EMBO/sd-character-level-ner huggingface dataset:
Figure 5: Memory decline in 8-month old Fmn2 -/- mice correlates with deregulated transcriptome plasticity B. Top GO domains and pathways affected in 3-month old Fmn2 -/- mice when compared to wild type control animals. D. Top GO domains and pathways deregulated in 8-month old Fmn2 -/- mice when compared to an age-matched control animals. GO:CC; gene-ontology domain "cellular compartment", GO:MF; gene-ontology domain "molecular function", GO:BP; gene-ontology domain "biological process", pathway "KEGG pathways".
Representative immunoblots from protein extract of GC muscles of 4-month-old control, HSA-Cre untreated and HSA-Cre Bezafibrate-treated mice, with the indicated antibodies.
A) Oocytes were fixed for chromosome spreads 8 hours after GVBD, and stained for PP2A-c (red), Sgo2 (green), CREST (blue) and DNA (Hoechst, shown in grey). Spreads were classified into metaphase I and anaphase I, depending on whether chromosome segregation had taken place, or not. Arrowhead indicates fused sister kinetochores, arrows indicate separated sister kinetochores.
(G) Western blot of whole‐cell lysates from control and Beclin‐1 siRNA‐treated cells. siRNA, small interfering RNA.
(I) Grk5, Nppa, and MEF2 targets Nr4a1 and Xirp2 mRNA levels in NRCMs after Raptor KD. Analyzed by t-test, n=3 biological replicates per conditions. Data information: Error bars indicate means ± SEM; * - P ≤ 0.05, ** - P ≤ 0.01, *** - P ≤ 0.001, **** - P ≤ 0.0001
Representative H&E staining in liver sections from tumor-bearing mice treated with ASO1 and siBMPR1A in orthotopic transplants of tumors from HCC#50 and HCC#51. Scale bar, 100 μm.
Mammalian two-hybrid assays between pACT-LRP130 and pBIND-PGC1α in A549 cells treated with DMSO or 100nM rapamycin. Samples were subjected to the luciferase activity assays.
M-P Representative images of lectin stained choroidal flat mounts 7 and 14 days after laser coagulation in C57BL6/J control mice (M, N) and Ifnar1-/- animals (O, P). Dashed lines indicate CNV areas and the asterisk marks the central optic nerve head. Scale bar: 200 µm.Q Quantification of lectin-stained CNV areas with ImageJ software. Bars show mean ± SD. (n = 4-11 RPE/choroidal flat mounts; One-way ANOVA followed by Tukey's post-test: *p = 0.0281).
(d) Gel filtration analysis. The supernatant fraction of mouse brain lysates was subjected to a Superdex 200 HR 10/30 column and each fraction was immunoblotted with the indicated antibodies. Relative amounts of each fraction determined by Odyssey software are plotted.
(F) Mobility of the Q15 and Q128 C. elegans lines upon overexpression of TBK1 or TBK1 KD (n= 26-29).
(I) Left: schematic representation of polar histogram analysis by clustering the traced axons (WT n=6 pups, crmp2-/- n=9 pups) into 3 groups based on the growth angles. Right: proportion of axons growing in selected clusters (WT, 0°-±20°: 67.3±10.3%; ±20°-±40°: 21.2±5.3%; ±40°-±60°: 6.22±3.2%; crmp2-/-, 58.5±5%, p=0.047, 27.7±4.3%, p=0.022, 8.64±2.25%, p=0.11), mean ± SD, *p<0.05, t-test.
(A) Double-immunolabeling of spinal cordneurons with ChAT (red) and N-terminal FUS antibody (green). Nuclei were visualized with DRAQ5 (blue). Cellular localization of FUS was analyzed in the ventral spinal cord of Fus+/+/ChAT-CRE (A1-A4), FusΔNLS/ΔNLS/- (A5-A8), and FusΔNLS/ΔNLS/ChAT-CRE (A9-A12).FUS was completely nuclear in ChAT+ neurons of Fus+/+/ChAT-CRE, while cytoplasmic in FusΔNLS/ΔNLS/-, In the ventral horn of FusΔNLS/ΔNLS/ChAT-CREmice, ChAT+ neurons (motor neurons, e.g. within the dashed square) displayed nuclearFUS immunoreactivity, while ChAT negative cells retained cytoplasmicFUS immunoreactivity (arrows)
Effect of knockdown of BLIMP1 and PRDM14 on PGCLC induction. Knockdown of BLIMP1 (F) and PRDM14 (G) was done using the lentiviral system with two individual shRNA vectors for each gene. The knockdown efficiencies were assessed by qPCR (left panel, each). The induction of d4 PGCLCs analyzed by FACS, gated for TRA‐1‐81 and cKIT (right panel, each). Data are presented as means ± SD (n = 3).
