EMBO/sd-character-level-ner huggingface dataset:
Quantitative real-time PCR analysis of CTGF, CYR61, and BIRC5 in HEK 293T cells with knockdown of endogenous HOXA4. ShLATS1/2 and shYAP were used as an experimental control. *P<0.05, **P<0.01 vs shCtrl, by ANOVA with Sidak's correction.
(c-d) UMAP and pie-charts showing the distribution of Trim28-KO and control cells over the seven different clusters. There were no major differences in proportions of the different cell clusters between Emx1-Cre/Trim28-KO animals and controls.
(C) Scatter plot shows the intensities of vDNA and vRNA in colocalizing foci with the Spearman correlation r and associated p-value.
D. Knockdown of SNAP23 by siRNA inhibits DnaJC5-mediated TDP-43 release in M17 cells as shown by dot blot. Quantification of extracellular levels are mean ± SEM, n=3, **p<0.01 one-way analysis of variance with Tukey's multiple comparison post-hoc analysis. DnaJC5 was detected by FLAG antibody.
H. Percentage of live (Annexin V-) and apoptotic cells (Annexin V+) in sh1 and sh2 mouse ESCs compared to shScr.
(d) Western blot revealed an increased expression of CD68 in the Emx1-Cre/Trim28-KO animals (n=5 per group), unpaired t-test, **p=0.0036, error bars mean ± SEM. The star indicates an unspecific band.
(I) GST-GSDMD and control GST were mixed with HEK293T cell lysate containing FLAG-tagged full-length nucleocapsid or truncated nucleocapsid lacking amino acids 70-160 and 290-360, followed by a GST-pulldown assay. Input and precipitates were immunoblotted as indicated.
(B) WT (n = 9), Irgm1-/- (n = 7), Irgm2-/- (n = 9) and Casp1-/-Casp11-/- (n = 7) mice were injected i.p. with LPS (8 mg/kg). Serum was collected 4 hpi and concentration of IL-1β, IL-18, and TNFα was measured via ELISA.
(C) QRT-PCR assay of SOX1-OT V1 in control and V1-PAKI cells on day 16 of dorsal neural differentiation, p=0.0059. Data information: Data are presented as mean ±SEM from three independent experiments (n=3). *p<0.05, **p<0.01, ***p<0.001 (unpaired two-tailed Student's t-test).
B Caspase activity in HCT116 cells treated as indicated for 24h (NEN 0.6 µM, Domperidone (Domp) 20 µM, A77126 (A77) 50 µM, JNK inhibitor II (Jnki) 1µM). Data information: data are presented as mean (SD) (N=3) and were analyzed by two-way ANOVA with Tukey post-hoc test
A proposed model where GPR15-C10ORF99 signalling initiates the first colonic Treg homing reaction in herbivorous amniotes.
Mouse YUMM1.7 melanoma cells were subcutaneously inoculated into C57BL/6 mice and when tumors reached 100 mm3 mice were treated with vehicle (Ctrl), Nintedanib/BIBF1120 (BIBF), MAPKi (BRAFi, Vemurafenib and MEKi, Trametinib) or BRAFi/MEKi plus BIBF (n=6). (B) Representative median graphics showing tumor growth following treatment (n = 6). Two-way ANOVA was used for statistical analysis. ** P≤0.01.
B) The WT-blot shows the expression of LRP6 upon upregulation of miR-424/503 in miR-cluster-Dox-MCF-10A cells (Dox+) when one or both of the conserved microRNA binding sites (#1 and #3) are blocked by target protection.
(I) Whole mount staining of LIFR and CD31 in mouse retina. The fluorescent staining for CD31 (green) and LIFR (red) is shown. White arrows indicate the co-staining of CD31 and LIFR on retinal ECs.
A. Top: graphs showing the change in cell diameter for MCF7 cells transfected with ZsGreen (left) or ZsRASSF1C (right) plasmids at 0 h and 12 h, connections indicate individual cell tracking. Bottom: example images diameter measurements (red line). Scale 20 μm.
(D) Grouping E. rectale individuals from the Danish (DK) and Swedish (SE) studies, based on this deletion shows a significant (*p < 0.05, **p < 0.01, ***p < 0.001) increase in BMI and blood fasting insulin levels as well as a decrease in overall community diversity in individuals who are predominantly colonised by the flagellum carrying subspecies (see Methods). The same trend is observed for E. eligens subspecies in the same studies, though not statistically significant (n.s.).
