Journal: bioRxiv

Article Title: Predictable clonal hierarchies from restricted progenitors provide a framework for cell type-specific therapies in glioblastoma

doi: 10.64898/2026.02.21.707071

Figure Lengend Snippet: Track-informed combination targeting of progenitor populations suppresses GBM growth a) LGALS1 expression across progenitor Tracks (left) and progenitor cell types (right) in the CellTag lineage-tracing dataset. b) FeaturePlot of LGALS1 expression in the GBM meta-atlas of primary tumor cells. c) Primary GBM meta-atlas cells were binned into LGALS1 -High (grey) and LGALS1 -Low (light blue) based on LGALS1 expression (STable6, Methods): cells were split by the median LGALS1 expression (High ≥ median, Low < median). Violin plot shows LGALS1 expression in each bin. Differential expression was then performed Low vs High (so positive avg_log2FC indicates genes enriched in LGALS1 -Low cells). Right, lollipop plot shows the top differentially expressed genes enriched in LGALS1-Low cells, highlighting CDK4 (dot size, −log10 adjusted P value; x-axis, avg_log2FC Low vs High). d) CDK4 expression across progenitor Tracks (left) and progenitor cell types (right) in the CellTag lineage-tracing dataset. e) FeaturePlot of CDK4 expression in the GBM meta-atlas of primary tumor cells. f) The combination of LGALS1 inhibition through OTX008 with CDK4 inhibition through Abemaciclib is predicted to target Track 3 progenitors (MES.Progenitor, NVP) and complementary Track 1-2 progenitors (IPC, Radial Glia). g) LGALS1 and CDK4 expression stratifies progenitor cells into complementary high-expression groups. (Top) Boxplots show LGALS1 and CDK4 expression in the CellTagging dataset comparing Progenitor vs Non-Progenitor cells. P-values are from two-sided Wilcoxon tests. (Bottom) Progenitor cells were additionally binned by global median splits of LGALS1 and CDK4 across all cells to define four mutually exclusive categories (Neither, LGALS1_high, CDK4_high, Both) and an OR category (Either_High = LGALS1_high OR CDK4_high). Lollipop plot reports the percent of progenitor cells in each category. h) Representative clones satisfying LGALS1_high or CDK4_high treatment categories across patients, as defined in panel g. Clone member cells are overlaid on the global UMAP (grey) and indicated by colored shapes, with each shape representing an individual cell within the clone. i) Representative clones multiple patients containing cells classified as Both (LGALS1_high and CDK4_high), as defined in panel g. j) Representative immunoblot of the patient-derived gliomasphere line GS187 treated for 7 days with Vehicle, Abemaciclib (CDK4/6 inhibitor), OTX008 (LGALS1 inhibitor), or the combination. Abemaciclib treatment reduced phosphorylation of RB at S780 (pRb) with corresponding effects on total RB, consistent with on-target CDK4/6 pathway inhibition. CCN2A and CDK4 levels are shown as additional markers in the CDK4/6 axis. OTX008 treatment targets LGALS1 and CYPB serves as a loading control. k) Quantification of immunoblot signals shown in panel 4j from GS187 gliomaspheres. Protein levels for pRB (S780), RB, CCN2A, CDK4, and LGALS1 were normalized to the loading control (CYPB) and expressed as fold change relative to Vehicle (dashed line at 1). l) Patient-derived gliomaspheres expressing a Gaussia luciferase construct are transplanted onto human cortical organoids, where tumor cells engraft and secrete luciferase into the surrounding media. Secreted luciferase activity in conditioned media provides a noninvasive readout of tumor cell burden over time. m) Schematic timeline of the treatment regimen used for growth assays in the HOTT system. Following a 7-day engraftment period, organoids transplanted with patient-derived gliomaspheres were treated with Vehicle, Abemaciclib, OTX008, or the combination of OTX008 and Abemaciclib. Conditioned media was collected every 48 hours for measurement of secreted Gaussia luciferase activity, with luminescence quantified to generate tumor growth curves. n) Patient-derived gliomasphere lines GS005 and GS025 (n = 2 independent lines) expressing Gaussia luciferase were transplanted onto human cortical organoids (n = 3 independent transplants per condition) and treated according to the scheme in . Conditioned media were collected every 48 hours and luciferase activity was normalized to the corresponding day 1 measurement for each transplant. Data are shown as mean ± s.d. across independent transplants. Statistical comparisons were performed between drug-treated and vehicle conditions at each time point.

