EMBO/sd-character-level-ner huggingface dataset:
ATPase stimulation for GFP-tagged Rad54, Rdh54NRad54, Rdh54 or Rad54NRdh54 in the presence of Rad51-ssDNA. Error bars represent s.d. of three independent experiments.
C mRNA expression in female Lin-Sca1+ cells, differentiated in the presence of 100 nM Rosi or vehicle for 8 days, as determined by qRT-PCR (n=3) t-test Cited4-/- vs. Cited4+/+ (Rosi) *P=0.013 (Ucp1), **P=0.004 (Cpt1b), *P=0.026 (Dio2)
A) Immunoprecipitations and Western blots were performed on MEFs stimulated or not with IFNγ (100 U/ml) and infected with an RH strain expressing type II GRA15-HA and as a control RH expressing GRA45-HA. The blots using antibodies against TRAF6 and TRAF2 were made after stripping the first blot. Left panel and right panel were run on a single gel; vertical white lines indicate excision of irrelevant lanes.
B. U2OS cells treated with HU in the presence or absence of ATR inhibitor (ATRi) were fractionated and immunoblotted with indicated antibodies. Relative RADX levels on chromatin were quantified and normalized to histone H3. See also Fig EV2A.
Experimental design for TSLP neutralization in vivo. TSLP neutralization was performed by triple intra-dermal injections of 20 μg of anti-TSLP or IgG to the right ears of DKO* and DKO*15 mice five days after of psoriasis-like induction. EdU was added into mice by IP injection 2 hour before euthanasia.
(C) Left panel, western blotting with HeLa and TRIM16KO cell lysates probed with indicated antibodies. Right panel, densitometric analysis (mean ±SD) of protein band intensity relative to actin, n=3, ***p < 0.0005 (Student's unpaired t-test).
D. TBK1 is required for EGF-stimulated mTORC1 and mTORC2 signaling: TBK1+/+ and TBK1-/- MEFs were stimulated with EGF as in A.
(c) STM of 30-d-old (30 d) Spd1mM+ and Spd5mM+ and Spd− flies (n = 8-9 independent experiments, F = 14.48, one-way ANOVA with Bonferroni correction).
BNIP3 levels in primary melanoma and metastases within the SKCM TCGA cohort, using Mann-Whitney's non-parametric test. The box represents the median and the 25th-75th percentile with the whiskers representing the minimum and maximum values.
C. The results of the luciferase reporting system showed that LncBMP4 could rescue the gga-mir-12211 inhibitory effects against BMP4-3'UTR (Data are shown as mean ± SEM, n =3 independent experiments, * p < 0.05, **** p < 0.0001, one-way ANOVA).
A. Unspliced RPL28, an NMD substrate, was enriched in Nmd4-TAP purification in comparison with a control untagged strain, as measured by reverse transcription followed by quantitative PCR. Bars correspond to the mean of pre-RPL28 enrichment for 3 independent experiments, as compared with RIM1, a non-NMD mRNA. Error bars correspond to SD. The indicated p-value was computed using the Welch t-test, single-sided comparison
(C) Prediction of population-wide, between-line, wing size variations from the mediator-linked genotypes. Mediator-linked eQTLs relevant for each condition (size traits, sexes) were used to predict wing size traits (absCS/relCS) of 143 DGRP lines for each sex. Spearman correlation coefficient and the P-value, and R2 from linear fitting are shown for each case (size traits, sexes). The dark and light grey zones indicate 50% and 95% prediction ranges.
Overexpression of Inh1 decreases ∆ψm in ρ0 cells. Cells were cultured in SCD or SCD plus 100 μM CuSO4 for 12 hours to mid-log phase. Cells were then stained with 125 nM TMRM for FACS analysis.
Indirect calorimetric measurement (n=10/group) of (H) heat productio at P77 Bar graphs represent mean±SD The dat were analyzed using Kruskal-Wallis and Mann-Whitney U tests for selected comparison. Significant differences between groups (p value) are indicated on graphs
D Correlation between gene expression and basal cell adhesion to VN and reduction in cell adhesion upon Plg treatment. Adhesion 4 h after seeding the cells on VN (expressed as cell index) was measured in the experiment described in panel C. The extent of cell adhesion reduction was calculated at the indicated time point in panel C as percentage of the cell index value measured in control wells treated with vehicle. Both parameters were correlated with the expression levels of the indicated genes. Gene expression data were downloaded from the CellMiner web tool. The table shows gene name, Pearson correlation coefficient (r) and p-value.
