EMBO/sd-character-level-ner huggingface dataset:
(B) Cell Counting Kit 8 (CCK-8) was used to assess the viability of BMDMs treated with different doses of LicoB for 24 h.
(A) Tetrad analysis reveals that the respiration defect of Sc+Sb-CCM1 cells can be rescued by mutations in mitochondrial or nuclear genomes. The suppressor clones were crossed with the Sc+Sb-CCM1-ρ⁰ strain and the tetrads from the cross were analyzed. A non-Mendelian 4:0 segregation pattern for improved respiration is expected if the suppressor mutation is in mtDNA (left panel). Otherwise, a 2:2 segregation pattern would be observed if the rescue effect involved a single nuclear mutation (right panel).
(A) Genomic structure of CG10967. The P‐element insertion site of EP3348 (DmATG11) is denoted.
D Clustal Omega sequence alignment shows evolutionary conservation of the p.His58 residue (highlighted) along with its neighbouring residues (human NDUFC2: NP_004540.1).
A, B) ELISA of the (A) RIPA soluble fraction of female APP/PS1 and APP/PS1 PD-1-/- mice for Aβx-40 (biological replicates with n=6 for APP/PS1 and n=5 for APP/PS1 PD-1-/-, mean+/-SEM, one-way ANOVA (DF = 1, F = 0.6, p=0.45), Tukey's HSD, ** p<0.01, *** p<0.001) and (B) of the SDS soluble fraction (biological replicates with n=6 for APP/PS1 and n=5 for APP/PS1 PD-1-/-, mean+/-SEM, one-way ANOVA(DF=1, F= 32.8, p=2x10-5), Tukey's HSD, ** p<0.01, *** p<0.001).
(F) Sphere formation assay results of MGC-803 (upper panel) and MKN-45 (bottom panel) cells incubated with 20 μg/mL sEVs from HEK293T cells (left panel), WT-LSD1 sEVs (middle panel), and LSD1 K661A sEVs (right panel) for 7 days. Scale bar = 100 µm (n = 3 biological replicates; mean ± SEM; **P = 0.0021 (MGC-803) and **P = 0.0020 (MKN-45); two-tailed unpaired Student's t-test).
(H-J) Quantification of fibronectin immunohistochemistry staining, fiber thickness and alignment scored of images presented in e. In all cases, histogram bars represent mean ± s.e.m.; *P<0.05,**P<0.01,***P<0.001 (t-test for A, B, C; Anova and Tukey"s post hoc test for H, I, J). Scale bar is 1
C2C12 cells were treated with 0, 0.5 and 2 mM SUC for 48 h. quantification of MyHC-I and IIb immunofluorescent staining (green) in C2C12 cells (n=16).
J Physical activity for the dark and light period in WT and FADD-D mice (n = 5 for each genotype). Data are expressed as means ± SEM. NS, not statistically significant (Student's t-test).
SID 26681509 inhibits the 1,25D3 mediated inhibition of HIV and M. tuberculosis replication.MDM were pretreated with SID 26681509 (SID) before treatment with 1,25D3 and subsequent infection with HIV and/or M. tuberculosis (TB). (A) ELISA performed for HIV p24 antigen release at days 0, 4 and 7.
(B) Microglia from newborn Becn1+/- and wild type mouse pups were kept for 2 h either in full medium or HBSS with or without Bafilomycin A1 (Baf). LC3 and ACTIN levels were determined by Western blot. LC3-II was significantly reduced in microglia from Becn1+/- mice after Baf treatment in full medium compared to wild type microglia; mean ± SEM, wild type n = 3, Becn1+/- n = 4; two-tailed t-test *: p < 0.05.
Plasma Free Fatty Acid (FFA) and Glycerol levels in WT fl/fl and QKI KO fl/fl:AP2-Cre mice fed the NCD or HFD for 20 weeks. (n = 8, per genotype)
D uPAR accelerates the generation of SMB-containing VN-fragments by uPA. VN immobilized in 96-well plates was incubated with 10 nM sc-uPA or tc-uPA together with increasing concentrations of soluble Fc-tagged uPAR (uPARWT) or a mutant form specifically deficient in VN-binding (uPARW32A/R91A). After a 1 h incubation, the supernatants were recovered and analysed for the presence of N-terminal VN-fragments by immunoassay. The release is reported as percentage of the maximal signal observed in the experiment (10 nM uPARWT + tc-uPA). Data points represent mean ± SD of three independent experiments.
