EMBO/sd-character-level-ner huggingface dataset:
D Western blot of Sec63, mCherry and Pgk1 from WT cells (SSY1404), cells harboring the estradiol-inducible system (SSY1405) or ∆opi1 cells (SSY1607), all of which expressed Sec63-mNeon and Rtn1-mCherry. Cells were untreated or treated with 800 nM estradiol for 6 h. Pgk1 served as a loading control.
(C) Coomassie‐stained gel of a liposome co‐sedimentation assay showing the lipid requirements of the Atg5-Atg12/Atg16 complex. Liposomes were composed of 40% POPC, 35% POPS, 20% POPE and 5% PI3P. In the liposomes containing no POPE or POPS, these lipids were replaced with POPC.
(A) Growth assay of the indicated cells with and without doxycycline-inducible overexpression of PLK4. Experiments were performed in wild-type or SAS6 monoclonal knockout cells. Data acquired across n = 3 biological replicates. Mean ± s.e.m.
umber of γH2AX foci, respectively, in control- and Molm-14-xenograft-derived: (K) KSL, n=101 / 204, and (L) LT-HSC, n=33 / 53. Images were processed similar to D-F. Scale bars are 3μm. Statistics: Student's t-test. (** P< 0.01).
Immunoblot probed with Siglec‐5 Fc and Siglec‐14 Fc to detect direct binding to Hsp70. B6N domain of GBS β‐protein was used as a positive control, and clusterin was used as the negative control.
4D) SH-SY5Y cells were grown in RPMI+5% FCS and the amount of nt and PINK1 knockdown (kd) cells in S-phase was determined by BrdU incorporation. No differences in cell proliferation were visible between cells without (nt) and with PINK1 kd; n = 3.
Wildtype myosin is phosphorylated in early sporozoites allowing the generation of optimal force transduction and gliding motility. Dephosphorylation is also important for optimal force generation as S19D shows lower force and speed. Non-phosphorylated myosin still allows sporozoite gliding but at reduced speed with too little force generated for efficient salivary gland invasion. Disruption of the interaction of the N-terminus with the Switch I and II (E6R mutation) has similar impact as constitutive phosphorylation as mimicked by S19D.
AFraction (left) and speed (right) of motile hemolymph sporozoites on glass . Dots correspond to individual experiments and bars indicate the mean. Box‐and‐whisker plots depict the 25% quantile, median, 75% quantile, and nearest observations within 1.5 times the interquartile range (whiskers). Significance for (A left) and (B left) determined by One-way analysis of variance with Tukeys Multiple Comparison test. Significance for (A right) and (B right) determined by Kruskal-Wallis test with Bonferroni's Multiple Comparison test.
(A, C-E) Changes in mRNA transcript levels of an array of adhesion molecules (A) in retinas from ONC eyes compared with contralateral noninjured retinas, 8 hours, and 1, 3 and 7 days after ONC. n = 6-13 per group. Data shown are representative of three independent experiments.
I Lysates from 293T cells transiently expressing GFP-CbpC or GFP, and HA-Atg14 were subjected to SDS-PAGE and analyzed by immunoblotting using antibodies against HA or GFP.
Four to six-week-old C57BL/6 mice were injected i.p. with 104-107 PFU of WNV-poly(A), 104 PFU of WT WNV or PBS (negative control) in a volume of 200 μL. body-weight changes in infected mice were monitored daily (n=5, the values represent mean ± sd in each group) Data information: two-way ANOVA analysis were used * p < 0.05, *** p < 0.001, ****p < 0.0001, ns represents not significant.
J. AlphaLISA-mediated quantification of p-Syk levels in human macrophages upon treatment with Ab1 and Ab2 with liposomes for 60 min (n=3). An isotype antibody was used as a negative control. Data points indicate individual patients. Isolated material from patient #3 did not yield enough cells to perform this experiment. Data information: Data represent mean ± SEM. For statistical analysis of patient samples in comparison to HC, the unpaired, two-tailed student`s t-test was performed. Statistical significance was set at *, p < 0.05; **, p < 0.01; ***, p < 0.001; ****, p < 0.0001; ns, not significant
(d) A COS-7 cell expressing EBFP2-parkin (cyan), AcGFP-sec61β (green) and TagRFP-DFCP1 (red) were treated with 10 μM CCCP for 4 h and imaged. Omegasomes (DFCP1) appeared where ER (sec61β) and impaired mitochondria (parkin) overlap. Scale bar, 10 μm.
