EMBO/sd-character-level-ner huggingface dataset:
F RT-PCR validation of Matrin3‐regulated alternative spicing events in the ST7, ACSL3, PLEKHA3, TCF12, VWA5A, PTBP2, PTBP3, C3orf17, ZMYND8, VEZT, PIGX and DMD genes. In each case, triplicates for each condition (C-control, M-Matrin3, PTB/nPTB and Matrin3/PTB/nPTB siRNA transfection samples) were analysed and exon inclusion (EI) percentage is shown beneath the corresponding lane, along with the standard deviation (s.d.).
Immunohistochemical staining for HIF-1α (brown) representative from CntlKD, BNIP3KD and ATG5KD, B16-F10 tumor tissues. Higher magnification of the highlighted (with a white square) stained sections is shown below.
(E) RNA expression levels 16 h after exposure to 3,4-DC of the indicated genes in HepG2 cells were measured by RT-PCR and normalized to the expression of the housekeeping gene (GAPDH). Data are means ± SD (* = p < 0.05;** = p < 0.01;*** = p < 0.001).
OCR (C) and ECAR (D) per µg of protein of B16-F10 cells assayed in medium containing either 25mM galactose (C) or 25mM glucose (D) medium using the Seahorse technology (n=4).
E,F. Effect of Nox4 knockdown or overexpression, respectively, on the tunicamycin-induced changes in mRNA levels of ATF4 target genes. n=4/group. Psat1, phosphoserine aminotransferase; Phgdh, 3-phosphoglycerate dehydrogenase; Asns, asparagine synthetase; Slc6a9, glycine transporter 1.
A. Experimental design for the whole genome sequencing of Rev3l-deficient cells. Populations of mouse embryonic fibroblasts Rev3l+/+ and Rev3l-/- were isolated from Rev3l+/+ and Rev3lflox/flox littermates and Rev3l was excised using CRE recombinase. The resulting Rev3l-deficient cells and Rev3l+/+ cells were expanded for 90 doublings. Rev3l+/+ and Rev3l−/− subclones were then isolated for deep sequencing.
(G) HEK293T cells were transfected with the indicated ESM1-GFP constructs. Cell extracts were pulled down with purified GST-ARM.
ion leakage (C) of the egr2-3 mutant and egr2/EGR2:EGR2-Myc complementation lines under non-acclimated (NA) and acclimated (CA; 4 d at 4°C) conditions. Two-week-old seedlings grown on MS medium containing 0.8% agar were treated at −5°C for 0.5 h (NA) or −8°C for 0.5 h (CA). Data information each bar represents the mean ± SEM of three independent experiments, each of which has three technical repeats. Asterisks indicate significant differences compared to the wild type with the same treatment (*P < 0.05, **P < 0.01, two-tailed t-test).
H, Dotplot showing expression of top 8 positive markers identified for each nonCM population.
E. Knockdown of the indicated proteins by siRNA in Drp1/OPA1DKO 293T cells was confirmed by Western blotting analysis.
(B, C) The ALP staining (B) and ALP quantification (C) of Cdc20f/f and Sp7-Cre;Cdc20f/f BMSCs after 7 days osteogenic differentiation. (n=6)
(E) At 48h after triple-transfection of H1, the indicated proteases and wtSPINK6 or mutSPINK6, BHK21 cells were lysed for the detection of HA cleavage.
A. Deconvolved inverted fluorescence micrographs Chm7-GFP and truncations in the indicated null strains. Scale bar is 5 μm.B. Plot of the percentage of cells with SD of Chm7-GFP (and truncations) NE foci from A. Data are from 3 independent replicates where >200 cells were counted for each strain. p values from un-paired student's T-test. ** is a p value ≤ 0.01; ****, p ≤ 0.0001.
E) Patterns of RUNX1, ETS1 and JUNB binding at RUNX, ETS and AP-1 motifs at the Trpm6 locus.
B) Replication of S. Typhimurium in Atg5-/- MEFs cells complemented with ATG5 or mock and treated with the TBK1 kinase inhibitor MRT68843 (10 nM) or DMSO. Fold replication was determined by counting bacterial colonies on agar plates at 2 and 8 h post inoculation (p.i.) following cell lysis.
