EMBO/sd-character-level-ner huggingface dataset:
(d) PTPL1 silencing inhibits the FBXL2-p85β interaction. HeLa cells stably expressing FLAG-tagged FBXL2 were transfected with either an siRNA targeting PTPL1 or a non-silencing siRNA (NS). Forty-eight hours post-transfection, cells were collected and whole-cell lysates (WCL) were immunoprecipitated (IP) and immunoblotted as indicated.
VgrG inhibition of Tle1H. Specific phospholipase A1 (PLA1) activity measurements of purified Tle1H in the presence of 1:10 molar ratio of lysozyme from chicken egg white (Lyso) and increasing molar ratio (0, 1, 5, and 10) of SVgrG or SVgrG1-490. Inhibition experiments with SVgrG were repeated three times with independent protein preparations, each measured in triplicate. Inhibition experiments with SVgrG1-490 were repeated twice with two independent protein preparations, each measured in triplicate. Mean values and standard deviation are shown. Statistical analysis relative to the Tle1 activity is indicated. ns, non-significant (P>0.05), *P<0.05, **P<0.01, ***P<0.001, unpaired two-sample Fisher-Pitman permutation test. (P values: Lyso, 0.7006; VgrG 1:1, 0.004946; VgrG 1:5, 1.448e-07; VgrG1:10, 1.448e-07; VgrG1-490 1:1, 0.5627; VgrG1-490 1:5, 0.2977; VgrG1-490 1:10, 0.002631).
A. Correlation of magnitude and direction of change of genes dysregulated (relative to wild type) in timeless vs. ddx11 DT40 cells. rs (Spearman rho) is shown for each correlation.
Parental MDCK cells or those transfected with Prom1 or K138Q mutant were grown for 7 dpc (A-C) or as indicated (D). confocal laser scanning microscopy after DAPI staining Domes of similar size were evaluated (C). Means and standard deviations are displayed. 15 domes per independent experiment were examined (n = 3). Cell density at a given time of culture (7, 10 and 14 days) was determined by counting DAPI-labeled nuclei per 0.1 mm2 (D, n = 4).
F Time course analysis of autoubiquitination reactions with unphosphorylated full‐length humanParkin (hParkin) and Ub (left), a 80% Ub/20% phosphoUb mixture (middle) and 100% phosphoUb (right).
(c) The lipidation reactions are highly dependent on the molar percentage of DOPE in the liposomes. Reactions are as in b, but run on 400 nm liposomes. Liposomes are composed of the indicated amount of DOPE, 10 mol% bl-PI, 0.15 mol% Rh-DOPE and POPC.
N-termini of Tap-1 share more than 30% overall amino acid sequence identity. The identity of the nucleotide and amino acid sequences across the indicated regions among tap-1 of 36 V. cholerae strains (sliding window = 1) is shown. Green bars indicate 100% identity, yellow bars 30-99%, and red bars < 30%. The percent amino acid identity across the indicated region, with the length of amino acids indicated, is shown at the bottom of the figure. The first 14 amino acids of class 1 and 2 Tap-1proteins were excluded from this analysis.
C. McIdas and Foxj1 specific antibodies were used for immunofluorescence on trachea from GemC1WT/WT (upper) or GemC1KO/KO (lower) P0 mice. Arrows show representative positive cells for McIdas (green) and FoxJ1 (red) in the GemC1WT/WT mice. DNA was stained with Draq-5 (blue). Scale bars, 10 µm.
HepG2 cells, HAT1 KO HepG2 cells, and HAT1 KO HepG2 cells reconstituted with either wild type HAT1 or mutant HAT1 (T188A) were subcutaneously injected into athymic nude mice Tumor volumes and average tumor weight were calculated. N = 6 biological replicates. Scale bar = 10 mm. In the boxplots, boxes extend from the 25th to 75th percentiles (inter‐quartile range (IQR)), central band represents the median, whiskers indicate the lowest and highest data within 1.5 × IQR from the lower and upper quartiles, respectively. Student's t-test, ***P < 0.001
+/- inhibitors: anti-MyD88 peptide inhibitor, anti-mouse TLR2 antibody, or lipopolysaccharide (LPS)-RS, an antagonist of TLR4 and anti-mouse IL-6 or JAK1/2 inhibitor (Ruxolitinib)
(E) Plasmablast response of patient TB7 (top) and IgG serum response against MTB cell lysate of patient TB7, TB19 and TB39 (bottom) and one HD at the indicated time points before and after treatment onset.
dHepaRG cells were infected at an MOI of 100 virions/cell and transduced at day 7 p.i. with an adenoviral vector for expression of shRNA targeting ISG20 (AdV-shISG20). After 2 days, cells were treated with 300 U/ml IFNα or 200 U/ml IFNγ. ISG20 expression was analyzed by western blot after 7 days of IFNα or 12 days of IFNγ treatment, respectively.