Left: representative conventional image of interphase MT network in the 1st quadrant of a Human Retinal Pigment Epithelium (HRPE) cell. Grey: α-tubulin; Yellow: TGN-46; Yellow dashed line: Golgi boundary. Right: the classified MT subgroups. Red: GaMTs; Green: non-GaMTs. Scale bar: 5 μm. Box-whisker plot presents the proportion of GaMT and non-GaMTs. (data were pooled from 3 independent experiments and n= 36 cells). The ends of whiskers set as the 10% and 90% of the entire population. ***p < 0.001, two-tailed Mann-Whitney.
The release of mature IL-1β (b) from THP-1 cells were measured by enzyme-linked immunosorbent assay (ELISA) following HSV-1 infection.
F 3' RACE analysis of polyA+ TERRA in ter1Δ cells grown for ~ 43 pds. The sequence at the top is the genomic reference sequence (gen) taken from the pNSU70 plasmid (nucleotide positions are indicated). The sequences below derive from all positive clones isolated. Sequences boxed in blue, green and yellow correspond to the oligonucleotide used for RACE (o3'RACE), subtelomeric DNA and telomeric repeats, respectively. Genomic adenines corresponding to putative RNA cleavage sites (CS) are highlighted.
(C) Confluency doubling times quantified from BV-2 cells with dox-inducible expression of Siglec-F constructs. Plots indicating doubling time (normalized to 2xY->F constructs) estimated from Incucyte bright-field images. Bars indicate mean ± SD; n = 8 replicates; *: p < 5e-2, **: p < 1e-2, ***: p < 1e-3, ****: p < 1e-4; ns: not significant, using unpaired Student's t-test, two-sided. Dotted line indicates mean of 2xY->F group.
(D). Interactions of the PTP-MEG2-trapping mutants with the MUNC18-1-Y145 mutants and DYNAMIN2-Y125 mutants. PC12 cells were transfected with FLAG-MUNC18-1-Y145, FLAG-DYNAMIN2-Y125 and different mutations of the FLAG-MUNC18-1-Y145A, Y145H, Y145E or Y145F, FLAG-DYNAMIN2-Y125A, Y125E, Y125F, 24 hours before stimulation with 100 nM AngII, respectively. The cell lysates were then incubated with GST-beads-PTP-MEG2-D470A complex for 2 hours with constant rotation. The potential PTP-MEG2 substrates were pulled down by GST-beads, and their levels were examined by the FLAG antibody with Western blot.
Using CRISPR/Cas9, MyD88 knock-out (KO) and AAVS1KO (control) pDCs were generated. MyD88 protein levels in KO and control pDCs were analyzed by western blotting
(C) Representative time-lapse images showing examples of CTL-tumor conjugates resulting in either no detectable response, transient calcium response or sustained calcium response in the target cell. Arrows show actin accumulation at the immunological synapse. Scale bar, 5 µm. Data information: Data were pooled from three independent experiments. (***p<0.001, ns, not significant, unpaired t‑test).
A, CheY crosslinks with FliM∆N-YPet in vivo. The cytoplasm of fliM∆N-YPet ΔcheZ cells overexpressing CheY (strain EW694) or FliMN-CheY (strain EW697) from a plasmid was crosslinked by glutaraldehyde and resolved by SDS-PAGE. 1, 2, 3 stand for three different experiments that underwent this procedure. The plus sign before ~14 and ~15 stands for +55 kDa of FliM∆N-YPet. Note that gel running suffered from parabolic distortion in band positions. The annotations relate to the lowest positions of the bands. The gel was imaged for FliM∆N-YPet fluorescence. To see the crosslinking products, the intense fluorescence of monomeric FliM∆N-YPet is shown at saturation.
c, Nuclear REST levels in PFC from cases with neuropathological AD (moderate/frequent plaques by CERAD score and intermediate/high likelihood AD by NIA-Reagan criteria) that had mild or no cognitive impairment (NCI/MCI), or AD dementia. Values are the mean ± s.e.m. *P 0.01 by Student's unpaired t-test; NCI/MCI n = 30, AD dementia n = 21.
