EMBO/sd-character-level-ner huggingface dataset:
Staining of VGLL4 and IRF2BP2 on human non-small cell lung cancer tissue arrays containing 71 samples was quantified as described in the Materials and Methods section. Correlation of VGLL4 and IRF2BP2 expressions was significant (Pearson correlation test; R = 0.6341, P < 0.001) Correlation analysis of VGLL4 and PD-L1 expression on human non-small cell lung cancer tissue arrays containing 71 samples
B Western blot of the overexpressed Matrin3 and its mutants probed with anti‐FLAG and anti‐actin antibodies.
(C) Western blot showing the expression of ANKRD26. Experiments were performed in monoclonal ANKRD26-/- PLK4Dox cells expressing the indicated ANKRD26 transgenes.
Proportion of CD4+Foxp3+ Tregs (B) from the spleens and kidneys of islet transplant mice receiving vehicle, IL-33, IL-33/DT, IL-33/PC61, or IL-33/DT/PC61 at day 5 post-islet transplantation. Data shown are the mean ± SEM (n=4-5 per group) and a one-way ANOVA was performed; NS: non significant, ***P<0.001.
(B, C) HEK293T cells were co‐transfected with the indicated constructs. Cell lysates were analysed by IP. IP, immunoprecipitation; ND, not determined.
G. CFLAR full length (FL) promoter ranging from -1179 to +281 and three promoter regions P1 (-1179 to -788), P2 (-788 to -288) and P3 (-288 to +281) were fused with a luciferase reporter and then co-transfected with an increase dose of Bclaf1 in HeLa-Bclaf1-KO cells. At 24 hours after transfection, the cells were collected and luciferase activity was measured. The experiments were performed in triplicates with a Renilla reporter in the transfection mixture for normalization and the activity in the control was arbitrarily set to 1. Data information: Data are shown as mean ± SD. n=3 biological replicates. *p<0.05; ***p<0.001; ****p<0.0001. One-way ANOVA test.
(a) Proliferation of B cells purified from Atg5f/fCD19-Cre and Atg5f/f control mice and activated for 3 d with LPS, assessed by flow cytometry analysis of dilution of the membrane dye CFSE. (b) Size of B cells purified as in a and activated for various times (horizontal axis) with LPS, assessed by the intensity of forward scatter (FSC) by flow cytometry. (c) CD138 expression of B cells purified and activated as in a. APC, allophycocyanin; PE, phycoerythrin.
(B) The graph depicts percentage change in body weight of CHIKV infected irgm1+/+ and irgm1-/- neonates for duration as indicated
(D) Heatmap showing phosphosites in CK-p25 which overlapped in their directional change with BV-2 Siglec-F-associated sites. Colors indicate fold change relative to 2xY->F controls.
Immunoblot (IB) analyses of the levels of β-catenin and RAS in DLD1, WT-HCT116, MT-HCT116, HepG2, and SW48 cells transfected with Myc-axin for 36 hr
(A,B) Splenocytes isolated from Bbs4+/+ (n=4 mice) and Bbs4GT/GT (n=3) B-cell transgenic B1-8 littermates were activated with 4-hydroxy-3-nitrophenylacetic acid succinimide ester-loaded T2-Kb cells in three independent experiments. Percentage of activated B cells (gated as CD69+ B220+ IgLλ+ viable cells) in the samples without T2-Kb (negative control), and in the samples with T2-Kb added in ratios 1:10 or 1:3 was determined by flow cytometry. (A) Representative mice are shown. (B) Mean±SEM. Statistical significance was calculated using two-tailed Mann-Whitney test.
(F and G) YFP-LC3 and mCherry-Parkin stably expressing WT (F) and TBC1D15−/− (G) cells were treated with valinomycin for 3 hr and then subjected to immunoelectron microscopy with anti-GFP antibody. The square in panel a shows enlarged areas in panel b Scale bars, 500 nm.
Δ_intron_retention values for the MVA patient cell dataset (compared to the healthy sibling) using all (significant and not significant) minor A-type introns (n=179 for the depletion and n=177 for the MVA patient datasets) and minor G-type introns (n=441 for the depletion and n=446 for the MVA patient datasets). Only introns with on average at least 5 intron-mapping reads were used in the analysis. See also Appendix Figure S12.
