EMBO/sd-character-level-ner huggingface dataset:
(c) Inhibition of etoposide-induced autophagy by silencing of Beclin 1. Bax/Bak−/− MEFs with silencing of Beclin 1 were treated with 20 μM etoposide at 18 h and were analysed by electron microscopy (×8,500).
Flow cytometry analysis of surface PD-L1 levels in control and VGLL4 knockdown A549 cells treated with IFNγ for the indicated times
F Model of the FAK oligomeric assembly placed on a lipid bilayer. The membrane is placed by considering the KAKTLRK basic sequence in the FERM F2 lobe as main membrane binding site (Cai et al., 2008; Goni et al., 2014).
C. Confusion matrix of the SVM model based on a large validation dataset (102,137 cells), illustrating the distribution of the SVM classifier output in comparison to the visual classification.
simulating the effect of perturbing a single phase-coupling factor by significantly increasing its abundance or activity. Perturbation was simulated by increasing the abundance of a phase-coupling factor by 10 fold.
d, Western blot analysis of LC3-I/II (non-lipidated and lipidated forms of MAP1LC3, respectively) and p62 levels in indicated tissue from mice at rest (-) or after maximal exercise (+). Skeletal and cardiac indicate skeletal and cardiac muscle, respectively.
A-C. Wild type embryos injected with control MO or with shox MO. (A) Lateral views of the embryos at 55 hours post fertilization (hpf). (B) Dorsal view and magnification on the lateral view of the embryos. Dotted line, pectoral fins. shox morphants show smaller fins compared to controls (n = 30 embryos).
B. The motor protein MyoA localizes to the periphery of motile Plasmodium stages. Images show parasites expressing GFP-tagged MyoA. Nuclei were stained with Hoechst. Scale bar, 5 µm.
(C Co-immunoprecipitation of ectopically expressed Myc-CDC20 with endogenous p65 and ectopically expressed Flag-p65 with endogenous CDC20 in HEK293T cells.
PCR array analyses were performed on LCM captured P7 CLE of Prom1 and Glis2 KO vs. WT mice (n = 3). The mRNA expression of gene significantly changed in the PCR array (in (C)) (D) was evaluated in WT, Prom1 and Glis2 KO mice by real-time RT-PCR analysis. Each sample was isolated from distinct mice (n = 3). The results are in arbitrary values after normalization for GapDH.
A Representative dendritic segment of a neuron expressing GFP-G375D and 3B11-immunostained endogenous gephyrin (red).B Quantification of density and (C) size of endogenous gephyrin clusters in neurons expressing GFP, GFP-G375D or non-transfected neighboring neurons. 20 GFP-G375 and non-transfected neurons and 15 GFP-expressing neurons from three independent cultures were used for quantifications. Results are expressed as mean ± SEM and data were analyzed by t-test.
D. Confocal microscopy images of PrimPol and γH2AX (damage control) immunofluorescence staining in control (UVA) or TMP-UVA-treated PRIMPOL KO cells stably expressing V5-tagged WT or RPA binding domain mutant (RBDm) PrimPol versions. Nuclear DNA is counterstained with DAPI. UVA laser path is indicated. Scale bar, 10 µm. Histograms (right panel) show the average percentage of PrimPol-positive cells and SD of two assays (n ≥100 cells per condition in each replicate). Circle dots in each column represent the values of individual replicates. Statistical analysis was conducted with one-way ANOVA followed by Bonferroni post-test. p-values of individual comparisons are indicated.
Experimental setup. TAM was applied to 6 weeks old Cx3cr1CreERT2:Rosa26-tdTomato mice leading to the excision of the stop sequence followed by robust Tomato expression in microglia. At the age of 14 weeks (8 weeks post TAM) three focal argon laser burns were applied to each retina to induce microglia activation and subsequent choroidal neovascularization (CNV). Analysis was performed on days (d) 3, 7, 14, 28 and 56, respectively.
H Cumulative frequency curves of the lengths of adjacent exons of 399 HSATIII-up-regulated internal introns. The lengths of whole annotated internal introns are shown as a reference.