Article Snippet: Organoids were treated with vehicle control (DMSO), abemaciclib (1 μM, MedChemExpress), OTX008 (2.5 μM, MedChemExpress), or a combination of abemaciclib and OTX008 for 7 days, with compounds refreshed at each media change.

Techniques: Expressing, Quantitative Proteomics, Inhibition, Clone Assay, Western Blot, Derivative Assay, Phospho-proteomics, Control, Luciferase, Construct, Activity Assay

Journal: bioRxiv

Article Title: Predictable clonal hierarchies from restricted progenitors provide a framework for cell type-specific therapies in glioblastoma

doi: 10.64898/2026.02.21.707071

Figure Lengend Snippet: Identification of progenitor-associated drug targets with tumor-selective expression a) Strategy used to identify candidate therapeutic targets from lineage-informed progenitor programs. Progenitor signature genes (n = 1,855) were first defined from the CellTagging dataset based on differential expression between progenitor and non-progenitor malignant cells. These genes were queried against the Drug-Gene Interaction Database (DGIdb) to identify targets with known inhibitor interactions, yielding 326 druggable genes. Druggable candidates were then ranked by tumor selectivity using a composite score that integrates progenitor specificity from the CellTagging genescore together with relative expression in a primary GBM meta-atlas and depletion in a normal adult brain meta-atlas, enabling prioritization of progenitor targets with maximal therapeutic window. b) Scatter plot shows progenitor-associated druggable genes identified by querying the Drug-Gene Interaction Database (DGIdb) for inhibitor-linked interactions among progenitor signature genes. The x-axis shows the CellTagging progenitor genescore, a composite metric reflecting both specificity and enrichment in progenitor cells, calculated as the ratio of the fraction of progenitor cells expressing a gene to the fraction of non-progenitor cells expressing the gene, multiplied by the average log 2 fold change. The y-axis shows a tumor-normal score calculated as the difference between z-scored mean expression in a GBM meta-atlas and z-scored mean expression in a normal adult brain meta-atlas. Each point represents a gene. Genes with positive tumor-normal scores (red) are enriched in tumor relative to normal brain, whereas genes with negative scores (blue) show higher relative expression in normal tissue. c) Kaplan-Meier survival curves for proneural GBM patients in the TCGA dataset stratified by LGALS1 expression using a median cutoff. Patients with LGALS1 High tumors (red; n = 81, events = 77, median survival = 11.1 months) exhibit reduced overall survival compared to the LGALS1 Low group (blue; n = 81, events = 58, median survival = 19.8 months). Significance was assessed by log-rank test (p = 3e−04) and Wilcoxon test (p = 5e−04); hazard ratio (HR) = 0.53 (95% CI, 0.38-0.76). d) Volcano plot summarizing differential expression in the primary GBM meta-atlas comparing LGALS1-Low versus LGALS1-High cells. e) Differential expression in the primary GBM meta-atlas comparing LGALS1-Low vs LGALS1-High cells (Low vs High). Each point is a gene (x-axis, avg_log2FC Low vs High; y-axis, −log10 adjusted P value). Positive fold-change indicates genes enriched in LGALS1-Low cells; CDK4 is highlighted/labeled. Differential expression used a Wilcoxon test with min.pct = 0.5 and logFC threshold = 0.25. f) Representative immunoblots from two additional patient-derived gliomasphere lines (GS025 and GS225) treated for 7 days with Vehicle (DMSO), Abemaciclib (1 µM), OTX008 (2.5 µM), or the combination.

Article Snippet: Organoids were treated with vehicle control (DMSO), abemaciclib (1 μM, MedChemExpress), OTX008 (2.5 μM, MedChemExpress), or a combination of abemaciclib and OTX008 for 7 days, with compounds refreshed at each media change.