(c) MALDI MS analysis of the ε-cleavage sites of wt and mutant TREM2 C-terminal fragments. Mass spectrometry reveals ε-cleavage C-terminal of A192 for the wt CTF. MS determination of the ε-cleavage site of TREM2 CTF K186A reveals major and minor ε-cleavage sites C-terminal of A195 and L193, respectively. The exact same cleavage pattern is observed for the K186L mutant. MS analysis of the cleavage pattern of the K186P mutant reveals major and minor ε-cleavage sites C-terminal of L193 and S191. Minor peaks that could not be assigned are indicated by an asterisk.
Nuclear accumulation of PBG observed under GFP excitation in the given genotypes. (C,D) Epi-fluorescence microscopy. (E,F) Confocal microscopy showing the size of the nuclear bodies. Scale bars equal 5 µm.
U87 cells were treated with increasing concentration of LXR623 in the presence or absence of cholesterol. Thereafter, whole cell protein lysates were collected and analyzed the protein levels of the respiratory complexes (OXPHOS) by standard western blot.
A. Scheme of the experimental approach to quantitatively capture gene expression changes during mESC differentiation towards EpiSCs.
(B) Heat map of PPARγ target genes upregulated in both HFD feeding and HF-R at ZT12 (n=4, Cyber-T test p<0.05).
C, D Representative H&E images (C) and the degrees of inflammation (D) of intestinal tissues from animals treated with SCH772984 or Bevacizumab. The inflammatory infiltrates were indicated by a yellow arrow. The edema area was indicated by a red star. Scale bar, 100 µm. For each group, n = 4. n, biologically independent samples (mice). Data information: All data are shown as mean ± SD. P values are determined by one-way ANOVA.
A. 3′ end counts for the indicated locus in the Drosophila melanogaster genome, corresponding to tRNA-Alanine(TGC) in libraries generated from total RNA or dmDis3l2CM-IP. PM, prefix-matching (i.e. tailed); GM, genome-matching.
In the probe trial 24 h after the last training day, the time mice spent in the target quadrant (TQ) was different from chance in all groups except for APP/PS1-Stat3WT mice (p < 0.05, one-tailed one-sample t test). APP/PS1-Stat3KO, WT-Stat3WT and WT-Stat3KO mice spent significantly more time in the target quadrant compared to the mean of all other quadrants (AO), whereas APP/PS1-Stat3WT spent equal times in the target and all other quadrants (Wilcoxon matched-pairs signed rank test for each comparison; APP/PS1-Stat3WT, n = 15 (8 female and 7 male) mice; APP/PS1-Stat3KO, n = 15 (9 female and 6 male) mice; age, 8-9 months).
B HSATIII ASO-mediated depletion of nSBs. Thermal stress-exposed HeLa cells (42°C for 2 h and recovery for 1 h at 37°C) were visualized by HSATIII-FISH and immunofluorescence using an anti-SAFB antibody or anti-HNRNPM antibody. The nuclei were stained with DAPI. Scale bar: 10 μm.
A. Left. Representative images of surface GluA2 and DARPP32 expression in striatal neurons from co-cultures treated either for 30 min with DHPG (DHPG) or for 30 min with DHPG and pretreated with Xestospungin C and S107 (XeC/S107 + DHPG). Right. Quantified expression of surface GluA2 under each condition, n = 3 replicates of 10 or 20 cells each, p < 0.0001, Student's t test.
Graphical summary of the alterations in the dynorphinergic system between healthy (top panel) and epileptic (middle panel) hippocampi and their consequences on neuronal signaling. The bottom panel indicates the proposed mode of action of AAV-pDyn gene-therapy. The incoming burst stimulus triggers the release of dynorphins in a "release on demand" mode.
A. Immunoblot analysis of U2OS/GFP-FAM111A WT cells treated with DOX for the indicated times.
(B) Ten micrograms of control and patient cell lysates were tested for their chymotrypsin-like activity by incubating them with 0.1 mM of the Suc-LLVY-AMC substrate at 37°C over a 180-h period of time in quadruplicates on a 96-well plate. Indicated on the y-axis are the raw fluorescence values measured by a microplate reader and reflecting the AMC cleavage from the peptide. Bars show the mean of 4 independent experiments +/- SD.