D. Internal structure of the mean and CV of width in island 16. The average gradients of phenotypes over the area of the island 16 are represented with arrows.
(C, D) Immunoblotting against the GFP (C) or the HA tag (D) or the GAPDH of proteins extracted from HEK293 cells transfected for 24 hours with 3, 10 or 100 C4G2 repeats embedded in the human antisense C9ORF72 sequence fused to the GFP in the PG frame.
(C, D) Heatmaps showing expression levels of genes involved in KEGG pathways (C) fatty acid degradation and (D) ketone body metabolism in cardiac endothelial cells isolated from male C57Bl/6J mice that were fed a ketogenic diet or control diet for two weeks.
E, F. Preference index was tracked and calculated using MATLAB and Optimouse. One sample t and Wilcoxon tests were used for statistical analysis. Data is presented as mean ± SEM. *** p<0.001. Total N=11, 13 mice were used for each genotype.
(A) GSCs contain the higher levels of stemness markers (Nestin, SOX2, Musashi-1, NANOG, and OCT4) compared with their DFCs. Total RNAs from GSCs and DFCs were subjected to real-time PCR. The average relative amounts of GSCs were normalized with those of DFCs. Shown are means +S.D. of the normalized mRNA levels of GSCs obtained from the three independent experiments.
C Transient expression assay in the infiltrated leaves of N. benthamiana showing OsPRR73 can repress OsHKT2;1 transcription. Left panel showing the bioluminescence signal of OsHKT2;1 and OsPRR73. Bioluminescence of co-transformation of either GFP or 35S: GFP-OsPRR73 (GFP-OsPRR73) with OsHKT2;1pro: LUC in N. benthamiana. D Quantiﬁcation of bioluminescence intensity of OsHKT2;1pro: LUC shown in (C). Data represent means ± SD. n = 10. The asterisks indicate the significant difference by student's t-test with (***) P ≤ 0.001. At least two biological replicates were conducted with similar results.
Microscopy of Tau:polyA, Tau:PEG, and Tau:PEG:polyA condensates (5 µM Tau, 10% PEG, 4.8 µg/ml polyA) formed at increasing NaCl concentrations and in X/2-buffer mimicking the axoplasm ion composition. Scale bar=10 μm.
(C G3BP1-mCherry HeLa-Kyoto cells were lipofected for 72 hrs with a non-targeting siRNA control or siRNAs specific for Hsp90 α and β. (C) Efficacy of Hsp90 knockdown and expression levels of HSPA1A were verified in total protein extracts. TUBA4A was used as loading control.
(A) Effect of 3‐MA on neutrophil phagocytic capacity of opsonized E. coli as observed by flow cytometry. Percentage of phagocytosing neutrophils after 3‐MA pretreatment (III) compared with cells incubated with opsonized bacteria (II). Data are representative of six independent experiments and are presented as mean±SD, (I: control unstimulated group), (IV) MFI representation (bar 1: control: 1±1.9, bar 2: E. coli: 387.7±33.3, bar 3: E. coli+3‐MA: 25.13±18, Wilcoxon matched‐pairs test, *p<0.05; bar 2 compared with bar 1 and bar 3 compared to bar 2).
D, F, Fraction of D4H area overlapping with lamp1 (D) and D4H area positive for internalized integrin β1 (F) in a peripheral region toward the leading edge (exemplary box as inset). Mean ± SD, n = 20-30 cells pooled from 2 independent experiments. Student's t-test.
c) Kinetics of YFP labeling in macrophages of the healthy eye. Symbols represent means ± s.e.m. rMG are shown as squares (2 weeks: n = 10 mice, 12 weeks: n = 9 mice , 24 weeks: n = 12 mice, Kruskal-Wallis ns p > 0.05), cbMΦ are depicted as triangles (2 weeks: n = 4 samples from eight mice, 12 weeks: n = 3 samples from six mice, 24 weeks: n = 6 samples from twelve mice, Kruskal-Wallis ns p > 0.05) and cMΦ as circles (2 weeks: n = 6 mice, 12 weeks: n = 8 mice, 24 weeks: n = 12 mice, one-way ANOVA ***p < 0.0001). Data were obtained from two (cMΦ: 2 weeks, cbMΦ: 2 and 12 weeks), three (rMG: 2 weeks, cbMΦ: 24 weeks) or four (rMG: 12 and 24 weeks, coMΦ: 12 and 24 weeks) independent experiments.
