EMBO/sd-character-level-ner huggingface dataset:
(G-I) Simultaneous expression of Y701F-STAT1 did not induced any further change on basal synaptic transmission (I/O curve) compared with expression of hTau alone, recorded in hippocampal CA3 (G). LTP magnitude was calculated as the average (normalized to baseline) of the responses recorded 40-60 min after conditioning stimulation. (I). (n=5 slices from 4 mice for each group). Data information: Data were presented as mean ± SD , two-way analysis of variance (ANOVA) followed by Bonferroni' s post hoc test *, p<0.05, **, p<0.01, ***, p<0.001 vs eGFP or hTau; #, p<0.05, ##, p<0.01 vs hTau.
C Numbers of T and B cells found in the blood of WT and Arhgap45-/- mice. Data information: In the results for each mouse are shown as a dot and correspond to three to four experiments involving a total of 12-25 mice. * P ≤ 0.033, ** P ≤ 0.002, *** P ≤ 0.001, **** P ≤ 0.0001; unpaired Student's t test. Mean and SEM are also shown.
(A) Immunoblot analysis and quantification of pTFEB S211 in HeLa cells stably expressing TFEB-GFP. Data are presented as mean ± SD, ***: P ≤ 0.0001, as determined by ANOVA (n=3 biological replicas ). GAPDH immunoblotting was performed as a loading control.
A. Representative images of mouse hippocampal neurons transfected with either GFP-expressing control or Lrig1 shRNA vector at 9 DIV and maintained for 3 additional days in vitro (9+3 DIV). Scale bar, 15 m. Boxed area represents a higher-magnification image showing the profuse proximal dendritic arborization of Lrig1-shRNA transfected neurons.B. Sholl analysis of the dendritic arbor from hippocampal neurons transfected with either control or Lrig1 shRNA-GFP vector at 9 DIV and maintained for 3 additional days in vitro (9+3 DIV). Data are shown as mean SEM of n=3 independent experiments. *p<0.05 and **p<0.01 by two-way ANOVA followed by Bonferroni multiple comparisons test.C-G. Quantification of primary (C), and secondary (D) dendrites as well as total dendritic branching (E), terminal dendritic points (F), and total dendritic length (G) of hippocampal neurons transfected with either control or Lrig1 shRNA-GFP vector. The results are shown as mean SEM of n=3 independent experiments. *p<0.05 by Students t test.
(F) HeLa cells infected with control or PAQR3-overexpressed lentivirus were treated with GS for 4 h. PI(3)P levels were determined as in Figure 2E(n = 5; **p < 0.01; ns, not significant).
PC and PC biosynthesis have become obsolete (blurred). The inhibition of Acc1 (highlighted in red) is essential for shortening average acyl chain length, which in turn is required for maintaining the physical properties of membranes faced with excess PE. The decreased non-bilayer propensity of PE is indicated by its reduced conical shape.
F. GFP IPs from U2OS cells transfected with indicated REV3-GFP expression constructs were immunoblotted with indicated antibodies.
B. FCS analysis yields a fluorescence autocorrelation function (G(τ)), which reports the average number of fluorescence molecule, N (N is inversely proportional to the correlation function amplitude G(0)) , and the mobility parameter of the molecules diffusing through the diffraction-limited volume (τD is the translational diffusion time, and D is the diffusion coefficient). Faster mobility correlates with smaller τD.
A 601-nucleosomal arrays were incubated in 0.5, 5 mM MgCl2, 5 mM MgCl2 + MNase, and analyzed by the differential centrifugation assay to determine the fraction oligomeric. The amounts of DNA in the supernatant fraction were measured. Note that for the MNase-digested oligomers the supernatant fraction also includes the digested free linker DNA. Each value is the mean of three measurements and the error bars represent the standard deviation.
% of telomere FISH signal loss in 30 months old wild-type mice and late generation Terc-/- mice (6 months old) in comparison to 4 months old wild-type mice. Data are from n=3 mice. >100 CMs were analysed per mouse.
E. Representative western blot of AKT phosphorylation in liver 7 minutes after intravenous injection of PBS or 1.5 U/kg insulin in control (n=3) and Rbpji∆EC (n=3) mice five weeks after recombination. F. Densitometric analysis of western blot in E. n=3, data represent mean ± SEM, unpaired t-test.