B shCtr and shM2 H1299 cells were treated by 5-FU (50 μM; 24 h). Then drugs were washed out and the cells were cultured in normal DMEM medium (Ctr) or conditioned medium from non-treated cells or co-cultured with non-treated cells in transwells (separated by the filter) for another 24 h. The cell viability of 5-FU treated cells was determined using MTT assay. Data information: data were analyzed using two-way ANOVA with Bonferroni post-test and shown as mean ± SEM; * P < 0.05, ** P < 0.01, *** P < 0.001, ns, not significant.
Cartoon representation of the 1.5 Å W. pipientis wMelOTU crystal structure with labeled termini, missing regions, and features of the active site.
CD4+ and CD8+ T cells were isolated from the spleens of WT, and EGR4KO mice by cell sorting. (H) Comparison of IFNγ levels in WT vs. EGR4-/- T cells.
Parental and VAR cells were treated with the indicated drug concentrations for 48 hours. Cells were then harvested, and lysates were immunoblotted for the indicated proteins.
G Production of c-di-GMP at the indicated time-point by SiaD with SiaC or SiaCT68A was determined by HPLC. To evaluate the effect of SiaB-mediated phosphorylation on SiaD DGC activity, SiaC or SiaCT68A was pretreated by SiaB in the presence of 1 mM ATP before reaction initiation.
A The indicated overexpression and RNAi constructs were co-expressed with markers for the plasma membrane (Src-GFP, green) and nuclei (DsRed2-Nuc, magenta) in the larval epidermis. The effects of upregulating autophagy (top row) are suppressed when autophagy is blocked by simultaneously downregulating Atg1 or Atg5. n=20-40 larvae each genotype.
(e) Top: IF for GFP and K63-linked ubiquitin (red) of SY5Y cells expressing GFP-p38 or -ANK1-p38 WT and mutant K385R (green). Arrows indicate colocalization. Bottom: percentage of Agm positive for K63-linked ubiquitin.
(D) A model of Wnt signaling regulation by MDMX. In the absence of stress, MDMX inhibits CK1α, increases basal expression of Wnt/β-catenin target genes and stimulates proliferation. Interaction with mutant p53 stimulates MDMX-CK1α binding and promotes proliferation. DNA damage promotes MDMX degradation and inhibits MDMX-CK1α binding, reducing Wnt signaling.
Human term placentas were dissected and cytotrophoblast cells were extracted and seeded. (B) Trophoblast cell fusion was quantified on days 1, 3, and 5 post-seeding. Values are means + SEM, derived independently from human placentas of three pregnancies.
(a) Relative acetylation of histone H3 Lys 9 and 14 residues determined by quantification of immunoblot analysis performed at day 20 of the ageing experiment shown in panel b. Data represent means ± s.e.m. (n = 3; *P 0.05). (b) Chronological ageing of wild-type (▪, o) and Δiki3Δsas3 (▴, ▿) with (open symbols) or without (closed symbols) addition of spermidine (4 mM) at day 1. Data represent means ± s.e.m. (n = 4). (c) Quantification (FACS analysis) of phosphatidylserine externalization and loss of membrane integrity (annexinV/PI costaining) as well as ROS production (DHE->Eth conversion) performed at day 20 of the experiment shown in b. Data represent means ± s.e.m. (n = 4; *P 0.001).
GOChord plot showing relationships between selected representative biological process GO terms and differentially expressed proteins identified by nanoLC MS/MS analysis. The representation shows up-(red) and down-regulated (green) proteins differentially expressed in UL1 relative to b-CTRL (-0.3≥log2FC≥0.3).
(C) Proportion of ER+ and ER- breast cancer cell lines that have ESR1 as a rCCS gene. P-value was calculated with the Fisher's exact test.