E The expression of Twi1p in wild‐type, COI12KO, and DCL1KO cells at the indicated time points of conjugation was analyzed by Western blot using an anti‐Twi1p antibody (top panel). The expression of Pdd1p was analyzed using an anti‐Pdd1p antibody as an indicator of the proper progress of conjugation (2nd panel), and the expression of alpha‐tubulin was analyzed by anti‐alpha‐tubulin antibody as a loading control (3rd panel). The expression of TWI1mRNA (4th panel) and RPL21mRNA (bottom panel) was analyzed by Northern blot.
E RT-PCR analysis for DUXAP8 expression in RNA extracted from WT and GS∆44 myocytes and from WT (WT#1), GS∆44 (GS∆44#2, GS∆44#8) and GSM (GSM#1) iPSCs induced to differentiation for 9 days. GAPDH was used as control. Lane (-) indicates the negative control. Representative results are shown (n=3).
(a,b). Representative fluorescent images of HeLa cells co-tansfected with GFP-tagged Beclin 1 wild type, MutM L178A/L192A or MutStab E189L/A217L/E224L/A255L (green) and AsRed-Atg14L (red) (a) or FLAG-UVRAG (red) (b); Co-localization of AsRed-Atg14L with GFP-tagged Beclin 1 wild type or MutM is shown in discrete puncta.
(A) Serum IgG ELISA reactivity with MTB (H37Rv) whole cell lysate, purified cell membrane fraction and secreted culture filtrate proteins (CFP) for TB patients and healthy donors (HD). ELISA graphs (left; TB: black lines; n=25; HD: red dotted lines; n=2) and area under the curve (AUC) values for all tested samples (right; TB: n=25; HD: n=17) are shown. Median is shown.
(D and E) HEK GFP-DFCP1 cells were starved or not starved for 50 min and immunostained for SNX18 and LC3 (D) or WIPI2 (E). Results shown are mean ± SEM (error bars), n = 3 with 30 cells in each experiment. *, P < 0.05.
D. Key residues involved in the formation of the catalytic center from MvcA (core domain: green, insertion domain: yellow, tail domain: blue) and their interactions with UBE2N-Ub (UBE2N, cyan; Ub, magenta). Left panel: the detail view of the interactions. Right panel: the 2Fo-Fc map of the left panel (it was contoured at 1.2 σ). Residues in the catalytic triad (Ala(Cys)83-His244-Q265, yellow), Ser82, Arg140, Gly242, Ser243, and Phe268 of MvcA, Lys92 and Asp93 of UBE2N, as well as Asp39 and Gln40 of Ub are shown in sticks. Hydrogen bonds are shown as dashed lines.
E. Microglial expression of P2RY12 in cortical sections of wt, Grn-/-and Trem2-/- mice. (9 months of age, female) F. Quantification of P2RY12 positive microglia. Data are shown as mean ± SD (n=3 per genotype, female, except one male for Trem2-/-).
Average fractions of disordered residues in the skipped exons in each RBP-depleted RNA-seq dataset. SRSF3-depleted datasets are indicated in red. The q-value between SRSF3-depleted datasets and other datasets was calculated according to the gene set enrichment analysis (GSEA).
(C) Recovery of mitochondrial networks upon Mic60 re-expression. Cells were induced with doxycycline hyclate for 72 h, immunolabeled for TOM20 and visualized by confocal microscopy.
Overexpression of Inh1 represses the proliferation of ρ0 cells. Serial dilutions (tenfold dilution) of the indicated strains were analyzed on SCD or SCD plus 100 μM CuSO4 plates at 30℃ for 2 days.
C Cell lysate from COI12KO cells at 3 hpm was incubated with (+) or without (−) hexokinase followed by radiolabeled double‐stranded 27‐nt RNAs and recombinant wild‐type Coi12p. Loaded RNA was analyzed as in (B). The intensities of the bands relative to the sample without hexokinase are shown.