(D) HeLa GFP-LC3 cells were transfected with the indicated myc-tagged SNX18 constructs for 16 h, starved for 2 h, and analyzed by confocal imaging. Bars, 10 µm.
Wild type and rad9∆ cells were synchronized in G1 and released into S phase with the addition of pronase in medium containing IdU and 200 mM HU to activate the DRC. Then, DSBs were induced by the addition of 100 μg/ml Zeocin to activate the DDC. HU was washed away 45 minutes later to inactivate the DRC and cells were resuspended in fresh medium containing CldU and 100 μg/ml Zeocin, in order to keep the DDC active. Samples were collected at the indicated times.
THP-1 derived macrophages were infected with the wildtype (Wt) and ΔF2 H5N1 (VN) virus at MOI 10. Viral protein expression for PB1-F2 (A) was detected by immunoblotting at 24 h post-infection (hpi) Equal loading was confirmed by detection of beta actin.
Tukey box plots of the mean cLuC ratios (C) obtained from PPI experiments with wild-type CSPα-mCit-PA and its mutant variants.
MECP2-KO cortical organoids plated on MEA (K; left: schematic depicts process of plating organoids on MEA; right: top-down view of organoid on MEA; scale bar = 200 µm) showed decreased population spiking
E. HeLa cells transfected with indicated siRNAs were treated with 5-azadC and/or SUMOi in late S phase as outlined in (A). Cells were then collected at the indicated times after 5-azadC withdrawal and analyzed by flow cytometry. Data are representative of three independent experiments. Proportion of cells with G2/M DNA content is indicated.
h, Representative haematoxylin and eosin images of Xbp1Dgr;PC and wild-type mice scored in i. Scale bars, 50 µm. i, Enteritis scoring in Xbp1fl/fl (WTfl), Defa6-cre+ (WTcre) and Defa6-cre+;Xbp1fl/fl (Xbp1Dgr;PC) mice (n = 21/26/29; median shown; Kruskal-Wallis with post-hoc Holm's-corrected Mann-Whitney U-test). Results represent two (b, d) independent experiments. *P 0.05, **P 0.01, ***P 0.001.
(I-J) ICP-MS quantification of total (I) and protein-bound (J) iron in mouse quadriceps (n=4-5). Data information: For all data, n represents the number of biological replicates. Statistical significance was calculated by unpaired, two-tailed Student's T-test. Data are mean ± SEM. ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001.
(A, B) A free energy diagram of the transport cycle (black) and its modulation (colors) by positive or negative allosteric modulators, PAMs (A), or NAMs (B), respectively. Cartoon representations of the low-energy states are below the diagrams and are colored as in Figure 1. The barrier heights are not to scale to the measured rates. Substrate binding to the apo OFS precedes isomerization into the IFS via the highest-energy TS (‡) that structurally resembles the IFS. Substrate release and recycling into the OFS complete the cycle. PAMs, shown as squares in the cartoons of the states, bind with higher affinity to the IFS (dark cyan squares) than to the OFS (light cyan squares). Therefore, they stabilize all IFS-like states, including the TS, and smoothen the energy landscape (cyan line). PAMs that bind too tightly to the IFS may become inhibitory, as apo OFS becomes a high-energy state (dotted blue line). NAMs bind tighter to the OFS ((B), dark magenta squares) than to the IFS (light magenta squares), increase the ruggedness of the landscape (magenta line), and slow down transport.
(E) HeLa cells expressing HA-Parkin with various pathogenic mutations were treated with CCCP, followed by immunocytochemistry. (A, D, and E) Higher magnification views of the boxed areas are shown in the insets. (F) Parkin colocalization with mitochondria was analyzed in >100 cells per mutation. Example figures indicative of robust colocalization (counted as 1), weak colocalization (counted as 0.5), and no colocalization (counted as 0) are shown. Error bars represent the mean ± SD values of at least three experiments.
A Schematic diagram shows how the SunTag-JARID1A system is recruited at the SNCA promoter. The dCas9-5xGCN4, scFV-JARID1A, and sgRNA plasmids are co-overexpressed in the cells. The dCas9-5xGCN4 is recruited to the SNCA promoter as directed by the specific sgRNA. Five scFV-JARID1A molecules in turn recognize the GCN4 polypeptide sequences of dCas9. Upon recruitment of the entire system, SunTag-JARID1A demethylates H3K4me3 at the target region.
