EMBO/sd-character-level-ner huggingface dataset:
Specific interaction of CLK1 with HSATIII during thermal stress recovery. HSATIII-ChIRP at various time points during and after thermal stress exposure. Endogenous CLK1, SRSF7, and SRSF9 were detected using anti-CLK1, anti-SRSF7, and anti-SRSF9 antibodies, respectively. HSATIII was detected by ChIRP-RNA purification, followed by RT-PCR. Input: 0.1% for CLK1, 1% for SRSF7 and SRSF9, and 100% for HSATIII.
(A) Schematic of KrasLSL-G12D/+; p53fl/fl (KP) mice intratracheally infected with pSECC lentiviruses containing sgNf1 or control sgTom. Mouse tumor burden was tracked by micro-computed tomography (micro-CT) for five months post-infection, and lungs were finally harvested 21 weeks post-infection. Tumors were dissected out for immunohistochemical (IHC) staining and generation of the tumor-derived parental KP cell line.
D-H The relative gene expression levels of growth factors in P5-treated DP cells (n = 4 (VEGF, PDGFA), 5 (IGF1), 6 (HGF, FGF7) biological replicates / group)
(B) Quantification by micro-CT of mean tumor volumes in KP mice derived from 50 randomly-selected tumors at 8, 12, 16, and 20 weeks post-infection with control sgTom, sgNf1.1, sgNf1.2, or sgNf1.3 (n = 18 mice, 21 mice, 21 mice, and 20 mice, respectively).
(E) Cytoplasm-mitochondrial fractionation assay was performed to determine the subcellular location of GDH1 with or without aa starvation. The fractionation efficiency and GDH1 location were determined by WB using antibodies against VDAC1 (mitochondrial membrane marker) and GDH1. Tubulin was used as loading control.
G Colony-forming units on YEPD plates with or without CPT at different concentrations. Plates were incubated 3 days at 25°C. Plotted values are the mean values with error bars denoting SD (n = 3)
E. Several amino acids are predictively important for SPOP dimerization. Mutations on the following residues might destroy the dimer interface for MATH domain: any residue in blue color to Pro at the strand where Q165 locates or any residue in green color to Pro at the strand on the dimer interface. Residues mutated in PCa patients F102, F133 and Q165 are in red.
(b) siRNA-mediated depletion of Atg6 (Beclin-1) and Atg7 from HeLa cells causes MR accumulations. The right panel shows the quantification of MRs per cell (mean ± s.d. of three independent experiments); the left panel the efficiency of Atg6 and Atg7 depletion.
Schematic of cardiolipin (CL) biosynthesis pathway in mitochondria. Phosphatidic acid (PA) is transported to the inner membrane by PRELID1 where it is converted to CDP-diacylglycerol (CDP-DAG) and glycerol 3-phosphate (G3P) by TAMM41. Phosphatidylglycerol phosphate (PGP) is dephosphorylated to phosphatidylglycerol (PG) by PTPMT1. PG is either degraded to DAG or reacts with CDP-DAG to form CL in a reaction catalyzed by cardiolipin synthase (CLS1). Tafazzin (TAZ) catalyzes the remodeling of monolysocardiolipin (MLCL) to mature CL. CL is transported to the outer membrane and converted to PA by mitoPLD. PA is converted to DAG by Lipin1. PA can be supplied to the inner membrane from DAG conversion by Acylglycerol Kinase (AGK).
A-F 22 days of treatment of DIO male mice with vehicle (white), liraglutide (10 nmol/kg) (gray), RM-493 (3.6 μmol/kg) (black), or liraglutide (10 nmol/kg) and RM-493 (3.6 μmol/kg) (checkered). Effects on (A) body weight. Compounds were administered by daily subcutaneous injections. Data represent means ± SEM;n = 8; *P < 0.05, **P < 0.01, ***P < 0.001.
Representative FACS plots of differentiation marker CD127/KLRG1 staining of the gated P14 CD8+ T cells and the statistical summary of SLEC subsets were shown to indicate CD8+ T cell differentiation. Data are shown as mean ± s.d. and n=5. * indicates significant difference (P<0.01, two-tailed unpaired Student's t-test). Data are from one representative experiment of two biological replicates.