(F) Immunoblot of SCOT, BDH1, CD31 and the loading control VCP in human cardiac ECs, HUVECs and adipose tissue ECs.
A. Root tip of Arabidopsis with distinct growth zones marked: meristematic (MZ, green), transition (TZ, blue), elongation (EZ, pink) and differentiation (DZ, yellow). Double arrow indicates the first expanded cortex cell considered as a start point of the TZ, which encompasses epidermal cells smaller than 45 µm. Epidermal cells reaching a length of more than 45 µm prior termination of the elongation are in the EZ. Scale bar 25 µm.
D-E) Principal component analysis (PCA) of all subjects based on their urinary proteome profiles. Female subjects are shown in purple and males in green.
(A-B) Immunofluorescence (IF) analysis of IκBα in sections from murine small intestine of 2 month-old WT (A) and Lgr5-GFP reporter mice (B). Scale bars, 50μm.
Back skin sections of P55 mouse skin immunostained for LYVE1 (red), Tenascin-C (green) and counterstained with DAPI (blue). n= 3 - 4 skin samples per mouse, n= 3 - 4 mice. Scale bar, 50 μm. TNC, Tenascin-C.
Representative H&E histological staining of sWAT at 20wks of age (scale bars represent 50 μm) Data are from male wild type (WT), Ucp1-TG (TG), and Ucp1-TGxGdf15-KO (TGxKO) mice.
D) Snapshots of a laser cut in the nest area. PIV arrows are shown in red. Scale bar = 5 µm.
Vascularized area. I. Vessel area in the outer 20% of the retinal vasculature; pink in F (vessel area normalized to vascularized area). Each dot represents one retina/mouse; n=3-4.
(C) CH058-, CH077- and vKB18-infected primary CD4 T cells were incubated with the indicated antibodies and NHS. After 24h, C3 surface levels on infected cells were analyzed by flow cytometry. Results are expressed as MFI of staining on infected (Gag+) cells. Each dot represents a donor of CD4 T cells. n=6 donors of CD4 T cells.
(F) Immunofluorescence staining of LC3 in WT or PAQR3-deficient MEFs after GS for 4 h. The arrowhead indicates representative LC3-positive puncta. Scale bar: 10 μm.
Workflow of tamoxifen (TAM)-induced Ythdf1 deletion in AOM/DSS-induced Lgr5-creERT2:Ythdf1fl/fl mice.
(B) Western blotting analysis of cellular extracts from HepG2 cells transfected with the indicated plasmids.
C and D) HEL cells primed live for 30 min with an anti‐CD235a‐Atto655 antibody before treatment with the Duolink reagents.
(E) Representative Hematoxylin and Eosin stained motoneurons in the coronally sectioned hypoglossal nucleus (white dashed line) of 36 weeks old mice with different genotypes. The motoneurons are dark purple with pyramidal shape within the nucleus. C: central canal. Scale bar = 100 μm.
D) Intracellular mycobacteria harvested and assayed for viability based on time to positivity (75 growth units) at day 0 and day 7 using the MGIT 960. All bar and line graphs are reported as mean ± s.e.m. of three independent experiments performed in triplicate. § P<0.05; * P<0.001.
Pulldowns of pointed end site 1-4 mutants using Strep-Hook3 (D) or Strep-BICD2 (E). Binding is shown relative to the binding of the wildtype pointed end construct (dashed lines). * shows p<0.05. For BICD2, p=0.06 for Site 1 mutant, and p=0.1 for Site 4 mutant. Data presented as mean ±SEM, n=3. Statistical significance calculated using ANOVA with Tukey's test for multiple comparisons.
(E) Expression of MAKR5-GFP fusion protein under control of the MAKR5 promoter in 5-day-old roots upon CLE45 treatment (3 h). Note accumulation of MAKR5-GFP in protophloem sieve elements (magnified) and its dependence on functional BAM3 and CLE45. The frequency of representative observations per total observations is indicated.
D. Proportions (Y-axis) and numbers (within bars) of cells arising from the different regions of a fusion are listed for each cluster. Numbers are down-sampled to 941 cells in the smallest region group for proper representation. UMAP depicting the fusion region from which the cells were isolated.