Human monocytic (THP-1) cells were induced to acquire an M2-like phenotype (see Methods) and treated with different concentrations of TLR7-54 or FA-TLR7-54 for either 48h or 2h In the latter case, after the 2h incubation, culture medium was replaced with drug-free medium and incubation was continued for 46h. cell supernatants were analyzed for secreted cytokines by ELISA. (B-C) Changes in CCL18 and IL-1β in the culture media induced upon treatment with TLR7-54 and FA-TLR7-54 for the treatment regimens (n=3, technical replicates).
A. Heatmap of IC50 values for cell viability. Human dermal fibroblasts (HDFB) controls and 4 MCC cell lines (PeTa, MKL-1, WaGa, MS-1) were treated with the 43 indicated small molecules targeting epigenetic modifiers. IC50 values are depicted as log10(IC50) in [mM]. n/a, IC50 values could not be calculated. n = 4 technical replicates.
Two representative images of eWAT dissected from Evans blue-injected obese (HFD 16 weeks) WT and CD169-DTR mice treated for 7 days with DT. Evans blue dye was extracted from eWAT using formamide and the absorption of the extract was measured at 620 nm (the absorption values were normalized to the tissue weight in grams). A chart showing the normalized mean optical density ± SD (n = 5-7 mice per group). Statistical significance was determined using an unpaired Student's t-test. ***P < 0.001.
Representative IF double staining and 3D reconstruction of the Prom1 (green) and AcTub (red) at the apical domain of polarized MDCK cells expressing Prom1 and its K138Q mutant (top panels). Black-white inserts show Prom1 signals only. Same cells were analyzed by SEM (bottom panels). Note that Prom1 is asymmetrically distributed along the primary cilium (white arrows) as observed in vivo (see Fig 2C) and mutation K138Q significantly impacts on the primary cilium length. MV, microvilli.
(A) Ovaries were stained with TUNEL (green) to detect DNA fragmentation. Clusters of cysts with TUNEL staining were observed in region 2 in nutrient-deprived w1118 files. In Dcp-1Prev flies, fewer TUNEL-positive cysts in region 2 were observed. Under well-fed conditions, numerous TUNEL-positive cysts were observed in BruceE81 flies. DAPI staining of nuclei is shown in white. (B) Numerous degenerating stage 8 egg chambers (arrows) with Bruce-positive staining (green) were observed in well-fed BruceE81 flies. DAPI staining of nuclei (white) is shown on the right.
(E) Immunoblot analysis of fibronectin, pSmad2/3, total Smad2/3, hepsin, and GAPDH (loading control) in cell lysates from MCF10A-pIND20-HPN cells with (DOX+) and without (DOX-) hepsin overexpression, and with or without fibronectin silencing (siFN1). The graph depicts quantification of pSmad2/3 normalized to total Smad2/3 levels (N = 3 biological repeats).
a-e) 16HBE cells were stably infected with lentiviral vector pLKO alone or expressing EMP1 shRNAs (1 or 2). All data are representative of n=3 independent experiments. (b) Cells were fixed and stained for ZO-1, E-cadherin and DNA. Scale bar represents 20m.
Schematic representation of BioID proximity biotinylation in HeLa-T-REx cells stably expressing H3.1-BirA*-HA. Randomly cycling cells were treated with biotin to label proteins proximal to nucleosomal (nucH3.1) or non-nucleosomal soluble (solH3.1). H3.1-BirA*-HA, and biotin-labeled proteins were purified on streptavidin-conjugated beads.
(N-P) The loss of progenitor TH and Ddc function using domeMESO-Gal4, UAS-GFP analysed at wandering 3rd instar, 120h AEL. Data information: DNA is stained with Hoechst in blue, domeMESO (representative of progenitors) expression in green, P1 (representative of mature plasmatocytes) in red. All image panels show a 20µm scale bar. AEL indicates After Egg Laying. For better representation, the primary lobe of the lymph gland has been represented and outlined in white dashed lines
F. Secondary grafting of tumor cells (GBM44-GFP+) isolated from vehicle or prazosin-treated mice bearing primary tumors. Mice injected with glioblastoma cells isolated from prazosin-treated mice developed tumors at a lower frequency (50% versus 100%). Moreover, mice injected with glioblastoma cells isolated from prazosin-treated mice presented a statistically significant survival benefit. Left Panel: Bioluminescent in vivo images of secondary grafts. Middle panel: Quantification of the bioluminescent signals. *P=0.0004, n=8, two-sided Mann-Whitney U-test. Right panel: Kaplan-Meyer survival curves of mice bearing secondary graft from glioblastoma cells isolated from vehicle- and prazosin-treated mice.
