Journal: PLoS Pathogens

Article Title: Memory like NK cells display stem cell like properties after Zika virus infection

doi: 10.1371/journal.ppat.1009132

Figure Lengend Snippet: ( A ) Hallmark pathway gene sets analysis in FACS purified CD27 + memory like and non-memory CD27 - NK cells a month post ZIKV infection. RNA-seq data are from 3 biological replicates for each group. ( B ) ATAC-seq tracks for selected loci of Wnt/β-catenin pathway genes in CD27 + memory like (green) and non-memory CD27 - NK cells (blue). ( C-D ) GSEA enrichment plots ( C ) and heat maps ( D ) for Wnt/β-catenin pathway ( C left ) and canonical Wnt targets ( C right ) among CD27 + memory like and non-memory CD27 - NK gene sets. (E - G ) Immunofluorescence images of FACS purified CD27 + memory like and non-memory CD27 - NK cells, isolated a month post ZIKV infection, and stained for TCF-1 (yellow) and β-catenin (red) show co-localization of both molecules in CD27 + cells. Scale bar corresponds to 10 μm. Top-CD27 + NK cells, Bottom-CD27 - NK cells. Data are representative of 2 independent experiments. ( G ) Relative fluorescent intensity of TCF-1 in CD27 + memory like and non-memory CD27 - NK. Data are representative of 2 independent experiments (n = 4 per experiment). ( H ) Transcription factor motif enrichment analysis of ATAC-seq from CD27 + memory like NK cells. ( I ) % of target sequences with TCF-1 motifs in genomic regions of CD27 + memory like and non-memory CD27 - NK cells. Chromatin opening by ATAC-seq ( J ) and gene expression by RNA-seq ( K ) of selected TCF-1 target genes in CD27 + memory like NK cells. Fold change values for peaks are plotted in ( J ). Mean ± s.d. two-sided Student’s t-test, *** P ≤ 0.001.

Article Snippet: This was followed by antibody staining step and cells were incubated with TCF-1-PE (4:100) (S33-966, BD Biosciences, #564217) and β-catenin-APC (4:100) (REA480, Miltenyi Biotech, #130124453) antibodies in PBS with 0.5% BSA for 45 min. Then, cells were washed with PBS containing 0.5% BSA, pelleted and subjected to cytospin for 2 minutes and taken on the slides.

Techniques: Purification, Infection, RNA Sequencing, Immunofluorescence, Isolation, Staining, Gene Expression

Journal: MicrobiologyOpen

Article Title: Therapeutic Impact of Caffeic Acid Phenethyl Ester and Acyclovir Combination on Human Gingival Fibroblasts (HGF‐1) Infected With Herpes Simplex Type 1 ICP0

doi: 10.1002/mbo3.70110

Figure Lengend Snippet: Alterations of Catenin‐β, IFN‐β, IFN‐γ, IRF 3, WNT protein levels for different study groups. C: Control, I: ICP0, I‐C: ICP0 and CAPE combination, I‐A: ICP0 and aciyclovir combination, I‐A‐C: ICP0, Acyclovir and CAPE combination.

Article Snippet: IFN‐β (BT LAB, Cat. No: E0154Hu), IFN‐γ (BT LAB, Cat. No: E0105Hu), IRF3 (BT LAB, Cat. No: E0105Hu), β‐catenin (BT LAB, Cat. No: E2396Hu), WNT‐1 (BT LAB, Cat. No: E2355Hu) protein amounts were measured using commercially available ELISA kits.

Techniques: Control

Journal: International Journal of Molecular Sciences

Article Title: Combined Therapy Versus Fortified Anti-VEGF Monotherapy in Type C Polypoidal Choroidal Vasculopathy: Long-Term Outcomes and Exploratory Biomarker Insights †