C Univalent-like chromosomes. Images were 3D-reconstructed and viewed from the top of the metaphase plate. Red surfaces with white arrowheads indicate univalent-like chromosomes. Scale bar = 3 μm.
(B) CCB02 but not conventional tubulin binders (Taxol, Bacatalin III, Docetaxel and Vinblastine; concentrations used 30nM) causes activation of extra centrosomes and prevents them from clustering. MCF10A cells with extra centrosomes (+Dox, extra centrosomes) were used. In contrast to CCB02-treatment, interphase centrosomes of tubulin binders-treated cells consistently display clustered centrosomes. Note, disrupted mitotic spindles were observed in tubulin binders-treated cells due to their general toxicity to microtubules. Cells were stained with CPAP (green), Cep152 (magenta) and microtubules (α-tubulin, red). Scale bar, 2µm. Three independent experiments (N)=3 with each at least 100 cells were examined per treatment
(A)-(C) The scattering profiles (A), the PDDFs (B) and the dimensionless Kratky plots (C) of DB12s from DENV2 (cyan), ZIKV (red) and WNV (blue). The inset in (A) shows the Guinier regions of the respective scattering profiles with linear fit lines. The dimensionless Kratky plot of ZIKV xrRNA1 (red dashed line) was included in (C) for comparison, indicating that the structures of DB12s of ZIKV and WNV are well folded, but that of DB12 of DENV2 is partially folded. The Kratky plots for the two PK3 mutants of DB12s, the ZIKV- DB12-PK3∆ (green) and WNV- DB12-PK3∆ (black), respectively, are also included for comparison, suggesting reduced compactness upon PK3 mutations.
Immunoblot from parallel samples in (C) utilizing antisera specific to the 33 amino acids generated by human CCND1 intron 4. Lamin B serves as a control. Arrow indicates the cyclin D1b band.
H Changes in the morphologies of livers and H&E staining depicted steatosis as circular white gaps caused when the dehydration process leaches the fat out of fixed livers.
Protein sequence alignment of human ATAD3A and ATAD3B. Candidate LIR motifs (W/F/YxxL/I/V motifs) are depicted in red, and different amino acids are depicted in green. Because ATAD3A just contains 586 amino acids (aa), the 594aa-617aa of ATAD3A is not exist and thus not shown.
A. Analysis of Fn colonization in mouse xenograft tumors by IHC. An inoculum of 5×106 HCT116 cells was injected subcutaneously and bilaterally into the nude mice. Once the tumors became visible (after 3-4 days), approximately 5×106 CFU of Fn 12230 washed in PBS or 1 mg/ml Congo Red (CR) were injected into the tumors. The tumors were extracted one week later, and the formalin-fixed and embedded (FFPE) tissues were stained with mAb 7H7. Note the brown stains in tumor injected with PBS-washed tumor, but not in CR-washed tumor. Scale bar = 20 μM.
C Intestinal barrier functional assays measuring serum FITC-dextran before DSS treatment (n = 5, P = 0.0117)
D Relative CpG methylation level [log2(fold change)] at each chromosome in the hippocampal DNA samples (ATO vs. Ctr), as determined by MethylC-seq.
(b) Binding of the EDA-ADP-ATTO 590 probe to wild-type VCP in the presence of different allosteric inhibitors or ADP.
Ni2+-NTA precipitation of HeLa cells transfected with indicated vectors. S13A-Myc-His, Myc/His6 double-tagged FUNDC1-S13A mutant.
(A) hCAP-G is composed of 1,015 amino acids and contains 19 HEAT repeats. hCAP-H is composed of 730 amino acids and contains 5 conserved motifs (I: hSMC2 binding region, II: hCAP-D2 binding region, III: DNA binding region, IV: hCAP-G binding region, V: hSMC4 binding region).
D. The best structural model for the helices α2-α3-α4 dimer is shown with the residue pairs replaced by cysteine pairs in (B) presented as in Figure 1A. The β carbon atoms of each residue pair are linked by a dashed line with the distance ranging from 4.7 to 5.2 Å.
(A) Proportion of inflammatory- and immune processes- associated mRNA in regard to the total number of significantly deregulated mRNA in miR-21-3p mimic versus scrambled control treated HaCaT cells.
