EMBO/sd-character-level-ner huggingface dataset:
A, B, E, F Immunoblot analysis with indicated antibodies of protein extracts prepared from root tips of 10-d-old Arabidopsis WT heat-stressed seedlings (39ºC) 0, 20, 40 and 60 min after the onset of HS. For CHX treatment in B, the seedlings were pre-treated with 200 ng μL-1 CHX for 30 min before HS. The charts show SnRK1 activity, expressed as the ratio of phosphorylated to total SnRK1 protein. The data represent mean ratios of integrated band intensities (for both isoforms) normalized to 0 min ± SD from at least four different experiments. P values denote statistically significant differences for comparisons to 0 min (two-tailed t-test).
F Paraffin-embedded sections of WAT and BAT from WT and FADD-D mice were stained with H&amp;amp;E. Scale bar = 50 μm. Shown are typical results from four different fields and three different experiments.
C. Gross morphology of testes from adult mice at 3 months postnatal with mutated MLS compared to their wild-type littermates.
NAT4 expression levels and N-terminal acetylation on Histone H4 are reduced under Calorie Restriction conditions. Lower levels of N-acH4 affect the methylation status at H4R3, with this arginine being a key regulator of the lifespan extension induced by the CR pathway. Under these conditions several stress-response genes, including PNC1, are induced. Lifespan extension is probably an effect of increased Pnc1 activity and the hormesis effect caused by enhanced stress protection previously described. Calorie Restriction also extends lifespan through rDNA stability and decrease in translation, pathways that are independent of Nat4.
(A) Tumor growth curve after later passage ICL cells were injected into flanks of athymic nude mice (n = 5 per group and error bars denote SD, p<0.0005 for Ch9, p<0.05 for Ch10 and p<0.005 for Ch14).
(B) Immunofluorescence microscopy experiment to determine transfection efficiency.
, F The percentage of cells with cGAS foci was quantified, n = 3 biological replicates (F). Data information: Error bars, mean with s.d.
A Representative fluorescence images showing the SHG signal from cross-linked collagen in untreated, LOX antibody-treated or isotype control-treated organotypic cultures of primary fibroblasts and rat tail fibrillar collagen I.B Chart showing the percentage of cross-linked collagen by depth, based on SHG signal, in organotypic matrices treated as indicated. Error bars indicate SEM.C Barchart showing total cross-linked collagen in organotypic matrices treated as indicated. The experiment was performed in triplicate with three different zones imaged for 80 μm, at 2.5-μm sections each. Data are shown as total pixels ± SEM.
F Upregulation of MAPK and YAP target genes in mouse intestinal organoids after induction of oncogenic BRAF. Wnt target genes is not significantly affected. For experimental details, see Riemer et al. (2015). Graph displays data points for signature gene expression values, mean and standard deviation. **** indicates p value of <0.0001 in two-tailed paired t test of gene expression ratios (luciferase control versus BRAF-induced). n.s.: not significant.
BMDMs were stimulated with TNF (100 ng/ml) in combination with TAK1i (125 nM) for the indicated time points. mixed supernatant and cell extracts were analysed.
Representative Ca2+ signals in sperm from a patient with deafness-infertility syndrome lacking functional CatSper channels (CATSPER2-/-) (red) and a healthy donor (black), evoked by progesterone, PGE1, NH4Cl, or ionomycin. NH4Cl increases the intracellular pH. Bar graph: Amplitudes (n = 4; mean ± SD) of Ca2+ signals in CATSPER2-/- sperm
B. Two views showing the conformations of the Sec61 complex (green) with the signal sequence (ss; red) bound to the lateral gate (upper panels) and in the apo state. The two Sec62 TMs (orange) are stabilized in ss-bound state. The plug is indicated by "P" in the apo state.
C, Confocal microscopy image of cryostat sections of C57BL/6J recipient retinas 21 days after transplant of C57BL/J6 photoreceptors infected with empty vector (n=5), RHOA overexpression (RHOA OE) (n=7) or RAC1 dominant negative (RAC1 DN) (n=7) lentiviruses. Quantification of MT in retinas transplanted with control, RHOA and RAC1 DN lentiviruses.