F. The bar plot shows the contribution of each organelle to total cellular protein mass, also accounting for unassigned proteins. Percentage of cytosol, mitochondria, nucleoli, plasma membrane and actin filaments is indicated.
(F) Western blot analysis of LAMP2 protein levels in WT and separate clones of STX6KO or VTI1AKO HeLa cells.
G. BiFC signal quantifications of the strains presented in (F). β'-COPVN yielded BiFC fluorescence signals with all tested complementation partners. This rules out the possibility that the lack of suppression observed in F simply reflects the inability of the BiFC partners to form a complex, and shows that the successful complementation of the split-YFP fragments does not per se suppress the synthetic lethal effect of the VN tag in dsl1-5xWA cells. Mean values + SEM of at least three independent experiments (n=3-8) are displayed.
D RCA products were resolved by denaturing agarose gel electrophoresis, transferred on a membrane and hybridized with a telomeric TG1-3 probe.
e, Number of recoverable c.f.u. per mouselung24 h after intranasal inoculation with 1 × 106 of wild-type M90T or each mutant Shigella strain as indicated. Limit of detection (LOD) for this assay is indicated by the dotted line. Error bars, geometrical means ± s.e.m. **P<0.001.
A. LysoTracker Red staining of the primary cerebella neurons from Cacna1atg-la mice and WT controls. The control cells show big bright punctae, while the mutant cells have much dimmer and smaller punctae. B, C and D. Quantification of LysoTracker relative intensity ("n" represents the counted cell number), LysoTracker positive punctae number and size per cell ("n" represents the counted image number)
(A) Scheme of ribosome footprint analysis using PACE reporter mRNAs. An example of a 28-nt footprint is shown. The relative ribosome density of each codon at the A site was calculated using the formula shown on the right.
(A-H) Graphs plotting predicted versus measured phenotypes are shown for the best-performing whole-transcriptome and metabolome models for each phenotype, based on the pooled R2 scores in Table 2. (A) Transcriptome e-net model for leaf 16 blade length, (B) metabolome e-net model for leaf 16 blade length, (C) transcriptome e-net model for leaf 16 blade width, (D) metabolome e-net model for leaf 16 blade width, (E) transcriptome e-net model for husk leaf length, (F) metabolome random forest model for husk leaf length, (G) transcriptome e-net model for ear length, (H) metabolome random forest model for ear length. The dot colors represent different outer cross-validation folds. Perfect predictions are located on the diagonal line in each panel.
E-F Acute cold test (4°C) after treatment with the β-adrenergic antagonist propranolol (Prop) in Cdk4+/+ (n=7) and Cdk4-/- (n=6) animals or with vehicle (NaCl) (Cdk4+/+ (n=7) and Cdk4-/- (n=6)) (E) and corresponding quantification of the area under the curve (AUC).
(A) IHC staining of Nfatc1 expression in HFs on P84 in Sirt7+/+ and Sirt7-/- mice with or without Cyclosporin A (CsA) treatment. The black dashed line indicates bulge (Bu) of hair follicle. (B) Quantitative analysis of Nfatc1 levels in (A, n=10 hair follicles) using ImageJ plus 6.0.
(B) KEGG enrichment analysis was performed by clusterProfiler in R language. Top 20 interested KEGG enrichment terms of 2511 QKI-targeted genes shown in left panel. A total of 22 genes were enriched in TGF-β signaling pathway, which were presented in right panel.
Neutrophils were mobilized into the murine systemic circulation within 30 min of injury in our murine fracture model. Compared to control and number of blood neutrophils at 3 h ***P = 0.0006 and at 6 h *P = 0.042, by one-way ANOVA with Dunnett correction.
Images of whole brain sagittal sections that were immunolabelled with anti-MBP at P17 from indicated mice (n=3 for each group). MBP staining (shown in gray) in cortex (green dotted line represents the border of the cortex), hippocampus and cerebellum is presented (magnified from the top panel).
Mitochondrial volume estimated by Tim 23 staining as in (c), and presented as % of total cell volume;
(d) Cells stably expressing the VPS29-GFP V90D mutant that cannot assemble with VPS35 were transiently transfected with mCherry-tagged WT VPS35, D620N and H675R constructs, along with an additional control of mCherry-FAM21 tail. Cells were lysed 48 h post transfection, and VPS29-GFP V90D and associated proteins were recovered by anti-GFP native IP. Blots shown are representative of experiments replicated at least twice.