Representative raw traces of epidural EEG recordings during hyperthermia (HT) from a WT and a CA VII KO mouse. Seizures were reliably induced in WT (n=9) but not in CA VII KO (n=7). Error bars denote s.e.m., all P-values are based on Student's t-test (***P<0.001), and animal number is given in bar diagrams. Rectal temperatures are given above the traces.
(D) The extraction of endogenous MITOL from depolarized mitochondria is blocked by the p97/VCP inhibitor NMS-873. Higher magnification images of the boxed regions are shown in the lower panel. Scale bars, 10 µm.
C Quantitative analysis of (A). The partition coefficient was calculated as the total fluorescence intensity of droplets / bulk fluorescence intensity of background. n = 3 biological replicates. Data information: Error bars, mean with s.d. , **P < 0.01, two-tailed t-test.
Internalization of Aβ (stained with IC16 antibody or methoxy-XO4) was assessed using an engulfment assay, in which glial and Aβ structures were surface-rendered and Aβ volumes co-localized with glial volumes were quantified. Scale bars, 10 µm.
(C) Inhibition of the interaction between endogenous TAB2, TAB3 and BCN1 by C‐terminal fragments of TAB2 and TAB3. Forty‐eight hours after transfection with pcDNA3.1 or plasmids coding for the indicated proteins, cells were lysed, TAB2 or TAB3 was immunoprecipitated and BCN1 was immunodetected. GAPDH levels were monitored to ensure equal loading. This experiment has been done three times, yielding comparable results.
D CDF4 expression level at various developmental stages of rosette leaves. YL, young leaf; NS, fully expanded, non-senescent leaf; ES, early-senescent leaf, with 1/4 leaf area turned yellow; LS, late-senescent leaf, with >50% leaf area turned yellow. Three independent experiments were conducted. Values are given as mean ± SD, n=3.
Immunoblot analysis confirming the successful siRNA depletion of CDK5 and indicating hypo-phosphorylation of DBN1S142 in response to CDK5 depletion The DBN1pS142/GAPDH ratio from (H) was densitometrically measured. Three independent experiments. Mean ± SD. * P≤ 0.05
(f) Dvl2 ubiquitylation is required for its direct interaction with p62. Dvl2 was ubiquitylated by the pVHL E3 ligase complex in vitro, followed by in vitro binding assay with recombinant p62.
C. GSTpulldown assay was performed as in (B) using truncated forms of Rbd2 C-terminus; Rbd2200-251, Rbd2200-225, Rbd2225-251 and Rbd2200-240. Unbound (1x) and bound (5x) fractions were analyzed by western blotting
D. Conceptual model of SPIN90-bound Arp2/3 complex in the short pitch conformation. The model was made by superposing subdomains 1 and 2 of Arp3 from the co-complex structure onto an actin subunit from a high-resolution structure of an actin filament (3J8I Arp2 (red ribbon) was then moved into the short pitch position based on the filament structure. Arp2 in its original splayed position (as observed in the crystal structure) is shown in grey ribbon representation. Shortest Cα-Cα distances from SPIN90 to either subdomain 2 or subdomain 4 in Arp2 in the hypothetical short pitch conformation are indicated
Confirmation of Brcc3 expression from knockdown samples in by RT-qPCR (technical duplicates)
(G) Atg5 KO MEFs were starved for 30 min. Differential centrifugation as shown in Figure 1D was performed to collect the 25K ×g and 100K ×g pellet fractions. The LC3 lipidation was performed on these two fractions with indicated concentrations of SAR1 (H79G). Quantification of lipidation activity is shown as the ratio of LC3-II to LC3-I (II/I).
The average microtubule length remains close to the maximum length 6 μm. The circles are obtained by averaging results from 200 stochastic simulations of the model equations and stars are the experimental data (blue stars are for (α2+, α2++, α2+++) strains). The error bar shows the standard deviation in the data and simulation results.
(A) PY79 (WT) and ET28 (PIPTG-sigX) cells were infected with SPP1 or Phi29 (t=60 min) at 1:20 (phages:bacteria) MOI, and OD600nm was followed at 2 min intervals. IPTG was added 30 min before infection (t=30 min). Shown is a representative experiment out of 3 biological repeats, and the average values and SD of 4 technical repeats.