G Excess of GRIp65-84 (10 μM) but not of GRIp31-96 or other peptides (GRIp31-51, GRIp47-68, GRIp80-96) competed the binding of 0.46 nM 125I‐Y‐GRIp65-84 to membrane extracts from Col‐0 (all bars show the average of two samples, triangles show individual data points).
I The levels of Ras, c-Raf, pMEK, ERK, pERK and p-P90RSK in Caco-2 cells treated with Control-Fc, Spike RBD-Fc or Spike RBD-Fc combined with SCH772984 by Western blot. Protein expression was normalized to β-actin. Data are from 3 independent biological experiments. Data information: All data are shown as mean ± SD. for (I), P values are determined by one-way ANOVA.
C) Disease symptom development in Pst-infected lines with estradiol inducible constructs of ind-MKKK7AA L8, ind-MKKK7AA L10, ind-MKKK7DD L1 and ind-MKKK7DD L3. Two independent transgenic lines for each construct were grown under short-day conditions and disease symptoms were scored 3 dpi. Data represents mean values ± SEM (n=20; *, p<0.05; **, p<0.01; paired t-test). The vertical axis represents the percentage disease symptoms. Experiments were done at least twice with similar results.
Heat map of the most regulated genes per cluster (adjusted p-value < 0.05 based on the negative binomial distribution). Clusters are arranged from the left to the right and represent microglia (light green), macrophages (purple) and monocytes /granulocytes/lymphocytes (grey). The scale bar represents color-coded z-scores. Genes that were subsequently confirmed on protein level in h) and i) are highlighted by asterisks.
A. Heatmap of selected proteins that were significantly downregulated in BMDMs from Tpl2[D270A] mice relative to WT (P < 0.05). Selected hits were grouped into clusters according to their molecular functions.
RPE1 cells were depleted for p53 in combination with the indicated proteins by siRNA, in conditions used for the primary screen (2 Gy of IR). Mitotic entry was analyzed by MPM2 and PI staining by flow cytometry. For normalization see materials and methods. Error bars represent the SEM of three independent experiments.
H. Genomic DNA was sheared to fragments by Biorupt (left). EMSA analysis of hTrmt13 and DNA fragments (15 ng/μL DNA was used).
(C) Analysis of chromosome spreads after auxin and EdU treatment and Giemsa staining.
Abolition of PTENε expression by disruption of the palindromic motif. (E) Disruption of the CUG816 downstream palindromic motif by mutagenesis.
Indicated cell lines were treated as depicted in Figure 2. Data are depicted as mean +/- standard deviation of three independent biological experiments. Statistical significance was determine by two-tailed Student"s t test where *=p<0.05, **=p<0.01,***=p<0.001, ****=p<0.0001. LNCaP: E2F1, p=0.0159; PCNA, p=0.0217; MCM7, p=4.0936e-6; CCNA2, p=0.0005. C4-2: E2F1, p=0.0074; PCNA, p=0.1258; MCM7, p=3.7471e-5; CCNA2, p=0
Schematic diagram depicting the procedure of compound screening during mouse chemical reprogramming.
C. Schematic depicts FBXO7 full length and FBXO7 deletion mutants used in mapping analyses. UbRD = ubiquitin-related domain, FP = FBXO7/PI31 domain, F-box = F-box domain, PRR = proline rich region.
A Comparison of the precursor and polymeric structures of UMOD shows how dissociation of the EHP triggers a major conformational change of the ZP module. This involves a significant rearrangement of the interdomain linker, which not only completely dissociates from ZP-C but also changes secondary structure upon conversion of α1 in the precursor to α1β in the polymer. Molecules are depicted in cartoon representation, with only one subunit of the UMOD precursor homodimer shown; structural elements are colored as in Fig EV1A, with the N- and C-terminal halves of the ZP-N/ZP-C linker colored bright and dark red, respectively.
Gene set enrichment analysis of HMGB1-KD data. Normalized enrichment scores (NES) and associated P-values for each gene set are shown.
Pearson correlation between S1P and apoM (C) Scatter plots, together with the fitted regression line, are shown. Pearson correlation was performed for statistical analysis. Exact p values or ****p < 0.0001 are reported.
