highlight their DAPI structure. Scale bar, 20 μm.
(G) Quantification of the percentage of calcineurin depleted ARPE-19 cells with nuclear TFE3 upon Tunicamycin (Tun.) or Starvation (Strv.) treatments for 16 h (mean ± SD of three independent experiments, one-way ANOVA analysis versus siNon-target treated cells within the indicated treatment, ns= not significant, *p < 0.05, **p < 0.01, ***p < 0.001; n>400 cells per condition).
A volume-rendered representation of the apoRyR1 (orange) and ryRyR1 (blue) structures with the highlighted conformational changes. The ryRyR1 reconstruction was mirrored in the right panel for a clear comparison to the aporRyR1. The left panel depicts the view down onto the receptor from the cytoplasm. The right panel depicts the section through the isosurface indicated by the dashed line, with red arrows indicating the conformational transition of the SR extensions (dark-orange and blue circles for apoRyR1 and ryRyR1, respectively). Red arrows indicate the conformational changes of the SR extentions.
100 nM paclitaxel treatment of human hair follicles (HFs) in organ culture for 24h does not significantly affect the total number of Ki-67+ cells (A) (S-phase) in the hair matrix. Unpaired t-test performed using N of 9-12 HFs from 3 patients.
(B) The distribution of LAMP‐2A through the sucrose gradient after extraction with 1% Triton X‐114 was calculated from the densitometric quantification of immunoblots as the one shown here. Values are expressed as percentage of the total lysosomal levels and are mean+s.e. of four experiments.
E-F. PI staining of and LDH release from LPS-primed primary BMDMs infected with log-phase S. typhimurium for the indicated timepoints in the presence of PEGs of the indicated molecular weight (numbers on the X-axis, 30 mM final concentration).* p<0.05 as determined by student's t test. Graphs show mean and s.d. of quadruplicate wells. Data are representative of at least three independent expeirments.
A) For each population (CD38- and CD33+ cells), Z stacks of two representative cells are shown in the left panel. Microtubules are shown in green, actin in magenta, centrosome in white and chromatin in blue. In the middle panel, inverted image the corresponding actin staining is shown. In the left panel, the corresponding 3D projection of microtubules is presented as inverted image. Scale bar 5 µm.
B. Confocal images of ZsGreen or ZsRASSF1C expressing MDA-MB-231 spheroids embedded in 3D rat tail collagen I. Cells were stained with NANOG (red). Zoom images show that RASSF1C expressing cells are also NANOG positive. Scale 100 μm.
(h-i) Quantification of cluster formation assays performed with mCherry-p62 and GST-4xUb in presence of the indicated free ubiquitin chains. Ubiquitin chains were either pre-mixed with p62 before the addition of GST-4xUb (h), or added 3 minutes after the addition of GST-4xUb to p62 (i)
(b) Southern blot analysis of PCR-amplified fragments with a Myc-specific probe from two independent experiments. CH12F3-2A cells were transfected with the indicated siRNAs. (c) Frequency of IgH/c-Myc chromosomal translocations derived from two independent experiments (mean ± sd; Fisher's exact test).
G. Schematic representation of EATR assay: eGFP fluorescence, but not mCherry, is lost at acidic pH. Chondrocytes with indicated genotypes (ctrl=wild type) were treated with FGF18 (50 ng/mL; 12 hours) and BafA1 (200 nM; 3 hours) where indicated. ER acidification was measured by FACS. Mean +/- standard error of the mean (sem) of N=3 biological replicates. Analysis of variance one way (ANOVA) p<0.0001; Tukey's post hoc test ***p<0.0005; **p<0.005; NS not significant.
(C-D) Representative images of immunofluorescence staining for CD31 (green) and SM -actin (red) or SM-MHC (red) in No/mild, moderate, and severe disease human left main coronary arteries. No: no-disease. Nuclei were stained with DAPI (blue). (b)&amp;amp;(d)&amp;amp;(f) are high-magnification view from (a)&amp;amp;(c)&amp;amp;(e). Images are representative of ten No/mild, nine moderate and ten severe disease human left main coronary artery samples. L: lumen. Scale bar: 16 m.
The graph shows the number of microtubules per centrosome in response to increasing concentrations of monomeric actin. Data were pooled from 2 independent experiments; 0 µM: n=21; 0.3 µM: n=17; 0.5 µM: n=17; 1.0 µM: n=17. ****:P<0.001 Mann-Whitney test.