Techniques: Expressing, Biomarker Discovery, Quantitative Proteomics, Labeling, Western Blot, Derivative Assay

Journal: bioRxiv

Article Title: Predictable clonal hierarchies from restricted progenitors provide a framework for cell type-specific therapies in glioblastoma

doi: 10.64898/2026.02.21.707071

Figure Lengend Snippet: Track-informed combination treatment predictably remodels clonal interaction architecture a) Schematic of the track-informed CellTag lineage tracing and drug perturbation workflow in HOTT. Primary IDH1 WT GBM cells from (n = 3) patient tumors are dissociated and transduced with a high-complexity CellTag lentiviral barcode library encoding combinatorial DNA barcodes and GFP. Barcoded tumor cells are directly transplanted onto human cortical organoids and allowed to engraft and invade toward the organoid center over a 5-7 day period. Following engraftment, organoids are separated and treated with vehicle (DMSO), abemaciclib (1 µM), OTX008 (2.5 µM), or the combination of abemaciclib and OTX008 for 7 days, with drugs refreshed at each media change. At the experimental endpoint, organoids are dissociated and GFP⁺ CellTagged tumor cells are isolated by fluorescence-activated cell sorting (FACS) for single-cell RNA sequencing (scRNA-seq). Lineage relationships are reconstructed by identifying shared CellTag barcode combinations across cells, enabling analysis of treatment-induced changes in clonal architecture. b) UMAP visualization of scRNA-seq profiles from CellTag-labeled GBM cells following treatment in the HOTT (n = 98,474 cells). Cells are colored by treatment condition. c) Fraction of cells assigned to each transcriptional cell type following reference-based mapping from the full CellTag lineage-tracing dataset. d) Clone-member composition shifts (n = 9,138 clones) by cell type following drug treatment. Dot plot shows the log₂ fold change in clone-member representation for each cell type relative to vehicle, computed from unweighted clone-member proportions. For each treatment, the proportion of clone-member cells assigned to each cell type was calculated and normalized to the corresponding vehicle proportion (log₂FC). Dot size represents the magnitude of the log₂ fold change (|log₂FC|), and color denotes directionality (red, enrichment; blue, depletion), with values capped at the 75th percentile. Statistical significance was assessed at the clone level by comparing the distribution of clone-level cell type proportions between each treatment and Vehicle using two-sided unpaired Wilcoxon rank-sum tests, with p-values corrected across all cell type × treatment comparisons using the Benjamini–Hochberg method (**** FDR < 1×10⁻⁴, *** FDR < 1×10⁻³, ** FDR < 1×10⁻², * FDR < 0.05; ns, not significant). e) Top enriched clonal co-occurrence interactions per treatment. For each treatment condition (vehicle, abemaciclib, OTX008, combination), edges represent cell type pairs that co-occur within inferred clones more frequently than expected by chance (log₂ observed/expected), computed from clone × cell type presence matrices. Interactions were filtered to retain pairs with log₂ enrichment ≥ 0.5 and the top 10 strongest enriched pairs per treatment were plotted. Edge thickness denotes log₂ enrichment, and edges are colored by the Track assignment of the recipient cell type. f) UpSet plot of progenitor-progenitor clonal co-occurrence patterns across treatments. Columns denote the top 20 progenitor-progenitor cell type combinations observed within inferred clones; filled circles indicate presence of each progenitor cell type in the combination. The upper bar plot reports intersection size as the fraction of all clones within each treatment exhibiting the corresponding combination, with bars stacked by treatment (vehicle, abemaciclib, OTX008, combination). Fractions are normalized independently within each treatment using the total number of clones in that treatment as the denominator; therefore, stacked bar heights can exceed 100% because per-treatment fractions are summed across conditions. Left bars indicate progenitor set sizes. g) Delta abundance-normalized log₂ enrichment of progenitor-progenitor (PP), progenitor-mature (PM), and mature-mature (MM) cell-cell pairings for each treatment relative to Vehicle. Enrichment values reflect pooled clone-derived cell-cell interactions normalized to overall progenitor abundance. Significance was assessed at the clone level using two-sided Wilcoxon tests with Benjamini-Hochberg correction (* q < 0.05, ** q < 0.01, *** q < 0.001). h) Weighted clone-member Track composition changes relative to Vehicle. Bars show weighted log₂ fold change in Track representation among clone-member cells for each treatment versus Vehicle, with weights defined as 1 / p(Track | Treatment) and baseline Track frequencies computed from all cells. Significance was assessed using clone-level replication (Wilcoxon signed-rank test against 0) with FDR correction (* FDR < 0.05, ** FDR < 0.01, *** FDR < 0.001). i) Clone-level Track interaction residuals for combination treatment. Bars show deviation of the observed Combo effect from the additive expectation of Abemaciclib and OTX008, defined as log₂FC_Combo − (log₂FC_Abemaciclib + log₂FC_OTX008). Residuals were tested against 0 using clone-level replication (Wilcoxon signed-rank test) with FDR correction (* FDR < 0.05, ** FDR < 0.01, *** FDR < 0.001).