GSC#9 were transfected with LC3B reporters (wild type WT or G120A mutant, which cannot be lipidated), treated 24 hours later with vehicle (DMSO) or MPZ (20 µM) for 6 more hours. Ratios of WT/mutant luciferase signals are presented as the mean + s.e.m of 3 independent experiments.
Cellular cholesterol content of ECs freshly isolated from Ldlr+/+ and Ldlr-/- mice stimulated for 15 min with VEGF-B186. Data presented as mean ± SEM from a representative experiment performed in triplicates. Statistical evaluation using one-way ANOVA and Tukey´s multiple comparisons test, p-value: *** <0.001 (compared to Ldlr+/+ control).
D SRM images of the paraspeckles in ∆16.6-20.2 kb and ∆20.2-22.6 kb cells detected by NEAT1_5′ (green) and NEAT1_3′ or 19k (magenta) FISH probes in the presence of MG132 (5 μM for 6 h). Scale bar, 500 nm.
(F) Summary of the predictive accuracy of the three cABNs progressively refined against experimental results, with the 0.717 cABN having the highest predictive accuracy for each set of the investigation
(C) ChIP-qPCRs at ARAP1, RFX5-GBAT2, WDR74 and HAUS5 promoters for IgG and DVL3 in MDA-MB-468 (NTC, shA DVL3, and shB DVL3).
L ERLAD schematics. 1. Synthesis and CNX-independent polymers formation; 2. CNX-regulated polymers segregation in ER subdomains (ES); 3. FAM134B-dependent (LIR-independent) formation of ER-derived vesicles (EV); 4. FAM134B:LC3II-mediated EV docking to RAB7/LAMP1-positive endolysosomes (EL); 5. STX17/VAMP8-controlled fusion of EV:EL membranes and polymers release in the EL lumen for clearance.
(E) Immunoblotting of ESM1 expression with different expressing patterns in the supernatant (S) of 22Rv1-P cells.
(A) Western blots for Ago2 (top) and HA tag (bottom) of parental Mavs-/- MEFs and two Mavs-/- Ago2-/- clones (clone 5.2 and 5.3; see Fig 4A) stably expressing d2GFP and transduced with an empty vector or a vector encoding HA-tagged wild-type (HA-mAgo2 WT) or catalytic mutant (HA-mAgo2 D597A) versions of mouse Ago2. β-actin served as loading control. The membrane was first analysed for Ago2 and β-actin, stripped and then analysed for HA tag.
Localization of Ams1 in WT, lap2Δ, ape2Δ, and ape4Δ cells. Scale bar, 3 μm.   Localization of Ape4 in WT, lap2Δ, ape2Δ, and ams1Δ cells. Scale bar, 3 μm.
D) MDA-MB-468 were infected with the indicated shRNAs targeting EGFR and selected by puromycin. cell viability was measured after 4 days of treatment with serial dilutions of AZD8186 (D). Average ± SD of triplicates and representative of three independent experiments.
Voronoi diagram showing the functional distribution of 145 proteins targeted for deletions present in JCVI-syn3.0 (black), M. florum only (dark grey), and JCVI-syn1.0 but not JCVI-syn3.0 (light grey). The shapes are sized according to transcriptomic data and the KEGG categories are represented by bright colors. The single protein associated with environment information processing is represented in black on the top part of the diagram between the genetic information processing and metabolism categories. Voronoi diagram showing the functional distribution of the retained proteins in the predicted reduced genome. Shape colors are as in b, and purple represents proteins shared with JCVI-syn3A but absent in JCVI-syn3.0. Section borders are colored according to KEGG categories depicted in c.
A MMS-induced checkpoint activation is not altered in irc5-Δ1 cells. The level of Rad53 phosphorylation was analyzed in wild type (W303-1a) and irc5-Δ1 (IL012) cells by Western blot with an anti-Rad53 antibody
HeLa CALCOCO1 KO cells stably expressing EGFP-CALCOCO1 were starved for 4 hours and then immunostained with anti-ATG13 and anti-WIPI2 antibodies. Scale bars in A are 5 μm for the confocal microscopy images and 2 μm for the airyscans.
F. The capacity of HctRNAs to be methylated by hTrmt13. Error bars represent mean ± SD for at least three independent experiments.
