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Journal: bioRxiv

Article Title: Menin maintains enhancer-promoter interactions in a leukemia-specific manner

doi: 10.64898/2026.01.16.698179

Figure Lengend Snippet: a , Menin ChIP-seq after 24 h treatment with DMSO or 250 nM Menin inhibitor VTP50469 (MENi) in SEM, RCH-ACV and OCI-AML3 cells. Metaplots show mean reference normalized reads per million (RRPM) centered on transcription start sites (TSS) genome-wide. b , Dose response curves to MENi recorded at 48 h using CellTiterGlo (n = 5 for SEM and RCH-ACV cells, n = 3 for OCI-AML3 cells). c , Colony forming units recorded after culture in Menin inhibitor (n=5). Error bars represent standard error. d , Violin plots depicting the log2 fold changes of differentially expressed genes (FDR < 0.05) after 24 h MENi (250 nM), split by Menin binding at the promoter. e , Upset plot representing the cell lines in which shared Menin-bound genes (centre of Venn diagram in ) are downregulated following MENi (250 nM) for 24 h. f , Intersections of all upregulated genes following 24 h MENi (250 nM) in SEM, OCI-AML3, and RCH-ACV cells. g , Correlation heatmap of genome-wide Menin ChIP-seq signal in cell lines (SEM, RCH-ACV, and OCI-AML3) and Menin ChIPmentation in primary patient samples (NPM1c-AML, iALL28349, iALL863388). h , Heatmaps and metaplots showing the mean Menin signal at promoters in SEM cells (ChIP-seq) and two primary patient samples (ChIPmentation), sorted and k-means clustered by Menin signal in SEM cells. i , Heatmaps and metaplots showing the mean Menin signal at promoters in OCI-AML3 cells (ChIP-seq) and one primary patient sample (ChIPmentation), clustered by Menin signal in OCI-AML3 cells.

Article Snippet: RCH-ACV and OCI-AML3 (DSMZ) cells were grown in RPMI supplemented with 10% FBS and 1X GlutaMax (Gibco).

Techniques: ChIP-sequencing, Genome Wide, Binding Assay

Journal: bioRxiv

Article Title: Menin maintains enhancer-promoter interactions in a leukemia-specific manner

doi: 10.64898/2026.01.16.698179

Figure Lengend Snippet: a , Volcano plots of transient transcriptome RNA-seq after 24 h of treatment with DMSO or 250 nM Menin inhibitor VTP50469. b , Mean Menin binding (RRPM = reference normalised ChIP-seq reads per million) in SEM, RCH-ACV, and OCI-AML3 cells at promoters of differentially expressed genes in control (DMSO) or Menin inhibitor treatment (MENi). c , Proportion of differentially expressed genes (n.s. = not significant) following MENi with Menin binding at the promoter (± 2 kb around the TSS). Reported p -values are from a Pearson chi-square test. d , Intersections of all Menin-bound genes in the cell line panel. e , Intersections of downregulated Menin target genes in the cell line panel. f , Examples of Menin ChIP-seq in cell lines (SEM, RCH-ACV, and OCI-AML3) and ChIPmentation in primary patient samples (NPM1c-AML, iALL28349, and iALL863388) at down-regulated genes after 24 h MENi in the indicated cell lines.

Article Snippet: RCH-ACV and OCI-AML3 (DSMZ) cells were grown in RPMI supplemented with 10% FBS and 1X GlutaMax (Gibco).

Techniques: RNA Sequencing, Binding Assay, ChIP-sequencing, Control

Journal: bioRxiv

Article Title: Menin maintains enhancer-promoter interactions in a leukemia-specific manner

doi: 10.64898/2026.01.16.698179

Figure Lengend Snippet: a , UpSet plot representing significantly enriched proteins (FDR < 0.01 compared to IgG controls) co-immunoprecipitated with Menin in SEM, OCI-AML3, and RCH-ACV cells. b , Heatmap of statistically enriched Menin interactors in SEM, RCH-ACV and OCI-AML3 cells. c , Global enrichment of select complexes involved in transcription in Menin co-immunoprecipitations. d , Correlation between the gene effect scores reported in DepMap for SEM and OCI-AML3 CRISPR screens. Proteins within complexes specifically enriched in SEM cells are colored. Genes with an effect score of < -1 in both cell lines are labelled.