(d) Comparison between calpain activity, EGFP-HDQ74 aggregation and autophagosomes as seen in a-c. The control condition for all the assessments was set at 100%. Calpastatin lowered the increased calpain activity and EGFP-HDQ74 aggregation caused by (±)-Bay K8644 in a dose-dependent manner with a simultaneous increase in LC3-II levels (autophagosomes).
Experimental designs for lineage-tracing of control, Lats1/2 double knockout (dKO) and Raptor;Lats1/2 homozygous triple-knockout (tKO) lungs. Specific time points for tamoxifen treatment and analysis are indicated.
(B1) Schematic of the two Atg30 molecules, one with an Atg8‐binding site mutated and a second with an Atg11‐binding site (A11‐BS) mutated, used to complement Δatg30 cells by co‐expression. P: indicates phosphorylation in vivo.
Representative immunoblot and quantification of sera collected at the indicated times from DBA/2J mice fed a high fat (60% fat) diet after a 18 h fast. A schematic of the fasting/refeeding experimental setup is shown above. The quantification was normalized for each mouse to the amount of ERdj3 in the serum draw immediately prior the fast. *indicates a p-value < 0.05; (n = 6).
H The interaction between RBM47 and the three targeted RNA fragments from the 3'UTR of IFNAR1 mRNA was tested using the luciferase reporter assay. The U to A mutants of these three sequences (as shown in Table EV1) were also used as negative controls.Data are represented as the means ± SD of n = 3 biological replicates. Data information: Data are representative of n = 3 independent experiments. NS, non-significant; **P ≤ 0.01, and ***P ≤ 0.001 (Student's t-test).
(j-m) CftrF508del mice (n = 3 per group) administered intranasally with a lentiviral vector encoding beclin 1 (LV-beclin 1) or GFP (LV-GFP). (k) Confocal microscopy of TG2 activity. Representative stainings from at least five airway epithelial areas per mouse from three mice per group. L, lumen. Scale bar, 10 μm.
H Graphs showing threshold cycle number of KLK3 plotted over housekeeping genes, semiquantitative RT-PCR performed with human-specific primers on RNA extracted from control (n=6) and LNG-treated (n=3) xenografted glands.
K, Quantification of THEM6 expression in PCa tissue samples according to Ki67 expression in the patients analysed in F. L, Quantification of THEM6 expression in PCa tissue samples according to Ki67 expression in the patients analysed in I-J. Data information: Centre line corresponds to median of data, top and bottom of box correspond to 90th and 10th percentile, respectively. Whiskers extend to adjacent values (minimum and maximum data points not considered outliers). Statistical analysis: two-tailed Mann-Whitney U test. Data reproducibility: K: n = 269 tumours for Ki67 low and n = 270 tumours for Ki67 high. L: n = 35 tumours for Ki67 low and n = 29 tumours for Ki67 high.
C. Delineation of the Sae2 domain responsible for interaction with Sir3 by two-hybrid assays. The GAL4-BD fusions with indicated Sae2 fragments were tested in combination with a GAL4-AD-Sir3 fusion; "+" indicates an interaction.
(E) Co-immunoprecipitation in confluent DU145 cells between endogenous β-TrCP, Ubch5c, YAP and β-catenin. DU145 cells were transfected with the indicated siRNA (control, siCTRL; UBTD1, siUBTD1pool or siUBTD1single). β-TrCP was used as bait. IgG isotype was used as a negative control. Immunoblot of UBTD1 shows the level of siRNA-mediated depletion.
(C) The Venn diagram represents overlap between differential phosphosites identified in the different GALNT isoform KOs.
D Immunocytochemistry analysis of sperm stained with anti‐ApCatSper 3, anti‐GC, or anti‐CNGK antibodies; superposition of images obtained by fluorescence microscopy and bright‐field light microscopy; scale bar = 10 μm. The DNA was stained with DAPI (blue).
(A, B) t-SNE visualization of 20,009 human retinal cells colored by (A) annotation of 18 transcriptionally distinct clusters (C0-C17) and (B) their distribution in 3 donor retina samples.