Correlation of mRNA expression of USP28 and TP63 in lung SCC (left, n=498), ADC (right, n=513) and normal, non-transformed tissue (normal SCC=338, normal ADC=348). R: Spearmans correlation coefficient; m=Slope. Xena UCSC software.
A, Representative photomicrographs taken from the dorsal striatum 13 weeks after AAV-injection. In mice injected with GFP control virus, virtually all GFP positive cells depict an astrocytic morphology, many GFP positive cells in ALNe-218 and ALN-treated animals show a neuron-like morphology. Data information: Scale bars indicate 20 µm.
Graphical summary showing muscle mitochondrial stress induced secretion and diurnal variation of GDF15 to drive a daytime-restricted anorexia, affecting in turn metabolic flexibility, adiposity, WAT browning and systemic insulin sensitivity. Parts of this cartoon were created using Servier Medical Art (http://smart.servier.com). Data shown are from male wild type (WT) vs. Ucp1-TG (TG) mice sacrificed at day (10am) or night (10pm).
Number of ookinetes in the mosquito midguts. The midguts were dissected at 8 hour post blood-feeding and stained with P28 antibody to visualize the crescent-shaped mature ookinete. n represents the number of mosquitos dissected.
A. Phase contrast images of representative cultures for B6 and D2 strains maintained in conditions supporting naive pluripotency and after transitioning to formative EpiLCs. B6 ESC colonies adopt a classical ground state morphology, whereas D2 ESCs grew with a flat morphology and fewer cells per colony. Morphological differences persisted in EpiLCs (Scale bar = 50 µm).
C Immunoprecipitation analysis of the interaction between USP33 and p97 in RAW264.7 treated with additional NaCl (+34 mM) for 12 hrs. Data information: Data are representative of at least two biological replicates.
(C) CSD threshold and CSD velocity in cortical slices from P30-33 KI mice that were injected with saline (Ctr KI, n = 38; N=7) or Cef (Cef KI, n = 31; N=6). CSD threshold is 12% higher (Mann-Withney U test: P = 0.02) in Cef-treated compared to saline-treated KI mice. CSD velocity is not altered by Cef treatment (P = 0.90).
I BMDMs were pretreated with NF-κB inhibitor BAY11-7082 (1 μM) for 1 h and infected with VSV (MOI 1) for 6 h. The percentage of lincRNA-EPS transcripts downregulation in the VSV-infected group compared with the Mock group was calculated.
(F) Succinate Dehydrogenase activity staining in transversal sections of mouse gastrocnemius and corresponding intensity quantification (n=3-4). Scale bar= 50µm. 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.
Human T cells from two healthy donors, P1 and his mother were expanded and cultured in the presence of C. albicans and IL-2 for 2-4 weeks. (D) Fura-2 loaded T cells were stimulated with thapsigargin (TG) in Ca2+-free buffer followed by readdition of 2 mM Ca2+ to induce SOCE. Bar graphs represent the mean ± SEM from two independent experiments.
(E) Immuno-blot analysis of fractions collected during preparation of SVs from brain of Clcn3ven/ven mice. VenusClC-3 (detected with GFP antibody) co-purified with SV marker protein synaptophysin.
(A) Transcript mRNA expression of Col1a1 and Fn1 in sham and post-MI hearts. Hearts were obtained at day 7 after surgery. Error bars represent mean ± SEM (n=13-16 for each group). Statistical analysis was performed by two-way ANOVA. Post Hoc test was performed by Tukey test.
(c) F1 survival after control (black diamonds) or bec-1 RNAi (red squares) in N2 and msh-6(pk2504) mutants. The survival curve shows the mean±s.d. for each data point from three independent experiments.
A Schematic of microtubule regrowth assay during mitosis in RBM14-depleted U2OS cells.
(A) 293T cells were co-transfected with HA-GRWD1 wild-type (WT) (0.5 ug) or HA-GRWD1 Δ1-136 (3.5 ug) and RPL11-FLAG (1.5 ug) as indicated for 42h, and then immunoprecipitated with an anti-FLAG antibody. Immunoprecipitates (IPs) and 1.6% of inputs were immunoblotted with the indicated antibodies.
