EMBO/sd-character-level-ner huggingface dataset:
S. indica induced eATP release in different Arabidopsis transgenic lines. Culture medium was collected from mock treated or S. indica inoculated seedlings growing in liquid medium at 5 dpi and released eATP was measured. RLU: relative light units. Error bars represent ±SE of the mean from three biological replicates. Asterisks indicate significance to all other samples within the same treatment group (ANOVA, p<0.05).
(g-i) Echocardiography analysis of cardiac dimensions and function for α-MHC-miR-212/132 TG mice and WT controls (n=16-18) (g) end-systolic area, (h) end-diastolic area, (i) fractional shortening. All values in e-i represent mean±s.e.m. *P0.05; **P0.01; ***P0.005. DAPI, 4′,6-diamidino-2-phenylindole; WGA, wheat germ agglutinin (membrane stain).
Quantification of ZO-1 levels (grey dots) in four independent Western blot experiments by ImageJ. * P-value < 0.05 (Student's t-test), bars correspond to Mean ± Standard Deviation (N=4).
(1) Iron (red circle) enters the chloroplast and is then captured by the conserved cysteine residues in the CR domain of DJA6/5 proteins. (2) During ATP binding, dimerization of SUFC occurs, which induces a large conformational change of the SUFBC2D complex and exposes the buried assembly sites to the SUFB-SUFD surface. (3) This conformational change facilitates the recruitment of the NFS2-SUFE1 complex. Then the sulfur (yellow circle) is extracted from the substrate L-cysteine by the action of NFS2, and further delivered via SUFE1 to SUFB. (4) Iron-loaded DJA6/5 proteins directly interact with SUFE1 and SUFC via their J domain and deliver iron to proposed iron recipient SUFD. (5) Arrival of the electrons allows the building of Fe-S cluster at the SUFB-SUFD interface. After assembly, DJA6/5 protein and NFS2-SUFE1 complex are released and ready for a new cycle. (6-7) The nascent Fe-S cluster (red and yellow circle) is transferred by carrier proteins (NFUs, SUFA, GRXs and HCF101) to client proteins (such as PetC, PsaA/B, PsaC, Fd, PAO).
A and B IFNβ1 luciferase assays (upper panels) in HEK293T (A) and HEK293T-IRF3 KO (B) cells transfected with the indicated plasmids or infected with VSV. Immunoblot analysis showed the indicated constructs in HEK293T cells (bottom panels). n=3, respectively. Data information: *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001 and ns, not significant (P > 0.05); using a one-way ANOVA Data are from three independent experiments Error bars mean ± SEM).
O. Quantification of three categories of midguts treated with the pH indicator Bromophenol Blue in Drosophila with indicated genotypes. The numbers of quantified guts from left to right are 90, 90, 90, and 90. Error bars show the SD of three independent experiments. Data information: Error bars represent SDs. p-values for lifespan curves (N) were calculated by the log-rank test. The statistical tests used in other panels were student's t-tests. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001, and non-significant (NS) represents p > 0.05.
(D) RT-qPCR were performed on total RNA extracted from 1603MED cells 48 hours after transfection with siRNA targeting INHBB. Relative INHBB expression was assessed. siCTRL condition was set at 1. The p-values were determined by unpaired t-test. *p < 0.05, **p < 0.01, ***p < 0.001. Bars represent the mean ± SD. Number of replicates is n≥3.
A) Manhattan plot of genome-wide association for the levels of hepatic Pex16 transcript, where the only significant locus appears directly surrounding the genomic location (red arrow). Significant cut-offs are shown for FDR (blue) and Bonferroni (red). The peak SNP (rs27364570) is highlighted with a dark red box. Y-axis shows the -log10(pvalue) vs x-axis showing each SNP measured. P-values for GWAS associations were calculated using FaST-LMM.
, F 3rd instar larval fat bodies were stained by BODIPY (green) for lipid droplets and DAPI (blue) for nuclei. Scale bars represent 25 µm. (F) RDH/CG2064 overexpression increases lipid droplet size in ppl>DGAT1 larvae. (G) Quantification of the lipid droplet size in (F). data were analyzed by one-way ANOVA with a post hoc Turkey's multiple-comparison test. Each point represents data from one fat body, and at least 30 cells were examined in each fat body. Error bars represent ± SEM. ***: P < 0.001; **: P < 0.01; NS: non-significant.