Article Snippet: Organoids were treated with vehicle control (DMSO), abemaciclib (1 μM, MedChemExpress), OTX008 (2.5 μM, MedChemExpress), or a combination of abemaciclib and OTX008 for 7 days, with compounds refreshed at each media change.

Techniques: Transduction, Isolation, Fluorescence, FACS, Single Cell, RNA Sequencing, Labeling, Clone Assay, Derivative Assay

Journal: Cell reports

Article Title: Neuronal hyperactivity becomes mTORC1 independent due to transcriptional changes in tuberous sclerosis complex disease models

doi: 10.1016/j.celrep.2025.116664

Figure Lengend Snippet: (A and B) Plots showing the weighted mean firing rate of hiPSC-derived neurons of the indicated genotypes ( TSC2 +/+ blue; TSC2 +/− purple; TSC2 −/− red) with the designated treatments (DMSO, squares; rapamycin, asterisks) over time. The arrows above the plot represent the start of treatment with either DMSO or rapamycin, which began earlier (A) or later (B) during neuronal development. Points represent mean per condition, and error bars represent SEM. (C and D) Weighted mean firing of the indicated genotypes and treatments at the end of recording with either earlier (C) or later (D) rapamycin treatment. (E and F) Bar plot of burst frequency of the indicated genotypes and treatments at the end of recording with either earlier (E) or later (F) rapamycin treatment. (G) Bar plot of the day when the synchrony index reaches half maximal in the indicated genotypes and treatments with early rapamycin treatment. For all bar plots, each dot represents a separate well of neurons across three separate differentiations. Bar plots show mean ± SEM ( n = 16–20 independent wells per genotype per treatment from three separate differentiations; p < 0.05 ANOVA with post hoc Dunnett’s test).

Article Snippet: DMSO Vehicle control, rapamycin (MedChem Express HY-10219) 0.2nM, 2nM, 20nM were added to the media beginning at either day 10 (Chronic Treatment) or 30 (Acute Treatment).

Techniques: Derivative Assay

Journal: Molecular and cellular biology

Article Title: Loss of function mouse models reveal a novel regulatory function for ULK1 in myeloproliferative neoplasms

doi: 10.1080/10985549.2025.2529837

Figure Lengend Snippet: ( A ) Schematic illustration of the Jak2 V617F knock-in MPN transplant mouse model used, treatment regimen, and analyses performed. ( B ) Hemoglobin (Hb) levels, ( C ) hematocrit (HCT) percentage and ( D ) red blood cell (RBC) counts in peripheral blood of recipient mice are shown for each treatment group four weeks post treatment initiation. ( E ) Percentage of Ter119 med CD71 high proerythroblasts (R1), ( F ) Ter119 high CD71 high basophilic erythroblasts (R2) and ( G ) Ter119 high CD71 med late basophilic and polychromatophilic erythroblasts (R3) and Ter119 high CD71 low orthochromatophilic erythroblasts (R4) in the BM of recipient mice four weeks post treatment initiation. ( H ) Spleen weight and percentage of ( I ) R1, ( J ) R2 and ( K ) R3+R4 cells in the spleen of recipient mice four weeks post treatment initiation. ( B-K ) Box plots show distribution of data from 10 mice per group. Statistical analyses were performed using Mann-Whitney test. Statistically significant p -values are reported. See also supplemental figures 6 and 7 . ( L-M ) Cellular viability of JAK2 V617F -positive ( L ) HEL and ( M ) SET-2 cells treated with either DMSO-vehicle control (Ctrl) or with increasing doses of the ULK1 inhibitor SBP-7455 for five days, as indicated, was measured using WST-1 cell viability reagent. Data are expressed as percent cell viability relative to Ctrl-treated cells and represent means ± SEM of ( L ) four and ( M ) three independent experiments. IC50 values are shown. ( N ) Clonogenic capability of HEL cells treated with either vehicle-control (DMSO) or with increasing doses of the ULK1 inhibitor SBP-7455, as indicated. Data are expressed as percent colony formation relative to DMSO-treated cells (control) and represent means ± SEM of three independent experiments. Statistical analysis was performed using Welch’s ANOVA test that accounts for unequal variances followed by Dunnett’s T3 pairwise multiple comparisons test. Statistically significant p -values are reported. Test for linear trend based on the one-way ANOVA model showed a significant decrease in colony formation with increased dose of ULK1 inhibitor ( p <0.0001). See also supplemental figure 8 .