Article Snippet: RCH-ACV and OCI-AML3 (DSMZ) cells were grown in RPMI supplemented with 10% FBS and 1X GlutaMax (Gibco).

Techniques: Immunoprecipitation, CRISPR

Journal: bioRxiv

Article Title: Menin maintains enhancer-promoter interactions in a leukemia-specific manner

doi: 10.64898/2026.01.16.698179

Figure Lengend Snippet: a , Pearson correlations between nuclear proteome samples (left) and Menin immunoprecipitation (IP) samples (right), computed on log2-transofrmed and imputed data. b , Correlation in the abundance of differentially enriched complex components in the nuclear proteomes of SEM and OCI-AML3 cells. The grey dashed line represents a slope of 1. Pearson R values are shown for each complex. c , Comparison of proteins enriched in Menin IPs in SEM versus RCH-ACV cells (left) and SEM versus OCI-AML3 cells (right). Only proteins that were statistically enriched over IgG controls in at least one cell line (FDR < 0.01) were included.

Article Snippet: RCH-ACV and OCI-AML3 (DSMZ) cells were grown in RPMI supplemented with 10% FBS and 1X GlutaMax (Gibco).

Techniques: Immunoprecipitation, Comparison

Journal: bioRxiv

Article Title: Menin maintains enhancer-promoter interactions in a leukemia-specific manner

doi: 10.64898/2026.01.16.698179

Figure Lengend Snippet: a , Heatmaps of Menin ChIP-seq at promoters and enhancers in SEM, RCH-ACV, and OCI-AML3 cells. Regions are sorted by H3K27ac signal and centered on ATAC peaks. b , Heatmaps of Menin ChIPmentation at promoters and enhancers, centred on H3K27ac peaks, in primary samples from two infant MLL-AF4 ALL patients (iALL28349, iALL863388) and one adult NPM1-mutated AML patient. c , Association between Menin binding at intragenic enhancers and differential gene expression from the nearest TSS following 24 h of MENi. p -values are reported from a Pearson chi-square test. d , Mean Menin, MLL/MLL-AF4, and H3K27ac at intragenic enhancers annotated to differentially expressed genes by nearest TSS after 24 h of MENi in SEM and OCI-AML3 cells.

Article Snippet: RCH-ACV and OCI-AML3 (DSMZ) cells were grown in RPMI supplemented with 10% FBS and 1X GlutaMax (Gibco).

Techniques: ChIP-sequencing, Binding Assay, Gene Expression

Journal: Turkish Journal of Medical Sciences

Article Title: Neuroendocrine effects of exogenous adropin administration on the hypothalamic pituitary testicular axis in male rats

doi: 10.55730/1300-0144.6164

Figure Lengend Snippet: Dose-dependent effects of ADR administration on circulating reproductive hormones: A) high-dose ADR significantly decreased LH versus control/sham, B) FSH levels remained unchanged across all groups, C) testosterone concentrations were significantly elevated following high-dose ADR treatment, D) activin A levels demonstrated a significant reduction in the high-dose ADR group, E) inhibin B levels significantly increased in the high-dose ADR group. Data are presented as mean ± SD with individual data points (n = 8 per group). One-way ANOVA with Bonferroni-adjusted omnibus α = 0.006 (0.05/8); Tukey’s HSD pairwise comparisons are reported only when the corresponding omnibus test met this adjusted threshold. *p < 0.001 vs. control; #p < 0.001 vs. sham. “ns” over a bracket denotes a nonsignificant Tukey comparison (p ≥ 0.05). Horizontal lines above bars indicate significant pairwise comparisons.

Article Snippet: The measurements were carried out using LH (catalog no. E-EL-R0026), FSH (catalog no. E-EL-R0391), testosterone (catalog no. E-EL-R0389), inhibin B (catalog no. E-EL-R0521), and activin A (catalog no. E-EL-R0001), Elabscience, Beijing, China, commercial ELISA kits in accordance with the manufacturer’s instructions.