The profile of EphA2 expression in different cells is indicated. (B) Murine B cells and T cells were purified from spleens using a cell sorter, total RNA was isolated from murine B cells, T cells, BMDCs, BMDMs, AMs and AECs. Shown is mean ± SD. Data represent three independent biological replicates.
(G-J) Anterograde (red) and Retrograde (blue) velocities of ECFP-TrkA (G), TagRFP-Rab3QL (H), TagRFP-synaptotagmin (I), and mitochondria labelled with MitoBright (J). ns, p > 0.05; **, p < 0.01; ****, p < 0.0001. ECFP-TrkA, n = 25­-72; TagRFP-Rab3QL, n = 31-71; TagRFP-synaptotagmin, n = 33-62; Mitochondria, n = 21-49 moving particles were quantified from at least three independent cultures and statistical analysis performed using unpaired t test. Error bars show SEM.
A Neutral red and trypan blue stainings of FI, CI, PI and PI+MVF. CI incubated for 24 h with 0.2% H2O2 served as control. Scale bar: 100 µm.
Reduction in apical Arl13b in the electroporation site (white arrowheads) indicates loss of apical belt integrity and disruption of apico-basal polarity upon Ece2 KD.
Representative images (A and E), histological sections of dorsal back (B and F) and clinical scores (C and G) and quantitative PCR analysis of mRNA levels in dorsal skin (D and H) from wild-type (n=6) and M-Shp2-/- mice or DC-Shp2-/- mice (n=6) treated with IMQ for 4 days. Scale bar: 100 μm. Left: H&E (hematoxylin and eosin) staining data; right: statistical data (mean ± SEM). Results were normalized to Gapdh expression. Data information: Data are represented mean ± SEM. P values were calculated by Tukey multiple comparison test (B, D, F, H) or Bonferroni multiple comparison test (C, G). *P<0.05, **P<0.01, ns, not significant.
E: Immunofluorescence of paxilin (green) and phalloidin (red) in podocytes stimulated with control medium, supernatant (SN) from glomerular endothelial cells from early (p9) or late (p17) passage and treated either with vehicle or Tiplaxtinin, a PAI-1 inhibitor (upper panel). Quantification of focal adhesions (lower panel) was performed by counting the number of paxilin-positive spots in 30 cells from three independent experiments. Original magnification X1000. Scale bar = 20 μm. Data information: Data are means ± SEM. Statistical analysis: ANOVA followed by the Tukey-Kramer test
D) KLF5 signal intensity at genomic regions where ELF3 or FOXA1 signal is reduced in KLF5-KO clones relative to WT clones. Central values represent the median.
Percentages of occurrence of the indicated motifs in the PIF, BES or PIF+BES target loci, as compared with all Arabidopsis genes (genome, in gray)
(A) Table shows the total number of pups, the number or frequency of human HC-, human LC-and human BCR- KI pups after One-step CRISPR/Cas9 microinjection of CLK09 and CLK19.
Western blot analysis of the supernatant (S) and insoluble pellet (P) fractions of ShRNA MICU1 HeLa cell mitochondria transfected with the indicated constructs, following carbonate extraction at pH 10. The established integral membrane protein TIM23 and the soluble protein cytochrome c (Cyt. c) were analyzed as markers. The cells were treated with 5 μM MG132 for 4 h before fractionation
S X-Gal staining on mature artificial muscle (arrowhead) and the underneath host TA (arrow) revealing no tendon development at the extremity of the artificial tissue; implanted LacZ-positive Mabs are present within the host TA. Scale bar: 200 μm.
C. EGF time course analysis of mTOR auto-phosphorylation: TBK1+/+ and TBK1-/- MEFS were serum starved, EGF stimulated for 0-60 min, and analyzed as in A.
(B-D) mRNA expression levels of lineage-specific marker genes upon KD of Yap1 and Taz. Data are represented as mean SD.
(A) Schematic diagram of histone H3 indicating the position of Y41. The pY41-peptide (amino acids 37-46, red) was used for immunizing mice and the subsequent generation of the hybridoma cell line 8B2-C1 The longer phosphorylated (pY41) and non-phosphorylated peptides (amino acids 29-53, black) were used for ELISA and immunoblot analysis.