A) ROC curve shows the capability of plasma oxLDL concentration in discriminating ACM vs. HC subjects (data as in Figure1A). The red dot shows the point where the difference between sensitivity and specificity is minimized; this value, corresponding to the oxLDL cut-off = 86 ng/ml, was used to part the whole ACM cohort in two subpopulations.
(B) The stiff or soft cells were isolated from ALDH- or ALDH+ 4T1 cells by microfluidic chip. Then, these cells were injected into the mammary fat pads of NSG or BALB/c mice mice (100 cells/mouse). Twelve weeks later, the tumor formation was recorded. n = 10.
F) Expansion of a vacuolar fusion pore in real time. pmc1∆/vcx1Δ cells were labeled with FM4-64 and immobilized in a 50 µL flow chamber (Ibidi). The osmotic value of the medium was changed by perfusion with water, using a pump with a flow of 30 µL/s. A frame was acquired every 2 s for a total period of the 30 s, using the laser at minimal intensity.
(D) Consequence of SIX4 depletion in PEO1 cells on E-cadherinplasma membrane accumulation 48 hours after transfection. Cells were counterstained with phalloidin and DAPI.
D) UCSC genome browser shot of the human IL3/CSF2 locus showing DNase-Seq and ChIP-Seq in CD4 TN and TB with (red) and without stimulation (black) with PMA/I for 2 hours, plus the ENCODE Jurkat T cell DNase-Seq data (Thurman et al, 2012b). Black arrows represent stable DHSs and red arrows are inducible DHSs, with the distances in kilobases of the DHS from either the IL3 or CSF2 promoters.
A Dose response curves of ID188 (p27-29) and ID211 (p26-28) organoids treated with FOLFIRINOX over three days. ATP was measured with CellTiter-Glo assays. Shown is the mean ± SD of three independent experiments.
C Elongation response of seedlings of the indicated lines grown for 7 days in continuous W or 2 days in W then transferred for 5 days to W+FR (R:FR, 0.02). The mean hypocotyl length in W (HypW) and W+FR (HypW+FR) of at least four biological replicates was used to calculate HypW+FR-HypW. Error bars represent SE. Data information: Different letters denote significant differences (one-way ANOVA with Tukey test, p-value <0.05) among means.
(A) NF-κB activation during MZT. Immunofluorescence staining of p65 shows nuclear translocation of p65 at the two-cell stage and thereafter. Scale bar = 25um.
E HUVEC transduced with lacZ or with SHP2 were either untreated (-) or treated (+) with thrombin for 30 min followed by immunoblotting either VE-cadherin immunoprecipitates or cell lysates for the indicated antigens on the right.
D-E WT donor derived Gr, B, CD4 T, and CD8 T cells in the peripheral blood Data information: Data are shown as percentages of the total number of white blood cells (WBCs). Data were collected at month 7 post transplantation for the uMT-/- group and month 8 post-transplantation for the NSG group, and presented as mean ± SEM. n=7 mice for the uMT-/- group and n=6 for the NSG group. *p<0.05, **p<0.01, ***p<0.001 (two-tailed and two-sample equal variance Student"s t-test)
Quantification of actin levels from Westernblot of whole CO lysate reveals a reduction in ECE2 KO COs (n=4 independent batches of CTRL and ECE2 KO COs with 3 pooled COs each sample; *P = 0.021 in Kruskal-Wallis One Way Analysis of Variance on Ranks and Dunn's Pairwise Comparison).
Ribbon diagram of the VgrG and Tle1 pseudoatomic structure, coloured according to the chain and in different orientations
E Bioenergetic profiles measured with Seahorse flux analyzer showing the contribution of OCR and ECAR to cellular bioenergetics upon the aforementioned treatments. Data represent the mean ± SEM of n=3 independent experiments.
D-F, Adipose tissue measurements on hematoxylin-eosin (H&E)-stained adult zebrafish sagittal sections. (D) Adipose tissue area per total section area (average of three sections/biological replicate) and (E) adipocyte size (average of 20-30 adipocytes of ventral adipose tissue per biological replicate) (Δ1 +/+ n=3, Δ2 n=8). scaf1Δ1 and scaf1Δ2 are represented with circles and squares, respectively.