doi: 10.3390/ijms27031224

Figure Lengend Snippet: Various vascular markers for type C PCV, CSCR, and nvAMD. Before intravitreous injection (IVI), aqueous protein levels of VEGF/PlGF/HIF-1α/β-catenin/Wnt1 were detected using ELISA on patients with AMD, PCV, or CSCR. In ( A ), the PCV ( n = 17) or nvAMD ( n = 41; control) levels of VEGF were median [Q1, Q3]: 106.19 [80.00, 203.81] or 191.91 [116.68, 289.96]. In ( B ), the PCV ( n = 13) or nvAMD ( n = 29) levels of PlGF were median [Q1, Q3]: 1.39 [0.72, 18.45] or 15.48 [11.25, 17.90]. The PCV/CSCR/nvAMD (pre-IVI; n = 9/4/16) levels of β-catenin ( C ) were 983.77 ± 329.68/1224.33 ± 743.69/3622.41 ± 499.70. The PCV/CSCR/nvAMD (pre-IVI; n = 5/4/20) levels of HIF-1α ( D ) were median [Q1, Q3]: 6096.66/8705.06/1091.28 [5173.83/5939.04/803.69, 7811.37/14,239.77/3210.46]. Additionally, the PCV/CSCR (pre-IVI) levels of Wnt1 ( E ) were 1180.66 ± 172.41 ( n = 6)/1387.12 ± 289.54 ( n = 4). Significance was * p < 0.05.

Article Snippet: Protein levels in aqueous humor were quantified using commercial ELISA kits [ , ]: VEGF (BMS227/2, Bender MedSystems, Wien, Austria), PlGF (CBS-E07400r, Cusabio, Houston, TX 77054, USA), HIF-1α (M00013-2, Uscn Life Science, San Jose, CA 95123, USA), β-catenin (DYC1329, R&D Systems, Minneapolis, MN 55413, USA), and Wnt1 (RHF128CK, Antigenix America, Huntington Station, NY 11746, USA) [ ].

Techniques: Injection, Enzyme-linked Immunosorbent Assay, Control

Journal: Biochimica et biophysica acta

Article Title: Oestradiol signalling through the Akt-mTORC1-S6K1.

doi: 10.1016/j.bbamcr.2012.12.019

Figure Lengend Snippet: Fig. 3. The overexpression of β-catenin is not sufficient to favour axonal elongation in the presence of ICI. (A) Morphology of 5 DIV neurons co-nucleofected with GFP and wt-βcat or S33Yβcat plasmids. Neurons were stained with antibodies against an axonal marker (SMI-31) and identified by GFP fluorescence. Scale bar: 50 μm. (B) In parallel experiments, neu- rons were transfected with GFP plus either pcDNA3.1 plasmid or β-catenin plasmids. These transfected neurons were cultured in the absence or presence of ICI. After 5 days, neu- rons were fixed and the axonal length (SMI-31 positive extensions) was determined in those GFP-expressing neurons. The graph represents the mean±s.e.m. axonal length in 3 independent experiments. Note that the expression of wt β-catenin showed longer axons, however the differences with control situation (pcDNA3.1 transfected neurons) was not statistically significant. Whereas ICI generated shorter axon, statistically significant (***pb0.001), the expression of wt-βcat did not recover the blocking effect of ICI. (C) Plasmid expression was corroborated by Western-blot, and the expression and activity of S33Y β-catenin in neurons, were inferred by the increase in total Axin2, a direct target on β-catenin (right panel). Total levels of β-catenin were also tested in N2a neuroblastoma (left panel), Akt, GSK3 and actin were used as loading controls.

Article Snippet: Mammalian expression vectors for the expression of RhebQ64L [17], S6K1 wt (Sigma), β-catenin S33Y and wt β-catenin (provided by B. Vogelstein), S6K1-HA wt, S6K1ΔCtE389 (Addgene) [18] pEGFP-N1 and pcDNA3.1 (Invitrogen)were introduced into the cells by electroporation (Nucleofector, Lonza) or using lipofectAMINE 2000 (Invitrogen) in the case of N2a neuroblastoma cells.