G, H Immunofluorescent analysis (G) and statistical quantifications (H) of the vascular endothelial cell marker Glut1 in xenografts derived from T387 GSCs expressing shUSP33 or shNT. Disruption of USP33 in GSCs reduced vessel intensity in GBM xenografts. Scale bar, 80 μm. (n = 5 tumors for each group; ***, p < 0.001; mean ± s.e.m.; two tailed unpaired t-test).
A. Labeling of non-permeabilized (top) and permeabilized (bottom) cells demonstrate that surface labeling does not label internal proteins. GluA2 labeling (green) is visible both on the surface and internally, while DARPP32 labeling (red) is only visible internally.
D. Liver-stage development of concavin(-) parasites compared to wildtype, both expressing cytoplasmic GFP (white). Parasite size was measured 24h and 48h post infection. Data points represent individual parasites from 4 independent biological replicates. Shown is the mean ± SEM. P-values calculated using the Mann Whitney test. Scale bar: 5 µm.
A. A set of different constructs of PTEN, PTENα, PTENβ, and PTENε with a C-terminal GFP tag. The AUG start codon of canonical PTEN was mutated to AUA in PTENα, PTENβ, and PTENε constructs to abolish the expression of canonical PTEN and the corresponding start site of these PTEN isoforms was mutated into AUG to enhance their expression.
E Stable HEK293 cells treated as in (D) and transiently expressing GFP-tagged YOD1-wt or the YOD1-C160S catalytic mutant (CS) were processed for co-immunoprecipitation with GFP nanobodies. Asterisk, unspecific band. Note that the YOD1-CS mutant stabilized p97 binding and, in the p97-EQ background, also associated with UBXD1 and PLAA.
E. qPCR results showing mRNA expression of FT in the genotypes indicated. The transcript levels in Col are set to 1.0. Samples were collected from 7-day-old seedlings of the genotypes indicated at ZT16. Data information: error bars indicate standard error within three biological replicates and for each of these two technical replicates were performed.
Sholl analysis of apical and basal dendritic arbors of CA1 pyramidal neurons from Tardbpfx/fx and CamKIIaCRE;Tardbpfx/fx mice. Results are presented as average ± SEM (N=3 mice per condition, 20 neurons per mouse). *, p<0.05; **, p<0.01. Data information: Results are presented as average ± standard error of the mean (SEM). All statistical tests were performed using 2-way ANOVA with Sidak post hoc analysis.
A Gene expression of LGR5 and EPHB2, along activity gradients of LGR5-ISC or MAPK target gene signatures.
C Experimental method schematic representation. CAFs or PaSC was treated or not with SOM230 (10−7 M) for 48 h. Conditioned media (CM) were collected. Pancreatic cancer cells were incubated for 48 h with the indicated CM, in the presence or not of gemcitabine (100 μg/ml).
(B, C) Venn diagrams showing the overlap between DMS-53 RNA-seq (Blue circle) and either ASCL1 ChIP-seq (Orange circle) (B) or NEUROD1 (Green circle) (C) ChIP-seq promoter annotated peaks in untreated conditions (t=0). Top panels. Tables showing the common and unique features from Venn diagram. According to RNA-seq data, a gene has been considered transcribed, if it has a coverage (number of reads per base of the gene) of more than 1 and a cut off value of TPM (transcript per million reads) of 4. DMS53 RNA-seq: genes being transcribed; ASCL1- and NEUROD1-Chip-seq: genes targeted byASCL1 or NEUROD1; DMS53 RNA-seq and either ASCL1- or NEUROD1-seq: genes bound by either ASCL1 or NEUROD1 and being transcribed; DMS-RNA-seq only: transcribed genes not targeted by ASCL1 or NEUROD1; ASCL1- and NEUROD1-Chip-seq only: non-transcribed genes in our experimental conditions. Lower panel : Venn diagram showing the overlap between ASCL1 and NEUROD1 (Dark green Circle) targeted and downregulated genes (3470 genes) in untreated conditions.
(C) Immunohistochemical staining for PECAM-1 (red), cleaved Caspase-3 (green) and DNA (blue) of B16Bl6 tumors after p.l. treatment with 50µg mCD13-AFR and 23.8µg mCD13-AFN-II. Scale bar is 100µm.