C DNA breaks were measured using alkaline comet assay in BRCA2-proficient (+BRCA2) or -deficient (-BRCA2) human DLD1 cells treated with 2 µM pyridostatin (PDS) for 16 hours and released into fresh medium without pyridostatin. Representative images are shown. Scale bar represents 100 µm. D Quantification of DNA breaks shown in (C). Graph and error bars represent the mean and SEM of n = 3 independent experiments. A minimum of 50 cells were analysed per condition per experiment. P values were calculated using an unpaired two-tailed t-test. *, P ≤ 0.05; NS, P > 0.5. E Quantification of γH2AX foci visualised using immunofluorescence staining in cells treated as in (C). A minimum of 200 cells were analysed per condition per experiment. Graph and error bars represent the mean and SEM of n = 3 independent experiments. P values were calculated using an unpaired two-tailed t-test. ***, P ≤ 0.001; NS, P > 0.5.
Number of Us11-GFP expressing neurons at 3 days post-LY294002-induced reactivation in P6 SCG neuronal cultures infected with HSV-1 in the presence or absence of IFNα (600 IU/ml), then treated with an α-ΙFNAR1 neutralizing antibody. n=9 biological replicates. RT-qPCR for viral mRNA transcripts at 3 days post- LY294002-induced reactivation of SCGs infected with HSV-1 in the presence or absence of IFNα. n=9 biological replicates. RT-qPCR for viral mRNA transcripts at 20 hours post-LY294002-induced reactivation in SCGs infected with HSV-1 in the presence of absence of IFNα. n=9 biological replicates.
Expressing a SUMOylation-deficient Fis1 mutant reverses the effect of SENP3 knockdown on DFP-induced LC3-II induction. pcDNA3, Flag-Fis1 WT or Flag-Fis1 K149R mutant was transfected into HeLa cells in which SENP3 was depleted using siRNA for 48 h (Nsi, non-specific siRNA; SENP3i, SENP3 siRNA (I); siRNA concentration, 20nM), and the cells were treated with DFP for a further 24 h (DFP, 1mM). Lysate samples were blotted as indicated.
C Fit of two Gaussian distributions to the peak intensities for peptic peptides 159-168 (left), 169-175 (middle), and 176-189 (right). Representative plots of 3 independent experiments.
Confocal imaging of FITC-labelled GBS A909 strain adhesion to human CC1-expressing or empty vector control HeLa transfectants. Cell membranes were stained with AF-647 conjugated wheat germ agglutinin (WGA) (red) and nuclei with DAPI (blue). Scale bar: 26 μM.
C. Anti-C5b-9 immunostaining of RPE/choroid whole mount preparations 48 hours after laser damage showed strong MAC deposition in the laser lesions of vehicle-injected controls. PolySia avDP20 treatment reduced MAC formation in a dose-dependent fashion independent of SIGLEC11 presence. Scale bar: 100 µm.D. Quantification of C5b-9 fluorescence signal intensity in the laser lesions. In comparison to the high amount of MAC deposition in vehicle-injected controls, the pixel intensity is reduced in polySia avDP20-treated eyes in a dose-dependent fashion and regardless of SIGLEC11 presence. Data show mean +/- SD. *** p< 0.001, One-way ANOVA followed by Fisher's LSD. WT PBS (n = 12 laser spots), WT 0.2 µg Sia (n = 12 laser spots), WT 3 µg Sia (n = 7 laser spots), SIGLEC11 tg PBS (n = 6 laser spots), SIGLEC11 tg 0.2 µg Sia (n = 10 laser spots), SIGLEC11 tg 3 µg Sia (n = 12 laser spots); all statistical comparisons p < 0.0001 except SIGLEC11 tg PBS versus SIGLEC11 tg 0.2 µg Sia p = 0.0004.
H Schematic diagram of LHL1m, LHL2m and LHL12m mutants, which have D1N, D3A, E12N mutations in LHL1 and/or LHL2.
Physical interaction network of proteins significantly upregulated in Fam134 knockout MEFs. The network was generated using the STRING plugin in the Cytoscape environment with a confidence score set to 0.4. Nodes are protein entities while lines represent physical interactions Red, orange, green: Collagen, stress fiber, ER associated.