Article Snippet: To assess the effects of drug-targeted inhibition of ULK1 on cellular viability of JAK2 V617F -positive leukemic cells, SET-2 cells (20,000 cells/well) or HEL cells (1,500 cells/well) were plated in quadruplicate in 96-well plates and treated with vehicle-control (DMSO), ULK101 (TargetMol), SBI-0206965 (Cayman Chemical) or SBP-7455 (TargetMol) at increasing concentrations, for 5 days.

Techniques: Inhibition, Activity Assay, In Vivo, Knock-In, MANN-WHITNEY, Control

Journal: Molecular and cellular biology

Article Title: Loss of function mouse models reveal a novel regulatory function for ULK1 in myeloproliferative neoplasms

doi: 10.1080/10985549.2025.2529837

Figure Lengend Snippet: ( A-B ) Immunoblotting analysis of the indicated proteins in lysates from non-targeting (NT) control, Atg7 KO and Ulk1 KO Jak2 V617F -positive Ba/F3-EpoR + GFP-LC3-RFP-expressing cells. ( C ) Percentage of autophagy measured as percentage of GFP negative cells assessed by flow cytometry analyses of NT control, Atg7 KO and Ulk1 KO Jak2 V617F -positive Ba/F3-EpoR + GFP-LC3-RFP-expressing cells cultured under normal nutrient conditions (RPMI 1640 media supplemented with 10% FBS and 10 ng/mL of IL-3, no starvation) or under starvation conditions (RPMI 1640 media without serum and IL-3) for 48 hours. Scatter dot plot shows means ± SD. Statistical analysis was performed using Welch’s ANOVA test that accounts for unequal variances followed by Dunnett’s T3 pairwise multiple comparisons test. Statistically significant p -values are reported. ( D-F ) Immunoblotting analysis of the indicated proteins in lysates from ( D ) Cas9-control compared to ULK1 KO HEL cells and from ( E ) HEL cells treated with either DMSO-vehicle control (C), 5μM SBP-7455 (S), 100nM bafilomycin A1 (B) or with the combination of SBP-7455 and bafilomycin A1 (S+B) for 4 hours under either nutrient-starvation conditions (HBSS) or normal complete nutrient-conditions (RPMI). Immunoblots shown are representative of three independent experiments. ( F ) SET-2 cells treated with either DMSO-vehicle control (C), 5μM SBP-7455 (S), 100nM bafilomycin A1 (B) or with the combination of SBP-7455 and bafilomycin A1 (S+B) for 4 hours under either nutrient-starvation conditions (HBSS) or normal complete nutrient-conditions (RPMI). Immunoblots shown are representative of three independent experiments.

Article Snippet: To assess the effects of drug-targeted inhibition of ULK1 on cellular viability of JAK2 V617F -positive leukemic cells, SET-2 cells (20,000 cells/well) or HEL cells (1,500 cells/well) were plated in quadruplicate in 96-well plates and treated with vehicle-control (DMSO), ULK101 (TargetMol), SBI-0206965 (Cayman Chemical) or SBP-7455 (TargetMol) at increasing concentrations, for 5 days.

Techniques: Inhibition, Western Blot, Control, Expressing, Flow Cytometry, Cell Culture

Journal: Molecular and cellular biology

Article Title: Loss of function mouse models reveal a novel regulatory function for ULK1 in myeloproliferative neoplasms

doi: 10.1080/10985549.2025.2529837

Figure Lengend Snippet: ( A-B ) HEL cells were treated with either vehicle (DMSO, Ctrl), 5μM SBI-0206965 (SBI) or 5μM ULK101 for 6 hours followed by RNA-seq and analysis of transcript expression. ( A ) Heatmap of differentially expressed genes between treatment groups (adj. p val. < 0.01). ( B ) MA plot of genes significantly changed by drug-targeted inhibition of ULK1 in HEL cells versus control (adj. p val. < 0.01). In purple are represented up-regulated genes and in green are represented down-regulated genes. ( C and D ) Enriched ontology clusters for genes that are ( C ) increased or ( D ) decreased after drug-targeted inhibition of ULK1 in HEL cells. ( A-D ) Data are from 4 biological replicates per condition. See also supplemental figures 9 – 11 .