C, D Clinical chemistry plasma concentrations of parameters related to acid-base balance (Lactate and Ammonia) and metabolic state (Glucose) n = 15 Uqcrh-/- and 16 WT pups 1-2-week-old (C); n = 15 f, 15 m Uqcrh-/- and 15 f,15 m WT mice aged 8-9 weeks (D); sex not differentiated. Data shown as scatter dot plots with line at median. * p < 0.05, ** p < 0.01, **** p < 0.0001, Wilcoxon rank sum test.
A. Relative abundance of miR species in human naive CD4 T cells. Cell purity was >97%.
A summary bar graph showing the quantitative real-time PCR data for TMEM16A, TMEM16B, and BEST1 with cDNA samples prepared from the mHb and hippocampus of adult mouse brains (N=3, n=3 each, unpaired Student t-test, data are presented as mean values ± s.e.m.).
Immunoblot showing LC3-II formation MB-3-treated HeLa cells in the presence or absence of the lysosome inhibitor Baf.
C. Electron microscopy images of control and NaB (2mM) treated HCT-116 cells. ER, endoplasmic reticulum; Mt, mitochondrion; AL.
Cortical extracts from rTg4510-Mapt0/0 brains had significantly less phospho-tau (CP13, PHF1, 12E8) than rTg4510 extracts. Compared to WT mice, both transgenic tau lines had high levels of phospho-tau. Mean±SEM, n=3 mice/group.
E Serum cholesterol concentrations of each group. Liver cholesterol concentrations (F) of each group were examined.
(C) Venn diagram illustrating the overlap of differentially expressed (FC>1.5, p<0.05) transcripts between any of the three comparisons: EV to SOX9-WT (upregulated: 145+308+21; downregulated 146+333+44), EV to SOX9-T236/T240A (upregulated: 294+308+95+21; downregulated 345+333+95+44), or SOX9-WT to SOX9- T236/T240A (upregulated: 112+95+21; downregulated 114+95+44). Each oval represents the number of transcripts either upregulated or downregulated in the respective comparison, where the direction of differential expression is indicated by the inequality sign in the label. Numbers in overlapping regions signify the number of transcripts commonly differentially expressed in all contributing comparisons.
A) Schematic representation of the peptide design used in this study. An aggregating peptide core (or APR, red) is flanked on either side by one of four charged residues (Arg, Lys, Asp or Glu), an Ala on either side, or no flanking residues (noGK).
(B) Immunoblot of protein lysates of ARPE-19 cells treated as shown in (A). Data are representative of three independent experiments.
BODIPY staining of neutral lipid stores in the indicated melanoma cell lines, which present increasing degrees of aggressiveness (from left to right). DAPI was used to counterstain nuclei. Scale bar: 20µm.
(E) Heatmap showing non-conversion rates of small non-coding RNA positions methylated in stoichiometry higher than 50%. Data information: In E), n = 3 independent biological replicates.
E. Area under the curve calculated from individual cells as measured in (D). Bars indicate mean±s.e.m. Data information: *p<0.05, **p<0.01, ***p<0.001 , Kruskal-Wallis Anova with Dunn's multiple comparison test Data (total number of cells, n) were obtained from at least three independent transfections with several technical replicates each.
e-g, Western blots show that CPAP targeting siRNA treatment depletes endogenous CPAP. Both low -and high -exposures are given (e). Increased cilia length and NPC differentiation upon expression of RNAi-resistant CPAP E1235V compared to WT CPAP (f-g). Error bars are s. e. m. *** p<0.001 (cilia length), * p<0.05 (differentiation), t-test. For cilia length: n = 4 independent experiments. 25 cells for CPAP, 47 cells for CPAP E1235V. For differentiation: n = 4 independent experiments. 145 for CPAP and 81 for CPAP E1235V. Scale bar 1 μm.
(C) P-Smad2 staining by IHC in 3 representative tumors per group after 25 days of treatment. The scale represents 500μm and 100μm on the left and right panels, respectively.