C. The effect of the IDAP2 mutation on the recruitment of IDM1 to its target loci. ChIP was performed in the wild-type, IDM1-HA-YFP/idm1-3 and IDM1-HA-YFP/idap2-1 transgenic plants with an anti-HA antibody. The transgene was introduced into idap2-1 by crossing.
D, E. Luciferase assay in 293T cells transfected with an IFN-β luciferase promoter and TK-Renilla together with mutant HDAC6 or HDAC6-CDM (100, 200, 400, or 800 ng), followed by PR8-GFP (MOI = 2) infection (D) or by poly(I:C) (E) (1 μg/ml) transfection for another 12 h.
J: Brain homogenates from panel C were immunoprecipitated with anti-VAC14 antibodies. FIG4 and PIKfyve did not co-precipitate in prion-infected brains at terminal disease.
Jurkat cells were exposed to either DMSO, or dieldrin in DMSO for 30 min. RNA-seq was then performed on cDNA libraries prepared after depletion of ribosomal RNAs. Screen captures from IGV showing an example of a HERV becoming a site of divergent transcription upon exposure of the Jurkat cells to dieldrin. Top tracks show coverage from sequencing of poly(A)-enriched libraries for comparison. All coverage tracks are at the same scale and all the sequencing result files are of comparable size. Blue and red reads (rds) are in opposite orientation. CAGE peaks use the same color code. Reads mapping inside a series of 4686 HERVs located away (30Kb) from protein-coding genes were quantified both in the poly(A)-enriched and the ribo-depleted data. Read counts from each replicate were then summed and plotted.
(B-I) Association of Jumpy CS mutant with autophagic organelles. C2C12 cells were transfected for 24 h with GFP‐Jumpy C330S (Jumpy CS) and tdTomato‐LC3 (LC3), fixed and immunostained with anti‐G58K (Alexa 648‐labelled secondary antibody). Jumpy CS (green), LC3 (red) and G58K (white in D, H or blue in E, I). Boxed areas (B-E) are shown at higher magnification in the corresponding panel below (F-I). Scale bars, 2 μm. White arrows indicate colocalization between Jumpy CS, LC3 but not G58K, blue arrow indicates colocalization between Jumpy CS and G58K but not LC3.
(C) Graphs showing the quantification of FACS analysis of infiltrating F4/80+ tumor macrophages and average percentage of median fluorescence intensity (MFI) of TNFα+ or INOS+ on F4/80+ cells after ex vivo stimulation with PMA and ionomycin in vehicle (n=4 tumors) and COMBO (n=6 tumors), *P < 0.05 versus vehicle (TNFα P = 0.037; INOS = 0.038).
C) Expected log2(H/M) values over the course of 24 hours for proteins with half-lives ranging from 1 to 10 days. Compare with the actual measurements shown in Fig. 7 A-C.
E) Left panel: representative images of internalization of oxLDL (red) in ACM C-MSC cultured in AM or AM+5μM GW9662 and subjected to 10μg/ml DiI oxLDL treatment. Nuclei are counterstained with Hoechst33342 (blue). Right panel: quantification of the DiI fluorescence normalized on nuclei number for each sample (n=3 biological replicates, arbitrary units; Two-tailed Student's t-test). Data information: mean ± SEM. * p<0.05; ** p<0.01.
Proline abundance in NIH-3T3 cells expressing empty vector or HA-P5CS cDNA, measured by GC-MS. Values are relative to mock-treated empty vector expressing cells.
B) PBMC of a healthy donor (HD1) cultured for 6 days in the presence of 6.5 mg/ml C. albicans protein. At day 6, PBMC were restimulated with PMA and ionomycin in the presence of 10 μM GSK-7975A or DMSO for 6 h and CD4+ and CD8+ T cells were analyzed for cytokine production by flow cytometry. Bar graphs represent the mean ± SEM from two independent experiments.
H) Cortex glial (NP2222-GAL4>) overexpression of two independent hh RNAis significantly rescue EdU incorporation defects caused by htlACT overexpression (n=10, 16; 7, 12; 14, 11 brain lobes).
(d-f) Death of Ifng−/− and Irgm1−/−Ifng−/− T cell populations activated with mAb to CD3 and expanded in IL-2, then treated with IFN-γ (d), agonistic mAb to CD3 (e) or Fas ligand (FasL; f), assessed by propidium iodide staining at 48 h after treatment. Open bars, Ifng−/−; filled bars, Irgm1−/−Ifng−/− (a,b,d-f). Data are representative of three independent experiments with similar results (mean and s.d. of triplicate cultures a,b,d-f).