C Cells prepared as in (B) were treated with 50 µM antimycin A for 2 h. Arrows indicate OCT-DsRed2-positive/TOM20-negative MDVs that colocalize with GFP-parkin, while circles indicate MDVs that are parkin-negative. Arrowheads indicate nascent vesicles, adjacent to mitochondria, exhibiting cargo selectivity and parkin recruitment. Open arrowheads indicate parkin-negative MDVs containing the reciprocal cargo (TOM20-positive/OCT-DsRed2-negative). Cell boundaries are delineated in the GFP-parkin single-channel image. Scale bars, 30 µm.
Metaplots of 5hmC Enrichment for Cluster 1 (Left) and Cluster 2 (Right) regions for Day 0, 2 and 10 of AA+2i treatment.
SV-AUC (D) Kap114p and (E) the Kap114pyTBP complex. The experimental data were analyzed using the Sedfit program and are presented above molecular weights calculated using standards (in brackets).
(a-g) Four-month-old C57BL/6 male mice kept on HFD for 2 months were subjected to daily administration of phosphate-buffered saline (Con, n=4) or verapamil (Ver, 25 mg per kg body weight, i.p., n=4) for 10 days. Systolic blood pressure (a), LV wall mass (b), diastolic LV volume (c), systolic LV volume (d), ejection fraction (e, % EF), stroke volume (f, SV) and cardiac output (g, CO) were analysed by tail-cuff method (a) or echocardiography (b-g). All data are shown as mean±s.e.m. *P0.05 (Student's t-test).
E) Michaelis-Menten analysis of USP1 deletion mutants (+UAF1) against Ub-Rho shows that all deletions mutants have similar catalytic activity (n=2, biological replicates).
(G and H) Immunostaining assay of SOX1 (red) after SOX1-OT V1, SOX1-OT V1-5P or SOX1-OT V1-3P overexpression in V1-PAKI cells on day 16 of dorsal neural differentiation (G), and quantiﬁcation of SOX1+ cells (H), p=0.0001 (V1-PAKI), p=0.0001 (ptV1+dox), p=0.0001 (pt5P+dox). Scale bar, 100 μm. (I and J) Immunostaining assay of SOX1 (red) after SOX1-OT V1, SOX1-OT V1-5P or SOX1-OT V1-3P overexpression in V1-PAKI cells on day 16 of ventral neural differentiation (I), and quantiﬁcation of SOX1+ cells (J), p=0.0001 (V1-PAKI), p=0.0001 (ptV1+dox), p=0.0001 (pt5P+dox). Scale bar, 100 μm. Data information: Data are presented as mean ±SEM from three independent experiments (n=3). *p<0.05, ***p<0.001 versus Ctrl group ; #p<0.05, ##p<0.01, ###p<0.001 versus -dox group (one-way ANOVA).
B Western blot analysis showing FBXW7 and c-MYC expression in control, Mettl5 KO (KO-6B) and KO+HA-MT5WT Day7 EBs, respectively. α-TUBULIN was used as a loading control.
Quantification of mCherry-positive cells in the regenerated epidermis (n=3 biological replicates). The data from individual mice are connected by lines. *0.01 test.
(J) Quantification of the probe association ratios with old versus new H3 for each candidate gene in bam mutant germ cells. Data gathered over 4 separate experiments for dad, 3 for bgcn, and 2 for ss.
Live confocal imaging of Myosin-II shown by Zipper::YFP (A at the apical cortex of follicle cells during egg chamber elongation showing a transition from cell to tissue-level organization during stage 6
F), Schematic depicting stepwise neurons to NBs reversion in nerfin-1 type I lineages where neurons express Elav, NBs express Dpn, and reverting neurons express both markers.
E: RT-PCR analysis in zebrafish of total embryos and larvae showing the expression of Igsf10 mRNA at different time points. Expected band size: 905 bp.