Article Snippet: To assess the effects of drug-targeted inhibition of ULK1 on cellular viability of JAK2 V617F -positive leukemic cells, SET-2 cells (20,000 cells/well) or HEL cells (1,500 cells/well) were plated in quadruplicate in 96-well plates and treated with vehicle-control (DMSO), ULK101 (TargetMol), SBI-0206965 (Cayman Chemical) or SBP-7455 (TargetMol) at increasing concentrations, for 5 days.

Techniques: Inhibition, Activity Assay, Gene Expression, RNA Sequencing, Expressing, Control

Journal: Molecular and cellular biology

Article Title: Loss of function mouse models reveal a novel regulatory function for ULK1 in myeloproliferative neoplasms

doi: 10.1080/10985549.2025.2529837

Figure Lengend Snippet: ( A-E ) Scatter dot plots of PIM1 , ID2 , HES1 , CTR9 and PDCD2 expression in healthy individuals (normal, n = 11) and patients with ET (n = 47), PV (n = 28) and MF (n = 18). Data extracted from GSE5464672. Shown are means ± SEM of Log2 mRNA expression. Statistical analyses were performed using one-way ANOVA followed by Dunnett’s multiple comparisons adjustment comparing each MPN group vs. Normal group. Statistically significant p -values are reported. ( F-J ) mRNA expression of the indicated genes was assessed by qRT-PCR analysis for HEL cells treated for 6 hours with either vehicle (DMSO, Control) or SBP-7455 (SBP), as indicated. Data are means ± SEM from three independent experiments. Fold changes relative to control (dashed line) were calculated for each experimental replicate (SBP/DSMO), and fold changes were compared to FC=1 using a one-sample t-test, p values are reported. See also supplemental figure 12 .

Article Snippet: To assess the effects of drug-targeted inhibition of ULK1 on cellular viability of JAK2 V617F -positive leukemic cells, SET-2 cells (20,000 cells/well) or HEL cells (1,500 cells/well) were plated in quadruplicate in 96-well plates and treated with vehicle-control (DMSO), ULK101 (TargetMol), SBI-0206965 (Cayman Chemical) or SBP-7455 (TargetMol) at increasing concentrations, for 5 days.

Techniques: Inhibition, Expressing, Quantitative RT-PCR, Control

Journal: Molecular and cellular biology

Article Title: Loss of function mouse models reveal a novel regulatory function for ULK1 in myeloproliferative neoplasms

doi: 10.1080/10985549.2025.2529837

Figure Lengend Snippet: ( A-E ) qRT-PCR analysis of the indicated genes mRNA expression in murine c-kit + bone marrow Jak2 V617F/+ VavCre + cells from 3 mice treated for 6 hours with either vehicle (DMSO, Control) or 5μM SBP-7455 (SBP), as indicated. Data are means ± SD across three different mice. Fold changes were calculated relative to gene expression from one randomly selected vehicle control-treated mouse sample. Statistical analyses were performed using two-tailed unpaired t test with Welch’s correction. Statistically significant p -values are reported. ( F-J ) qRT-PCR analysis of the indicated genes mRNA expression in Cas9-control and ULK1 KO HEL cells, as indicated. Data are means ± SD across three independent experiments. Fold changes were calculated relative to gene expression from one randomly selected Cas9 control sample. Statistical analyses were performed using two-tailed unpaired t test with Welch’s correction. Statistically significant p -values are reported. See also supplemental figures 13 – 15 .

Article Snippet: To assess the effects of drug-targeted inhibition of ULK1 on cellular viability of JAK2 V617F -positive leukemic cells, SET-2 cells (20,000 cells/well) or HEL cells (1,500 cells/well) were plated in quadruplicate in 96-well plates and treated with vehicle-control (DMSO), ULK101 (TargetMol), SBI-0206965 (Cayman Chemical) or SBP-7455 (TargetMol) at increasing concentrations, for 5 days.

Techniques: Inhibition, Quantitative RT-PCR, Expressing, Control, Gene Expression, Two Tailed Test