D, Longitudinal monitoring of ICG intensity in control and steatotic livers (time interval: 5 minutes; total length: 60 minutes). Each data point represents the mean from 5 animals at each time point. For each curve, data is normalized to the highest intensity acquired. Data information: In the figure, A.U. = arbitrary units
Dmxl1 was knocked down in WT iBMDMs or Tpl2[D270A] iBMDMs by RNA interference using a SMARTpool ON-TARGETplus siRNA for 48 h. ON-TARGETplus non-targeting pool functioned as siRNA control. (C) qRT-PCR analysis of RNA extracted from iBMDMs was used to check the efficiency of Dmxl1 knockdown (D, E). Dmxl1 mRNA levels were normalised to Hprt mRNA levels and fold changes calculated (ΔCt values) (n = 4). Data Information: One representative experiment out of three shown. Error bars and shaded areas represent SEM. **** P < 0.0001.
B. The distribution of mean H3K79me2 amongst different gene sets (6A, left panel) from activated and naïve B cells depicted by box plots. Boxes in Box plot indicate Inter quartile range (IQR) and whiskers show 1.5 IQR of highest and lowest quartile. Central horizontal line within the bars represent median of the TMM normalized H3K79me2 counts + 1 values of the respective genes for each condition. Results represent the data generated from three biological replicates for each group.
F Co-immunostaining of CHL1 and NB-3 in FG-labeled corticospinal neurons (arrowheads) of NB-3+/+ and NB-3−/− mice 14 days post-injury (dpi).G Quantification of the fluorescence intensity of CHL1 in (F). *p < 0.05, and **p < 0.01; one-way ANOVA followed by Bonferroni post-test. The intensities of more than 300 corticospinal neurons from 3 mice in each group were quantified.
A) t-SNE maps showing clustering based on differentially expression analysis and highlighting cell type identification of bronchioalveolar cultures based on cell makers. Each color represents a cluster or different cell type. Number indicates number of cells in cluster identified as cell type presented.
Left graph shows the multiplication rate of P493-6 (-Tet) cells expressing either a scrambled control sh-RNA or a TSC1-specific sh-RNA determined by viable cell counting 3 days after seeding of equal number of viable cells (determined by Trypan blue exclusion; mean ± st.dev., n=3 biological replicates). Right graph shows percentage of apoptotic P493-6 (-Tet) cells expressing scrambled control shRNA or a TSC1-specific sh-RNA determined by FACS analysis of AnnexinV/7AAD stained cells (mean ± st.dev., n=3 biological replicates).
(A) Phosphorylated Myosin-II Regulatory Light Chain (p-MLC; purple) detected by antibody staining reveals high levels around the cortex of rounded mitotic cells (pH3, red) in wild-type wing discs, and aurA homozygous mutant wing discs, but not upon inhibition of both AurA and AurB by treatment with VX-680. Note increased numbers of mitotic cells in aurA homozygous mutant wing discs, due to delayed mitotic progression. Scale bars ~20µm (low mag.) and ~1µm (high mag.). n > 15 independent biological replicates.
(A) Structure of the reported PP2Aγ-B56-hSgo1 binding interface (top) and residues mutated in the B56α 5A mutant are shown (bottom).
(C) H2O2 'acute stress' assay. Wild-type, Δprx1, Δglr1 and Δglr1Δprx1 cells pre-grown in SGal medium complemented with all amino acids to early exponential phase. Cells were treated with H2O2 at the indicated concentrations for 30 mins. Subsequently cells were diluted, and a fixed volume plated on YPD plates. The number of viable colonies was counted after 2 days growth at 30°C, here represented as a percentage relative to the 0 mM pre-treatment. Error bars represent standard deviation (n = 3 biological replicates, with cells taken from independent cultures for each individual biological replicate). An inset with a different scale on the y-axis is presented for the 1 and 5 mM concentration to allow better interpretation.
E. Quantification of colocalized GFP-LC3 and mCherry-capsid puncta normalized to the number of mCherry-capsid puncta per cell (% colocalization) at 8 h after Sindbis virus (AO28 strain) infection in MEFs of the indicated genotype. Bars are mean ± SEM of triplicate samples (~100 cells analyzed per sample). Similar results were observed in more than three independent experiments. *p<0.05; two-tailed unpaired t-test. See Fig EV1G and H for quantification of mCherry-capsid puncta per cell and GFP-LC3 puncta per cell from the same experiment.