(A) Western analysis for on-target effects for Everolimus (EV, P-RPS6) and CX-5461 (p53). Each lane represents equal amounts of protein from lymph node tissue isolated from a single mouse that received drug vehicles (everolimus vehicle: 1% methylcellulose; CX-5461 vehicle: 25 mM NaH2PO­­­4) (V/V; mouse #1-6), 5 mg/kg everolimus (EV; mouse #7-12), 35 mg/kg CX-5461 (mouse #13-18) or both drugs (CX-5461+EV; mouse #19-24) for 2 hours (n=6 per treatment group). Actin was used as a loading control.
Peptide array dot blot analysis to identify LIR motifs in the indicated SNARE proteins. Amino acids for the identified LIRs from positive signals are marked on each SNARE. Amino acids are denoted as amino acid single letter codes in the blot.
(C Organ damage parameters were determined in the plasma of female C57BL/6J mice injected with 14.5 mg/kg LPS (normoxia) or 5 mg/kg LPS (hypoxia) 6h and 2h after LPS injection, respectively. N=4-5 per group. Data information: All bars represent mean ± SEM. P-values were calculated using two-way ANOVA followed by post-hoc Šídák's multiple comparisons test to correct for multiple testing during the pairwise multiple comparisons, except if otherwise stated. Survival curves were analysed with Fisher's exact test. ****P<0.0001, ***P<0.001, **P<0.01, *P≤0.05.
(D) Correlation plots of the indicated differentially expressed gene (DEG) sets obtained in expression microarray (5 technical replicates of a minimum of two organoids per genotype were analyzed). Values for DEG in fetal and adult organoids were obtained from Mustata et al, 2013.
A PKAr is predicted to possess two cAMP binding sites. A single glycine to glutamic acid change in the site B of the cAMP binding domain is known to abolish cAMP binding and to prevent activation of the holoenzyme in the presence of cAMP. In PKAr the conserved glycine residue is Gly321.
C. Schematic diagram illustrating how unphosphorylatable Rb∆K11 allele or control wildtype Rb DNA was introduced in vivo (top) or ex vivo (bottom) into retinal progenitors. i.v.c., in vitro culture.
(A) Number of proteins identified after analysis by mass spectrometry in the six fractions of EVs from control and HIV-infected cells. The majority of proteins were quantified in both samples.
C: STV changes (left) and representative examples of QT interval oscillations plotted over 30 consecutive beats (right) in the presence of AST and AST+LUF7346 20 µM. * = p<0.05 vs Baseline. ° = p<0.05 vs AST. N = 7-24.
(A) MAP4K4 associates with PP2C38 in vivo by Co-IP. MAP4K4-GFP and PP2C38-HA were co-expressed in protoplasts. GFP trap beads were used for immunoprecipitation, and target proteins were detected by western blots using anti-GFP or anti-HA antibodies. The predicted molecular weight of MAP4K4-GFP and PP2C38-HA is 103.8kDa and 48.1 kDa respectively.
Mice were injected with Ctrl MC38 cells or Ifn-DKO cells and treated with 5-FU or PBS. (H) Tumor and spleen weights at the endpoint for (G), with each dot representing a mouse.
Correlation between ChgB puncta per neuron and total neurite length for hippocampal (green) and striatal (red) neurons.
Basic fuchsin staining of protoxylem (unfilled arrowheads) and metaxylem (filled arrowheads) in WT, shr-2 or hst-1 roots. *: protoxylem gap. Scale bars: 10 µm.
(G) ZIKV NS1 expression 48 h after ZIKV infection of hNSCs expressing control siRNA (NTC) or siFANCC-targeting siRNA. Scale bar = 100 µm. (H-I) ZIKV NS1 expression 48 h after ZIKV infection of hNSCs expressing control (NTC) or siE2F4-targeting siRNA. Mean ± SEM of six imaging fields of biological triplicates, **p < 0.01 by Student's t test, Scale bar = 100 µm,
In vitro dephosphorylation of DBN1 by purified hCDC14A. DBN1-GFP was transfected into HEK293T cells and expressed for 48 h. DBN1-GFP was immunoprecipitated from cell lysates with GFP binder. The immunoprecipitated phospho-DBN1 was then incubated with and without recombinant hCDC14A in vitro. The DBN1pS142/DBN1 ratio was densitometrically measured. Three independent experiments. Mean ± SD. **** P≤ 0.0001
A schematic diagram demonstrating the serial replating experiment. KSL were sorted from primary recipient control mice (black, n=4), or Molm-14-xenografts (red, n=4) and plated in triplicate (500 cells/plate/mouse) in methylcellulose media. Seven days later, colonies were counted and serially replated in triplicate (5000 cells/plate/mouse). The replating process was repeated twice for a total of three rounds (labeled week "WK" 1, 2 and 3).