Kaplan-Meier analysis of breast cancer patients (combined GSE2603 and GSE5327 datasets) showing a link between high SPP1 and TNC expression and poor lung metastasis-free survival. Patient samples, SPP1 and TNC low n = 70; SPP1 and TNC high n = 70. HR, Hazard ratio.
G, Gel mobility shift assays of bacterially expressed, purified HP1γ-Hinge domain, fused to GST proteins, and tested for its direct interaction with the Cy3-labeled dsDNA oligonucleotide probes The probes in the gels, either free (white arrowheads) or as shifted protein/RNA complexes (red arrowheads) were detected by their Cy3 fluorescence. Representative of 3 independent experiments.
(H) H&E and SOFG staining of new bone in hind paws. Data information: CB: Cortical bone; NB: New bone
Layers of epidermis (left) and Trans-epidermal water loss (TEWL) (right) were analyzed in the back skin of indicated mice. (Left: n = 8-14, right: n = 6-14; ≥ 2independent experiments). Data information: Data are shown as mean ± SEM. P‐values were calculated by one-way ANOVA with Tukey Statistical significance: ns > 0.05, *P < 0.05, **P < 0.01, ***P < 0.001, **** P < 0.0001. See Appendix Table S3 for exact P‐values.
A The mRNA value of AKT2 was analyzed in the GEO Profiles from the liver explant of Hepatitis B virus (HBV)-associated acute liver failure (ALF) patients (GDS4387/225471_s_at), and from bronchial epithelial cells with pandemic and seasonal H1N1 influenza virus infections in vitro (GDS4855/203808_at). normal, n=10; HBV, n=17; control, n=3; influenza A, n=9. Data information: *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001 and ns, not significant (P > 0.05); using unpaired t-test Error bars mean ± SD
E. Proportions of the families of CACACA-containing SINE repeats within each family, as a percentage of total intragenic sense SINEs.
M238P cells were transfected with two different sequences of siRNAs vs FSCN1 or with a control siRNA (72 h, 100 nM). (C) Western Blot analysis of cell cycle markers on cell lysates from M238P cells cultured for 72 h following transfection with the indicated siRNAs.
Two independent primary mouse fibroblast isolations FB1 (black) and FB2 (grey) were cultured in collagen gels for 3 days before being released by collagenase treatment and plated on TCP for 4 days (triangle). Controls were kept on TCP for 3 days before plating (circle). Fold increase in confluency 24 hours after plating of collagen gel released cells and cells kept on TCP is shown (n= 3 technical replicates).
A. HEK293T cells were transfected with MYC-FOXP3 and FLAG-USP44 encoding expression constructs using Polyethylenimine. 48hrs post-transfection, cells were harvested, lysed, and anti-FLAG or anti-MYC antibody coated beads were used to immunoprecipitate the given labeled protein along with its binding partner. Co-IP'ed proteins were subjected to SDS PAGE followed by immunoblot analysis. Antibodies recognizing FLAG or MYC tags were used to probe for USP44 and FOXP3, respectively.
RPE1 cells stably expressing centrin1-GFP were plated for 3 h on coverslips coated with different ratios (100:0; 50:50 or 1:99) of fibronectin and PLL-PEG prior to fixation and staining for F-actin (top line and magnified views around centrosome below. Scale bars: 10 µm and 2 µm, respectively) and α-tubulin (bottom line. Scale bar: 10 µm).
(N) The SMAD3 inhibitor decreased melanoma cell density. Cell lines have been exposed to SMAD3i (0, 3, 10, 15 or 20 µM, 84h). The cell lines defined as S and R to BRAFi in the item 5M are indicated in blue and red. Normal human melanocytes (NEHM) have been used to evaluate the effect of SMAD3i on normal cells (n=3 independent donors). The SMAD3i effect on NHEMs is weak and manageable for these normal cells (NHEM).
Nesting behavior of mice at 10-14 months of age was scored 0-7 by an investigator blinded to genotype. n = 17 NTG, 12 CaMKII-tTA, 13 hTau-WT(L32), and 10 hTau-A152T(L1). Nest building was significantly impaired only in hTau-A152T(L1) mice (P < 0.01 at 2 and 6 h) and CaMKII-tTA mice (P < 0.05 at 2 h, P < 0.01 at 6 hours) by nonparametric Wilcoxon rank-sum test with gatekeeping approach and Holm adjustment. Values are means ± SEM.
SQLE protein expression and mRNA levels were examined in p53+/+ and p53-/-HCT116 cells (D) Actin was used as loading control.