Quantification of vDNA foci detected by click chemistry at time of reactivation (8dpi) in SCG neurons infected with HSV-1 in the presence or absence of IFNα (600 IU/ml). n=60 genomes from 3 biological replicates. LAT mRNA expression at time of reactivation (8dpi) in neurons infected with HSV-1 in the presence or absence of IFNα (600 IU/ml). n=9 biological replicates.
C. Identify direct targets of Tfcp2l1 by integrating Tfcp2l1 bound genes (ChIP-seq) and dependent genes (RNA-seq). Pathway analysis is done by using Tfcp2l1-activated and -repressed genes.
(A) Side view of NHE9 monomer constituted by 6-TM core transport domain (blue), dimerization domain (orange) and linker helix TM7 (grey) showing the extracellular hydrophobic gate in the inward-conformation between TM12b (yellow spheres) and TM3 (purple spheres and black boxes in alignment). The hydrophobic barrier is made up of highly conserved residues in TM3 of the dimer domain that face towards the transport domain; indicated as purple spheres. The asterisk (*) indicates hydrophobic residues in TM5b of the transport domain that are likely to form an intracellular hydrophobic gate in the outward-facing state as based on outward NapA.
The blood urea nitrogen (BUN) concentrations were higher in Foxd1Cre::Pdgfrb+/J mice compared to wt mice, apart from 25 weeks old group. Bar graphs show means ± SD, 10 weeks n = 7 wt and n = 5 Foxd1Cre::Pdgfrb+/J, 14 weeks n = 3 per group, 25 weeks n = 11 wt and n = 12 Foxd1Cre::Pdgfrb+/J, 35 weeks n = 3 per group
(A) Heat map representation of the TNF-α-up-regulated genes. Genes were classified based on the TNF-α-treated time points, using the algorithm "HOPACH".
SIRT5-deficient or WT H1299 cells (SIRT5 -/- or SIRT5 +/+) were infected with VSV-GFP viruses (MOI = 0.1) for 12 h and viral infectivity western blot analysis (P) Data information: ll data are presented as the mean values based on three independent experiments, and error bars indicate S.E.M. (unpaired two-tailed Student's t test).
(A) Schematic of Casparian strip development (magenta). Casparian strips start to appear as centrally aligned discontinuous dots in the endodermal cell layer, progressing into a network of fused rings functioning as a root apoplastic barrier.
(A) THP-1 cells infected with VN Wt and ΔF2 virus at a MOI 10 for 24 h or treated with 6.7 μM of nigericin (nig) for 45 min were analyzed by immunoblotting. Detection of the full-length gasdermin D. Equal loading was confirmed by beta actin. One representative blot of five independent repeats is shown. (B) Quantification of band intensity for the gasdermin D full-length isoform. The mean ± standard deviation five independent experiments is shown. Statistical analysis was performed by the paired two‑tailed Student's t test., The asterisk (*) marks a significant difference when compared to the mock group ** p < 0.01.
(C) Frequency of live HIV-1-infected cells (NLAD8 WT or ΔVpu strain) 6 days after incubation with the indicated antibodies, and with NHS or HIHS. Each donor of CD4 T cells is represented by a different symbol. n=8 donors of CD4 T cells.
(D) Phase contrast of extracellular parasite cultures. Serial passage of T. gondii in 40-80 μM parabulin induces accumulation of aberrant tachyzoite forms. These arise with MT defects that disconnect coordinated nuclear division and daughter cell budding.
C. A volcano plot showing that 23 proteins are at least two-fold significantly more abundant in the CSF of P15-21 Mpdz-/- mice (red circles, protein names are indicated) whereas only two proteins were more abundant in the CSF of Mpdz+/+ mice (green circles). The CSF composition was analyzed in 3 Mpdz-/- and 3 Mpdz+/+ mice.
B) Quantification of the proportion of connected vs. unconnected pyramidal neurons in slices from wildtype (wt) and Nrg3 mutants. Data are presented as bars and the numbers of connected/tested neuron pairs from 20 wildtype and 30 mutant mice are displayed. Chi-square test was performed to assess statistical significance (****P<0.0001)
A) Representative MEA trace (left) showing the effect of 100 nM AST and increasing concentrations of LUF7346 in the presence of AST on FP contour, measured in LQT1R594Q-CMs. Average data (right) of the effect of AST and LUF7346 in the presence of AST on QT interval duration compared to baseline in CMs derived from all the hiPSC lines used in this study. * = p<0.05 vs respective baseline. ° = p<0.05 vs AST. Colour in the heatmap defines the magnitude of QT prolongation (red) and QT shortening (blue), respectively, after treatment with AST and with increasing concentrations of LUF7346 in the presence of AST. N: 5-10.
e-g, LAMP1-YFP NRK-LC3 cells starved for 2 h and then treated with 100 nM rapamycin for another 4 h (total, 6 h) or 6 h (total, 8 h) analysed by blotting (e) as in b or microscopy (f; scale bar, 5 µm) with quantification (g). Error bars, s.e.m.; n = 3.