D. Dissociation constants for interactions between PBP1A and LpoA with NlpI, MepM, MepS, PBP4 and PBP7 as determined by MST. The values are mean ± standard deviation of three independent experiments. 1PBP1A was used as fluorescently labelled protein in all assays. 2LpoA was used as unlabelled ligand in all combinations, except with MepM and PBP4.
i-m) Mice were treated by intravenous injection of NILV-S/MAR(Mock), LV(CD19CAR) and NILV-S/MAR(CD19CAR)-transduced T cells (8x106 cells/injection) at days 18, 21, 24 after tumor implantation. Tumor growth was monitored by caliper measurements. i-k) Tumor volume of individual mice in each treatment groups are presented. l) The average tumor volume of each treatment group is presented and the values on day 37 were statistically compared (n=12 in LV group, n=9 in NILV-S/MAR group and n=11 in Mock control group). m) The survival of mice is shown as Kaplan-Meier curves.
F Schematic diagram depicting induction of c-MYC expression using rtTA-dependent system in WT mESCs.
A Time‐dependent changes in nucleoside contents under nitrogen starvation. Nucleosides in wild‐type, atg2Δ, atg7Δ, atg11Δ, atg17Δ, atg19Δ, atg32Δ, nvj1Δ, and pep4prb1Δ cells under nitrogen starvation. All data are means of triplicates. The error bars represent the standard deviation.
The emerging timeline for highly pathogenic viruses and the proposed Disease X. b. Schematic representation of SARS-CoV-2 S protein. Its S1 subunit contains NTD (14-305 aa), RBD (319-541 aa), and RBM (437-508 aa). Its S2 subunit contains FP (788-806 aa), HR1 (912-984 aa), HR2 (1163-1213 aa), TM (1214-1237 aa) and CP (1238-1273 aa). c. The formation of syncytium in Huh-7 cells 24 h after SARS-CoV-2 infection, with scale bar of 200 μm.
A. Schematic representation of the RASSF1 gene showing the domains in RASSF1A and C. Bars shaded dark and light green denote the CpG islands associated with RASSF1A and RASSF1C respectively.
(H) Workflow depicting the validation step: 501Mel cells overexpressing SMAD3, BIRC3 or SLC9A5 (obtained by CRISPR-SAM) were xenografted on nude mice and tumor volume was monitored using caliper. 3x106 cells/mouse. n= 7, 6 and 6 mice, respectively.
Depletion of LOC113230 in Caco-2 cells using specific shRNAs and stable cells were established with puromycin selection. The resulting cells as mass pools were used for cell migration assays. Scale bar represents 100 μM.
f, Seckel cells show delayed mitotic entry. Note that an unresorbed Arl13b-positive ciliary remnant (ciliary membrane, green) is present with one of the centrosomes(Paridaen et al, 2013). Bar diagram shows mitotic index of WT and Seckel cells 24 hrs after serum stimulation. n = 3 independent experiments, n> 300 cells for WT and Seckel. Error bars are s.e.m. Scale bar 1 μm.
Western blotting analysis showing the effect of HPV16E6 (400 nM, 48 h) on YAP protein levels in HT3 cells transfected with non-targeting control siRNA (siCtrl) or YAP siRNA (siYAP).
A U2OS cells stably expressing HA‐Flag‐ATG9A transfected with siRNA targeting AP2A1 (40 nM), or siRNA AllStar control (40 nM) were treated with KU0063794 or DMSO (6 h) 4 days post‐transfection, fixed, and stained with anti‐HA antibody.
(A) Anti-CHIKV IgG titers from the vaccination phase were determined with a CHIKV virion-based ELISA. Sera from four animals were pooled and diluted 1:500 for the assay. Statistical analyses were performed using two-tailed paired T-test (*P =0.029 RH-CHIKV 6 dpv, *P =0.029 RH-CHIKV 90 dpv, *P =0.029 RHEV-CHIKV 6 dpv, *P =0.029 RHEV-CHIKV 90 dpv, *P =0.029 EV-CHIKV 90 dpv).
Overall view of the IAPV-IRES/80S complex class 1 with 60S represented as cyan ribbons, the 40S as yellow ribbons and the IAPV-IRES represented as solid Van der Waals surface colored by secondary structures motifs.
C Endogenous RBPJ co-purifies specifically with HA-L3MBTL3 but not with HA-EGFP, HA-TBL1X or HA-HEY2. IPs of HA-tagged L3MBTL3, EGFP, TBL1X or HEY2 in U87-MG cells followed by Western blot analyses using HA or RBPJ antibody. The experiment was independently replicated twice. EV: Empty Vector control; WB: Western blot; IP: immuno-precipitation.