Techniques: Over Expression, Staining, Marker, Transfection, Plasmid Preparation, Cell Culture, Expressing, Control, Generated, Blocking Assay, Western Blot, Activity Assay

Journal: Nature neuroscience

Article Title: Social Deficits in Shank3 -deficient Mouse Models of Autism Are Rescued by histone deacetylase (HDAC) Inhibition

doi: 10.1038/s41593-018-0110-8

Figure Lengend Snippet: ( a ) Quantitative real-time RT-PCR data on the mRNA level of class I HDAC family members (HDAC1, 2, 3, 8) in PFC from WT and Shank3 +/ΔC mice. t 16 =3.75, ** P =0.0017 ( HDAC2 ), n=9 each group, two-tailed t -test. ( b ) Immunoblots and quantification analysis of the protein level of HDAC1 and HDAC2 in the nuclear fraction of PFC neurons from WT vs. Shank3 +/ΔC mice. t 16 =3.00, ** P =0.0085 (HDAC2), n=9 each group, two-tailed t -test. ( c ) qPCR and Western blot data showing HDAC2 mRNA and protein levels in PFC from WT and Shank3 e4-9 mice. t 14 =3.24, ** P =0.006 (mRNA), n=8 each group; t 16 =3.79, ** P =0.0016 (protein), n=9 each group, two-tailed t -test. ( d ) qPCR and Western blot data showing HDAC2 mRNA and protein levels in PFC infected with one of the two different HDAC2 shRNA lentiviruses or a scrambled shRNA lentivirus. shRNA-1: t 10 =7.28, *** P <0.0001 ( HDAC2 mRNA), n=6 each group; t 10 =10.84, *** P <0.0001 (HDAC2 protein), n=6 each group; shRNA-2: t 14 =11.33, *** P <0.0001 ( HDAC2 mRNA), n=8 each group; t 10 =12.47, *** P <0.0001 (HDAC2 protein), n=6 each group, two-tailed t -test. ( e, f ) Plots showing the time spent investigating either the social (Soc) or nonsocial (NS) stimulus (e) and the social preference index (f) during 3-chamber sociability testing of WT or Shank3 +/ΔC mice with PFC injection of one of the two different HDAC2 shRNA lentiviruses or a scrambled shRNA lentivirus (n=8-10 each group). In (e), F 5,92 =5.1, P =0.0004; In (f), F 2,46 =26.2, P <0.0001; +++ P <0.001 (Soc vs. NS), ** P <0.01, *** P <0.001, two-way ANOVA. ( g ) Representative heat maps of the 3-chamber sociability tests of WT or Shank3 +/ΔC mice injected with different viruses. All animals used are males (5-8 weeks old). Data are presented as median with interquartile range (a,b,c,d,e) or mean ± SEM (f). Each set of the experiments was replicated for at least 3 times. See for blot source data.

Article Snippet: The shRNA lentivirus targeting mouse β-catenin gene (GCCTTCAGATCTTAGCTTA, CAGCTGGAATTCTCTCTAA, CTGCAGAACTCCAGAAAGA, GTCGAGGAGTAACAATACA) was obtained from Santa Cruz Biotech (sc-29210-V).

Techniques: Quantitative RT-PCR, Two Tailed Test, Western Blot, Infection, shRNA, Injection

Journal: Nature neuroscience

Article Title: Social Deficits in Shank3 -deficient Mouse Models of Autism Are Rescued by histone deacetylase (HDAC) Inhibition