C-D) RT-qPCR analysis for cells treated as shown in panel A. (C) RT-PCR for the p21 (top), or PARD6G mRNA (lower). (D) RT-PCR for primer pairs spanning subtelomere18q as indicated below. Lower panel shows the No-RT control for 18qsubtelomere primers. RT-qPCR was quantified as relative to Actin with error bars indicating SD and * indicating p value <.05 using student t-test comparing etoposide (24 hr) relative to untreated for specific primer pairs.
Systemic C. albicans infection. WT and Stim1fl/fl Cd4Cre mice were injected i.v. with 2x105 CFU C.albicans or PBS as control. (J) Frequencies of CD4+ T cells isolated from the spleens of mice at day 6 p.i. producing the indicated cytokines after restimulation with 20 nM PMA and 1 μM ionomycin for 6 hours and analyzed by flow cytometry.
(E) RagA/B KO HEK293A cells were co-transfected with HA-tagged ArfGAP1, HA-tagged ArfGAP2, or HA-tagged RFP1 (control) with Myc-tagged S6K1. Cells were starved of amino acids (-AA) for 2 hours and then 4mM of Gln or Asn were added for 2 hours. mTORC1 was analyzed similar to (B). IP or WCL samples were probed for HA, Myc, and phosphorylated S6K1 at Thr 389. Actin serve as a loading control.
(A) Primary hippocampal neurons (DIV6+4) were transduced with shRNA targeting TDP-43 (shTDP) or control (shCtrl) and surface expression levels of glycoproteins was analyzed by metabolic labeling followed by surface biotinylation and subsequent streptavidin purification. Volcano plot depicts proteins that are significantly (p < 0.01, t-test, Benjamini-Hochberg, FDR: 0.05) decreased or increased on the cell surface in three independent experiments with two technical replicates. For full dataset see Table EV2.
C. Mechanisms of H2O2 degradation by peroxiredoxins. Auranofin inhibits thioredoxin reductase and thus the reductive half reaction in the detoxification of H2O2. Arrows indicate the "flux" of electrons.
(E) Correlation of poison isoform inclusion and GE levels for temperature-dependent poison skipped exon events. Shown are the log2 fold change (FC) in GE versus the ∆PSI of the poison isoform. Decay targets were identified by using data from CHX-treated plants. R² and P(deviation from zero slope) are indicated. N=80
D, Western blot of BT308NS showing phosphorylation of ATM, Chk2, and AKT (pAKT), and accumulation of RAD51 24 h after IR (5 Gy) in the absence (vehicle, veh) or in the presence of MAPK (PD98059, 20 M), AKT (Ly294002, 20 M), MET (JNJ38877605), or ATM (CGK733, 10 M) inhibitors. Total ATM and AKT are also shown. β-actin was used as loading control. Ctrl: non-irradiated cells.
G,H Expression of mRFP via the col-19 promoter in C. elegans hypodermis at (G) L4+24 hours or (H) L4+48 hours. Wild-type animals are shown. Puncta containing mRFP aggregates are indicated by arrows. Scale bar, 100 microns. I,J Similar analysis as in (G,H) for cat-2(e1112) mutants. Scale bar, 100 microns.
G Immunoblotting of protein extracts from SKMEL5 cells cultivated as described above on plastic, Coll-1 or the indicated fibroblast-derived ECMs in the presence or not of BRAFi or BRAFi/MEKi for 96 h, using antibodies against P-ERK1/2, ERK2 or cell cycle markers (P-Rb, Rb, Cyclin D1, p27KIP1, Survivin, p53). HSP60, loading control.