HMDM were stimulated with AdV (50 000 pp/cell) complexed with antibody at indicated doses for 2h and viral genomes were measured by qPCR. (n = 4, mean ± s.e.m)
Micrograph of coronal sections of E16 mouse cerebral cortices electroporated at E14 with GFP-empty vector control, GFP-Cstb or GFP-R68X mutant, analyzed 2 dpe and immunostained with GFP and Tbr2. Ventricle (V) is indicated. The dashed lines represent the apical surface of the ventricles. Quantification of the total number of Tbr2+ cells/ cortical area (µm2) in (L). Data shown as Z-scores relative to the mean of GFP control vector.
(E) PARP1, but not PARP2, mediates the ADP-ribosylation on H2AX. Wild type (WT) cells, PARP1-null cells or PARP2-null cells were treated with H2O2.
(G) Statistic analysis of IMA numbers of vehicle or phenformin (Phen) treatment group in KLN mice (n=11 per group). Results were shown as mean.
D BMMΦ were stimulated with LP and with repeated LP stimulation on day 3 where indicated and transcript levels of inos relative to gapdh were quantified by qRT-PCR at indicated timepoints as fold change to unstimulated. Depicted are means ± SEM from 3 independent experiments.
Lack of differences in body weight among groups registered along time in the SW1417-derived CCR model and the regression of metastases protocol (N=10 mice/group). Lack of differences in body mouse weight among groups registered along time in the SW1417 cell line-derived model and the prevention of metastasis protocol (Buffer (N=11; Free oligo-FdU (N=12), T22-GFP-H6-FdU (N=12)). Lack of differences in body mouse weight among groups registered along time in the M5 patient-derived model and the prevention of metastasis protocol (Buffer (N=6); Free oligo-FdU (N=17); T22-GFP-H6-FdU (N=8). Scale bar, 100 μm
B PIPKIγi5 specifically interacts with LAPTM4B, but not LAPTM4A or LAPTM5. Top: schematic diagram of all three LAPTM members. Bottom: each Flag‐tagged LAPTM protein was immunoprecipitated from HEK293 cells cotransfected with Myc‐tagged PIPKIγi5 and empty vector or Flag‐tagged LAPTM, and the co‐immunoprecipitatedPIPKIγi5 was examined by immunoblotting.
Boxplots with outlier calling showing the significant codon biases in Dnmt2 down-regulated and up-regulated proteins in the DML and dSILAC datasets. For the dSILAC (S-All) dataset, we display the plot for all identified proteins or stromal (S-St) and suspension (S-Ss) cells. A significant increase or decrease of a codon frequency in up- or down-regulated proteins relative to the average frequency of that codon in all identified proteins is displayed as a colored dot. Codons showing no deviation from average values are grouped together in the box.
CD4+ and CD8+ T cells were isolated by negative selection from WT or EGR4-/-mice. (A) CD4+ and CD8+ T cells were loaded with Fura-2AM and plated on poly-D-lysine (2 hrs) before treating with biotinylated anti-CD3ε, followed by streptavidin where indicated. The average response of the majority of CD4+ (WT 74.2±3.2%; EGR4-/- 77.8±2.9%) and CD8+ (WT 79.4±3.5%; EGR4-/- 78.2±2.5%) cells that responded to streptavidin crosslinking of CD3 (mean±SEM; 40-60 cells/coverslip; 7 to 8 separate experiments).
Northern blot analyses of the 7S RNA levels in 4- and 8-week-old control and Tefm knockout mouse hearts (n= 12 mice for each group). 5S rRNA was used as loading control. RNA from tissue-specific Mterf4 knockout mouse hearts and tissue-specific Polrmt knockout mouse hearts were loaded as positive and negative control, respectively.
(A) Infection data for THP-1-IFIT-1 cells transduced for 24 h with HIV-1 GFP (0.1-3 U/ml RT) in the presence of DMSO vehicle or PF-74 (10 μM).
(g-j) Immunofluorescence analysis of the indicated proteins and cell type markers in IPF (n=3) and control samples (n=3).
