Journal: Journal of Virology

Article Title: PKC inhibitors reveal PKC isoforms involved in HIV latency reversal and immunomodulation

doi: 10.1128/jvi.00500-26

Figure Lengend Snippet: Summary of pharmacologic PKC isoform inhibitors used ^a

Article Snippet: The following commercially available PKC isoform inhibitor compounds were used based on their reported biological activities against PKC isoforms: PKCε inhibitor V1-2/εV1-2 (MedChemExpress and Cayman Chemicals) ( , ), ζ-Stat (MedChemExpress) ( , ), PKCθ inhibitor (MedChemExpress and Selleck Chemicals) , PKCβ inhibitor 1 (MedChemExpress) ( , ), and Go-6983 (MedChemExpress) ( , ). summarizes the specific inhibitor used and the complement of PKC isoforms inhibited by the compound at the concentrations used in this study.

Techniques: Concentration Assay

Journal: Stem Cell Reports

Article Title: CCL5 exposure promotes acute and transient megakaryopoiesis and hematopoietic progenitor expansion

doi: 10.1016/j.stemcr.2026.103014

Figure Lengend Snippet: CCL5 administration induces transcriptional changes in megakaryocytes (A) Mice were treated with CCL5 as previously described, and bone marrow MKs were isolated after 24 h following lineage depletion and enrichment by flow cytometry sorting. RNA was extracted using TRIzol purification, and RNA sequencing was performed (4n vs. 4n). (B) Volcano plot shows genes that are significantly up- and down-regulated. The points highlighted in purple are genes that have padj <0.05 and a log2-fold change >1. Points in blue have a padj <0.05 and a log2-fold change <1. Gray points are non-significant. The dashed lines correspond to the cutoff values of log2 fold-change and padj chosen. (C) Differentially expressed genes associated with mitochondrial metabolism. Expression values are presented in log 2 scale, and statistical significance was determined using padj. N represents a pool of 2 mice. (D) Male mice received retro-orbital injections of CCL5 (0.05 mg/kg) or vehicle ( Ctrl ). After 24 h, MKs were isolated by size exclusion, lysed, and analyzed using a RayBio Mouse JAK/STAT Pathway Phosphorylation Array. Signal intensity was quantified with Fiji. N represents a pool of 5 mice per group. (E) Representative histograms of TMRM in MKs by flow cytometry after CCL5 administration (Gray: FMO; Black: Ctrl; Red: CCL5). (F) MKs were identified by flow cytometry, and the mean fluorescence intensity of TMRM was quantified ( n = 4–5). Data are presented as mean ± SD. Statistical analyses were performed using an unpaired, two-tailed Student’s t test. N represents an individual mouse. Illustrations were created with BioRender. padj, adjusted p value.

Article Snippet: After 24 h, MKs were isolated by size exclusion, lysed, and analyzed using a RayBio Mouse JAK/STAT Pathway Phosphorylation Array.

Techniques: Isolation, Flow Cytometry, Purification, RNA Sequencing, Expressing, Phospho-proteomics, Fluorescence, Two Tailed Test

Journal: Acta Pharmaceutica Sinica. B

Article Title: Targeting NAT10 with Remodelin reshapes the pro-fibrotic microenvironment in renal fibrogenesis via inhibiting exosome oversecretion from tubular cells

doi: 10.1016/j.apsb.2026.05.020

Figure Lengend Snippet: Targeting acetyltransferase NAT10 with Remodelin breaks the TEC-fibroblast pro-fibrotic chain (A) The graph indicating the selection strategy of screen based on in vitro model of TEC-fibroblast communication with epigenetic inhibitor compounds. (B) The heatmap of viability of NRK-49F cells incubated with CM from HK-2 cells with indicated treatments respectively (left panel). The dots indicated the average fold of viability of NRK-49F cells incubated with CM from HK-2 cells treated with TGF- β and epigenetic inhibitors, in relative to the NRK-49F cells incubated with CM from HK-2 cells treated with TGF- β and DMSO (right panel). The red dots indicated the selected inhibitors for further screen. (C) The heatmap of viability of NRK-49F cells incubated with CM from HK-2 cells with indicated treatments, respectively. (D) The heatmap (left) and table (right) demonstrating the details of 13 effective epigenetic inhibitors. (E) The immunoblot analysis of NAT10 in kidneys from sham mice ( n = 5) and UUO mice ( n = 5). (F) The dot blot analysis of ac4C in kidneys from sham mice ( n = 2) and UUO mice ( n = 2). (G) The immunohistochemistry staining of NAT10 in kidneys from sham mice and UUO mice. (H) The immunofluorescence staining of NAT10 in kidneys from sham mice and UUO mice. LTL was used as marker of proximal tubular cells. (I) The immunoblot analysis of NAT10 in kidneys from CKD patients ( n = 18) and non-CKD control ( n = 5). (J) The dot blot analysis of ac4C in kidneys from CKD patients ( n = 18) and non-CKD control ( n = 5). Data are presented as mean ± SD. Student's t test was used for comparison between two groups and one-way ANOVA was used for comparison between multiple groups; ∗ P < 0.05; ∗∗ P < 0.01; ∗∗∗ P < 0.001.

Article Snippet: HK-2 cells were seeded in 96-well plates at the density of 10,000 cells per well, and then treated with TGF- β (5 ng/mL) in the presence of each inhibitor (1 or 5 μmol/L) of Epigenetic Compound Library (TargetMol, MA, USA).

Techniques: Selection, In Vitro, Incubation, Western Blot, Analysis, Dot Blot, Immunohistochemistry, Staining, Immunofluorescence, Marker, Control, Comparison