(C) Coverage of expressed genes by PolII S5P ChIL-seq peaks. The stacked bar chart shows the proportions of detected genes in the RNA-seq only (RNA-seq: blue), PolII S5P ChIL-seq only (ChIL: red) and both (Common: green).
A-B) NK cells were activated with IL-2 or IL-15 for two days in the presence or absence of PGE2 (1µM) and analyzed for A) the levels of phosphorylated S6 (pS235/pS236), STAT3 (S727), STAT5 (Y694), Akt (S473) (n=4, biological replicates) and B) 16 categories of phosphorylation array showed. Red box indicates category 1 (pS6+, pSTAT3+, pSTAT5+, pAKT+).
(E) The load of aggregated SQSTM1/p62 is also reduced by the treatments in ALSC9orf72 cultures (one-way ANOVA followed by Dunnett's multiple comparison test). n=3 independent treatments for each cell line. Scale bar: 20 µm. Data information: *p<0.05; **p<0.01; ***p<0.001. Error bars represent SEM. Arrow indicates the structure displayed at higher magnification. Exact p-values are reported in Appendix Table S1.
A Representative APs at 1 Hz of VM and AM CMs in response to vernakalant. Inset shows dV/dtmax.B, C Average APAplat (B) and dV/dtmax (C) in the absence and presence of vernakalant at 1-4 Hz. AP parameters are shown in Supplementary Table S6. Abbreviations as in Figs3 and 6.Data information: Data are presented as mean ± SEM. *P < 0.05 by Mann-Whitney rank-sum test for (B). P = 0.01, 0.008, 0.008 and 0.007, respectively, for comparison of APAplat between VM and AM groups at frequencies of 1.0, 2.0, 3.0 and 4.0 Hz. Two-way repeated measures ANOVA followed by pairwise comparison using the Student-Newman-Keuls test for (C). P = 0.686 between VM and AM groups and hence not statistically significant. For VM, P = 0.06 for 1 versus 2 Hz; P < 0.001 for 1 versus 3 Hz; P < 0.001 for 1 versus 4 Hz; P = 0.001 for 2 versus 3 Hz; P = 0.002 for 2 versus 4 Hz; and P = 0.857 for 3 versus 4 Hz. For AM, P = 0.03 for 1 versus 2 Hz; P < 0.001 for 1 versus 3 Hz; P < 0.001 for 1 versus 4 Hz; P = 0.02 for 2 versus 3 Hz; P = 0.02 for 2 versus 4 Hz; and P = 0.621 for 3 versus 4 Hz.
D, E) SOD1 filter trap assay (D) of spinal cord homogenates at 130 days and quantification of dot intensities (E), showing that PKO/G93A mice have less SOD1 aggregates than G93A. Results are expressed as mean ± SEM and as percent of Non Tg; n= 8 (4 males and 4 females); **p= 0.0078 by paired Wilcoxon's test.
(C) GSEA of RNA seq data demonstrating the enrichment of gene sets related to Wnt signaling in 22Rv1-P cells expressing ESM1-NLS. NES, normalized enrichment score. The p values for the GSEA test statistics are calculated by permutation.
I. The binding profiles of hTrmt13, H3K4me3, H3K27Ac, and other transcription factors (MYC, E2F1, TP53, FOSL1, EZH2, FOXM1) from ChIP-seq and ATAC-seq on representative target genes TGFB1, MEF2A, and PKN2. hTrmt13 track were average across 2 biological replicates.
(C) Kaplan-Meier survival curves of the 4 groups of mice shown in panel B. Statistics: Gehan-Breslow-Wilcoxon test.
(A) Inhibition of SARS-CoV-2 infection by ACE2-Fc in the plaque assay. Mixtures of ACE2-Fc and SARS-CoV-2 were incubated for one hour before adding to Vero E6 cells for another 1 hr at 37°C. The ACE2-Fc and SARS-CoV-2 premixtures were removed, and the cells were washed once with PBS and overlaid with methylcellulose with 2% FBS for 5-7 days before being stained with crystal violet. Those results showed increase of plaque formation was regarded as no inhibition of plaque formation. TPCK-treated trypsin: N-tosyl-L-phenylalanine chloromethyl ketone-treated trypsin.
(F) ACTN2 immunostaining of CTRL-, TECRLHet- and TECRLHom-hiPSC-CMs. Scale bar: 25 μm.