(A) Polarographic measurement of KCN-sensitive oxygen consumption, driven by NADH in isolated coupled mitochondria. Mitochondria were isolated from cells expressing the wild type form of Cor1 (Cor1WT) or the mutant Cor1N63A, N187A, D192A, V189A, Y65A, L238A, K240A (Cor1**). Thereby, strains either overexpressed cytochrome c (Cyt cOE) or harbored the empty plasmid as a control (Empty). Measurement was performed in the absence (basal respiration) or presence (phosphorylating condition) of ADP.
Quantification of cytoplasmic TDP-43 levels, each dot represents an independent differentiation, ratio paired-t-test.
B Principal component analysis (PCA) of the mean-centered transcriptome profiles. The share of variation captured by each principal component is mentioned in the axis labels.
(G) MPO release from intradermally injected WT or Tlr2 KO mice (n=5-15 biopsies each) Data information I represent data (mean+SEM) combined from 'n' technical or biological replicate mic ), Student's t-tes
(G) Quantification of percentage of cells observed in (E) and Figure EV6C with the indicated GFP-COP1 construct exhibiting nuclear (Nuc), nuclear and cytoplasmic (Nuc/Cyt), or cytoplasmic (Cyt) localization. Mean values ± S.E.M. are shown for three independent experiments where 50 individual cells per experiment were analyzed.
E Integrated analysis of transcriptome profiles of primed and naïve hPSCs, including primary human embryonic cells. Each point represents a biological sample; the colors represent the cell type. Naïve and primed samples are depicted in red and blue, respectively. Samples from pre-implantation embryo are shown in different colors. The number inside each circle indicates the study from which the data is obtained. The study of Tang et al., 2013 demonstrated as empty circle. Large dash circle indicates morula stage of human embryo which is almost in line with our data (small dash circle). All empty points are from dataset (9) Tang 2013.
(D) Cand2 mRNA levels in NRCMs treated with PE and Torin 1 measured by RT-qPCR. n=6-9 of biological replicates per conditions. Data information: Error bars indicate means ± SEM
(h) Atg5 is not cleaved in apoptotic HeLa cells (5 h staurosporine treatment) lacking the small subunit of calpain, which was silenced by using specific siRNA.
Snapshots of ChIP-seq signals of the RNAP3 subunits Rpc1 and Rpc2 in the presence or absence of Sen1 across a representative (A) tRNA gene, (B) 5S rRNA gene and (C) srp7. Boxed regions highlight the increased density of reads in the downstream region of genes in the absence of Sen1.
Monocyte recruitment in the draining lymph node requires collective DC activation (A) Representative dot plots showing the percentage of monocytes (CD11b+ Ly6Chigh cells, black box) present in popliteal dLN of WT:Irf3‑/‑Irf7‑/‑ chimeric mice injected with poly(I:C) (middle and right) or with PBS (left). CD11b+ Ly6Clow/int cells corresponded to neutrophils and were not included in the analysis.
THP-1s were stimulated with a constant dose of AdV-GFP (50 000 pp/cell), and complexed with decreasing antibody concentrations as indicated. A single experiment representative of 2 independent experiments is shown.
(C) Localization of Atg8 relative to Atg9 during nitrogen starvation. dsl3 cells expressing mCherry-tagged Atg9 and carrying a CEN plasmid expressing GFP-Atg8 were grown at 23°C in SDC and then shifted to SD-N for 2 h at 24°C or 37°C. Cells were analyzed by fluorescence microscopy. Scale bar, 5 µm. Scale bar for inset is 0.6 µm.
Quantitative RT-PCR expression analysis of miR-17 in human CD34+ thymocyte progenitors after 5 and 2 days, respectively, of coculture on OP9-DLL1 stromal cells in the presence of 5 µM DAPT (GSI). Graphs show mean expression, relative to the sample cultured in the presence of control DMSO (F) (n=2 independent experiments with different donors; error bars indicate SEM - the two data points are shown).
G, Metabolic reactions of glycolysis and the urea cycle; differentially expressed (treated patients vs. healthy tissue; Benjamini-Hochberg-adjusted p < 0.1) enzymes are highlighted in red. An empirical Bayes moderated t-statistic was computed from a gene-wise linear model fit with generalized least squares , comparing treated patients (n=4 samples), which cluster closely with the mouse samples (encircled in f), with healthy breast tissue (n=10 samples). Differential expression data from mouse in vitro transcriptome data of residual versus normal samples (RNA-seq; normal, n=8; residual, n=4) are shown (two-sided Wald test (Love et al., 2014), Bonferroni-adjusted p < 0.1).