(B) Schematic model of the distinct motor sets regulating EE (above) and LE (below) retrograde transport, along MTs. Stars indicate EB1-binding SxIP motifs.
A Simulation of SDD model, where after reaching steady-state (black line, insets), either production was stopped (left) or degradation increased (right). The gray arrow shows the direction of time, the color of the lines reflects the mCherry/sfGFP ratio (y axis).
A. Inhibition of Cdk1 at anaphase I. CDC20-mAR and CDC20-mAR cdc28-as1 cells were released from the metaphase I-arrest with CuSO4 at 7 h in SPM (t = 0) and treated with 1NM-PP1 at t = 40 min to inhibit Cdc28-as1 (arrows). Top, time-lapse series from the imaging of Mpc70-GFP, SPBs (Cnm67-RFP), and nuclei (TetR-RFP). Bottom, quantification of meiotic events.
Structures of RyR1 determined in presence of increasing Ca2+ concentration (1 mM and 5 mM), all with intra-SR extensions. Scale bars: 10 nm in (A) and (E), 20 nm in (C).
Detection of CAR T cells by vector copy numbers (VCN). Genomic DNA was isolated from peritoneal cavity, spleen and blood cells. VCN were determined in technical duplicates by qPCR for two individual mice of each group. Presence of B cells in the transplanted PBMC is indicated below.
A. HPLC-based PG digestion assay representing EPase activity. The graph shows the relative percentage of the muropeptide TetraTetra present at the end of the incubation period for each protein as described in materials and methods. MepM and PBP4 were incubated with sacculi, whilst MepS and PBP7 were incubated with soluble muropeptides, both from E. coli MC1061, respectively. Values are mean ± standard deviation of three independent experiments. To calculate significance, the data were fit using a linear model. Calculated means were compared using Tukey's HSD test, resulting in p-values corrected for multiple testing. Relevant p-values are highlighted directly in the figure (*<0.05; **<0.01, ***<0.001)
m) Representative immunoFISH (Telomere-FISH and 8-oxodG); n) mean number of 8-oxodG co-localizing with telomeres in hepatocytes; o) Mean telomere FISH intensity in hepatocytes.
C, ChIP-qPCR assay of TOC1 binding to promoter of pre-dawn-phased PIF3 target genes at ZT14 in Col-0, native promoter TOC1 and 5X lines. D, ChIP-qPCR assay of the chromatin residence of native promoter TOC1-GFP at target promoters in toc1 vs. pif3/4/5 toc1 (pif345t1) mutant backgrounds. Data information: 3-d-old SD-grown seedlings were harvested at ZT14, TOC1-GFP was immunoprecipitated by α-GFP and magnetic protein G beads. Data from 3 independent trials were averaged, error bars indicate SEM. Asterisks indicates significant differences (** p<0.001, *** p<0.0001, Student's t test), n.s=not significant.
(H, I) Gene set enrichment analysis of the top enriched gene signatures (H), including (I) Cholesterol homeostasis signature in MDA-MB-231 TMEM33 OE (#1) cells using KEGG and hallmark gene sets in GSEA databases. Adjusted p-value and normalized enrichment score (NES) were generated by GSEA.
E, Measures related to behaviour and neurological function, data generated by the Open Field test (8 weeks old, E) n = 7f, 8m Uqcrh-/- and 8f, 9m WT animals. Prepulse inhibition of the acoustic startle as a parameter associated with sensorimotor gating (10 weeks, E right panel), n = 7 f/5 m Uqcrh-/- and 8 f/ 9 m WT mice. Sex is not differentiated. Data are shown as scatter dot plots with a line representing the median. *** p < 0.001, **** p < 0.0001, Wilcoxon rank-sum test.
d-f, Representative images of WNV envelope antigen and TdT-mediated dUTP nick end labelling (TUNEL) staining (d) (T, Tat alone), quantification of cell death in brain (e) and survival curves (f) for 5-day-oldC57BL/6Jmice infected with WNV (Egypt strain 101, 1 p.f.u. intracerebral (i.c.)) and treated daily with peptide (D-amino acid forms, 20mgkg−1 i.p. beginning 1day post-infection). Images in d are from cerebral cortex day 6 post-infection. Similar results were observed in all regions of the brain for three mice per group. Scale bar, 20μm. Bars in e represent mean±s.e.m. TUNEL-positive cells per unit area of brain for three mice. g
C Immunohistological staining of liver sections from P120 PR-SET7ΔHepA mice and control littermates (WT) with FGF7 and A6 antibodies.