B Representative fluorescence microscopy images of BSP and its subconstructs (20 μM) at varying pHs. PEG 8K concentration is 2 %. Scale bar, 20 μm.
STK38 kinase activity is required and sufficient for its cytoplasmic accumulation upon nutrient starvation. (A) HeLa cells silenced for endogenous STK38 were transfected with myc-STK38(wt) expressing plasmid, myc-STK38(K118R) (STK38 kinase-dead version) plasmid or with HA-STK38(PIF) (STK38 constitutively active version) plasmid. 24 hours later, cells were incubated with DMEM or EBSS for 4 hours, fixed and stained for myc-tag or HA-tag. Representative images are shown and scale bars are 40 µm.
Proposed model of FYCO1 function in the MT-dependent transport of autophagic vesicles.
72h after stimulation with anti-CD3 and anti-CD28, the cells were re-stimulated with P+I for 2h, and the mRNA was subjected to qRT-PCR using the indicated primers for the lineage specifying transcription factors (B) or cytokines (C). The graphs represent an average of at least 4 independent experiments. In each graph, the expression level in the control was set as 100%. P-value was calculated by t-test. * p<0.05, ***p<0.005
(D) Representative transmission electron micrographs from bile canaliculi of healthy control (sham) and septic animals (PCI) treated with vehicle or the PI3Kγ inhibitors, free AS, or T-LipoAS. The asterisk marks a bile canaliculus where typical brush borders are lost due to sepsis.
Serum-starved HaCaT keratinocytes were treated with FGF7 different concentrations as indicated (B)) and/or IFN-α (500-1000 U/ml) for 12-16 h. RNA was analyzed by qRT-PCR for ISGs relative to RPLP0
(D) Percent of IFN-γ+ NK cells within the tumor in mice treated or not with LPS and with FTY720. n (number of animals per group)=4. Error bars depict SEM. FTY: FTY720. Statistical significance was determined with a two-tail t test. NT, untreated.
(c) Stable Bif-1 shRNA clones or control HeLa cells were transfected with Flag-PI(3) KC3 alone or in combination with Flag-tagged Beclin 1 and UVRAG for 48 h and subjected to an in vitro PI(3) KC3 lipid kinase assay. The results were quantified and are shown as relative activities (mean ± s.d.; n = 3).
F Detection of endogenous chromatin-bound and nucleoplasmic 53BP1 protein from WT and SirT7-/- MEFs before and after IR (8Gy) by western blot. Histone H3 was used as loading control, and tubulin as control for fractionation.
O Quantitative analysis of newly formed bone volume versus original bone volume (%). Results are shown as mean ± SEM; n=8; **: p<0.01 by t test
F. Secondary structure of pre-hsa-let-7i, with both 5p and 3p mature products highlighted in bold. The intramolecular ligation position is indicated in dash line between nt 28 and 61. It corresponds to cleavage positions of RNaseT1, which leaves 3'-terminal guanosine residues.
(A) Cy5 and Cy3 fluorophores were introduced into the clamp of SecA (PDB 3DIN; red space filling model) at position 233 and into the N-terminal half of SecY (blue) at position 103, respectively. The PPXD and NBD2 making up the clamp are shown as a violet and magenta ribbon models, respectively. (B) Rotated view of (A) with SecY masked except for the labeled residue 103.
(E) Western blot for the indicated proteins on tissue lysates from eyes, esophagus or tongue from RDEB mice treated as in A. Data information: β- actin or β-tubulin was used as loading control
Representative images (A) or traces (B-D & E-G) of changes in fluorescence of synaptophysin-pHluorin upon stimulation of neurons (scale bar in panel (A) = 2 µm).
(H) NTRAS and hnRNPL co-regulated alternative splicing (AS) events. Data points with an FDR < 0.05 are circled (n = 2 independent biological replicates).
E) DSB-SPB interaction involves a proficient DNA damage checkpoint activation. D1, D2 and D3 distances were scored in wild-type, sml1Δ and sml1Δ rad53Δ backgrounds using Ddc2-GFP and Spc110-RFP as DSB and SPB markers respectively. Measurements were performed by using a maximum projection of nine z-planes images. Graphs denote the average distribution of D1, D2 and D3 from three independent experiments where at least 100 cells for each sample were scored. P values were calculated using a 2-tailed unpaired Student t test.