Techniques: Control, Comparison

Journal: Science Advances

Article Title: Transition of pseudorabies virus from latency to reactivation state selectively triggered by pathogenic bacteria

doi: 10.1126/sciadv.adw4206

Figure Lengend Snippet: ( A ) Succinct overview of PRV quiescent infection in N2a cells. ( B ) Fluorescence microscopy images depicting N2a cells infected with different doses of HuBXY/2018-mCherry with or without ACV and IFN-α treatments. The images were acquired on 8 dpi. ( C ) Fluorescence intensity of N2a cells infected with different doses of HuBXY/2018-mCherry with or without ACV and IFN-α treatments. ( D ) LAT transcript levels in N2a cells after establishing quiescent infection with HuBXY/2018-mCherry at 0.01 and 0.005 MOI. ( E ) Relative mRNA transcription levels of the early genes IE180 and the LAT in N2a cells after establishing quiescent infection with HuBXY/2018-mCherry at 0.01 MOI (694× indicates that LAT transcription levels are approximately 694-fold higher than those of IE180 transcription). These levels were normalized to the internal reference gene 28 S RNA and calculated using the 2 -ΔΔCt method (Livak method). ( F to I ) Fluorescence microscopy images obtained from HuBXY/2018-mCherry quiescent cells infected with G. parasuis –CF7066, G. parasuis –Nagasaki, and G. parasuis –SH0165 (F); S. suis –SC19, S. suis –P1/7, and S. suis –43 (G); ETEC- C83549 , ETEC-E66, and ETEC-10667 (H); and ExPEC-RS218, ExPEC-PCN033, and medium control (I). Scale bars, 100 μm. All data were analyzed using t test; *** P < 0.001 indicates significant differences.

Article Snippet: Subsequently, the infective medium was removed, and the infected cells were cultured in a medium containing ACV (MedChemExpress, NJ, USA) and IFN-α2a human recombinant (IFN-α, PROSPEC, Rehovot, Israel) for 8 days.

Techniques: Infection, Fluorescence, Microscopy, Control

Journal: Science Advances

Article Title: Transition of pseudorabies virus from latency to reactivation state selectively triggered by pathogenic bacteria

doi: 10.1126/sciadv.adw4206

Figure Lengend Snippet: ( A ) Differentially expressed genes in N2a cells upon ExPEC-induced reactivation of quiescent HuBXY/2018-mCherry. ( B ) Read counts and qPCR validation of CXCL1 transcriptional alteration. ( C ) mRNA transcriptional changes of CXCL1 in N2a cells during ExPEC-induced HuBXY/2018-mCherry reactivation. Data were analyzed using the 2 −ΔΔ C t method. ( D ) CXCL1 transcript levels in each group at 6 and 96 hpi. Data were analyzed using the 2 −ΔΔ C t method. ( E ) Differential transcription of IE180 and LAT in N2a-WT and CXCL1 -KO cells during establishment of HuBXY/2018-mCherry quiescence. ( F ) Fluorescence microscopy and bright-field imaging confirmed ExPEC-induced reactivation of quiescent HuBXY/2018-mCherry in N2a-WT cells, but no reactivation was observed in CXCL1 -KO cells. mCherry fluorescence indicates reactivated HuBXY/2018-mCherry within cells. Scale bar, 100 μm. ( G ) Quantification of HuBXY/2018-mCherry reactivation in N2a-WT and CXCL1 -KO cells by gE copy number ( n = 6). ( H ) Proliferation of HuBXY/2018-mCherry during quiescent infection (ACV + IFN-α) in N2a-WT and CXCL1 -KO cells, assessed by qPCR of gE genome copies. Infected cells were sampled from 0 to 11 dpi. Analyses were performed using t-test (** P < 0.01; *** P < 0.001; ns, P > 0.05). ( I ) Proliferation of HuBXY/2018-mCherry during natural infection in N2a-WT and CXCL1 -KO cells. Samples were collected from 0 to 11 dpi. Analyses were performed using t test (*** P < 0.001; ns, P > 0.05). ( J ) Effect of pEGFP-CXCL1 and pEGFP-vector on HuBXY/2018-mCherry reactivation in CXCL1 -KO cells. Scale bar, 100 μm. ( K ) Quantification of HuBXY/2018-mCherry gE copies in CXCL1 -KO cells transfected with pEGFP-CXCL1 or pEGFP-vector. Analyses were performed using t test (*** P < 0.001; ns, P > 0.05).

Article Snippet: Subsequently, the infective medium was removed, and the infected cells were cultured in a medium containing ACV (MedChemExpress, NJ, USA) and IFN-α2a human recombinant (IFN-α, PROSPEC, Rehovot, Israel) for 8 days.

Techniques: Biomarker Discovery, Fluorescence, Microscopy, Imaging, Infection, Plasmid Preparation, Transfection