B MDA-MB-231 cells were treated with the indicated amounts of P5091 for 48 h, LSD1 protein levels were assessed by immunoblotting.
q-RT-PCR reveals upregulation of miR-181a/b targets in the eyes of miR-181a/b-1-/- vs. miR-181a/b-1+/+ animals. n≥5 animals/genotype.
A Overlap between differentially expressed (DEG) and spliced (DAS) genes in RNAi-ASCO and 35S:ASCO as compared to WT.
A Live cell imaging reveals that expression of GFP‐KSHV‐TK, but not GFP induces contraction of HeLa cells (see Supplementary Movies S1 and S2). The time from the start of imaging is indicated above each panel, and the scale bars represent 18 μm. Quantification of GFP‐KSHV‐TK‐induced cell contraction. The graphs show cell area (μm2) of cells expressing the indicated protein, and error bars represent SEM from three independent experiments in which n = 224 for GFP and n = 203 for GFP‐KSHV‐TK. ***P 0.001.
(C A549 cells were infected with S. pneumoniae R6 WT or ΔcbpC for 2 h and fixed and stained with DAPI and an anti-Atg14 Representative epifluorescence images are shown. Scale bars, 10 µm. The percentages of perinuclear-localizing Atg14 containing cells were quantified.
A | Schematic overview over the procedure of mouse immunization with 2,4,6-trinitrophenyl hapten conjugated to ovalbumin (TNP-Ova) and analysis of germinal center (GC) reactions at different time intervals. Control animals were injected intraperitoneally (i. p.) with PBS and quantified as day 0 of immunization.
Physical appearance of wild type (WT), Wwox null injected either with AAV9-hSynI-GFP (the control virus) or AAV9-hSynI-mWwox-IRES-GFP virus at P17.
(D,E) Proportion and numbers of locally transplanted CD45.2+ST2+ ILC210 in islet grafts of islet transplant mice over time. Data shown are the mean ± SEM (n=4-5 per group) and a one-way ANOVA was performed, **P<0.01, ***P<0.001.
F. Quantitative TMT-based proteomic analysis of control and patient fibroblasts. Proteins from three control and three patient fibroblast cell lines were TMT-labelled, quantified and analyzed separately as described in Materials and Methods; the data from control and patients were averaged after the analysis and presented as -log10 of the adjusted p-value vs log2-fold change (logFC). Mitochondrial proteins were selected according to human MitoCarta 2.0 (Calvo et al, 2016) and highlighted in blue; lysosomal proteins were selected according to hLGDB database (Brozzi et al, 2013) and highlighted in yellow.
A. Yb bodies (Yb in green) disappeared after 1,6-hexanediol treatment of OSCs, as did P bodies (Dcp1 in red). Nuclei are shown in blue. Scale bar: 5 μm.
A: Cal27 or JHU029 cells were transfected with control or ELDR siRNA, and EGFR mRNA expression was examined by qRT-PCR. 18S gene was used as internal control. n = 3 biological replicates and 3 technical repeates.
Western blotting showing accumulation of CMV CP in systemically infected leaves at 14 dpi. Bottom values represent relative accumulation (RA) of CMV CP. RbcL served as loading controls.
C. Apparent decrease in insertion efficiency for the TMD mutant version. While the WT otoferlin glycosylation amounted to 3.84 ± 0.53, the TMD mutant had only 2.13 ± 0.65 (n=3, p<0.05). Data are represented as mean ± SEM.
a-e) 16HBE cells were stably infected with lentiviral vector pLKO alone or expressing EMP1 shRNAs (1 or 2). All data are representative of n=3 independent experiments. (a) Total RNA was isolated and analysed for EMP1 expression using Taqman/qPCR with a GAPDH control. Wild type cells treated with 500nM GSK1120212 or siSOS1 for 4 days were also analysed. Error bars denote mean ± SEM, dots indicate individual data points. ***, p <0.0002 (GSK = 0.0002, siSOS1 = 0.0001); ****, p <0.0001.