A The procedure of CHAF1A depletion-mediated HIV-1 reactivation in primary CD4+ T cells. On Day -4, primary CD4+ T cells were isolated from PBMCs of healthy donors, and activated by PHA. On Day 0, activated CD4+ T cells were washed and infected with pseudotyped HIV-1. Another two days later, cells were treated with shluc and shCHAF1A lentiviruses respectively. Two weeks later, one part of naïve CD4+ T cells was treated with αCD3/αCD28/IL-2. One part of shluc-treated cells and one part of shCHAF1A-treated cells were further treated with 500 nM SAHA. On day 16, all the cells were proceeded to FCM analysis.
Pleural fluid cell pellets and supernatants from 45 patients (called ASK #) with pleural effusion from Munich, Germany (Klotz et al, 2019a and 2019b) were subjected to digital droplet polymerase chain reaction (ddPCR) for the detection of mutant (MUT) copies of KRAS codon 12/13 (KRASG12/13) and KRAS codon 61 (KRASQ61), as well as copies of TP53 and TERT. Diagnoses were benign pleural effusion (n = 5), lung adenocarcinoma (LUAD; n = 16), MPM (n = 12), as well as other extrathoracic cancers (n = 12). The assays were designed for detection of down to 1:20000 copies using EKVX (KRASWTTP53G610T), A549 (KRASG12STP53WT), NCI-H460 (KRASQ61HTP53WT), NCI-H3122 (KRASWTTP53E285V), and NCI-H3255 (KRASWTTP53G560-1A) human LUAD cells as controls. Shown are individual patient (KRAS plot) and individual sample (TP53 plot) allelic frequencies with color code and limits of normal TP53 allelic frequency as vertical dashed lines in the TP53 plot (A) Any number of KRAS-mutant droplets detected in any sample (KRAS plot in A) and any patient that failed to achieve normal TP53 ploidy by any sample (TP53 plot in A) was deemed altered.
Survival, gain of weight and mobility plots for Armadillidium vulgare during 75 days post-injection.There were no significant differences between animals injected with wVulC, wDil or control treatment for all these life history traits: Survival (A), Gain of weight (B) and Mobility (C).
(A) Western blot analysis of FLIP, Caspase 8 and FADD recruitment to the TRAIL-R2 DISC in U20S parental cells (EV) and 3 independent caspase 8 null clones (#1, #2, #3) after incubation with AMG655 conjugated beads for 30, 60 or 180 minutes.
E. Purified HAT1, PGAM1 or PGAM1 mutant, and succinyl-CoA were mixed in the in vitro succinylation assays and relative PGAM1 activity was measured by PGAM1 activity assays in vitro. N = 3 biological replicates. Data are presented as mean ± SD. Student's t-test, **P < 0.01.
protein expression of TSLP in different epidermal cell subpopulations sorted at mid-term (D7) or late-term (D30) of psoriasis-like progression in DKO* mice. n=2-3.
(A) Primer extension reactions on the Tg template with 5 nM Pol δ or Pol ε and either dATP, dCTP, dGTP, or dTTP.
(A) Lung cancer cells PC-9, prostate cancer cells 22RV1, bladder cancer cells UMUC3, breast cancer cells MCF-7, colonic adenoma-derived non-cancerous cells AA/C1 (aka C1) and AA/C1/SB (aka SB), or cancerous cells AA/C1/SB/10C (aka 10C) were incubated with wild-type F. nucleatum 12230 (Fn), the fadA-deletion mutant US1 (US1), or E. coli DH5α (E. coli) at multiplicity of infection (MOI) of 1,000:1. Cells numbers are mean values ± SEM. The experiment was performed in triplicates and repeated three times. **p<0.01, ***p<0.001, compared to untreated controls; #p<0.05, ### p<0.001, compared to US1-treated cells (two-way ANOVA).