Proportions and numbers of IFN-γ-secreting CD8+ T cells following restimulation ex vivo with SIINFEKL peptide were quantified. The upper panel of bar charts F) show the percentage of co-stained CD8+ T cells and the lower panel G) the absolute cell counts. Bar charts show mean values (±SEM) from representative experiments (*, p<0.05; **, p<0.01; ***, p<0.001; one-way ANOVA with Tukey's multiple comparison test). See Appendix Table S4 for exact p-values.
(A) Mouse survival curve after MI and sham surgery. The mortality of the WT and Fstl1-cfKO mice after MI surgery was 27.1% and 46.7%, respectively. Log-rank (Mantel-Cox) test was used for statistical analysis (n=16 for WT sham, n=15 for Fstl1-cfKO sham, n=59 for WT MI and n=30 for Fstl1-cfKO MI).
(L) Discrimination index (DI; %) in the novel object recognition test at 6 weeks of age (before pump implantation) and 11 weeks of age (4 weeks after cholesterol infusion) of wt (N=16 at 9 weeks, N=21 at 11 weeks), R6/2 ACSF (N=28 at 9 weeks, N=23 at 11 weeks), R6/2 chol-low (N=21 at 9 weeks, N=13 at 11 weeks), R6/2 chol-medium (N=10 at 9 weeks, N=7 at 11 weeks), and R6/2 chol-high mice (N=18 at 9 weeks, N=16 at 11 weeks). DI above zero indicates a preference for the novel object; DI below zero indicates a preference for the familiar object. Data information: The data are from five independent trials and shown as scatterplot graphs with means±standard error. Each dot corresponds to the value obtained from each animal. Statistics: one-way ANOVA with Newman-Keuls post-hoc test (*p<0.05; **p<0.01; ***p<0.001; ****p<0.0001).
C. Electrophysiological example traces (control = black; hTauAT = red) of excitatory postsynaptic field potentials (fEPSP) depicts examples of depolarizations that are induced by a single high potassium chloride application in stratum pyramidale (s.p.) of area CA3 in slices in which calcium imaging experiments were conducted. The example depolarization evokes averaged calcium influxes into neurons depicted in the calcium imaging graph. The graph shows the mean of [Ca++]i changes in response to high KCl in stratum radiatum and stratum pyramidale of area CA3 in Fura2-AM loaded hippocampal slices. After depolarization [Ca++]i rises up to ~600 nM in hTauAT slices (red trace, n=6 slices, prepared from at least three animals), compared to ~300 nM in control slices (black trace, n=6 slices; prepared from at least three animals). Note that even under resting conditions [Ca++]i is elevated to ~120nM due to hTauAT expression.
(b) Performance of the 5-gene classifier when predicting the class membership of the validation cohort.
C-H Gametangiophore morphology (C, E and G) and gametangium development (D, F and H) of plants with the designated genotypes. Scale bars, 1 mm (C, E and G), 20 µm (D), 50 µm (F), 100 µm (H).
B. Extracts of RPE-1 cells treated with the indicated siRNA for 72 hours, serum starved for the last 24 hours and treated either with DMSO (-) or 10 µM MG-132 (+) for the very last 6 hours. Left: Representative blot. Right: Quantification of MCAK/Uba2 signal ratio normalised to non-targeting control with DMSO of 5 independent experiments. Error bars indicate standard deviation, asterisks the p-value of a two-tailed unpaired Student's t-test (**P < 0.01, ***P < 0.001).
When ZIKA virus infects the pregnant woman, the virus can reach the placenta and transmit to the fetus. In the ZIKV replication cycle, it starts with the virus binding to host cell surface receptors, leading to endocytosis of the virus. Internalized viral particles release the viral RNA into the cytoplasm of the host cell and start replication. During its replication, rISG20-Fc degrades ZIKV RNA and inhibits the subsequent transcription and translation. Therefore, less new virus particles are released from the placenta to fetus.
G) Barplot showing the number of TM specific genes which have an iDHS within 150 kb of the 683 pDHSs.
(D) Strategy to generate Sox4 S316 phospho-antibody (pSox4) by phosphopeptide injection into rabbits.
Formaldehyde survival of wild type (wt), dvc-1, gcna-1 loss-of-function (lof) and gcna-1; dvc-1 double mutant C. elegans (mean±SEM; n=4 independent experiments).