(G) Confocal immunofluorescence microscopy of cleaved caspase 3 (red) in MM cells treated for 24 hours with MTX (1 μM) or increasing concentrations of BoxA. Nuclei were stained with Hoechst (blue) and cytosol with phalloidin (green). Scale bar 50 μm.
(B) Global increase in RNA Pol II signals after silencing of DDX5 (lv-shD) in HGC-27 cells. Average RNA Pol II ChIP-seq signal at all RNA Pol II peak regions. Upper subpanel: negative control, Lv-NC; lower subpanel: silencing of DDX5, lv-shD.
(f-i). Drp1 is dispensable for recruitment of parkin to mitochondria. Drp1WT and Drp1KO HeLa cells were transfected with GFP-parkin. Cells were treated with 150 μM actinonin for 6 hours (h), followed by immunodetecting mitochondria (TOM20, red) and parkin (GFP-parkin, green). Nuclei were labeled with DAPI (blue). Cells treated with solvent (DMSO) were used as a treatment control. Representative images were shown, scale bar=25 μm. Cell with mitochondrial parkin (%) in different experimental group was quantified (g, i). One-way ANOVA followed with Tukey's test. ***p<0.001, ns: no significance. Data was presented as mean ± SEM of three independent experiments. For each condition, >100 cells were analyzed.
F, G Representative TEM images of EP4i-treated spheroids. (F) The basal plasma membranes are outlined in orange solid lines, lateral plasma membranes are indicated with orange arrowheads, and nuclei are outlined with wide yellow dashed lines. Insets show a magnified view of the apical cell surface. (G) Higher power image of the cytoplasm. Single mitochondria are outlined with a narrow blue dashed line, vacuole structures are indicated with red asterisks. Scale bars, 1 µm.
Glial neurotrophic functions potentiated by SGK1 downregulation were mediated in a paracrine manner. VM-glia transduced with sh-Sgk1 (or sh-cont as a control) were challenged with H2O2+LPS for 3hr or not. Glial conditioned medium (GCM) was prepared in each glial culture condition and administered to mDA neurons primarily cultured from mouse VM (E) Cell viability of the neuronal cells was estimated using CCK8 assays and TuJ1+ cell counts. Data are represented as mean ± SEM. n=3 cultures; One-way ANOVA. Significantly different at p=0.0002*, 3.29E-08**, 0.0003***, 3.66E-06#, 0.0029## (TuJ1+ cell counting), 0.0127+, 5.98E-06++, 0.0002+++, 0.0005&, 0.0078&& (CCK8 assays) in graph E.
(C) ChIP samples from (B) were analysed by qPCR. Shown are averages (bars) of 3 independent experiments (dots)
D. CACNA1A is concentrated in the lysosomal fractions isolated from mice cerebella with iodixanol gradient.
(C) Airyscan analysis of Saos2 cells expressing GFP-LC3 (green) and immunolabeled for PC1 (405, blue) and CANX (647, red). The insets show higher magnification (x5.26) and single colour channels of the boxed area. Scale bar = 10 µm.
representative images of MyHC immunofluorescence (N), fusion index (O) and the distribution of nuclei per myotube (P) in C2C12 myocytes transfected with mGPDH plasmid with the AMPK inhibitor CC a 72 h (N-P) after differentiation
(K) neutrophils migrated in the presence of 10 nM CXCL12 alone and with 10 nM Gal-3, Gal-3 CRD and Gal-1
(B) LMP1 protein expression was evaluated by confocal microscopy in pDCs untreated (un) or infected by EBV−GFP. Right panels show the corresponding cells by using traditional differential interference contrast (DIC) microscopy. One representative experiment is shown out of three performed, having similar results. Scale bar: 20 μm.
(B) Quantification of AURKB gene transcripts in isolated fibroblasts from non-IPF and IPF lung stromal cell cultures. **P < 0.005, unpaired t-test, (n=6).
(c) Basal and maximal O2 consumption rates in cells as described in b. *P0.05 (mean±s.e.m.; n = 3).
(F) Graphic displays that ALYREF interacts with Lsm11 and facilitates U7-snRNP recruitment.