doi: 10.1038/s41593-018-0110-8

Figure Lengend Snippet: ( a ) Co-immunoprecipitation data from cortical lysates of WT mice showing the specific binding of β-catenin to Shank3. ( b ) Immunoblots and quantification analysis of the level of β-catenin in synaptic membrane, cytosol or nuclear fractions of cortical slices from WT and Shank3 +/ΔC (Het) mice. t 10 =3.35, ** P =0.0074 (synapse), t 10 =2.78, * P =0.0194 (cytosol), t 10 =4.01, ** P=0.0025 (nucleus), n=6 each group, two-tailed t -test. ( c ) Quantification analysis of synaptic and nuclear β-catenin levels in cortical slices from WT and Shank3 e4-9 mice. t 10 =4.33, ** P =0.0015 (synapse), t 10 =3.82, ** P =0.0034 (nucleus), n=6 each group, two-tailed t -test. ( d ) PCR images showing the ChIP (β-catenin-occupied DNA), input (total DNA) and no-template control (NTC) signals with 3 primers (P0, P1, P2) designed against different regions of the HDAC2 gene, including the promoter region containing (P0) or lacking (P1) the TCF/LEF binding motif (labeled with vertical lines) and a down-stream intron (P2). TSS, transcriptional start site. GAPDH was used as a control. ( e ) ChIP assay data showing the binding of β-catenin at HDAC2 promoter region (containing TCF/LEF binding motif) in PFC lysates from WT and Shank3 +/ΔC mice. t 12 =2.6, * P =0.02, n=7 each group, two-tailed t -test. ( f ) Quantitative real-time RT-PCR data on the mRNA level of other β-catenin target genes ( Vegf , Jun , Ccnd1 , and Neurod1 ) in PFC from WT and Shank3 +/ΔC mice (n=8 each group). ( g ) Images showing the β-catenin (GFP-tagged) adenovirus-infected medial PFC region (top) and PFC neurons (bottom). ( h ) qPCR data on the mRNA level of HDAC2 and other β-catenin target genes in PFC of WT mice with the overexpression of GFP-tagged β-catenin (n=10) or GFP control (n=8). t 16 =13.44, *** P <0.0001 ( HDAC2 ), two-tailed t -test. ( i-k ) Representative heat maps (i), plots of social interaction time (j) and social preference (k) in 3-chamber sociability tests of WT mice with the overexpression of β-catenin (n=12) or GFP control (n=10) in PFC. j: F 1,40 =20.5, P <0.0001; +++ P <0.001 (Soc vs. NS), ** P <0.01 (GFP vs. β-catenin), two-way ANOVA. k: t 20 =6.4, *** P <0.0001, two-tailed t -test. ( l, m ) qPCR and Western blot data showing the mRNA and protein level of β-catenin (l) and HDAC2 (m) in Shank3 +/ΔC mice with the stereotaxic injection of β-catenin shRNA or a scrambled shRNA lentivirus into the PFC. In (I), t 10 =6.47, *** P <0.0001 ( β-catenin mRNA); t 10 =4.88, *** P=0.0006 (β-catenin protein). In (m), t 10 =6.20, *** P =0.0001 ( HDAC2 mRNA); t 10 =5.05, *** P =0.0005 (HDAC2 protein), n=6 each group, two-tailed t -test. ( n-p ) Representative heat maps (n), plots of social interaction time (o) and social preference (p) in 3-chamber sociability tests of Shank3 +/ΔC mice injected with β-catenin shRNA (n=11) or a scrambled shRNA (n=11) lentivirus into the PFC. o: F 1,40 =15.0, P =0.0004; +++ P <0.001 (Soc vs. NS), *** P <0.001 (β-catenin shRNA vs. scrambled shRNA), two-way ANOVA. p: t 20 =4.36, *** P =0.0003, two-tailed t -test. All animals used are males (5-8 weeks old). Data are presented as median with interquartile range (b,c,e,f,h,j,l,m,o) or mean ± SEM (k,p). Each set of the experiments was replicated for at least 3 times. See for blot source data.

Article Snippet: The shRNA lentivirus targeting mouse β-catenin gene (GCCTTCAGATCTTAGCTTA, CAGCTGGAATTCTCTCTAA, CTGCAGAACTCCAGAAAGA, GTCGAGGAGTAACAATACA) was obtained from Santa Cruz Biotech (sc-29210-V).

Techniques: Immunoprecipitation, Binding Assay, Western Blot, Membrane, Two Tailed Test, Control, Labeling, Quantitative RT-PCR, Infection, Over Expression, Injection, shRNA

Journal: Nature neuroscience

Article Title: Social Deficits in Shank3 -deficient Mouse Models of Autism Are Rescued by histone deacetylase (HDAC) Inhibition