G Position of the ultimate eIF3j C-terminus in the mRNA entry tunnel (upper panel) and steric clash with mRNA as positioned in an 80S ribosome stalled during translation (PDB 5MC6); for clarity, in the lower panel only eIF3j and mRNA are shown, A/P/E respectively indicate the positions of aminoacyl, peptidyl, and exit site in the 80S ribosome.
K Relative mRNA expression levels for indicated genes were measured by qRT-PCR in wild‐type and Ccno‐deficient mTEC cultures at indicated days after differentiation‐onset. Relative values were calculated as in (J) relative to day 0 of ALI cultures.
(A) HeLa cell lines stably expressing eGFP-sNASP, eGFP-ASF1 and eGFP-HAT1. Scale bars represent 10 μm
(E) Representative images of wild-type or JfkKO mice fed on HFD. Arrows indicate abdominal SAT under MRI. EWAT and PRAT were dissected, and the sections from EWAT were stained with H&E. Scale bar, 100 μm.
Lysates of HEK293T cells transiently transfected with HA-tagged wild-type FAM134 genes were subjected to pulldown experiments (representative data; WB detection against HA; n=3) purified GST, wild type GST-LC3s, GST-GABARAPs, GST-Ubiquitin (Ub), GST-Tetra-Ubiquitin, A representative Ponceau staining is shown.
Kaplan-Meier survival curve for mice treated as in (C), with each treatment group containing n = 6 mice. Statistical significance was assessed by Log-rank test (****P <0.0001).
(B) The expression level of FAM210A mRNA in 15 human organs from the GTEx Portal database. TPM: transcripts per million of reads. The central band shows the median value and the box indicates the first and third quartiles. The sample size of human samples used for quantification in GTEx Portal database (from testis to pancreas): n=361/429/432/555/803/240/432/226/406/578/241/202/85/328/755.
(g) 16HBE cells were seeded on glass coverslips for 10 days to form a mature, polarised monolayer. Cells were fixed and costained for EMP1 and ZO-1, then analysed by confocal microscopy. A representative z-stack is presented; arrows indicate ZO-1 positive tight junctions.
C-F; H-K; and N-Q. The tagged WT or mutant 7SK RNA was co-transfected with the indicated Flag--tagged proteins into HeLa cells. Anti-Flag immunoprecipitates (IP) were analyzed by immunoblotting for the indicated proteins and primer extension for the bound 7SK RNA.
Schematic diagram of miR-AB-based lentiviral (LV) and retroviral (RV) vectors. miR-AB shRNAmir expression is driven by a composite promoter composed of the endogenous 5' LTR of HIV and a eukaryotic promoter in lentiviral vectors, or by the endogenous 5' LTR of MSCV in retroviral vectors. Eight fluorescent proteins with emission peaks across whole visible spectrum are controlled by mouse PGK promoter. A woodchuck hepatitis post-transcriptional regulatory element (WPRE) is used to enhance transgene expression.
(D) Beclin 1 (WT) or K437R‐Beclin 1 (K437R) mutant was stably expressed in Beclin 1‐silenced HeLa cells. Beclin 1‐knockdown HeLa cells were infected with lentivirus encoding 3XFlag‐tagged WT Beclin 1 (WT) or K437R‐Beclin 1 (K437R).
C Growth assays of untreated WT, ∆hac1, Δice2, and Δhac1 Δice2 cells (SSY1404, 2356, 2805, 2806). Numbers represent areas under the curves and serve as growth indices. Mean + s.e.m., n = 3 biological replicates.
C | The Random Forest analysis shows the highest impact of the hFwe-Lose biomarker in the multivariate analysis of outcome prediction. The plot shows the Mean Decrease in Gini coefficients for the factors that were incorporated in the statistical model for the multivariate CART analysis. The Gini coefficient is a measure of the miss-classification rate. The importance of a predictor is assessed by how much the predictor reduced this mis-classification rate. The hFwe-Lose expression has the highest score, followed by age and blood biomarkers. Comorbidities show the least impact on reducing the misclassification rate.
(C) Media samples were taken from the same cultures (n=3 for both strains) at the 8 hr timepoint and the remaining glucose was quantified. The consumed glucose was calculated based on the amount of glucose measured in the same, fresh media and normalised to the OD of each culture at the time of sampling.