(D) Ubiquitination of AGIA-PLZF in AGIA-PLZF and FLAG-CRBN expressing CRBN-/- HEK293T cells treated with DMSO or thalidomide (Tha) in the presence of MG132 for 10 h. AGIA-PLZF was immunoprecipitated using anti-AGIA antibody and the polyubiquitin chain on AGIA-PLZF was analysed by immunoblot.
C Comparison of the cryo-EM structure of H2A.B-NCP with the structure of canonical nucleosome in gyre view. Arrows indicate the direction of H2A.B-NCP DNA movement during nucleosome gaping transition. The dashed lines indicate the ~10 degrees rotation of H2A.B DNA at SHL 5. H2B N-tail refers to H2B residues 26-32 which are exclusively observed in the canonical nucleosome structure. Histones H2B in H2A.B-NCP are colored in warmpink, Their counterparts in canonical nucleosome are colored in red. H2A.B-NCP DNA in green is shown in surface mode for clear comparison.
(A) Schematic illustrates the size and location of the retinal explant (dashed line).
Representative immunofluorescence of primary cilium in WT or Mecp2 null MEF cells. Cells were starved for 48 h before staining with anti-γ-tubulin (green) and anti-acetylated α-tubulin (red) antibodies. Merge of all channels and DAPI staining (blue) is depicted for both genotypes. Scale bar 20 µm, and 10 µm in the enlarged image. Arrows indicate not ciliated cells.
A. Total protein copy number of the oxidative phosphorylation complex I-V in bulk liver tissue (n=6 independent biological replicates) and primary cell types (isolated primary cells from n=3 individuals for each cell type). Values are presented as mean ± s.d. B. Protein copy number for members of the oxidative phosphorylation complex I-V in hepatocytes and Kupffer cells with Pearson correlation coefficient indicated.
G RBM47+/+ and RBM47+/- mice were infected with HSV-1 (1× 107 pfu) via caudal vein injection. Viral genome DNA and progeny titers were tested using blood samples from infected mice. Data are represented as the means ± SD of n = 6 biological replicates. H qRT-PCR analysis of IFNAR1 and Cig5 mRNA in blood samples from HSV-1-infected mice. The PCR results are represented as the means ± SD of n = 6 biological replicates. Data information: The data shown are representative of n = 3 independent experiments. NS, non-significant; * P ≤ 0.05, **P ≤ 0.01, and ***P ≤ 0.001 (Student's t-test).
D. NH1 cells containing the integrated HIV-1 LTR-luciferase reporter and expressing Tat were transfected with siDKC1 or siNT. ChIP-qPCR analysis was performed to determine the levels of the indicated factors bound to the HIV-1 promoter. The signals were normalized to those of input and plotted.
Schematic model of the differences between a cell expressing one or two actins to perform two cellular functions. (Top) A model of the molecular mechanisms by which two actin isoforms may segregate to different actin networks. On the left, a system carrying wild-type actin is able to generate both the branched- and linear-networks. On the two central panels, defective interactions of an actin isoform with one or several ABPs, affect branched- or linear-network assembly. On the right, combining these two actin variants in one cell should trigger a natural segregation of actins and rescues the wild type actin organization. (Bottom) Effect of perturbing an actin assembly pathway for cells using one or two actin variants. On the left, when one actin is shared for two actin functions, the inhibition of one actin assembly pathway (for example branched-networks with CK-666) leads to a reinforcement of the other actin assembly pathway. On the right, when two actin variants are used for two different actin functions, this effect is limited as both actin networks assemble more independently. In other words, having a system with two actin variants can buffer against the addition of the drug.
B The Na+ and K+ contents and Na+/K+ ratio in roots and shoots of three groups of 369 accessions after treatment with 150 mM NaCl for 1 d.
c, IpaJ or its catalytic mutants were expressed from a galactose-inducible promoter (pGal413 vector) and assayed for a growth arrest phenotype on galactose or glucose (control) carbon source.