doi: 10.1038/s41593-018-0110-8

Figure Lengend Snippet: ( a ) Quantitative real-time RT-PCR data on the mRNA level of NMDAR and AMPAR subunits and Shank3 in PFC slices from saline-injected WT (n=8), saline-injected Shank3 +/ΔC (n=8), romidepsin (RMD, 0.25 mg/kg, 3×)-treated Shank3 +/ΔC (n=10) and RMD-treated WT (n=6) mice. F 1,28(treatment) =5.96, P =0.021 ( Grin2a ); F 1,28(treatment) =0.52, P =0.48 ( Shank3 ); * P <0.05; ns, not significant, two-way ANOVA. ( b, c ) Quantification analysis and representative immunoblots of the protein level of NMDAR and AMPAR subunits and Shank3 in PFC slices from WT or Shank3 +/ΔC mice injected with saline or romidepsin. F 1,20(treatment) =5.58, P =0.030 (Grin2a); F 1,20(treatment) =0.62, P =0.44 (Shank3); * P <0.05, two-way ANOVA, n=6 each group. ( d ) ChIP assay data showing the acetylated histone H3 level at Grin2a and Grin2b promoter regions in PFC lysates from saline-injected WT (n=6), saline-injected Shank3 +/ΔC (n=6), RMD-treated Shank3 +/ΔC (n=6) and RMD-treated WT (n=4) mice. F 1,18(treatment) =5.88, P =0.026 ( Grin2a ); ** P <0.01, two-way ANOVA. ( e, f ) Input-output curves of NMDAR-EPSC (e) and AMPAR-EPSC (f) in PFC pyramidal neurons from WT vs Shank3 +/ΔC mice treated with romidepsin or saline (n=16 cells/4 mice each group). Recordings were performed at 4-5 days post-injection. In (e), * P <0.05, ** P <0.01, *** P <0.001 (Shank3 +/ΔC +RMD vs. Shank3 +/ΔC +saline), two-way rmANOVA. Inset: representative NMDAR-EPSC and AMPAR-EPSC traces. ( g ) Box plots showing the NMDAR-EPSC to AMPAR-EPSC ratio in PFC pyramidal neurons from WT vs Shank3 +/ΔC mice treated with romidepsin or saline. Inset: representative EPSC traces. F 1,36 =4.8, P =0.036; * P <0.05, two-way ANOVA, n=10 cells/3 mice each group. ( h ) Input-output curves of NMDAR-EPSC in Shank3 +/ΔC mice treated with fluoxetine (5 mg/kg, i.p., 14×). Inset: representative NMDAR-EPSC traces. * P <0.05, ** P <0.01, *** P <0.001 (Shank3 +/ΔC +fluoxetine vs. WT+saline), two-way rmANOVA, n=12 cells/3 mice each group. ( i ) Input-output curves of NMDAR-EPSC in PFC pyramidal neurons of WT or Shank3 +/ΔC mice with the PFC injection of a HDAC2 shRNA or a scrambled control shRNA lentivirus. ** P <0.01, *** P <0.001 (Shank3 +/ΔC +HDAC2 shRNA vs. Shank3 +/ΔC +scrambled shRNA), two-way rmANOVA, n=12 cells/3 mice each group. All animals used are males (5-6 weeks old). Data are presented as median with interquartile range (a,b,c,g) or mean ± SEM (e,f,h,i). Each set of the experiments was replicated for at least 3 times. See for blot source data.

Article Snippet: The shRNA lentivirus targeting mouse β-catenin gene (GCCTTCAGATCTTAGCTTA, CAGCTGGAATTCTCTCTAA, CTGCAGAACTCCAGAAAGA, GTCGAGGAGTAACAATACA) was obtained from Santa Cruz Biotech (sc-29210-V).

Techniques: Quantitative RT-PCR, Saline, Injection, Western Blot, shRNA, Control

Journal: medRxiv

Article Title: Biallelic germline variants in the hematologic malignancy predisposition gene DDX41 cause retinal dystrophy through dysregulation of retinal homeostasis