SuperTop reporter assay showing fold change of Relative Luminescence Units (RLU) in Wnt3a conditioned culture media normalized to empty pcDNA3.1+ in the respective control (Ctrl) media after transfection of HEK293T cells with empty vector (violet), GPR56 FL (light turquoise) and GPR56 CTF (turquoise). Shown are means, standard deviation (stdev), and individual values of four technical replicates performed in either complete media or 1:3 diluted Wnt3a conditioned media. Unpaired t-test, **** p<0.0001, *** p<0.0005, ** p<0.005.
(K&L) miR-CTL, miR-195, or miR-195 + pLYS1-MICU1-Flag transfected cells were stained with MitoSOX Red, and mitochondrial ROS levels were determined by flow cytometry. The histogram shows representative staining and bar graph (right) shows results of three independent experiments. Mean ± SEM; . n=3, biological repeats. *P<0.05 when comparing with miR-CTL, # P<0.05 when comparing with miR-195 by Student's t-test.
(F) Separation of Vtn+/ CD45+ HepELs from tumour-bearing FX+/- and FX-/- mouse livers by a cell sorter (Moflo Astrios). Sorted Vtn+CD45+HepELs cells obtained from a littermate (3 animals each) were pooled, and 8 x 103 Vtn+CD45+HepELs cells were i.v. injected into a tumour-bearing mouse. Right graph shows fibrinogen depositions in the lung. Shown are averages (N = 3/ group, 9 fields/ sample) with SEM. 1-way ANOVA
(A) C-09.10 short-term culture cells were infected with retroviruses expressing ZEB1. Western blot analyses of ZEB1 and p75. GAPDH was used as a loading control.
D Representative scanning electron microscopy micrographs showing the basal regions of cochleae from CDDP-treated p53wt and p53-/- mice after 5 days. Scale bar=15µm.
Percentages of axons that initiated regeneration 24 h after laser surgery are shown. The numbers (n) of animals examined are shown. Error bars indicate 95% CI. Data information statistical significance was determined by Fisher's exact test; *P < 0.05; **P < 0.01; ***P < 0.001; NS; not significant.
B. Scatter plot showing the expression of canonical transposable elements from RNA sequencing data obtained from white virgins versus Rpp3018.2 ovaries. Arrows point to P-element (P-ele) and I-element (I-ele). Transposons are indicated as red or black dots (significant or not significant fold change, respectively). Genes are indicated as yellow or grey dots (significant or not significant fold change, respectively).
(F) PGC1α OE did not decrease αSMA protein neither without nor with TGFβ1 in COUP-TFII OE cells by WB (n=3).
(H) Binding-rates of Gal4 are concentration dependent, but are similar for UASwt and UASmut: kon UASwt = 0.011 ± 0.002 s-1 nM-1, kon UASmut = 0.009 ± 0.001 s-1 nM-1. n = 2 for all, except n = 4 for UASwt 10 nM Gal4 and n = 3 for UASwt 20 nM Gal4. Error bars indicate SD.
8-week-old female C57Bl/6 mice were infected intranasally with 150 pfu of influenza A/Scotland/20/74 (H3N2) virus (IAV) and treated or not simultaneously with 4 mg of succinate (Suc; by the intranasal route). Some mice were euthanized at 4 days post-infection and lungs were collected to determine: (h) tissue lesions in lung sections stained with hematoxylin-eosin and further assessed by microscopy. Scale bar: x6/20 µm. All data are represented as the mean or the mean ± SEM and are cumulative of 2 independent experiments with 5 animals each. Data information: Statistical analysis was performed using the Mann-Whitney test , h, , (*P < 0.05).
A) Expression of the 21U sensor in the indicated genetic backgrounds. Gonads are outlined by a dashed line. The mCherry signal is represented in pseudo-colours [LUT fire (ImageJ)] to reflect differences in the intensity of the signal. The panels on the right are DIC images of the respective animals. Scale bar: 25 μm.
H Heat map of top differentially expressed genes in the major immune/stromal cell clusters, identified in (A). BRCA1+/- preneoplastic cells, blue; BRCA1-associated tumor cells, yellow.
Analysis of Mif2 N-terminal and swap mutant using the anchor-away technique as for (B). Phenotypes of the indicated Mif2 constructs were observed in an otherwise wild-type or ctf19∆ background.
qRT-PCR for PHD1 showing silencing efficacy with both siRNAs 1 (*P = 0.0017 toward Scr) and 2 (*P = 0.0023 toward Scr) compared to the scrambled control in HCT116. A two-tailed unpaired t-test was performed with n = 3/group.