(E) Analysis of differential glycosites identified with the TMT labeling approach using the Qluqore Omics Explorer software. The heatmap represents O-glycosites most significantly contributing to sample variation, using ANOVA with a q value cutoff of 0.1, where each compared sample consists of three individual KO clones. Each horizontal line depicts the median quantification of glycopeptides contributing to the same glycosite. Alternative differentially glycosylated site positions are separated by semicolons on sites derived from glycopeptides with multiple HexNAc/HexHexNAc modifications.
I Immunoblotting using an anti-P-Akt, anti-P-S6 or anti-β-actin (loading control) antibody of protein extracts from SOM230-treated or SOM230-untreated CAF incubated or not with IL-6 neutralizing antibody (representative of n = 3).
(G) SHP2 shRNAs #1, #2, #3 reduce BMEC, not B16F10 cell proliferation; representative of 3 experiments; error bars: ± S.D.; 5 replicate cultures/experiment.
quantification of hypocotyl lengths (G) of 4-day-old seedlings grown with or without supplemental UV-B. The scale bar for all lines represent 5 mm except for cop1-5 where the scale bars represent 1 mm. Violin and box plots are shown for n > 60 seedlings; upper and lower hinges correspond to the first and third quartiles, the horizontal line in the interior of the box indicates the median. Data Information: lines used: wild-type (Ws), uvr8-7, cop1-4, cop1-5/Pro35S:YFP-COP1 (WT), cop1-5/Pro35S:YFP-COP1Lys422Ala, cop1-5/Pro35S:YFP-COP1Tyr441Ala, cop1-5/Pro35S:YFP-COP1Trp467Ala and cop1-5. #1 and #2: independent transgenic lines.
(E) (I) Percentage of neutrophils with LC3B punctuated structures. E. coli (bar 1: 84±2.2%) compared with E. coli+3‐MA (bar 2: 4±1.95%). Data are representative of six independent experiments and presented as mean±SD. Wilcoxon matched‐pairs test, *p<0.05. (II) Formation of LC3B puncta in phagocytosing neutrophils and (III) in cells treated with 3‐MA before incubation with opsonized E. coli, as observed by immunofluorescence confocal microscopy (1. LC3B: red; 2. FITC conjugated E. coli: green; 3. DAPI: blue; and 4. merge). Solid line arrows point the colocalization of LC3B puncta with E. coli bacteria. Dashed line arrows point LC3B aggregates that are not colocalized with E. coli.
B H3K9me3 immunostaining in the indicated HepG2 cell lines with nuclear counterstaining in DAPI. The indicated areas are zoomed-in for a better observation of the H3K9me3 signal profile. All images are maximum intensity Z-projections of confocal stacks.
Representative immunostaining of Arl13b (red) and γ-tubulin (green) in the P14 mouse cortical layers. Nuclei were stained with DAPI (blue). Scale bar 10 µm.
(c) CD39, Atg5 and as a control β-actin protein expression in isolated Atg5fl/+, Atg5fl/fl, KRas;Atg5fl/+ and KRas;Atg5fl/fl pneumocytes. Protein lysated were analysed at 4 days after AdCre infections by western blot. Quantifications of the CD39/β-actin ratios are shown for each lane, normalized to the Atg5fl/+ samples. Two independent blots are quantified.
D: Top: Basal area (black line) and total force F (blue line) as a function of time, for the same cell as in A. Inset: Temporal cross-correlation function (CF) of the area and F (blue) and of the area change rate and F (magenta). Bottom: Kymograph of T along the cell outline.
Immunofluorescence stainings of PNRC1 (red) and Ki-67 (green) performed on a malignant lymphoma (D). DAPI was used to stain cell nuclei. Scale bars:50µm.
LN229 were transfected with siNT, siNoxa 1, siNoxa 2 or BAK-siRNA for 72h. Thereafter, cells were treated with the combination treatment of 1 µM ABT263 and 20 µM LXR623 for another 24h. After conclusion of the treatment, cells were harvested, fixed, stained with propidium iodide and analyzed by flow cytometry for DNA - fragmentation.
B Plasma total cholesterol levels in mice that received adenovirus GFP (control) or PLTP. Blood and tissues were harvested seven days after adenovirus infection. n=8 in mice on RD and n=7 in mice on HFD for 14 weeks. ***P<0.001 relative to GFP by Student's t-test.