(A) Immunoprecipitation of DIC followed by Western blot analysis of CRMP4 in SOD1G93A compared to WT P90 sciatic nerves under physiological conditions. IgG antibody was used as a control. (B) Quantification of the blot in A. 3 repeats, 12 sciatic nerves per condition were used in each repeat. The CRMP4 intensity band was normalized to the DIC intensity band in each repeat. Data presented as mean ±SE (Ratio Paired t-test, *p = 0.0416).
J-L The migration speed of the (J) 1st, (K) 2nd, or (L) 3rd-5th macrophages along the first 25-30µm into the germband between the mesoderm and ectoderm. In schematics, analyzed macrophages--light blue, other macrophages--red, ectoderm--green, mesoderm--purple, and yolk--beige. For (J): control n=6 movies, mutant n=5, p=0.012. For (K): control n=5 movies, mutant n=5, p=0.03. For (L): control n=5 movies, mutant n=4, p=0.17. Data information: Unpaired t-tests. Graphs show mean±SEM; ns=p>0.05, *p<0.05, ****p<0.0001.
B-F: TEM images o MOSPD2, VAP-A and VAP-B (F: siVAP-A/VAP-B/MOSPD2) -silenced HeLa cells. An interpretation scheme representing contacts between organelles is shown on the right; the ER, endosomes and ILV are in dark, light and medium gray, respectively. Mitochondria and Golgi are in pink and light green, respectively. Scale bars: 500 µm
(e) COS-7 cells expressing Xpress-tagged ataxin-1 with 92 polyglutamine repeats (Q92) for 48 h were doubly labeled with antibodies to Xpress (green) and to mTOR (red).
(G) Left panel: a scheme illustrating the principle of the thiol modification-based 'redox shift' assay, for which reduced thiols (but not thiols oxidized to a disulphide bond or a sulfinic or sulfonic acid) can be irreversibly modified by the alkylating agent mmPEG24 leading to a ~2.4kDa increase in mass and thus decreased mobility on an SDS-PAGE gel. Right panel: redox shift assay to assess the oxidation state of the Prx1 catalytic cysteine residue performed in Δprx1+Prx1-WT, wild-type + empty vector and Δprx1+Prx1-C91A.
B Flow cytometry based on CD49f and EpCAM staining separates lineage-negative breast tissue cells into stromal (CD49f-EpCAM-) and epithelial cells, which includes basal (CD49f+EpCAMlo/-), luminal progenitor (LP) (CD49f+EpCAM+) and mature luminal (ML) (CD49f-EpCAM+) cells.
(H) Western blot analysis for HOPX in control, mFoxm1 and mutants in mice primary neural progenitors 3 days after lentiviral infection. β-actin was detected as loading control.
(F) Primary B cells of BrafAVKA mice show reduced CD69 surface expression upon LPS and anti-IgM stimulation. n = 3, mean + SEM, test, ** p < 0.01.
I) Real-time PCR analysis of the expression of EMT-associated markers (E-cad, vimentin) and transcription factors (Twist1, Snail, Slug, Zeb1) in SNU719 and SNU-4th cells.
A, B. Depletion of Ccdc108 markedly affects bead movement by decreasing velocity Fluorescent beads were applied to the dorsal surface of Xenopus embryos. Bead tracks every 500 ms over 2 s are shown (A). Plot of average bead velocity shows significantly reduced bead flow in ccdc108 morphants, which can be fully rescued by co-injecting with Xenopus ccdc108 mRNA (B). 150 beads from 15 embryos for each condition. Arrowheads indicate beads that showed no movement on the embryo surface through the recording. Data information: Quantification data were collected from three independent experiments. Unpaired two-tailed t-test was performed (*** p<0.001). Mean ± s.d. values are presented.
B HEK-293T cells expressing Flag-DENND2B were treated with DMSO or 250 nM OA and cell lysates were incubated with GST-14-3-3. Total proteins and bound proteins were detected by Ponceau S staining and Western blot, respectively.