doi: 10.64898/2026.01.28.26344834

Figure Lengend Snippet: Immunolabeling of DDX41 and Müller glia markers in the retina of wild-type and Ddx41 I396T/I396T mice. (a, b) Western blot analysis and quantification of DDX41 expression in retinal protein extracts from wildtype (WT) and Ddx41 I396T/I396T mice (n = 4 per genotype) at 1 and 9 months of age. (a) Representative Western blot; β-catenin was used as a loading control, and molecular weight markers are indicated on the right. (b) Quantification of DDX41 levels normalized to β-catenin, showing reduced expression in Ddx41 I396T/I396T mice compared with WT at both time points. Data represent mean ± SEM, **, p = 0.0042, ***, p = 0.0002 (two-way ANOVA with Tukey post hoc test). (c-f) Immunolabeling and quantitative analysis of DDX41 and Müller glia organization in retinas from 8-month-old WT and Ddx41 I396T/I396T mice. (c-e) Immunofluorescence staining showing (c) DDX41 (orange), (d) glutamine synthetase (GS; cytoplasmic Müller glia marker), and (e) SOX9 (nuclear Müller glia-specific transcription factor). Scale bars, 50 µm. (f) Quantification of Müller glia nuclear spatial dispersion within the inner nuclear layer (INL) based on SOX9 staining between WT and Ddx41 I396T/I396T . The ratio between the convex hull area encompassing SOX9-positive nuclei and the total INL area was calculated using QuPath (version 0.5.1) . This dimensionless index reflects glial spatial organization, with higher values indicating broader nuclear dispersion. Bars represent mean ± SEM (n = 3 per genotype). *, p = 0.0307 (unpaired two-tailed t-tests). (g) GFAP immunostaining of retinal sections from 12-month-old WT and Ddx41 I396T/I396T mice, indicating gliosis. Scale bar, 50 μm.

Article Snippet: Western blotting was performed as described above, except that DDX41 abundance across samples was normalized to β-catenin, using a polyclonal goat anti β-catenin primary antibody (1:500; AF1329, R&D Systems) and an HRP conjugated donkey anti goat IgG secondary antibody (1:10,000; Invitrogen).

Techniques: Immunolabeling, Western Blot, Expressing, Control, Molecular Weight, Immunofluorescence, Staining, Marker, Dispersion, Two Tailed Test, Immunostaining

Journal: International Journal of Clinical and Experimental Pathology

Article Title: Correlation of Wnt antagonist sFPR1, Slug and β-catenin with prognosis and metastasis in colorectal carcinoma

doi:

Figure Lengend Snippet: Expression of the proteins in colorectal carcinoma (×400 magnification). A. Positive sFPR1 expression in the cytoplasm of “normal” mucosa cells. B. Positive sFPR1 expression in the cytoplasm of cancer cells. C. Positive Slug expression in the cytoplasm of “normal” mucosa cells. D. Positive Slug expression in the cytoplasm of cancer cells. E. Positive β-catenin expression in the membrane of “normal” mucosacells. F. Positive β-catenin expression in the membrane of cancer cells. G. Positive β-catenin expression in the nucleus of cancer cells. H. Positive β-catenin expression in the nucleus and cytoplasm of cancer cells.

Article Snippet: The membrane was blocked using 5% skimmed milk for 1 h. Primary antibody sFPR1 (1:1000), Slug (1:1000), and β-catenin (1:1000) were added at 4°C overnight, followed by horseradish peroxidase-labeled rabbit anti-goat secondary antibody (1:10000), and shacked for 2 h. The Bio-Rad imaging system was used for imaging and acquisition.

Techniques: Expressing, Membrane

Journal: International Journal of Clinical and Experimental Pathology

Article Title: Correlation of Wnt antagonist sFPR1, Slug and β-catenin with prognosis and metastasis in colorectal carcinoma

doi:

Figure Lengend Snippet: The relationship between expression of sFPR1, β-catenin, Slug and clinicopathogical characteristics of (CRC)

Article Snippet: The membrane was blocked using 5% skimmed milk for 1 h. Primary antibody sFPR1 (1:1000), Slug (1:1000), and β-catenin (1:1000) were added at 4°C overnight, followed by horseradish peroxidase-labeled rabbit anti-goat secondary antibody (1:10000), and shacked for 2 h. The Bio-Rad imaging system was used for imaging and acquisition.