COX activity in cerebrum, kidneys and muscle (A) of Coq9+/+, Coq9R239X and Coq9Q95X mice.
C. Representative immunofluorescence staining of Lamp1 (red) in RCS chondrocytes treated with vehicle (5% ABS), FGF18 (50 ng/mL; 16 hours) and Actinomycin (1μg/mL; 4 hours). Nuclei were stained with DAPI (blue). Scale bar 10 μm. Representative images of N=3 biological replicates. Scale bar 10 μm.
Venn diagram showing overlap between genes that were significantly (P < 0.05) induced more than 1.5-fold in response to paclitaxel treatment of MDA231-LM2 cells and genes that were significantly (P < 0.05) induced in MDA231-LM2 cells after formation of oncospheres. Significant fold changes were determined by two-sample empirical Bayer tests with Benjamini-Hochberg correction for multiple testing. PAX.
B HEK293 cells were transfected with increasing amounts of Flag-FBXW7 expression vectors and 48 hours after transfection, cell lysates were subjected to immunoblotting (IB).
(d-g) Quantification of particle number, size and estimated volume determined from the data shown in (c)
(E, F) Optical section (E) (scale bar: 5 µm) and distribution of the fluorescence signal intensity (F) of A. castellanii infected with mCherry-producing L. pneumophila JR32 (Ptac-mCherry-PflaA-gfp) for 48 h. The plot profile was analyzed for an optical section in the center of an infected host cell and shows the intensity of the green and red channels, respectively (representative of n = 10). The GFP signal mainly localizes to the periphery of the bacterial cluster.
(D) WT, Irgm2-/-, panIrgm-/- and Casp11-/- mice (n = 8 mice/genotype) were injected i.p. with LPS (8 mg/kg body weight). Morbidity and mortality were observed for 48 h at 3-h intervals.
(f-h) Relative mRNA expression was analysed from eWAT of indicated mice through quantitative reverse transcription-PCR.
Immune response and physiology of monkeys immunized with recombinant adenovirus vaccine. ELISPOT analysis of IFN-γ response in PBMC samples. Pool A and B contain peptides corresponding to S1-orf8 fusion and N, respectively. Data represent two animals from each group.
Bone marrow cells from WT and Akt2 KO mice (CD45.2) were adoptively transferred to lethally irradiated CD45.1 mice and infected with VSV. VSV copies (G, n=9) were analyzed Data information: *P < 0.05, **P < 0.01; using a unpaired t-test Data are representative of three independent experiments respectively , in which the different groups of mice were sacrificed and quantified for indicated experimental purposes Error bars , mean ± SD).
C qRT-PCR for mRNA expression of the anoikis-related markers Bim and Bmf in sorted n-B (non-bulge), bBSC (basal BSCs) and sbBSC (suprabasal BSCs) (n=3 biological replicates; mean ± standard error of mean (SEM); * p<0.05, ns=not significant, two-way ANOVA test).
F, The refined structure of the partial translocon, generated by docking and refinement of ColE9 residues 85-580 (PDB ID 5EW5), OmpF (PDB ID 3K19), and TolB-ColE9 TBE (PDB ID 4JML). ColE9 residues 3-67 were built de novo.
Experimental treatment schedule of mice after cancer cell implantation in the mammary gland to address the role of SPP1 in resistance to PAX.
Identification of proteins with altered phosphorylation patterns in Spatc1l-KO testis by PMF. SS, standard spot; Seq. cov., sequence coverage calculated based on the amino acid count; MW, molecular weight; pI, isoelectric point.
N The protein levels of VEGF-A in METTL3-knockdown HCCs. O The protein levels of PDGF-B in METTL3-knockdown HCCs.
G. Immunoblot analysis of ALKAL2 induction of pSRF in NB1 cells. Cells were treated for 0 and 1h in the presence and absence of lorlatinib as indicated. RNA-Seq analysis was performed using 3 biological repeats. Immunoblots are representative of at least 3 independent experiments.
D The flexibility of SM proteins in domain 3a and domain 1. Structures of rat Munc18-1 WT in complex with closed Syx1, human Munc18-2, nSec1 from squid, and rat Munc18-1 WT in complex with mouse Syx4 N-peptide were aligned and superposed with rat Munc18-1 K332E/K333E. Enlarged views of domain 3a and domain 1 are shown in dashed boxes.
