Journal: bioRxiv

Article Title: Spatial mapping of RNA turnover kinetics and regulatory landscapes of mRNA stability in the mammalian brain

doi: 10.64898/2026.01.29.702431

Figure Lengend Snippet: a. Bar graph showing the fraction of uniquely mapped reads from the experiments either using optimized 2 nd SS (scNT-seq2) or the original Klenow-based 2 nd SS reaction (scNT-seq). b. Fitted line plots illustrating library complexity by comparing genes (left) or UMIs/transcripts (right) detected per cell as a function of aligned reads per cell across experiments in (a) . c. Box plot comparing nucleotide substitution rates in 4sU-labeled K562 cells from experiments in (a) . d. UMAP visualization of cortical cells (n=8,931 cells) from four UPRT transgenic mice colored by annotated cell types (left) or experimental conditions (right). DMSO injection (marked as DMSO) serves as the control for the 4tU-labeled mouse, while saline injection (marked as saline) is the control for the 4sU-labeled mouse. e. Dot plot representing RNA expression levels for 20 marker genes across distinct cortical cell types in conditional UPRT transgenic mice ( NEX/Neurod6-Cre; CAG-LoxP-GFP-3xstop-LoxP-UPRT) at postnatal day 12 (P12) versus wild-type mice. Uprt , the transgenic gene coding for uracil phosphoribosyltransferase, which is specifically expressed in Neurod6 -expressing excitatory neurons. Dot size indicates the percentage of cells expressing the gene in that specific cell type, while color intensity reflects mean gene expression level for that specific cell type. CR, Cajal–Retzius cells; Ex-L2/3/4/5/6, layer specific excitatory neurons; CGE, caudal ganglionic eminence (CGE)-derived interneurons; MGE, medial ganglionic eminence (MGE)-derived interneurons; MG, microglia; Astro, astrocytes; RG, radial glial cells; OPC, oligodendrocyte precursor cells; Oligo, oligodendrocytes; Fib, meningeal fibroblast; EC, endothelial cells. f. Scatterplots showing new-to-total RNA ratio (NTR, uncorrected) between in vivo labeled E16.5 cortical tissues (y-axis) and in vitro labeled cultured E16.5 cortical cells (x-axis).

Article Snippet: Human K562 cells (ATCC, CCL-243) were cultured in RPMI media supplemented with 10% fetal bovine serum (FBS, Sigma, F6178).

Techniques: Labeling, Transgenic Assay, Injection, Control, Saline, RNA Expression, Marker, Expressing, Gene Expression, Derivative Assay, In Vivo, In Vitro, Cell Culture

Journal: Frontiers in Immunology

Article Title: SARS-CoV-2 spike antibodies cross-react with dengue virus and enhance infection in vitro and in vivo

doi: 10.3389/fimmu.2025.1724625

Figure Lengend Snippet: Cross-reactivity and ADE of dengue virus infection by the SARS-CoV-2 anti-RBD antibody CR3022. (A) Confocal digital images of DENV-2 (NGC) infected C6/36 cells stained with CR3022 along with the controls, 4G2 and Rabishield ® (taken from Figure 5 to show the comparison) and the Mean Fluorescence Intensity (MFI). (B) Binding kinetics of (i) CR3022 with SARS-CoV-2 spike protein and (ii) DENV-2 protein E. (C) ADE of DENV-2 infection by different concentrations of CR3022 (2 µg and 4 µg) in K562 cells by flow cytometry. Statistical significance was determined using one-way ANOVA followed by Dunnett’s test. Asterisk (*) indicates a statistically significant difference between the control and treatment. P-value = 0.1234 (ns), 0.0332 (*), 0.0021 (**), 0.0002 (***), <0.0001 (****).

Article Snippet: Human myeloid cell lines K562 (ATCC CCL-243) and U937 (ATCC CRL-1593.2) were cultured in Iscove’s Modified Dulbecco’s media (IMDM, HIMEDIA) and Roswell Park Memorial Institute (RPMI, Gibco) 1640, respectively.

Techniques: Virus, Infection, Staining, Comparison, Fluorescence, Binding Assay, Flow Cytometry, Control

Journal: Frontiers in Immunology

Article Title: SARS-CoV-2 spike antibodies cross-react with dengue virus and enhance infection in vitro and in vivo

doi: 10.3389/fimmu.2025.1724625

Figure Lengend Snippet: ADE of dengue virus infection by SARS-CoV-2 positive patients’ sera in K562 cells. ADE due to convalescent plasma samples collected in the (A) first interval (samples collected from May 2020 to Jan 2021), n = 21, (B) second interval (samples collected from May 2021 to June 2021), n = 17, and (C) third interval (samples collected from February 2022 to April 2022), n = 10. (D) IgG purified (10 µg) from the four convalescent samples showing the strongest ADE activity was assessed for its potential to enhance DENV infection using a dengue clinical strain (IND-60). The bar graph represents the average percentage increase in DENV-positive cells with respect to VC for each sample, with standard deviation for duplicates. Statistical significance was determined using one-way ANOVA followed by Dunnett’s test in GraphPad Prism 8.4.2. Asterisk (*) indicates statistically significant difference between the viral control and serum samples. P-value = 0.1234 (ns), 0.0332 (*), 0.0021 (**), 0.0002 (***), <0.0001 (****). (E) Representative dot plots of patient samples from the first interval (#143, #155), second interval (#96), and third interval (#2, #7). Data was analyzed on FlowJo version 10.8.1.

Article Snippet: Human myeloid cell lines K562 (ATCC CCL-243) and U937 (ATCC CRL-1593.2) were cultured in Iscove’s Modified Dulbecco’s media (IMDM, HIMEDIA) and Roswell Park Memorial Institute (RPMI, Gibco) 1640, respectively.

Techniques: Virus, Infection, Clinical Proteomics, Purification, Activity Assay, Standard Deviation, Control

Journal: Science Advances

Article Title: Synergistic intragenic epigenetic deregulation by IDH2 and SRSF2 mutations causes mis-splicing of key transcriptional regulators

doi: 10.1126/sciadv.adu8292

Figure Lengend Snippet: ( A ) Venn diagrams showing the overlap of genes with CEs, CE circles, with the DEGs, DE circles, per genotype as compared to WT samples. ( B ) Venn diagram showing the enrichment of DNA binding protein motifs at the promoters of the DEGs. ( C ) Bubble plot showing the enrichment of DNA binding proteins unique to the double-mutant expression signature and interacting with genes with CEs. The binary matrix on the right side shows which protein (row of the heatmap) physically interacts with which protein coded in a mis-spliced gene (columns of the matrix). ( D ) Bar plot showing the percentage of DNA binding proteins interacting with proteins that contain CEs. ( E ) Bar plot showing the number of chromatin modifiers found with CEs at each genotype. ( F ) Bar plot showing the relative survival of K562 cells carrying IDH2 R140Q and/or SRSF2 P95H mutations in response to treatment with different doses of romidepsin. Asterisks indicate statistical significance [ P adj < 0.05 as per analysis of variance (ANOVA) followed by Tukey’s post hoc; shown are only the significant results with respect to the double mutant; N = 3 replicates]. ( G ) Graphical summary of the results of our whole study. Mutations in both IDH2 and SRSF2 genes cause the abnormal promotion of CCNG-rich exons, which code for proteins physically interacting with TFs or complexes that, in turn, regulate the expression of downstream genes, including signaling genes.

Article Snippet: The K562 human myeloid leukemia cell line was purchased from American Type Culture Collection (ATCC; #CCL-243).

Techniques: Binding Assay, DNA Binding Assay, Mutagenesis, Expressing