Violin plots of the log scale normalized expression of LIF receptor subunits, IL6ST (A), LIFR (B), LIF (C), IL6R (D) in all cell types in the human choroid Note the wide distribution of IL6ST (gp130), the common subunit to all receptors of the IL-6 family (A). In contrast, LIFR is strongly expressed in ECs and to a lesser extent in fibroblasts and pericytes (B). LIF is expressed in fibroblasts, macrophages/monocytes and pericytes and minimally in ECs (C). The specific IL-6 receptor (IL6R) is highly expressed in macrophage/monocytes (D), while LIFR has little expression in these cells (B).
Quantitative phosphoproteomics dataset showing that most phosphorylation events induced in rad9Δ cells are dependent on Mec1. These phosphoproteomic analyses were conducted in the presence of 0.02% MMS for 2 hours.
Treatment scheme: LM7 OS cells (106 in 25µl PBS) were intratibially injected; mice were treated for 21 days with vehicle or Erlotinib (50mg/kg) 42 days after injection, when the tumors started to grow
(a,b) Multiple MBds associate with a PC3 cell (a) and a B-lymphoblast (b). Insets: MBd labelling (a) and merged differential interference contrast microscopy image with MBd labelling to show cell boundaries (b). MKLP1, MBd marker (a,b; red); CD44, membrane (a; green); DAPI, DNA (a; blue). Scale bar, 5 μm (a) and 2 μm (b).
Immunoblot of H3K9me1/2 histone demethylase in WT or Kdm3b CRISPR targeted pre-iPSC clones. These pre-iPSCs carry a Nanog-GFP reporter. Parent line (WT), and two Kdm3b-KO clones using gRNA targeting either exon 1 (KO#1) or exon 2 (KO#2) are shown. RNA Polymerase II levels are the loading control.
(E) Western blotting profiling of MB002 expressing EV, SOX9-WT, or SOX9-T236/240A following 48 hours treatment with cisplatin, AZD2014, and their combination. The set of blots shown is representative from 3 independent experiments.
E. Working model for the contribution of BES1 to heat stress signaling. BES1 is de-phosphorylated and activated by heat stress, utilizing ABI1 and redundant ABA-repressed PP2C phosphatases. It then interacts with HSFA1s, which are also activated by heat, for binding to HSEs in promoters of HSP70s and HSP90s genes, which induces them and increases heat stress resistance. BRs, while not needed for the activity, can promote it.
H-I. Western blot analysis of Phospho- or total JNK and c-Jun in BMDCs of indicated genotype pre-treated with DMSO (1: 1000) or SP600125 (JNKi, 25 µM) for 1h and stimulated with IMQ (5 µg/mL) for 15 min.
C. Heatmap of missense score correlations for all possible non-synonymous SNVs at CpD Cysteine (29,541 missense) for eight pathogenicity scores. Overall, Spearman's rank r were between 0.36 and 0.91. Data information: color intensity represents two-tailed Spearman's rank-order correlation coefficients between 0 and 1.
Non-cullin neddylated species accumulate after oxidative stress in WT U2OS cells with the most highly induced species detected at 25 kDa (as indicated by the arrow). WT U2OS cells were treated with the indicated concentration of H2O2 for 30 minutes and then lysed in LDS sample loading buffer and processed for Western blot analysis.
Two sets of representative images showing fluorescent microtubules and actin filaments assembled from isolated centrosomes. Centrosomes were isolated from Jurkat cells expressing centrin1-GFP. Upper and lower lines show actin filaments and microtubules radiating from two distinct centrosomes with low (top) and high (bottom) densities of actin filaments. Scale bars: 10 μm.
B. Giemsa stained thin blood smears prepared at indicated hours post-infection (h.p.i) from assay. Arrows indicate parasites exhibiting abnormal morphology, which were observed at the beginning of each replication cycle.
E MAGE-A3/6 protein instability upon nutrient deprivation is not rescued by knockdown of its associated E3 ubiquitin ligase, TRIM28. HeLa cells were treated with control or TRIM28 siRNAs for 6 days before incubation in EBSS for the indicated times.