(E) Top view of cartwheel reconstruction from C. reinhardtii. Scale bar, 50 nm. Dark orange arrow marks the D2-rod. Purple arrow marks part of the pinhead. Dotted yellow box with arrows denotes the central hub-focused reslice shown in panel F; dashed white box with arrows denotes the spoke-focused reslice shown in panel H.
D) Untreated U2OS cells or cells exposed to either HU (2 mM, 24h) or IR (15 Gy, 2h recovery) alone or together with ATM inhibitor (KU55933, 10 μM) or inhibitors to ATR (ATR#1: ETP-464, 1 μM; ATR#2: AZ-20, 3 μM) were harvested and lysates were prepared. The inhibitors were added 30 minutes prior to HU or IR treatment. Immunoblots were performed with indicated antibodies.
(g,h) Representative images from movies of HEK293T negative shRNA or shHK5 cells showing cytosolic (green) and mitochondrial (red) [Ca2+] before, during and after ionomycin exposure. Scale bar, 20 μm.
(F) Log2 values of the calculated Pol II traveling ratios for each actively transcribed gene were arranged in order from low to high and then plotted against percentile.
e, Western blotting analysis of the protein levels of ISX, PCAF, and EMT markers in DOX-inducible ISX expression system A549 cells treated with TH1834, Garcinol, C646, MB-3 for 8 h after DOX induction. Data information: Each experiment was repeated at least three times.
(D and E) Proportions of the total recovered cell γ-secretase activity in different subcellular fractions after serum deprivation (D) or in uninduced (+serum) or induced (−Leu/−His) cells (E). Comparison of +serum versus −Leu and −His conditions shows the redistribution of γ-secretase activity from the tubulovesicular to AV fractions after macroautophagic induction. G, Golgi; A, AV.
B, C. Specific pharmacological inhibition of HDAC3 facilitates DRG neurite outgrowth (average neurite outgrowth after 24h in culture, Tuj1 positive neurons) on PDL-laminin or Myelin substrates. Scale bars, 100 μm. Data information: Data expressed as average neurite length ± s.e.m. N= 3-9 biological replicates. (*p<0.05, **p<0.01, ***p<0.005) indicate significant difference of 966 versus vehicle Student's t-test)
The corresponding α-synuclein levels (B were evaluated in SH-SY5Y cells expressing dCas9-5xGCN4 with (sgA-dCas9) or without scFV-sfGFP-JARID1A (sgA-dCas9-JA). B The levels of α-synuclein (α-SYN) in SH-SY5Y cells were evaluated using RT-PCR. The level of α-SYN was normalized to β-actin expression. A significant reduction of α-SYN in cells expressing scFV-sfGFP-JARID1A was observed. Four independent repeats were performed. *P < 0.05. Data were analyzed using non-parametric t-test followed by Mann-Whitney post-hoc corrections. Two-tailed p-values were calculated. Data information: All data are presented as mean ± SEM.
Relative luciferase activities of indicated constructs in differentiating C2C12 cells.
(K) Opti-prep purified supernatants from (J) were incubated with SupT1 target cells for 4 hours and virus-cell fusion was scored by flow cytometry. The mean + SD of 3 experiments is shown.
(c) Immunoblots using an α-Lc3 antibody detecting Lc3-I and conjugated Lc3-II. 4-OHT-treated and control-treated MEFs of the indicated genotype were incubated with leupeptin and ammonium chloride (lys PI) for 2 h in DMEM (+amino acids) or in EBSS (−amino acids) medium. The expression of α-tubulin (upper panels) or α-vinculin (lower panels) was used as loading control.
Changes in WT and variant FOXL2 mRNA expression were assessed by RT-PCR (top) and real-time RT-PCR (bottom) (A) after transfecting KGN cells with anti-miRNAs for 48 h.
(B) Negatively stained electron micrographs of fractions 3-7 and 27 directly derived from size exclusion chromatography showing the structural signatures and their structural integrity within the fractions. Decreasing molecular weight correlates with increased protein concentration as a function of protein complex elution is highlighted.
(E) Growth curves for MCF10A cells were transfected with either control siRNA or two independent siRNA targeting EPCAM, SCD, or USP3. Note that the control cell growth curve is the same in all graphs and were plotted separately for clarity and does not represent independent experiments. Two-way ANOVA was used to test for significance (n=3).