Left, representative western blot data of nuclear acetylated-histone H3 (Lys 9/14) and total-histone H3 in 6-mon-old of WT and FTLD-TDP Tg mice. Right, quantification of nuclear acetylated-histone H3/total-histone H3 ratio. N = 5 mice per group, data are presented as mean ± SEM (%), * p = 0.0147 by t-test.
A-C. Three-dimensional reconstruction (left) and Imaris-based morphometric analysis of CX3CR1+ brain microglia or F4/80+ liver and kidney MΦ in adult Irf8-/- or Irf-8+/+ mice, respectively. Quantification of cell density of Iba1+ microglia and F4/80+ liver and kidney MΦ in adult Irf8-/- or Irf-8+/+ mice, respectively (left). Scale bars = 10 µm. For morphological measurements each symbol represents one mouse with at least six examined cells per mouse. Data represent mean ± s.e.m. Significant differences were examined by an unpaired t-test and marked with asterisks (*P < 0.05, **P < 0.01, ***P < 0.001); n.s.: not significant.
(B) CLK21 KI mice F0 and F1 generations. Squares represent male mice and circles represent female mice. Upper halves of squares or circles represent Ig κ, and the lower halves represent Ig H, as shown in the schematic. F0 generation mice genotyping results showing 7, 9 and 14 are HCLK21/WTκWT/WT, 1 and 4 are HWT/WTκCLK21/WT, and 2, 3, 6, and 12 are HCLK21/WTκCLK21/WT. Mouse 3 was crossed with WT to obtain 11 F1 progeny: Five F1 mice are HWT/WT κCLK21/WT, four are HCLK21/WTκCLK21/WT and two are WT. (C) Single cell sequencing for naïve B cells from heterozygous CLK21 double KI mice. Left column shows the gating strategy for sorting naïve B cells (upper) and eOD-GT8 specific naïve B cells (lower). Right pie charts show the frequency of paired HC and LC sequences among total naïve B cells (upper) and eOD-GT8 specific naïve B cells (lower).
Quantitative RT-PCR analysis of selected (C) known HSPC metabolic regulators expression in bone marrow HSPCs (n=4 mice per genotype). Data information: The statistical significance of difference was assessed using Two-tailed Student's unpaired t-test analysis for comparison of control and PKCδ cKO HSPCs. All data are presented as mean± SEM., *p<0.05, **p<0.001.
D qPCR quantification of TIMM50 transcript levels in control and TIMM50 mutant fibroblasts. Data are shown as mean ± SD, n = 4.
(G) Network pathway analysis using IPA. The molecular network of genes connected with the top 5 functions/diseases associated with genes upregulated in Irgm1 knockout mouse brain.
Q-R Quantitative analysis of the incidence of monopolar spindles during the first (Q) and second (R) meiotic divisions for each experimental condition. Percentage of monopolar spindles functional analysis are represented for 100µM BI2536 and 10µM MLN8237 for 8h treatments on organotypic cultures of seminiferous tubules. Experiments were conducted in three different biological replicates.
(B) GSEA analysis of RNA-Seq results from PtenΔC/ΔC and WT mice (P21). Transcripts ranked by levels of expression (ΔC/WT ratio) were tested for enrichment in precurated gene sets in the C5 (gene ontology) category. NES, normalized enrichment score; positive and negative enrichments indicate a greater contribution of up- and downregulated genes, respectively, to the enrichments (see also Dataset EV2for the full GSEA results).
B Reporter assays: HepG2 cells were transfected with plasmids as indicated and treated with GW4064, and luciferase activities were measured. Values are presented as mean ± SEM (n = 3); two‐tailed Student's t‐test, *P 0.05, **P 0.005, NS, not significant.
GFP+ (CRE) and Tomato+ (CRE-) total bone marrow cells were sorted on day 8 after first TAM-administration and processed for Western Blot using the indicated antibodies. Sorted cells from three animals - mT/mG Vav-CreERT2 (WT) and mT/mG Vav-CreERT2 Chk1fl/fl (Chk1fl/fl) - were pooled per lane.
A-D Localization of PKG-3Ty shown by IFA using an anti-Ty antibody. Antibodies against GAP45, IMC1, cb-GFP, and myc-GAP70 were used as markers of the plasma membrane, IMC, residual body, and apical pole, respectively.Data information: Scale bars = 2 μm.
(C) GST pulldown of recombinant Sept2 with GST-Drp1 or GST alone showing that Sept2 is able to interact directly with Drp1.