In the 3-chamber test, the subject mouse of the PBS-treated mice and the CNO-treated mice explored freely the three test chambers. The time spent in each chamber during two sessions was measured. The CNO-treated ChAT(+)-cre::hM4D(Gi) mice exhibited a decreased interest for a stranger mouse (S1) against objects (O) compared to the PBS-treated group (left two panels) (nCTL=6, ncKO=9, unpaired Student t-test). I. When CNO-treated ChAT(+)-cre::hM4D(Gi) mice were exposed to a new stranger mouse (S2) against the familiar S1 mouse, they also showed a decreased interest for the S2 mouse compared to the PBS-treated control group (right two panels). The preference index showed decreased sociability of the CNO-treated group in both sessions (nCTL=6, ncKO=9, unpaired Student t-test;).
(A) Cisplatin dose response curves of (i) MB002, (ii) Daoy, and (iii) MIC in the absence (EV) or presence of SOX9 by Alamar blue. Cells were pre-conditioned with doxycycline to induce expression of SOX9 (or EV) prior to treatment with increasing concentrations of cisplatin. The IC50 were calculated following 5 (MB002 and MIC) or 3 days (Daoy) of treatment. Data are mean + standard deviation from 3 independent repeats, each containing 5 technical replicates.
(G) Respiratory control ratio (RCR) was calculated as maximal oxygen consumption rate (OCR)/H+ leak OCR (n= 3 independent experiments). Data are presented as mean ± SEM (H) Spare respiratory capacity was calculated as maximal OCR- basal OCR (n= 3 independent experiments). Data are presented as mean ± SEM. Data information: *p<0.05, one-way ANOVA followed by Tukey's post hoc test.
(D Immunostaining of TFE3 and IBA1 in the spinal cord sections from 5-month-old WT, Tmem106b-/-, Grn-/-, and Tmem106b-/-Grn-/- mice.
WT and Mfn1/2 double KO were transfected with: GFP and the indicated plasmids. (F) After 48 h, mitochondrial membrane potential was determined by measuring TMRM fluorescence. The values were normalized to surrounding untransfected cells. (n= 90 cells analyzed in 3 independent experiments).
SQR protein levels (D, E, F) in cerebrum (A, D), kidneys (B, E, G) and muscle (C, F, H) of Coq9+/+, Coq9R239X and Coq9Q95X mice. Note that SQRwestern-blots were performed in isolated cerebralmitochondria due to the low levels of this protein in cerebrum. In kidneys and muscle the western-blots were performed in tissue homogenates.
Immortalized MEFs (MEFi) deficient (−/−) or not (+/+) for TP53INP1 were left untreated (NT) or treated with 3-methyladenine (3-MA, 5 mM) during 4 h.Histograms show mt ROS level measured by flow cytometry upon MitoSox staining. P (−/− versus +/+; NT) = 0.019; P (−/− versus +/+; 3-MA) = 0.025; P (3-MA versus NT; +/+) = 0.031.Histograms show mt mass evaluated by flow cytometry in KO or WT MEFi using MitoTracker staining. P (−/− versus +/+; NT) = 0.012; P (3-MA versus NT; +/+) = 0.036.Histogram shows MitoSox fluorescence normalized with MitoTracker fluorescence. P (−/− versus +/+; NT) = 0.041; P (−/− versus +/+; 3-MA) = 0.030; P (3-MA versus NT; +/+) = 0.045.
E. Depletion of SHMT-M leads to significant changes in intracellular levels of many metabolites in iRBC. m/z features are plotted as the log2 ratio of treated/untreated intensities and the Benjamini-Hochberg corrected P values across six biological replicates plotted as -log10(P).
(D) Outline of strategy to map single MNs to a position along the AP axis (see also Materials and Methods). Upper panel: Intensities of Hox protein expression along the ventral nerve cord measured by immunofluorescence (upper left panel) and co-expression patterns of Hox gene transcripts measured by scRNA-Seq (upper right panel) were used as input. Upper right panel depicts a heatmap of color-coded Hox gene expression levels; columns correspond to n=758 single twitlow MNs. Lower panel: AP position is inferred form scRNA-Seq data by probabilistically mapping Hox gene expression pattern in each individual cell to the immunofluorescence reference data.
(B) Immunoblot analysis of the levels of P‐ACC and tubulin (loading control) in lysates from MCF10A cells left untreated or treated with 500 ng/ml TRAIL for 24 h, 1 mM AICAR for 4 h (positive control) or 5 μM rapamycin for 24 h (negative control).