Representative Masson's trichrome staining of lung sections from Bumetanide-treated control and F-CRTH2 KO mice. Scale bars, 100 µm.
(j) Model of system to measure degradation of GFP-tagged substrates by autophagy.
(b) Expression levels of FoxO1 and Atg7 conjugate in mice tumours were determined by western blotting.
Under normal growth conditions, MPK3/6 are less active and ARR1/10/12 maintains optimal cytokinin response to control plant growth and development. Exposing plants to high salinity activates MPK3/6, which interact with and phosphorylate ARR1/10/12. Phosphorylated ARR1/10/12 are degraded through the 26S proteasome-dependent pathway, eventually repressing the cytokinin response and leading to growth inhibition. X represents inhibited signaling or process.
I Bar chart depicting significantly enriched GO terms (analyzed first by Gorilla followed by Revigo) based on the 379 differentially expressed transcription factor genes (DeSeq2, cutoff pAdj0.01) comparing DIE and CTX GM astrocytes. Terms related to cell division, cell proliferation etc. are highlighted in red. (P-value threshold was set to 0.01
G Immunofluorescence images showing typical nuclear staining (DAPI, blue) and SOD2 staining (red) from WT, Aldh5a1−/− mice treated with vehicle and Aldh5a1−/− mice treated with rapamycin. Bar, 10 μm.
qRT-PCR analyses of KLF5 (left) and Sp1 (right) expression in FaDu cells transfected with control or KLF5 vectors. Data represent the mean (±SD) of three independent experiments performed in duplicate and unpaired t test was used to verify the statistical significance.
(D) Immunofluorescence analysis of adult chic/+ and chic/+; Ythdf#0/Ythdf#0 using anti-FasII antibody. Scale bar: 50 μm. Pink dashed lines highlight the normal and fused β-lobes.
(D) The body weight of male wild-type or JfkKO mice fed on HFD. Error bars represent mean ± SEM (n = 6, *p < 0.05, paired two-tailed Student's t-test).
MDM were treated with 5μM ETO for 18h and infected in the presence of ETO with VSV-G pseudotyped HIV-1 GFP viruses wild type (wt) HIV-1 capsid mutants (N74D or P90A), HIV-2, SIV sooty mangabey (SIVsm E543), replication competent Adenovirus type 5 AdV (AdV), Semliki Forest Virus (SFV) and HSV-1. The percentages of infected cells were determined using an automated cell‐imaging system Hermes WiScan and ImageJ and normalized to untreated control ~100%. (n = 3, mean ± s.e.m.; **P‐value ≤ 0.01; ***P‐value ≤ 0.001; (ns) non‐significant, paired t‐test). Cells from a representative donor were used for immunoblotting.
(B) Immunostaining of HP1 protein in fixed mouse ES cells that were stained with Hoechst to reveal condensed patches of heterochromatic DNA (examples marked by arrows; colocalization of HP1 and condensed DNA in 83 % of cells, n = 103).
(G) Control or CITK-depleted cells immunostained for ASPM (green), γ-tubulin (red) and DNA (blue).
(D) Immunostaining and quantification of the area of TUBG and PCNT signals from E5.5 and E6.5 centrosomes in epiblast cells. The separate channels for the marked centriole are shown in the insets. *** p < 0.001, ** p < 0.01 (two-tailed student's T-test). Bars represent mean ± s.d. Scale bar = 2 μm. Quantification of PCNT at E5.5: 0.22 ± 0.01 μm (n=103 centrosomes from 3 embryos); E6.5: 0.31 ± 0.02 μm (n=342 from 3 embryos). Quantification of TUBG at E5.5: 0.15 ± 0.02 μm (n=108 from 4 embryos); E6.5: 0.25 ± 0.01 μm (n=311 from 3 embryos).
Impaired re-epithelialization of the wounds in αSMA-TK mice at day 17 post-wounding. (I) Measurements of the distances between epithelial tips in the wounded skins of WT and αSMA-TK mice at days 17 post wounding. WT, N=7; TK, N=8 biological replicates. Black line denotes median value. Mann-Whitney test performed.
(B) HeLa cells were transfected with siRNA duplexes targeting PELP1, TEX10, WDR18, MDN1 or a control siRNA as indicated. Downregulation of the respective proteins was analysed by western blotting as indicated (WB, three lower panels). At 72 h after transfection, cells were pulse labelled with 32P‐orthophosphate for 1 h and chased for 2.5 h. RNA was separated on a denaturing agarose gel and detected by ethidium bromide (EtBr) staining and autoradiography after drying of the gel.