G-I. Representative plots (G) and quantification of the frequency (H) and absolute number (I) of Tfh cells (CD4+CD44+PD-1+CXCR5+) in the spleen after primary immunization (day 7) with NIP-OVA (n = 7).
Co-inertia analysis of transcriptome and proteome levels of all 29 tissues (arrow base: transcriptome; arrow head: proteome) showing that the information carried by transcriptomes and proteomes were closer to each other in the same than across different tissues. Grey lines are used to aid identifying tissue names for the respective arrows. Shaded areas highlight tissues that are related by their molecular profiles.
(A) Schematic representation of D-loop-Lux reporter construct used for luciferase assays.
A. Detection of polyubiquitylated species of endogenous Sufu co-immunopurified from DAOY cells transfected with Myc-tagged ubiquitin (Ub) either in the presence of non-targeting siRNA (Control) or two siRNAs against Fbxl17 (1) and (2). MG132 (10µM) was added in all samples.
(B) qPCR analysis of CIP2A and MYC mRNA levels in MCF7 cells treated as in A. AA-starv, amino acid starvation; a.u., arbitrary unit. Error bars show SDs for three independent experiments.
(F) HaCaT keratinocytes were transiently transfected with an ISRE-Luciferase reporter construct and starved 24 h after transfection for 9 h. They were then incubated in the presence or absence of FGF7 (10 ng/ml) for 20 h. Lysates were analyzed using a DualGlo Luciferase Assay.
In unstressed cells, p14ARF is predominantly sequestered in the nucleoli, bound to its nucleolar interaction partner NPM. Upon genotoxic stress, the interaction between p14ARF and PRMT1 is reinforced and the C-terminal NLS/NoLS of p14ARF is methylated by PRMT1. This stress-induced arginine methylation promotes the release of p14ARF from NPM and nucleolar sequestration, leading to p53-independent apoptosis.
(B) The experimental scheme for the Rfa1-13MYC ChIP in the indicated yeast strains.
A Aggregated sequencing tag distribution of ARChIP‐exo and H3K4me2 MNaseChIP‐seq around the four precisely defined ARBEs. ChIP‐exo density plot is shown as forward (blue) and reverse (red) strands, respectively. H3K4me2 signal is shown in green. The window indicates ± 500 bp regions from the ARBE motif (0).
Interaction interface of the MICU2 homodimer in the Ca2+-bound state. The left box (gray dotted line) shows residues involved in electrostatic interactions, the right box (gray line) residues involved in hydrophobic interactions. Molecule 1 and molecule 2 in the dimer are colored in purple and yellow, respectively. Side chains of residues that make crucial intreractions are shown in stick representation.
Frequency of IAHC categories based on the number of Kit+ cells forming a cluster. Quantification of confocal images. Bars represent the mean±SE (n=6)
(F) Venn diagram showing the overlap between MCF7 DVL3 ChIP-seq peaks and H3K4me3 ChIP-Seq
(k) Cells from g were analysed for Pearson's co-localization coefficent (R(r)) by Olympus Fluoview. n = 30 cells from three independent experiments. Error bars indicate the s.d. Uncropped images of blots are shown in Supplementary Fig. S6.
(A-B) Diagram of the organization of the tracheal system at the onset of terminal cell branching (A) and one hour later (B).
Analysis of Tfh cell development in the spleen (SPL), mesenteric lymph nodes (MLN), and Peyer´s patches (PP) of Pou2af1-/- and Pou2af1+/-mice following immunization with sheepred blood cells. (A and B) Generation of Tfh cells characterized by the coexpression of CXCR5 with either ICOS, PD1, or BTLA on day 7 after immunization. (A) Representative flow cytometry plots indicating the frequency of CXCR5hiICOS+, CXCR5hiPD1+ and CXCR5hiBTLAhiTfh cells in Pou2af1-/- and Pou2af1+/-mice. Dot plots show gated CD4+7AAD-T cells. (B) Summarized data for the analysis shown in A (n=17 for ICOS+, n=14 for PD1+ and n=10 for BTLA+Tfh cells from at least 4 independent experiments; mean ± SEM).
G) Annexin V assay showing the percentage of apoptotic CrizR1 cells upon MYC downregulation using siRNA. Early apoptosis P =0.002, late apoptosis P=0.04, alive P =0.0008.