Selected EKAR2G ratio time series illustrating, from top to bottom, sustained, oscillatory, or transient ERK activity dynamics. ER is color‐coded as in bar. Scale bar = 20 μm.
dHepaRG cells were infected with HBV at an MOI of 500 virions/cell, treated with 600 U/ml IFNα or 400 U/ml IFNγ from day 7 to 9 p.i. and stained by immunofluorescence for ISG20 and PML (C) or ISG20 and nucleophosmin (D).
(B) Biofilm formation of Newman WT and isogenic mutant strains after static incubation at 37 °C for 20 h. The histogram shows the amount of biofilm biomass attached to the microtiter plate when cells were grown in MHB-ca supplemented with 10% human plasma, 0.5 % glucose and 2% NaCl. Data are expressed as average ± SD of four independent experiments performed by octuplicates. ** Denotes p < 0.005, ns denotes no significant compared to WT via one-way ANOVA with Dunnett's posttest.
A. Drp1 oligomerization by chemical crosslinking in wild-type CNs with or without rIFN-β for 2 h.
(A&B) Non-biased proteomics of TGFβ-treated naïve (WT) and COUP-TFII overexpressing (COUP-TFII-OE) cells revealed that COUP-TFII promotes the expression of proteins enriched in metabolic process critical for myofibroblasts, in particular, suppression of FAO and enhancement of glycolysis. Top pathways ranked by NES (gene set enrichment with FDR < 0.05) altered in COUP-TFII-OE compared to naïve C3H10T1/2 cells (n=2).
B. Theoretical distribution of root growth computed when NEZ correlates with 1/ln(rEZ) (as in panel C) and when it does not (as in panel D). In the correlated case, the values extracted for real wild type plants for Rprod, l0EZ , rEZ and NEZ were used (n=24, white symbols in panel C). For the non-correlated case, the real values of rEZ and NEZ were randomly coupled in pairs and the Rprod ,l0EZ values for the associated rEZ were used.
Cytokine secretion of macrophages incubated with the indicated stimuli for 24 h. RBCL, iRBCL, XO were added to macrophages for 24 h. Each symbol represents the value obtained for cells from an independent donor in an independent experiment. Insets show paired samples by donor in two different conditions. Blue asterisks indicate significance when values were compared with RBCL (a) n=7 One-way ANOVA with Tukey test for multiple comparisons was performed to determine statistical significance (*p<0.05, **p<0.01 and ***p<0.001).
B. The size of hearts isolated from Ctrl or FIJs-treated mice; heart/body weight ratio of Ctrl or FIJs-treated mice.
(B) Heat map indicates which TFs significantly affects hypocotyl length, root length and the composite trait of root to total length in dark-grown seedlings and whether the effects of TFs are dependent on condition. TFs are hierarchically clustered using Euclidean distance.
A. Sequence of RNA substrate used for in vitro exoribonuclease assays. N, randomized nucleotide.
Scatter plot showing Log2 fold-change enrichment of mRNAs associated with tsGlnCTG over Scramble (Scr1) in LIF- versus RA-treated mESCs.
B. MTS was performed to compare the growth between EV and Q165P DU145 cells after the treatment with indicated inhibitors (2 µM of JQ1, 2 µM of CPI-637, 2 µM NEO2734) for 72 h. All data shown are means ± SEM. The P value was calculated by the unpaired two-tailed Student's t-test; * P < 0.05, *** P < 0.001.
Analysis of shScramble (gray, n = 2,400 cells)‐, shIP3R(1,3) A (blue, n = 1,611 cells)‐, and shIP3R(1,3) C (green, n = 1,454 cells)‐expressing DCs migrating in the device described in Supplementary Fig S3I, stained with Hoechst and imaged every 2 min during 24 h at 10× magnification. Values were obtained from three independent experiments. Cell trajectories were obtained by tracking their nucleus.D Path persistence (calculated as the ratio between the effective length and the total length of the cell trajectory) of migrating DCs. P‐values were determined with a t‐test analysis.
(g) Western blot of siRNA-transfected HeLa cells used in c-f demonstrates the efficiency of p62 silencing. β-Actin probing served as a loading control. WT, wild-type.