(b) Beclin-1 alone or bound to ATG14L was purified as described in a. Equal amounts of ULK1 were added to each complex and reactions were quenched at the indicated time points. Western blotting was performed with the indicated antibodies.
B-D Kaplan-Meier survival analyses of the humanpatients (n = 3,935) divided into two groups based on the expression level of the genes of each overrepresented class determined in Fig A: cell cycle genes, DNA replication genes, or p53 target genes.
The structure of the lower subdomain from the shoulder showing the organization of p150 (purple), p24 (yellow) and the two copies of p50 (p50-A in red, p50-B in pink). The N and C termini of each chain are shown. A Gaussian surface rendering of the lower subdomain is colored by feature (blues and magenta, inset).
(E) Quantitation of Rpb1-GFP fluorescent intensity expressed as percentage over the G1 level. SEM is indicated (n=106 for WT and n=102 for mec1Δsml1Δ).
TNF measurement in the serum of GRfl/fl (n=4) and GRVillinKO mice (n= 4). Mice were treated with 5 mg/kg LPS and blood was drawn 2 hours later.
Scatter plots of percent distal polyA site usage indices (PDUIs) in control cells (siCont), Srsf3-silenced cells (siSrsf3; left panel), and both Srsf3- and Hnrnpk-silenced cells (siSrsf3 + siHnrnpk; right panel). PDUIs of all 3′ UTRs are plotted. The 3′ UTRs shortened and extended by siSrsf3 exceeding the thresholds of |ΔPDUI| > 0.2 and p < 0.01 are indicated in red and blue, respectively.
Ubqln4 interacts with LC3. Confocal images of (A) Hela cells transfected with GFP‐LC3 and RFP‐Ubqln4 and starved for 1 h or
(D) Immunoblot analysis of BBS4 expression in testes and thymi lysates of Bbs4+/+ (WT), Bbs4GT/+, and Bbs4GT/GT mice. β-actin staining serves as a loading control. A representative experiment out of three biological replicates in total is shown.
(B) Bcl6 expression by Tfh cells in Pou2af1+/+:Pou2af1-/- mixed bone marrow chimeras seven days after immunization with SRBC. The graphs illustrate the proportion of Bcl6hi CXCR5hiICOS+ Tfh cells within the population of Pou2af1+/+ and Pou2af1-/- CD4+ T cells from bone marrow chimeras (n=7).
(B) In the OFT, Cox6a2-/- mice travelled a longer distance and moved faster than WT mice. Cox6a2-/- mice also moved more often from the outer zone to the inner zone of the arena. Two-tailed unpaired Student's t-tests.
PCA of genes in the molecular signature of MPNSTs. All primary-xenograft pairs cluster together. The first component distinguishes between sporadic and NF1-related tumors; the second component differentiates primary tumors (and derived orthoxenografts) from the cell line (and the derived orthoxenograft).
(A and B) Quantitative analyses of ATF4, Parkin, and PINK1 gene expression in HCV-infected cells. Huh7 cells infected with HCVcc for 5 days or treated with CCCP (10 or 20 µM) for 24 h were used for analysis of ATF4, Parkin, and PINK1 gene expression. (A) Intracellular mRNA levels of ATF4, Parkin, and PINK1 were analyzed by real-time qRT-PCR. GAPDH was used to normalize changes in Parkin and PINK1 gene expression (mean ± SD; n = 3; *p<0.01, **p<0.05). P values were calculated by using an unpaired Student's t-test.
(A) left panel, map4k4-1 shows enhanced resistance to Pseudomonas syringae pv. tomato DC3000. The growth of Pst DC3000 after inoculation in the indicated genotypes (Col-0, white bars, map4k4-1, green bars). Bacterial titers were determined 2 hours (day 0) and 3 days after inoculation. Right panel, disease symptoms of wild-type and map4k4-1 at 3 days after inoculation. Values are the means ± SD, n = 6 (biological replicates), p < 0.01. Data information: Statistical analysis were performed using a one-way ANOVA with Newman-Keuls multiple comparison tests or t-tests. n.s. indicate non-significant.
A) Expression analysis by qRT-PCR (mean ± SD) of the indicated intestinal epithelial cell markers regulated by the Wnt and Notch signaling pathways that are involved in stem cell homeostasis, regionalization, and Goblet cell differentiation (n=3).