The ability to form ub-hotspots is crucial for endogenous EUC1 function. The genetic interaction of EUC1 with SDS3 (Rpd3L complex) was rescued with plasmid-borne EUC1-alleles and serial dilutions were spotted on selective media. (-) denotes empty vector.
D U2OS cells stably expressing mCherry−ATG9 were transiently transfected with GFP−Dynamin 2 or GFP−Dynamin 2 (K44A), 20 h post−transfection cells were fixed and with anti−TBC1D5 antibody. ATG9A and Dynamin 2co−localization is indicated by arrows.
(D) Sirt5 deficiency decreases cell growth. MEF cells were seeded in 6-well plates at a density of 50,000 cells/well, and cell growth rate was carefully monitored every 1-2 days by cell counting for 8 days. The results are average ± SD of 3 independent experiments *p<0.05, ***p<0.001 (two-tailed unpaired t-test).
(C) Distribution of sgRNAs in BRAFi-resistant cells (before xenograft) and in the 7 tumors emerging from the BRAFi-resistant cells (log10(sgRNAs counts)). Blue and red lines indicated the enrichment ≥10 fold or ≥100 fold (tumors versus BRAFi-resistant cells (in vitro)).
(g) Spearman correlation coefficients computed in the same cell pairs from Venus::HES5 and H2B::mCherry (control) nuclear intensity timeseries; markers in each condition indicate pairs; black dots indicate median correlation coefficients per experiment (4 pairs, 3 pairs and 7 pairs), lines show median of 14 pairs from 3 experiments; paired t test with significance p=0.0058.
F. Quantification of [13C3]-lactate using LC-MS/MS in siCON (blue) or siMCT12 (orange) treated HBVPs after 20mM [13C3]-Lactate treatment (2hr). (n=3 from independent experiments. Error bars indicate the standard error of the mean (SEM) from unpaired Student's t test.)
CD69 expression, an early marker of lymphocyte activation, in CD3+ T cells infected with shNC, shNF45 or shNF90 lentivirus upon stimulation with P/I for 12 h.
(A) Representation of the SNARE complex with Asp68 highlighted (top). BET1Asp68 is involved in a hydrogen bond with SEC22bLys169, with the most probable conformation of His68 in the mutant variant (bottom).
A: Levels of Igsf10 expression in native NIH3T3 cells, and cells stably expressing a scrambled (sh-scr) or Igsf10 (sh-Igsf10) shRNA.
K Numbers of myonuclei in cross sections of TA and EDL muscle (TA: n = 6 KO/6 WT, EDL n = 3 KO/3 WT animals, Mann-Whitney test one-tailed, **p<0.01, *p = 0.05) Data are mean ± S.E.M.
(C-F) Measures of calcium in treated living LmnaG609G/+ VSMCs (C), treated fixed LmnaG609G/+ VSMCs (D), untreated living LmnaG609G/+ VSMCs (E), and untreated fixed LmnaG609G/+ VSMCs (F).
(D-F) THP-1 cells stably expressing the nucleocapsid gene or control vector were stimulated with 10 μM nigericin for 30 min following pretreatment with 1 μg/ml LPS for 3 h. Supernatants and cell pellets were collected and immunoblotted with antibodies against the indicated proteins (D). The percentage of viable cells was determined through checking cellular ATP levels in cell pellets (E). The percentage of cells undergoing pyroptosis was calculated through checking released LDH in the supernatants (F). For E, F, Student's t-test was used and data were shown as means±SD of three technical replicates. **, P<0.01; NS, non-significant. Data information: control vector used here was empty vector corresponded to the nucleocapsid-containing vector. Student's t-test was used and data were shown as means±SD of three technical replicates. **, P<0.01; NS, non-significant. Similar results were observed for at least three times.
D) Scheme showing contacts (putative H-bonds and hydrophobic contacts) and energetics between the Sen1 NIM peptide and Nrd1 CID. Equilibrium binding experiments with the protein mutants were monitored by FA. L20D mutant disrupts the hydrophobic contact with F17 and impairs the overall geometry of the α1-α2 loop that contributes to the interaction with the upstream electronegative stretch of NIM. KD (wild type Nrd1 CID-Sen1 NIM) equals 1.20 ± 0.02 μM. E) Alignment of RNAPII CTD and CTD mimics (Trf4 NIM, Sen1 NIM, and Mpp6 CTD mimic). Blue and grey boxes highlight the upstream electronegative stretches and hydrophobic regions, respectively. Previous structural works reported that S/NPXX motifs form the β-turn conformation (Kubicek et al., 2012; Tudek et al., 2014).