F. Exon skipping event of Cdk1-3ExS in LincGET-depleted 2C is confirmed by RT-PCR. Injection of LincGET fragments at the pronuclear stage was unable to inhibit the exon 3 skipping of Cdk1, while injection of full-length LincGET1 lacking LincGET-LNA2 target site partially inhibited the exon 3 skipping of Cdk1. For each lane, about 50 embryos were used. Three experimental replicates were performed. Two tailed student's t-test was used for the statistical analysis.
(c) Pathogenic Parkin mutations fail to poly-ubiquitylate endogenous VDAC1 in response to CCCP treatment. Western blot analysis of a time-course experiment with inducible Parkin SH-SY5Y cells after CCCP treatment. Total lysates were prepared, and western blots were probed with specific anti-Parkin and anti-VDAC1 antibodies. β-Actin probing served as a loading control in a-c. WT, wild-type; Ub, ubiquitin.
(F) Summary of the Vav1-regulated signaling pathways that contribute to promote the proliferation of primary CD4+ T cells that have been unveiled in this work. The other downstream effectors and pathways of Vav1 are indicated. The main primary effectors as shown in red.
(G) Per cell Pearson Correlation between GFP:RAB21 and EEA1 or VPS26; SEM, n=3 independent experiments. Statistical tests used: (G) - Mann-Whitney tests. All error bars are SEM. Number of cells presented on each graph represents the total number of cells analyzed for all repeats.
(b) Miz1 binds predominantly to core promoters. The panel shows a histogram of the percentage of promoters with the indicated distances between the peak of the Miz1-binding site and the next TSS. Of all the peaks, 140/261 (54%) are located in core promoters (±1.5 kb).
Reactivation from HIV-1 latency (A) and relative cell viability (B) in primary Th17 cells following 24 h treatment with the Trx inhibitor auranofin (AF; 500 nM), the GSH inhibitor buthionine sulfoximine (BSO; 250 μM), or a combination of the two. GFP-HIV-1 expression was determined by FACS. Data are expressed as mean ± SD of three replicates and were analyzed by One-Way ANOVA followed by Tukey's post-test (A) or Two-Way ANOVA followed by Sidak´s post-test (B). Solid lines represent the means.
(E) Representative epifluorescent images of HeLa cells transfected with a control siRNA or a siRNA against CLEC12A and infected with DsRed-labeled Salmonella for 1 hr. (F) Quantitation of ubiquitin-bacteria colocalization at 1 hr post-infection in cells shown in (E). Data are shown as means ± SEM from three independent experiments.
(f) Beclin1 binds UVRAG through its CCD. After transfection with Flag-UVRAG together with full-length or fragments of Beclin1-V5, WCLs were used for immunoprecipitation with anti-V5 followed by immunoblotting with anti-Flag.
Volcano plot of DEGs in female ESCs (#A4, #A10, #A11) versus males (#A6, #A13, #A17). The definition of up (red dots) or down (blue dots) genes is as follows: the ratio of up or down genes is > 1.5 and < two-thirds, respectively, with q-value< 0.05.
Normal presynaptic release in the hippocampal SLM region of Ptprd-meA-/- mice, as shown by the PPF ratio at the TA-SLM pathway (P20-24). (n = 15 slice from 5 mice [Ptprd-meA+/+] and 13, 4 [Ptprd-meA-/-], mean ± SEM, ns, not significant, two-way RM ANOVA).
(F) To induce sepsis via LPS injection (Shirey et al., 2013; Voss et al., 2016), age (9-10 weeks)- and sex-matched Atx∆ΜΕ/∆ΜΕ mice (n = 9) and Atx+/+ littermates (n = 21) were injected with LPS (i.p. 25 mg/kg). Survival was monitored for up to 16 h, and analyzed by the Kaplan-Meier method (Log-rank P=0.0004).
immunoblots of the expression of indicated proteins in the scramble and CD38 knockdown DC fibroblasts. The CD38 knockdown DC fibroblasts were treated with the PARP1 inhibitor Olaparib (400nM) and the SIRT1 inhibitor EX 527 (1 μM) for 24 hours. Data are representative four replicates. All values are presented as mean ± SD of four replicates. One-way ANOVA was performed on DC cells in indicated conditions.