C. Top. Representative immunoblots from GluA2 co-IPs probed for Sec23 and GluA2 after no treatment, 30 min DHPG, and 2APB/dantrolene followed by 30 min DHPG. Bottom. Quantification of Sec23 normalized to GluA2 under each of these conditions. For 30 min DHPG, n = 17; For 30 min DHPG + 2APB/dan, n = 14, p < 0.05, ANOVA.
Fluorescence image containing PDGFRαhigh MYO from sorted PDGFRα-GFP rMC within BALO derived from tdTomato+ mice at day 21 of culture. Scale bars represent 100 μm (left) and 50 μm (right).
mAb414 labeling of 5DO dTorKO fat body cells expressing the dTor cDNA, Luciferase RNAi, or RNAi against Nep1r1, Ctdnep1, or Lipin. Nuc, nucleus. The percentage of fat body cells with NE-localized mAb414. ** and **** indicate that Lipin, Ctdnep1, and Nep1r1 RNAi significantly increased the number of dTorKO cells with NE-specific mAb414 labeling compared to the Luciferase RNAi (Luc). Chi-square test followed by individual post hoc Chi-square tests. ** p < 0.01 and **** p < 0.0001. NE ultrastructure in 5DO dTorKO cells. Red arrows, nuclear pores; yellow arrows, abnormal INM herniations. Nuc, nucleus; Cyto, cytosol.
(B) TIRF image of TMR-labeled DDB molecules (green) on either WT (red) or CPA-treated (blue) pig brain MTs. Standard deviation map of the entire time sequence shows DDB preference for WT MTs and kymographs from either WT or CPA-treated are shown. Scale bars are 5 μm and 25 sec. (C) Quantification of the number of processive DDB complexes per μm MT per sec on the CPA-treated MTs, relative to WT MTs in the same chamber (n ≥ 7 MTs of each type quantified from at least three independent experiments). Error bars represent SD.
A. Representative Per2::Luciferase trace of Cry1-/- SCN slice at baseline (black) and after AAV-mediated (arrows) Cry1 complementation in Prok2+ cells (red) or ProkR2+ cells (yellow).
A schematic cartoon model of ZBD-relocation mechanism during σ28-mediated transcription initiation is presented. The ZBD-relocation shows an overall effect of facilitating the isomerization of closed RNAP-promoter complex (RPc) to open RNAP-promoter complex (RPo) by contributing to RNAP-promoter interaction. The RPc with the relocated ZBD (state 2) has a higher efficiency in isomerizing to RPo or is more stabilized than the one with the state 1 ZBD, consequently advancing transcription efficiency. The inset is the zoom-in view of ZBD relocation from state 1 to state 2.
Immune cell contexture in healthy colon and colon tumors of Apcfl/fl-Cdx2CreERT2 mice. Relative CD11b+ myeloid cell content in colon (n=16) and tumors (n=16). relative content of individual cell types was determined in tissue-derived single cell suspension using cell type specific antibodies and FACS analysis.
B, H1299 cells were transfected with Flag-tagged p53 for 24 h and then treated with 12 μM erastin or untreated for another 24 h. Co-IP analysis was performed with antibodies against Flag.
E. Release half times (t1/2) of target RNAs in panels (A-C) plotted against isomiR length. Data information: All plotted data are the means of at least three independent replicates. Error bars indicate SEM.
(A) Stills from time-lapse sequence of representative Hela cells expressing Lifeact-GFP and H2B-mCherry, exiting mitosis under different conditions i.e. Control siRNA, knock-down of centralspindlin protein RACGAP1, in the presence and absence of Aurora B kinase inhibitor (2µM ZM). Scale bar - 10 µm
qPCR analysis of glut1 and glut2 expression in liver tissue dissected from WT, yap-/- mutant and lf:Yap transgenic adults. n>3, *p<0.05, **p<0.01, two-sided Student's t-test; values represent the mean ± s.e.m
(B) HeLa cells were infected with Salmonella for 1 h or transfected with Effectene-coated latex beads for 3 h and then subjected to immunocytochemistry for LC3 and galectin3. Bar, 5 µm.
Representative DNA dot blot from C-circle assay on HuO9 cells, either mock transfected or transfected with 20nM siRAD54#2 for 48 hours. Quantification of C-circle assay in C. Signal was quantified with densitometry, background (- Φ29) was subtracted and signal was normalized to mock. N=5 biological replicates values shown are mean±sd. Conditions were analyzed using unpaired two-tailed student's t-test.