H. Gel mobility shift assays of bacterially expressed, purified HP1γ-Hinge domain, fused to GST proteins, and tested for its direct interaction with the Cy3-labeled RNA oligonucleotide probes The probes in the gels, either free (white arrowheads) or as shifted protein/RNA complexes (red arrowheads) were detected by their Cy3 fluorescence. Representative of 3 independent experiments.
A. Differentially expressed proteins in PtenStat3pc-/- vs. Ptenpc-/- proteomic samples. Colors indicate adj.p-value and log2-FC. (Black = Log2-FC ≤ 1 & adj. p-value ≥ 0.05, orange = Log2-FC > 1 & adj. p-value ≥ 0.05, red = Log2-FC > 1 & adj. p-value < 0.05). FC = fold change.
C) The WT-blot shows the expression of LRP6 and β-catenin in cells in miR-cluster-Dox-MCF-10A cells cultured in the presence of Dox and with and without WNT3a ligand (100ng/ml for 6 hours) when the microRNA binding sites #1 and #3 are blocked by target protection.
F. Control (ctrl) and RAB13 siRNA-treated HUVECs co-cultured on fibroblast monolayers. Endothelial cells were identified with an antibody against the endothelial cell marker PECAM-1. black arrowheads indicate filopodia (F)
D Ratio of toxicity and viability of HCT116, U87 and BxPC3 cells grown in spheroids (3D) and treated as indicated for 24h (BxPC3) or 48h (HCT116, U87) (NEN 1.2 µM; Domperidone (Domp), Imipramine (Imi), Desipramine (Desi) and Amitriptyline (Ami), each 30 µM; Clomipramine (Clomi) 20 µM). Data information: Data are presented as mean (SD) (N=3) and were analyzed by two-way ANOVA with Tukey post-hoc test Significance is indicated for multiple comparisons as indicated. * p< 0.05; ** p< 0.01;*** p< 0.001; **** p < 0.0001.
Reprogramming was also performed with mES-Vc or mES medium. Additional factors (Hif1α, Hif1α overexpression; TGFβ, TGFβ1/2/3 1 ng/ml each; 3F, Ctcf, Kdm2b, and Wdr5 overexpression) were used simultaneously with mES medium. The expression of Bmi1, Ctcf, Ezh2, Kdm2b, or Wdr5 was determined on day 6 with qPCR (K).
D. Crosslinked peptides obtained by sequential digestion of a synthetic 7-protein mix are smaller than their corresponding tryptic peptides.
Abundance changes of ribosomal proteins and their transcripts during aging. Cytoplasmic ribosomal proteins of large and small subunits are displayed separately and changes are shown for both the age comparisons as box plots. Transcripts are displayed as light blue and proteins as dark blue boxes. Changes of individual proteins are displayed as dots; orange dots identify significant cases (adj. p < 0.05, n=4 per age group for proteome and n=5 per age group for transcriptome). In boxplots, the horizontal line represents the median, the bottom and top of the box the 25th and 75th percentile, respectively, and the whiskers extend 1.5 folds the interquartile range.
Top, general overview of the non-rotated IAPV-IRES/80S class 1 structure. IAPV-IRES is depicted as solid Van Der Walls surface colored according to the secondary structure motifs. The PKI (green) is solidly anchored to the A site. Bottom, close up view of the IAPV-IRES PKI inserted in unsharpened map. Zoomed view of A3760, a nucleotide belonging to the helix 69 (H69) of the 28S rRNA interacting with PKI. Final refined model inserted in the post-processed map is shown. This interaction is not disrupted along the small fluctuations of the 40S. An apical view along the axis of the PKI of a superposition of class 1 versus class 2 shows the IRES displacements are minimal and are followed by the H69 which constantly interacts with the IRES.
(C) Quantification of the averaged tumor weights in (B) (n=5). Data information: Data are displayed as means ± SD. Statistical significance was assessed using a two-tailed Student's t-test, ∗p < 0.05, ∗∗p < 0.01 and ∗∗∗p < 0.001.
G) Metagene analysis of the distribution of the different Sen1 variants at mRNAs using either the TSS or the PAS as reference point. Values correspond to the median of Sen1 data normalized by the RNAPII signal obtained in the corresponding background.
B) Quantification of the percentage of cells presenting LC3 puncta upon the infection. These data are representative of three independent experiments.
E: Response times for IEGs, DEGs and ILGs. Genes on the same trajectory have the same response time, but response times are composed differently. For IEGs and ILGs, response times are solely determined by mRNA half-life, whereas DEGs have response times that are mixtures of half-life and transcriptional delay.