D) Larval VNCs at 24 h ALH from control (grh-Gal4 UAS-CD8-GFP) and msps924 with grh-Gal4 UAS-CD8-GFP were labeled with E-cadherin, Dpn, and GFP. NSC-neuropil contact were marked by dashed lines, and NSC-neuropil contact sites were circled. E) Quantification of E-cadherin basal localization at NSC-neuropil contact sites in qNSCs from genotypes in (D). "No E-cad" means absent or strongly reduced E-cad observed at the basal region of qNSCs. n=77 NSCs for control; n=30 NSCs for msps924. **p=0.0080. F) Quantification graph of the basal E-cad intensity at NSC-neuropil contact sites by normalizing against Dpn intensity in qNSCs from genotypes in (D). n=60 NSCs for control; n=37 NSCs for msps924. ****p<0.0001.
A. HuH7 cells were mock treated, treated with 10,000 U/ml of IFNα for three days, infected with HCV for six days or infected with HCV for six days and treated with IFN during the last three days of infection.
(B) Growth curves as in (A) for cultures supplemented with complete amino-acid mix (black), without any amino acids (red), or amino-acid mix without arginine (green).
K. Both AICAR treatment and glucose depletion impair the association between Prmt6 and Sirt7. MEF cells were cultured with or without glucose and treated with AICAR as indicated. Co-immunoprecipitation was performed using SIRT7 antibody. Input and immunoprecipitates were analyzed by western blot
Organoid morphology depends on Rspondin ligand type and concentration. Left panel: growth quantified as the percentage of elements present at day1 surviving at day4. A mean of 100 elements were analyzed per sample and per condition (n: 4 WT, 2 KO organoid culture samples, each originating from a given embryo). Right panel: organoid complexity measured by branching coefficient. Each symbol indicates the value of a given organoid (analysis was done on 4 WT and 2 KO organoid culture samples, each originating from a given embryo).
E-F. Echocardiography data (n=4-6/group) showing (E) ejection fraction (EF) and fractional shortening (FS). (F) Systolic (LV Vol;S) and diastolic (LV Vol;D) left ventricle volume in mice Bar graphs represent mean±SD Statistics One-way ANOVA followed by unpaired t-test with Welch"s correction for graph E
F Analysis of collagen type I fibers within infarcts identified by Sirius Red staining 7 days after ZT13 MI. Student`s t-test; n = 5 mice for isotype and n = 4 mice for Ly6G; *P = 0.0375.
Effects of DC and Beva treatments on Ren13, Ren86, Ren28 and Ren50-PDOX. Quantification of tumor necrosis in control and treated tumors from 4-5 samples/tumor/treatment group by Mann Whitney test. Box plots indicate median, Q1/Q3 and max/min value whiskers.
D. HeLa cells transfected with COX4-DsRed, mito-PAGFP, and empty vector control, GASZ or GASZ with MLS mutation, followed by photoactivation of PAGFP. Representative images of PAGFP and DsRed were taken at 0, 10, and 20 min post photoactivation. Scale Bar: 10 m. Insets show images with higher magnification. The averaged exponential decay constant (±s.e.m.) of normalized PAGFP fluorescence within the designated region (white circle) at photoactivation area over a period of 10 min was shown as a bar graph below. n>20 cells for each group.
(b) Proposed model of epiboly progression. The contractile E-YSL and the imbalance of stiffness between the EVL and the yolk surface account for epiboly progression. The vegetal boundary of the E-YSL is not mechanically free but linked to the tense yolk membrane. The tension originated by constriction of the actomyosin ring (E-YSL) is thus conveyed by the yolk membrane towards the vegetal pole leading to the progression of the less stiff EVL. Passive movements within the yolk arise as a result of force transmission from the surface.
(A) Measure of LDH and IL-1β release in WT, GBPChr3-/- and Casp11-/- BMDMs were Irgm2 was knocked down 16 hours after exposure to 2,5 µg/2.105 cells of OMVs. Si Scramble (siScr.) refers to RNAi pools with non-targeting sequences.