The relation of synaptic Ca2+ influx (B) and glutamate release (C). The bold lines show the means. (See also Appendix Fig S9 for individual plots)
WB analysis of smc5-AID clones in the absence or presence of Auxin using FLAG. Tubulin is used as loading control and wt cells is used as a negative control for the FLAG tag.
G Six-week-old C57BL/6N male mice were intravitreally injected with Sema3C-Fc (right eye) or control IgG-Fc (left eye), and retinae were collected 2 days later. The retinal vessel network was examined with CD31immunostaining. Scale bar, 100 μm (upper panel) and 20 μm (lower panel). Representative images of four retinae per group.
(A) Brains from E12.5 Foxg1 Cre MCL‐1 animals were analysed by western blot for the presence of the caspase‐cleaved fragment of the caspase‐3 substrate p130CAS and the autophagic markers LC3 and p62.
A. Overlap between Myc ChIP-seq peaks. For each time-point indicated at the bottom, the percentage of peaks overlapping over ≥1 bp with any other time-point (Reference sample) is reported. Peaks showed consistent distributions along the time-course, almost all those called in untreated cells being included in LPS-stimulated samples
A549 cells expressing either control shRNA or p53 shRNA were infected with lentiviruses expressing Flag-tagged full-length or truncated WDR63 proteins as indicated. Cells were then subjected to transwell invasion (F) assays. The shown images are representative of three independent experiments. Data shown are mean ± SD (n=3). *, P ˂ 0.05; ***, P ˂ 0.001; One-way ANOVA. Scale bar: 100 μm.
(D) dS6K activity in larval protein extracts measured by H2B target phosphorylation and (E) corresponding western blot of dS6K in the trans-heterozygote LBD-mutant combination (LBD), as compared to heterozygous larvae (Co).
(A) Volcano plot of up - (log2-fold change for transcripts with counts per million, CPM >1; red dots) and downregulated (log2-fold change CPM <1; blue dots) transcripts in LV after Cand2 KO. Differential expression analysis performed with edgeR; Benjamini-Hochberg method for p-value calculation, cut off 0.05. Cand2 and Grk5 marked among depleted transcripts in Cand2 KO vs. WT mice. Enrichment of Kyoto Encyclopedia of Genes and Genomes (KEGG Pathways) terms for differentially expressed genes in LV of Cand2 KO vs. WT mice.
A: Diamide is inducing the SUMO E1~E2 disulfide but not ATM phosphorylation. U2OS stable cell populations were depleted from endogenous Ubc9 by siRNA for 72 h before addition of 500 µM diamide or 500 µM H2O2. Cells were subsequently washed in PBS with 20 mM NEM and lysed in Laemmli buffer. The lysates were resolved by SDS-PAGE.
(H) Percentage of feeding, water intake and activity in the light time. (n=8 for each group). Data information: The data are representative of three independent experiments (mean ± s.d.). *: P<0.05. **: P<0.01 by unpaired student's t test.
(D) Quantification of electron microscopy imaging. Three independent experiments were quantified. Mitochondria were counted (cWT n = 232, PEX3-/- n = 266, and PEX3-/-+ATAD1 n = 257) and binned into 3 categories: mitochondria with many cristae and low electron density (Type 1), mitochondria with fewer cristae (Type 2), and mitochondria with high electron density and/or almost no cristae (Type 3).
(a) HEK293 cells were transfected with AMBRA1 or the empty vector, as a control. ULK1, AMBRA1 and actin were analysed by western blotting.
C and E. The oxidized mitochondria with the radioactive single-cysteine Bax proteins were prepared, subjected to Na2CO3 extraction, and analyzed as in Figure 1D.
B. Raw 264.7 macrophage cells transfected with eGFP(N-term)-Rab10 and Flag(N-term)-LRRK2 were sequentially lysed mechanically into buffer to create a 'soluble' protein fraction, and then insoluble material lysed into triton X-100 buffer to create a "triton x-100" fraction. The "soluble" and triton X-100 buffer solubilized fractions were analyzed using SDS-PAGE (TGX gels), and representative immunoblots from n=3 independent experiments are shown.