(E) Model for Rad52-mediated tolerance during DDT. The recombination factors Rad52, Rad51 and Rad57 promote efficient Rad6/Rad18 binding to chromatin under unperturbed conditions. In response to blocking lesions that impair replication fork advance the Rad6/Rad18 complex is mobilized to ssDNA lesions where, together with Mms2/Ubc13/Rad5, ubiquitylates PCNA and promotes TS. The ssDNA lesions that escape from this error-free pathway during S phase accumulate in G2/M, where they are filled in by two additional, less accurate mechanisms regulated by Rad52: UbPCNA-independent HR (recombinogenic) and TLS (mutagenic). Apart from facilitating Rad6/Rad18 chromatin recruitment, Rad52 plays an additional uncharacterized Rad51/Rad57-independent role in TLS.
C: SMC3 immunofluorescence showing cohesin on chromosomes of WT and Cnot6l-/- oocytes at 16 h after culture. Centromeres and DNA were labeled by CREST and DAPI, respectively. Scale bar, 5 μm
(A) Experimental setup for ESC based in vitro derivation of NPCs (4 days of differentiation condition, DDC) and GPCs (11 DDC). Time points for SOX3, SOX9 and H3K27Ac ChIP-seq experiments are as indicated
Analysis RAB2A expression was performed on the Invasive Breast Cancer Consecutive Cohort (n = 622) operated in the European Institute of Oncology, Milano, Italy, in the year 2000. Expression was measured by IHC on TMA.(b) Correlation of RAB2A expression with clinicopathological parameters. Only for 520 of 622 samples expression data for RAB2A was available. Note that the number of scored cases is lower than the total number of cases since: i) in some cases, individual cores detached from the slides during the manipulations; ii) clinical information was not available for all patients. In tumor tissues the IHC signal was associated with the tumor cell component and not with the adjacent or infiltrating stroma.
Splenic DCs were expanded in Rab39a KO and WT mice by injection of B16-Flt3L tumor. 10 days post tumor implantation, DCIR2+ (Cd8α-) or XCR1+ (Cd8α+) dendritic cells were isolated from spleens via magnetic positive selection. 5 x 104 cells were plated in a 96 well plate and incubated with the indicated amounts of Ova-Fe and 1:1 of Reporter CD8 or CD4 T-cells overnight before measuring luciferase activity. Error bars indicate SD of 2 replicate wells. Shown are representative graphs of 3 independent experiments. * p < 0.05 using two-way ANOVA.
Primary ILC3 cells were sorted from colonic LP cells and were stimulated with indicated cytokines. Productions of IL-22 were detected by ELISA. mRNA expressions of Il-22 were detected by qPCR.
(C, D) Histograms of the (C) number and (D) spreading distance of L. pneumophila released from infected amoebae. Spreading was quantified using the Imaris software ("surface" tool). One mask covered the heavily infected amobae (center: x, y, z = 0), another mask covered each single bacterium outside the infected host cell. The total number of released bacteria were for JR32 (n = 1240), ∆flaA (n = 33) and ∆lqsA (n = 214). The distance of each bacterium to the center was quantified by vector calculations. The red line marks the approximate cell diameter (5 µm). Data shown are means and SEM of four infected amoebae from one biological replicate (two-tailed Student's t test; * P < 0.05, ** P < 0.01, *** P < 0.001).
(G) UMAP maps color-coded for transcript counts of genes enriched in subsets of choroid plexus cells. The scale bars represent color coded sequencing depth-corrected log transformed transcript counts.
(D) Lysates from U20S or tetracycline-inducible VCP-WT, -RH, or -AE cells treated with vehicle or Baf for 4 h and immunoblotted for LC3 and α-tubulin. Note that Baf treatment does not increase the LC3II levels in IBMPFD mutant (RH and AE)-expressing cells. Bars, 15 µm.
(A) Two‐hybrid assay for interactions of Apg10p with Apg5p, Apg7p and Apg12p. Yeast cells (PJ69‐4A) harboring the indicated plasmids were streaked out on plates with medium lacking adenine to assay for interaction‐dependent activation of the ADE2 gene.
(D) The above cells were also IF stained for Pax7 (red) and MyoD (green). Quantifications of each population, Pax7+MyoD+, or Pax7-MyoD+, are shown on the right (n=3, each). Scale bar = 100 µm.