A. Unique residue pairs obtained by Wang et al. for the human 26S proteasome (PDB|5GJR).
Fig 3: TC randomization does not decrease gut microbial diversity in infants or mothers. Shannon diversity measures are plotted as the interquartile range with median for each TC exposure class and time point grouping for infants and mothers.
(B) FSCN1 immunofluorescent staining and quantification of fluorescence intensity in M238P cells treated or not with BRAFi (Vemurafenib, 3 μM) in the presence or the absence of LNA-based anti-miR-143 (LNA-143) or anti-miR-145 (LNA-145) (50 nM) or a combination of the two. Data are represented as scatter plots with mean ± SD from 10 independent fields representative of 3 independent experiments, Mann-Whitney U test was used for statistical analysis. ****P≤0.0001. Scale bar 40 μm.
C. A549 cells were infected with ZIKV (MOI=5) for 16 hrs and then transfected with an IFIT1 promoter-driven firefly luciferase plasmid (pGL3B/561) and a constitutively active renilla luciferase construct (pRL-TK), as well as 1 μg of poly(I:C). Eight hours later cell lysates were harvested and subjected to luciferase assay. Values are expressed as mean of two independent experiments, N=2
Relative mRNA expression levels in TB+ IL-2 and TB+ IL-2nil (A) and TB+ DMSO and TB+ Ruxolitinib (B). The expression level in the IL-2/DMSO TB+ sample is set to 1. (n=3, error bars represent standard deviation, P-values were calculated using a paired t-test with *p<0.05, **p<0.005, ***p<0.0005.)
HCT-116 (A) and HT-29 (B) cells were treated with the indicated concentrations of sodium butyrate (NaB) for 24 (grey bars), 48 (pink bars), or 72 (yellow bars) hours and cell proliferation was assessed. HCT-116
FACS plot of cell cycle distribution of day 6 Ronin del/del and Ronin fl/del, determined by EdU assay.
(E) H&E, SOFG and Immunofluorescence analyses of pathological new bone formation in hind paws. n=9 per group.
(D) EUC1 overexpression toxicity depends on DNA binding and transactivation. The indicated EUC1 alleles with endogenous or galactose-inducible promoters were integrated at the URA3 locus (YIplac211, euc1∆ background) and spotted on glucose control or galactose plates to induce EUC1 overexpression. See also Appendix Fig. S9A-C.
A-B. PBP4 has different interaction sites for PBP1A/LpoA and NlpI as shown by a single concentration MST assay. Plots show the FNorm or fluorescence values of fluorescently labelled PBP1A or LpoA with or without PBP4, NlpI or PBP4-NlpI. Values are mean ± standard deviation of three independent experiments.
to h. Inhibitory activity of EK1C4 in cell-cell fusion mediated by the S proteins of SHC014 (h).
(B) ssDNA repair efficiency of the indicated mutants as determined from the maximal and final percentages of cells with RPA foci during the time course (See Figures EV2D-E for the time course analyses; cells were synchronized in G1 and released into S phase in the presence of 0.033% MMS for 1 hour, treated with 2.5% sodium thiosulfate to inactivate the MMS, washed and released into fresh medium for different times). Data information: The mean and SEM of 3 independent experiments are shown. Asterisks indicate statistically significant differences according to an unpaired two-tailed Student's t-test. One, two and three asterisks represent p-values <0.05, <0.01 and <0.001, respectively.
Overexpression of LOC113230 in SW-1116 cells inhibited lung metastasis. Left: Exponentially growing SW-1116 - LOC113230-Luc and SW-1116-Vector-Luc cells were injected into the tail vein of 8-week-old nude mice and intensities of lung metastatic tumor cells at the 8th week were analyzed by in vivo photon flux imaging equipment. The red circles in images are to help to see the tumors. Right: Box plot (central band: median; box limits: first and third quartile; whiskers: minimum and maximum) of lung photon flux at the 8th weeks.