(D) BAX/BAK-deficient HeLa cells ectopically expressing BAX were treated and analysed
B RT-qPCR analysis of dMitf target gene expression in Drosophila larval fat body with silencing of dGcn5. Data information: In this Figure, data are presented as mean ± SEM; n = 3 independent experiments; *p < 0.05, **p < 0.01, ***p < 0.001, Student's t-test.
G) Comparing activity of USP1WT and USP1ΔL1L3 (+UAF1) on a peptide substrate i.e. LRGG-AMC (100µM). Addition of UAF1 allows cleavage of LRGG-AMC by both USP1WT and USP1ΔL1L3 (n=2, technical replicates).
(A) Schematic regimen for AOM/DSS-induction of colon tumorigenesis. At 8~12 wk of age, AhR WT (H, n=10) and KO (HV, n=10) mice were treated with a single dose of AOM (10 mg/kg) by s.c injection, followed by 3 cycles of 2% DSS in the drinking water for 5 d. Mice were terminated 6 wk after the third cycle of DSS.
C). The JAK inhibitor baricitinib reversed LIF-induced BAE growth inhibition. BAE cells pre-incubated with inhibitors for 1 hour were treated with vehicle and LIF (10 ng/ml, Sigma). Cell proliferation was analyzed after 6 days using alamar blue, n=3. Data information: Bars and error bars represent mean±SD. All experiments were carried out in three independent studies. siNegative, negative control siRNA not targeting any known genes. Two-way ANOVA was used as statistical test.
(A) Degradation of long‐lived proteins in mouse fibroblasts (NIH3T3 cells) treated or not with 25 mM MBCD. Where indicated, 15 mM NH4Cl/100 μM leupeptin (NH4Cl+Leup) were added into the medium. Values are the mean+s.e. of three experiments with triplicate samples.
D) FP based binding assays of USP1 mutants (+ UAF1) with PCNA-UbTAMRA show reduced binding of USP1ΔL1 and USP1PIP1 compared to USP1WT (n=2, technical replicates).
B. Western blot analysis for Mbp and P0 on lysates from Pmp22-/- and WT mice P20 shows decreased myelin protein expression levels at both time points in Pmp22-/- nerves, results are mean ± SEM, p=0.0500 with the exception of the P0 protein level at P20, for which the difference between Pmp22-/- and WT nerves is not statistically significant, p=0.1000, one-tailed Mann Whitney U test, representative of two independent experiments.
I) WT MEFs and Mfn1 or Mfn2 KO MEFs were incubated with 2-DG (10 mM) for 6 h, and ATP levels were measured (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.
I In vitro acetylation assays of TFEB. Purified recombinant TFEB was incubated with Myc-GCN5 or Myc-GCN5-E575Q immunoprecipitated from HEK293 cells.
(G) Overlap between ribosomal footprints and mapping of 5'OH ends from 35S:EVD in rdr6 cloned through RtbC ligation. Regions investigated are highlighted in grey. 5'OH ends were only successfully cloned from region #1. Alignment of sequenced clones to EVD is displayed in Appendix Fig. S9.
H&E (left), pan-cytokeratin (PCK, middle), and ITGA6 staining (right) at P2. The regenerated epidermis is indicated by arrowheads. Scale bar: 200 μm.
C Analytic PCR with primers flanking the splice site using cDNA's of tissues or cells as indicated. L denotes exon L of STIM1L, A denotes additional exon A.
C Prox1a and Eng expression in smohi1640 mutant embryos injected with mRNA encoding mSmo (n=10), mSmoSA (n=9) and mSmo14SA (n=6). Note the full recovery of SSFs and MPs compared to the un-injected controls. Scale bar, 50μm.
Heatmap of unsupervised hierarchical clustering based on Low Migration Signature (LMS) and High Migration Signature (HMS) gene expression.
K. Representative images showing mTFP (cyan) and Venus (yellow) fluorescence in HBVPs which have direct contact with control (upper panel) or MCT5 (lower panel) siRNA-treated BMECs. VECAD immunostaining was used for endothelial staining. L. Quantification of the mTFP/Venus fluorescence ratio of laconic in HBVPs which have direct contact with control (siCON) or MCT5 (siMCT5) siRNA-treated BMECs. (n=8 from independent experiments. Error bars indicate the standard error of the mean (SEM) from unpaired Student's t test.)