A) Schematic illustration of the sample collection. Samples were collected from eight different patient tumors. For each tumor, sections were processed with hematoxylin & eosin (H&E) staining to locate different growth patterns of lepidic (low-grade; group 1), acinar and papillary (intermediate grade; group 3), and solid and micropapillary (high-grade; group 3). Two to four growth patterns per tumor were selected and sectioned in two consecutive 5 μm iterations, to provide replicates with highest possible similarity, resulting in a total of 51 samples (one iteration was missing).
(A) Selection of Beclin‐1 fragments that interact with Bcl‐XL/Bcl‐2 in the yeast‐two‐hybrid system. Black lines indicate the fragments of Beclin‐1 (grey) that interact with Bcl‐XL (upper part of the graph) or with Bcl‐2 (lower part). ▪, CEMC7 library; •, human thymocyte library; ▴, placenta library and ★, human brain library. The minimal interacting domain required for interaction with Bcl‐XL/Bcl‐2 is situated between aa 112 and 159.
(A) Quantitation of Tollip vesicular clusters in SH-SY5Ys treated with 5 μM antimycin A/10 μM oligomycin B (AO) for 2 hours. The percentage of cells with vesicular clusters were quantified from 7-23 cells for each condition from 4 independent experiments.
F, G Knockdown of Nurr1 and Foxa2 synergistically aggravates H2O2-induced cell death of mDA neurons in culture. Representative image for Nurr1- and Foxa2-co-expressing mDA neurons (F) used in the loss-of-function study. Shown in right panels are the individual Nurr1-, Foxa2-, and TH-stained cells of the boxed area. Nurr1- and Foxa2-co-expressing mDA neurons were formed after 9 days of differentiation in VM-NPC cultures in vitro and transduced with lentiviruses expressing shNurr1 (shN), shFoxa2 (shF), shN + shF (shNF), or shControl (shC). Three days later, the cultures were treated with H2O2 (500 μM) for 8 h and cells positive for TH (upper) and cleaved (activated) caspase-3 (lower) were counted the following day (G). Insets, high-power TH+ cell images of the boxed areas. Significantly different from the control (shC)*, shN#, shF‡ at P < 0.05, n = 5 culture wells in each group. P-values: 0.038 (shN*), 0.026 (shF*), 0.013 (shNF*), 0.036 (shNF#), and 0.042 (shNF‡) for the % TH+ cells; 0.043 (shF*), 0.037 (shNF*), 0.019 (shNF#), and 0.029 (shNF‡) for the percent cleaved caspase-3-positive cells; one-way ANOVA followed by Bonferroni post hoc test.
Venn diagram showing the overlap between FOXA1/2-regulated genes in CFPAC1 and PANC1 cells.
A, B) Infectious virus titers can be observed by virus titrations on VeroE6 cells of apical washes at 2, 24, 48, and 72h after infection of bronchioalveolar-like cells from donor 1 (A) and donor 2 (B) at MOI 0.01 (red) or 0.1 (black) with SARS-CoV-2. The dotted line indicates the lower limit of detection. Error bars represent SEM. N=4 for all except donor 2 MOI 0.1, which is N=3. H p.i. = hours post infection.
E) Bar graphs showing the mean amplitude change (left axis) following 18°C exposure for 5h for each group of plate well profiles (grouped according to their distinct phase (a-f) prior to 18°C exposure, 10 wells per group) for both WT and KO cells from biological repeats 1 and 2. Mean changes are plotted to approximately align with the position of the control profile at the point of rewarming within the circadian period that is represented by the PER2:LUC (dashed line) and predicted REV-ERBα expression level (right axis) (grey shaded region (light grey indicates REV-ERBα deletion)).
C SOD activities were down-regulated by in vitro N-homocysteinylation. Flag-tagged SOD1, SOD1K23W,K122W,K128W (3KW) mutant, SOD2, and SOD2K44W, K51W,K98W,K106W,K178W (5KW) mutant were expressed in HEK293T cells, affinity purified, and incubated with or without 10 μM HTL in solution (in vitro). After 12 h, the reaction mixture was desalted and concentrated with filter tubes. N-Hcy levels and SOD activities were determined and normalized to untreated WT SOD1 and SOD2, respectively (n=4). Data are presented as the mean ± SEM and were compared using an unpaired Student's t test. nsnot significant, **P ≤ 0.01, ***P ≤ 0.001. One-way ANOVA with Dunnett's correction was used for multiple comparisons.