Immunoblot of phospho-S622 and pan-Drp1 in N2A cells depleted of STAT5 A and B by CRISPR/Cas9 (DKO) or with nontargeting control (NTC). Vinculin was used as a loading control. C. Quantification of B.
(C and D) Knockdown of Beclin1 in MEFs by shRNA inhibits HBSS-induced autophagy with and without pUNO1-HMGB1 transfection. Cells as indicated were stimulated with Earle's balanced salt solution for 3 h, and LC3 punctae formation (arrows) was assayed by immunofluorescence (D; n = 3; *, P < 0.05). Data are means ± SEM.
(D) Overexpression of SCOC-myc increases autophagy. Anti‐Actin, ‐LC3 and ‐Myc blots of HEK293 cells after transfection of pcDNA or SCOC-myc. Representative blot; quantification of LC3II/actin of averaged duplicates; error bars represent s.e.m. (n=5). SCOC-myc EL versus pcDNA EL, *P=0.0215.
C: The sorted E-GFPd1 ESCs populations were assessed by immunoblot for Esrrb and Nanog (left) or Oct4 (right) by fluorescence-based detection (Licor).
(E) Genome browser view of DNA methylation patterns of Hopx and Il10 loci for CD4+ naïve T cells, WT Treg cells and Tet2/3 DKO Treg cells. Differentially hydroxymethylated regions (DhmRs) and differentially methylated CpGs (DM-CpGs) are shown on top of the tracks. Conservation track (Cons) and denotation of all CpGs are shown at the bottom. WGBS data are from two biological replicate samples.
Typical E. coli cell displays foc expressed from the endogenous genetic locus of the F plasmid (F1-10B-mVenus). The nucleoid is labelled with Hu-mCherry (central). The overlay (bottom) combines the two fluorescent channels parSF inserted at the xylE locus on E. coli chromosome from DLT358
Sera were collected 3 months after transplantation and tested for ANA; percentage of mice with at least one ANA reactivity.
Direct targeting of HAG1:HA protein to WOX5 (I), SCR (J), PLT1 (K), and PLT2 (L) chromatin as determined by ChIP-qPCR.
C. The relative fluorescence was plotted over time for reactions with different ubiquitin acceptor molecules - for example in presence of K63-linked diubiquitin (K63‑Ub2) or K48‑linked diubiquitin. Initial reaction rates were determined as the slope of a linear fir of the fluorescence increase over 20 min.
(E) The number of soft 4T1 or MCF-7 cells from the outlet was calculated after treatment with or without Cyto (5 μM) or Jas (50 nM) for 4 hr or 12 hr, respectively. Data information: one-way ANOVA (E). The data represent mean ± SD of three independent experiments.
Control cell line (Tgfbr2wt; G&I) and the Tgfbr2-mutant cell line (Tgfbr2mut1; H&J) were orthotopically implanted in C57Bl/6 mice. Mice received rat IgG Mac48 or 2G8, n = 9-10/group for survival study (each 30 mg/kg 2x/week).
(C) HzTransib STC structure is shown as for RAG in (B). Three white arrows indicate the positively charged surface provided by HzTransib for target DNA binding.
b) MiR-29a and Dnmt3a expression in the cortex treated with scrambled or miR-29a mimic (N=3 mice). Data were normalized to the untreated cortex of the same animal. Mir-29a: scr vs mim29a, t-test, p=0.005; Dnmt3a scr vs mim29a t-test, p<0.0001.
E. Endogenous interaction of PCM1 and AURKA. Lysates from synchronous and serum-starved HEK293T were immunoprecipitated with AURKA antibody and rabbit IgG control. The initial sample and immunoprecipitated proteins were run on a gel and immunoblotted with antibodies against PCM1 and AURKA.
WOX5 transcript levels in Col and hag1-6 hypocotyl (D) and cotyledon (E) explants at indicated days on CIM.
E. Quantification of the level of 5'-Gly-CCC in shSCR, sh-1, sh-2, sh-1+hTrmt13, and sh-1+E463A assayed by RT-qPCR. Data information: Statistical analysis was performed using t-tests, and error bars represent mean ± SD for three independent experiments.