G Maximum intensity projections of fluorescent microscopy z-stacks of of 5-day-old nematodes expressing the indicated transgenes. White dashed lines outline the borders of muscle cells. Scale bar: 10 µm. M: muscle, H: hypodermis. Signal outside of muscle cells reveals spreading of α-Syn. H Quantification of animals showing α-Syn transmission at indicated ages. Displayed is the mean ± SEM (in %) (N = 4). Statistical analysis was done using two-way ANOVA with Dunnett's multiple comparison test. *** p ≤ 0.001.
A-H. Base pairing patterns for the sRNA-mRNA pairs identified by CLASH were calculated using IntaRNA software (Busch et al. 2008) and are shown (left) for chuA-Esr41 (F). Point mutations and predicted sRNA seed sequences (blue shading) are indicated. (Histograms, right) Median fluorescence intensity (MFI) was assessed by FACS for mRNA-sfGFP fusions with compensatory base changes. In each case, introduction of a point mutation into an sRNA or mRNA construct (M1) is expected to reduce sRNA repression, which should be restored by combining complementary point mutants (last bar, M1-M1). A two-tailed t-test was used to calculate significance from biological triplicate cultures. *p<0.05.
LDH release from WT and Cyld KO BMDMs primed with LPS and stimulated as indicated.
A. RT-PCR analysis of the expression of β-actin, Trpv1, Trpv2, Trpv3 and Trpv4 using mouse differentiated brown adipocytes after 29 (upper) and 35 (lower) thermal cycles with (RT (+)) and without (RT (-)) reverse transcription (RT). Control (Ct.) lanes indicate the results with each plasmid DNA as a template.
(E) relative immunohistochemical scores are shown. Student's t test was used to analyze statistical differences. Mean with ± SD. (G) relative immunohistochemical scores are shown. One-way ANOVA was used to analyze statistical differences. Mean with ± SD. Data information: in B, C, E and G, data were obtained from 4-5 tumors per group.
(D) MT intensity at MTOCs at the time of GVBD quantified from SiR-tubulin signal that was normalized to mean cytoplasmic SiR-tubulin signal. Mean of MT intensity on MTOCs was arbitrarily centered to 1 in the control group. Means ± SDs, Kruskal-Wallis, and Dunn's tests. 25 control oocytes with 264 MTOCs in total, 10 RanT24N-expression oocytes with 70 MTOCs in total and 19 RanT24N, T42A-expressing oocytes with 96 MTOCs in total were analyzed.
D. Quantification of the western blot in (C). Signals from the control and FBXL4-mutated cells were considered as biological replicates, normalized to the average of controls and displayed as mean ± SEM (n=3 for each). Student's t-test; *, p<0.05; **, p<0.01; ***, p<0.001.
Among genes with exactly three PASs in 3' UTR, genes with major PAS located proximally have lower sequence conservation in the core regulatory regions of the major PASs and are under weaker selective constraint in their coding sequence
E Tethering assay using the F-Luc-HhR-A95-C7-Hhr reporters containing an 8-nt or a 109-nt 5'-UTR and λN-HA-Me31B in S2 cells. F-Luc activity and mRNA levels were analyzed as described in Fig 2A and B.
(K-M) Cbl induces GSC differentiation. Immunostaining of germaria overexpressing Cbl with Hsp83-CblL (K) White arrows indicate a cyst in the GSC niche (K, outlined)
Percent body weight of male Prdx4-flox and Prdx4-∆LysMCre mice over the 48 h course of 4.5 mg/kg BW LPS ( i.p.). Each circle represents a mean of n=7 mice, vertical lines indicate SEM.
(a) Schematic representation of the rod and cone death kinetics found in the four mouse models of retinitis pigmentosa. The onset of cone death is set as time zero. The corresponding time windows on the x axis are given in weeks. The major cone death phase was the time period from onset until roughly 85% of cones had died. The end phase of cone death was the time period thereafter.
The levels of assembled ATP6V1A (R) (n = 3 independent experiments, *P = 0.0316) and ATP6V1C1 (S) (n = 3 independent experiments, **P = 0.0027) are quantified. Data information: Error bars represent ± standard deviation. Scale bar, 10 μm.