Control Western blot of HEK293 protein lysates obtained from cells transfected with mCherry (lane 1) or CASPR1-mCherry cDNA (lane 2) and probed with anti-mCherry antibody
Quantification of non-esterified cholesterol content by means of filipin staining in hearts of 12 to 16-week old male C57BL/6 wildtype (Vegfb+/+) (n=4), BKS.C57BL/6 db/+ Vegfb+/+ (n=8), db/db Vegfb+/- (n=10) and db/db Vegfb-/- (n=4) mice, normalized to db/db Vegfb+/+ (n=6) mice. Data presented as box-and-whisker plots. Boxes represents lower/upper quartiles with the median values indicated with a horizontal line. Whiskers represent min-max values. Statistical evaluation using one-way ANOVA and Dunnett´s multiple comparisons test, p-value: * <0.05, *** <0.001 (compared to db/db Vegfb+/+ mice).
USP36 promotes the binding of Nhp2 to snoRNAs. H1299 cells transfected with Flag-Nhp2 and V5-USP36 individually or together were assayed by RNA-IP with anti-Flag or control mouse IgG, followed by RT-qPCR detection of the indicated box H/ACA snoRNAs (C). The expression of Nhp2 and USP36 proteins is shown in (D). Shown is one representative experiment of three independent experiments. Data were presented as mean ± SD, n=3 technical replicates. *P<0.05; **P<0.01, compared to Nhp2 alone (Student's t-test).
(g) NSCs were isolated from C57B6/J E13.5 embryonic brains and then were infected with a lentivirus containing a TCF20 shRNA or with a control plasmids. Immunostaining of 5fC shows that TCF20 depletion increased 5fC levels. White dashed lines show the cells infected with lentivirus. Scalebar 25 μm (h) Statistical analysis of 5fC fluorescence level. n=20 cells, and P<0.0001 Data information: Error bars represent the means ± S.E.M. Two tailed unpaired T-tests were used to analyze the data, n.s. (no significant difference), p<0.05(*), p<0.01(**). and p<0.001(***).
M, Quantification and representative CK19 IHC of R211-luc lung micro-metastasis from vehicle or BYL-719 treated mice. n=6 in vehicle; n=5 in BYL-719 group.
(G) Endogenous miR-122 target CAT-1 (left panel) and Aldolase (right panel) mRNA levels in HA-HuR or pCIneo (control) injected mouse liver were quantified by RT-PCR (mean+/- s.e.m., n=4).
(C) Gene set enrichment analysis (GSEA) visualization of the common HP1 high-confidence interactors using Reactome pathways. Enrichment maps were developed with a ranked interaction network (p < 0.2, FDR < 0.5 and overlap coefficient = 0.75) and the cell cycle cluster is provided in this panel. The complete interaction network can be found in Expanded View Fig.1D. Pathways enriched in: (i) control conditions are represented in blue; (ii) NCS-treated conditions are represented in red.
(B) Kaplan-Meier survival curves for colon cancer patients with or without dysfunction of iron homeostasis in the GSE dataset (n = 590 samples, P = 0.016, Log-rank (Mantel-Cox) test). "Normal" represents the patients with unaltered expression of iron homoeostasis-related genes, including LTF, CP, FTH1, SLC30A1 and TFRC; "Dysfunctional iron homoeostasis" represents the patients with altered expression of iron homoeostasis-related genes.
B) KD values obtained by ITC measurements with full-length recombinant B56α and indicated ADAM17 variant peptides.
E mRNA levels of proinflammatory cytokines and NF-κB target genes from 6-7 week old retinas (WT, n = 5; NYKO, n = 5). Transcript levels were normalized to Hprt mRNA levels. Data were analyzed using unpaired t-test, *P ≤ 0.05, **P ≤ 0.01, ***P ≤ 0.001, ****P ≤ 0.0001, ns = not significant. Data are means ± SEM.
E,F. Serum insulin (E) and triglyceride (F) concentration was assayed in mice 24 h after one dose of CL316243 injection. n=5 mice each group. Data information: Data represent means±SEM. *P<0.05; **P<0.01; ***P<0.001; unpaired two-tailed Student's t test.
TNFR1 mRNA levels measured by qPCR in organs of B (n = 3) and S (n = 4). Affymetrix microarray data from hepatocytes (Affy Mo Gene 1.0 ST Array).