Techniques: Expressing, Membrane

Journal: International Journal of Clinical and Experimental Pathology

Article Title: Correlation of Wnt antagonist sFPR1, Slug and β-catenin with prognosis and metastasis in colorectal carcinoma

doi:

Figure Lengend Snippet: Correlation between expression of sFPR1, Slug, β-catenin in CRC

Article Snippet: The membrane was blocked using 5% skimmed milk for 1 h. Primary antibody sFPR1 (1:1000), Slug (1:1000), and β-catenin (1:1000) were added at 4°C overnight, followed by horseradish peroxidase-labeled rabbit anti-goat secondary antibody (1:10000), and shacked for 2 h. The Bio-Rad imaging system was used for imaging and acquisition.

Techniques: Expressing

Journal: International Journal of Clinical and Experimental Pathology

Article Title: Correlation of Wnt antagonist sFPR1, Slug and β-catenin with prognosis and metastasis in colorectal carcinoma

doi:

Figure Lengend Snippet: Kaplan-Meier analysis of the survival rate of patients with colorectal carcinoma. (A) Overall survival of all patients in relation to sFPR1 expression (log-rank = 17.415, P < 0.001). (B) Overall survival of all patients in relation to β-catenin expression (log-rank = 21.387, P < 0.001). (C) Overall survival of all patients in relation to Slug expression (log-rank = 10.415, P = 0.001). In (A-C) analyses, the green line represents positive expression of proteins and the blue line represents negative expression of proteins. (D) Overall survival of all patients in relation to the combination of sFPR1, β-catenin and Slug expression (log-rank = 34.157, P < 0.001). The green line represents positive expression of sFRP1 and negative expression of Slug, β-catenin and the blue line represents negative expression of sFRP1 and positive expression of Slug, β-catenin. The red line represents other positive or negative expression of the proteins. In all analyses, †represents censored observation.

Article Snippet: The membrane was blocked using 5% skimmed milk for 1 h. Primary antibody sFPR1 (1:1000), Slug (1:1000), and β-catenin (1:1000) were added at 4°C overnight, followed by horseradish peroxidase-labeled rabbit anti-goat secondary antibody (1:10000), and shacked for 2 h. The Bio-Rad imaging system was used for imaging and acquisition.

Techniques: Expressing

Journal: International Journal of Clinical and Experimental Pathology

Article Title: Correlation of Wnt antagonist sFPR1, Slug and β-catenin with prognosis and metastasis in colorectal carcinoma

doi:

Figure Lengend Snippet: Results of univariate analyses of (OS) time

Article Snippet: The membrane was blocked using 5% skimmed milk for 1 h. Primary antibody sFPR1 (1:1000), Slug (1:1000), and β-catenin (1:1000) were added at 4°C overnight, followed by horseradish peroxidase-labeled rabbit anti-goat secondary antibody (1:10000), and shacked for 2 h. The Bio-Rad imaging system was used for imaging and acquisition.

Techniques: Expressing, Membrane

Journal: International Journal of Clinical and Experimental Pathology

Article Title: Correlation of Wnt antagonist sFPR1, Slug and β-catenin with prognosis and metastasis in colorectal carcinoma

doi:

Figure Lengend Snippet: Results of multivariate analyses of (OS) time

Article Snippet: The membrane was blocked using 5% skimmed milk for 1 h. Primary antibody sFPR1 (1:1000), Slug (1:1000), and β-catenin (1:1000) were added at 4°C overnight, followed by horseradish peroxidase-labeled rabbit anti-goat secondary antibody (1:10000), and shacked for 2 h. The Bio-Rad imaging system was used for imaging and acquisition.

Techniques:

Journal: International Journal of Clinical and Experimental Pathology

Article Title: Correlation of Wnt antagonist sFPR1, Slug and β-catenin with prognosis and metastasis in colorectal carcinoma

doi:

Figure Lengend Snippet: The expression of sFPR1, β-catenin and Slug was determined by Western blotting in the SW480 cell line treated with 5-aza-dc.

Article Snippet: The membrane was blocked using 5% skimmed milk for 1 h. Primary antibody sFPR1 (1:1000), Slug (1:1000), and β-catenin (1:1000) were added at 4°C overnight, followed by horseradish peroxidase-labeled rabbit anti-goat secondary antibody (1:10000), and shacked for 2 h. The Bio-Rad imaging system was used for imaging and acquisition.

Techniques: Expressing, Western Blot