Assay to monitor for loss of GAL1 in tetraploid strain RBY18. Strain RBY18 is heterozygous for the GAL1 gene and only cells that have lost GAL1 function can grow on 2-DOG medium.
H Representative bright field images of angiogenic sprouting of hFI, hCI, hPI and hPI+MVF on day 3 of the sprouting assay. Scale bar: 150 µm.
(E) Caco-2 cells were infected with the indicated strains and treated with cycloheximide (CHX) for the indicated time. Whole cells lysates were analyzed by western blot using anti-c-Myc and anti-Actin antibody.
(B) [ATP]/[ADP] ratios in purified corticalneurons exposed to increasing SNOC concentrations (n=4).
C) Frequency of patients showing RV dysfunction (defined as in (31)) in the two ACM cohort subgroups (n=26 oxLDL<86ng/ml vs. n=41 oxLDL>86ng/ml; Two-tailed Student's t-test). D) Frequency of patients showing biventricular dysfunction in the two ACM cohort subgroups (n=26 oxLDL<86ng/ml vs. n=41 oxLDL>86ng/ml; Two-tailed Student's t-test). E) Frequency of patients showing RV wall motion abnormalities in the two ACM cohort subgroups (n=26 oxLDL<86ng/ml vs. n=41 oxLDL>86ng/ml; Fisher's exact test). F) RV ejection fraction % of the patients classified in the two ACM cohort subgroups (n=23 oxLDL<86ng/ml vs. n=39 oxLDL>86ng/ml; Two-tailed Student's t-test). Data information: mean ± SEM. * p<0.05.
(B) A histogram showing the percentage of gene pairs (y-axis; n = 3364) that have significant co-expression change according to the number of types (x-axis) in which each gene pair was significant. Colored bars indicate the 2.68% of gene pairs (n = 45) that were significant in at least 9 tumor types, and that were selected for more in-depth analysis.
B Migration of Cd53-/- pre-B cells transduced with empty, control, or mutant constructs in response to CXCL12 gradient, 3 days after transduction (n = 2-5 mice per group) over two independent experiments. Bars and error bars represent mean ± standard error of the mean. **p < 0.01 and ***p < 0.001 by two-way ANOVA.
Lyzs-Cre and p38γ/δLyzs-KO mice were fed a ND or a HFD for 10 weeks. (B) liver triglycerides (n=5-10).
(D-J) MBP (yellow, fully differentiated oligodendrocytes) IF on cross-sections of WT, HET and KO P7 optic nerves (ONs) at the chiasm (D-F) and between the chiasm and the eye (G-I). Note the dramatic decrease of MBP+ oligodendrocytes at the chiasm in HET and KO, quantified in (J). The ratio of MBP+ cells is calculated over the total DAPI+ cell number per chiasmal/ON section. data are represented as means ± SEM. N=4-5 Statistical significance was obtained by Student t-test or by two-way ANOVA when comparing 2 or multiple conditions, respectively (*P<0.05; **P<0.01; ***P<0.001). Nuclei (blue) were stained with DAPI. Scale bars: 50µm
A model of NLRP3 inflammasome regulation by PLK4 and Spata2/CYLD. Polyubiquitination of PLK4 suppresses PLK4 binding to and phosphorylation of NEK7. This polyubiquitination-mediated suppression can be reversed by Spata2 and CYLD-mediated deubiquitination of PLK4, thereby allowing for PLK4 phosphorylation of NEK7, which attenuates NEK7 binding to NLRP3 and NLRP3 inflammasome activation. Spata2 or CYLD deficiency would cause accumulation of PLK4 polyubiquitination, reduction of NEK7 phosphorylation, increase of NEK7 binding to NLRP3, and eventually hyperactivation of NLRP3 inflammasome.
Quantification of fluorescence intensity of PCNT positive centrosomes. Data were presented as mean ± SEM. Each plot represents the average intensity of two PCNT positive region in one dividing cell (n=11 for H9 cells; n=12 for RGCC-KO cells).Statistical significance was tested by one-way ANOVA. ****, p<0.0001.
L. Normalized entropy in STO and ATO. Data information: All data are presented in the box plot format. The central band in each box represents the median, boxes indicate the middle quartiles, whiskers extended to the minimum and maximum values. *p<0.05 and **p<0.01, determined using Student's or Welch t-test.