A, Co-IP assay of HDA15-TAP with TOC1-GFP and 5X-GFP in N. benthamiana. HDA15-TAP was immunoprecipitated with IgG resins and digested by HRV-3C protease. HDA15 and TOC1 were detected by α-MYC and α-GFP, respectively. B, Quantification of the interaction strength in A. Results from 5 independent trials were averaged. Error bar indicates SEM, asterisk indicates significant difference (*p<0.05, student's t test).
Quantification of proliferating (Ki67 positive) keratinocytes and fibroblasts during wound repair over time (n= 4 PW0, PW2, PW21; n= 3 PW4, PW10; n= 2 PW7, PW14 biological replicates).
Schematic representation of the symptoms and clinical presentation of patient III.2.
H Co-precipitation of GCN5 with TFEB. TFEB was immunoprecipitated from MEF cells using anti-TFEB, and the precipitates were analyzed using anti-GCN5.
B. Dot plot of the top three marker genes for each cell type. The dot size represents the percentage of cells expressing the gene; the color represents the average expression across the cell type.
qRT-PCR and western blotting assays showed stable expression or depletion of ASS1 in SW-1116 and Caco-2. NC, Negative control.
(A) Volcano plots representing transcript down- (red) or up-regulation (yellow) after 48 hours PTX in the somatic and process compartment. Representative transcripts are highlighted and labelled. Linear model was used to fit transcriptome data and subsequently contrasted using likelihood ratio testing for PTX-treatment effects across compartments.
(E) Log2-Ratios of the number of miRNA-binding sites found in significantly up- vs. downregulated genes in the somata (red) or processes (blue). Elevated ratio in processes indicates that miRNA-binding sites are more frequent in transcripts downregulated by PTX in processes. Non-parametric Mann-Whitney U-test was used to test difference (mean somata: 0.37 vs mean processes: 0.783); ***p-value < 0.0001; n=80 miRNAs, represented as colored datapoints.
(e) Total cell lysate from (c) were immunoblotted with antibodies anti-E-cadherin, which recognize either an epitope in the cytoplasmic domain (IC), an epitope in the extracellular domain of mature E-cadherin (SHE78-7), respectively, or anti-RAB2A, and anti-actin. An arrow indicates the unprocessed form of E-cadherin.
(B) Incidence of spinal ankylosis in PGIS model. n=5 per cage of total 3 cages per group, Fisher's exact test.
A. Knockdown of lnc-AP, as well as the endogenous pep-AP in HCT116 and SW480 cells (n = 3, biological replicates, mean±SEM, t test). Data information: * for P < 0.05; ** for P < 0.01; NS for no significance. si-NC was the abbreviation of commercial normal control of siRNA.
B: HIF-2α levels in HT29 primary tumors. Left: Example of immunostaining in vehicle-treated controls. Inset, high-magnification image of the region marked with a green asterisk (*). Right: Quantification of the effect of monotherapies or doublet LDM/MTD regimens on HIF-2α+ area. F(5,18) = 1.215 and P = 0.3424 (not significant) for overall treatment by Brown-Forsythe ANOVA.
C-D SDS-PAGE (C) and BN-PAGE (D) analyses from 143B cells and COX2∆ cybrids transiently transfected either with a COX5B-Myc-DDK construct or with the empty vector, followed by immunoblotting with antibodies against COX5B and CII subunit SDHA (loading control). The identities of MRC complexes and SCs are as in Figure 1. The red arrow points to the accumulation of over expressed COX5B bound to SC I+III2 in control cells.
G-I J774A.1 macrophages were pre-treated with cytochalasin D (CytoD, 10 μM) and infected with swollen conidia (MOI = 5) or zymosan (50 μg/ml). (H) For quantification of NF-κB translocation, nuclear extracts were separated by SDS-PAGE, followed by Western blotting. Membranes were probed with anti-NF-κB p65 and anti-HDAC1 antibodies.
C mRNA and protein levels of SQLE in different tissues of p53+/+ or p53-/- mice were determined by qRT-PCR and western blot respectively.
1.25 x 105 of DC3.2-Rab39a cells were incubated in a 12 well plate overnight ± dox (1µg/ml) to induce Rab39a. Cells were fed at 4 beads/cell of biotinylated-ova-6µm-magnetic-beads for 3 hours with or without 1:1000 BFA (golgiplug, BD). Phagosomes were isolated using the listed protocol. Isolated phagosomes were washed, permeabilized and stained. Shown are histograms of indicated stains as well as % of Rab39a positive phagosomes. Representative plot of two independent experiments.