• Tankyrase Inhibitors and Hippo Signaling in HCC

  2026-09-03

  The reference study shows that XAV-939 and G007-LK suppress hepatocellular carcinoma cell growth while reducing YAP activity and stabilizing the YAP inhibitors AMOTL1 and AMOTL2. These findings connect tankyrase inhibition to Hippo-pathway regulation and provide a mechanistic framework for combination studies with MEK or AKT inhibitors.

• GPR30 in Spinal CCK+ Neurons and Neuropathic Pain

  2026-09-03

  Chen and colleagues identify GPR30 in spinal cholecystokinin-positive neurons as a cell-type-specific regulator of neuropathic pain after nerve injury. By combining receptor manipulation, synaptic analysis, behavioral testing, and S1-to-spinal-cord circuit experiments, the study connects GPR30 to AMPA-mediated sensitization and a descending cortical pain pathway.

• NAT10–ac4C Control of Mouse Oocyte Maturation

  2026-09-02

  The reference study identifies NAT10-mediated N4-acetylcytidine (ac4C) as a post-transcriptional regulator of mouse oocyte maturation in vitro. NAT10 knockdown reduced ac4C modification and impaired first polar body extrusion, while RNA-interaction analyses nominated TBL3 as a potential ac4C-binding protein.

• (S)-Mephenytoin as a CYP2C19 Substrate

  2026-09-02

  (S)-Mephenytoin is a defined CYP2C19 substrate for measuring oxidative drug metabolism and mephenytoin 4-hydroxylase activity. Its reported kinetic benchmarks and compatibility with human intestinal organoid workflows support pharmacokinetic studies, but they do not replace model-specific validation or clinical testing.

• Dicloxacillin Activity Against Intracellular S. aureus

  2026-09-01

  The reference study compared dicloxacillin activity against intracellular and extracellular Staphylococcus aureus using complementary THP-1 cell and murine peritonitis models. Its central finding was that free-drug time above the MIC, rather than peak concentration or total exposure alone, best predicted efficacy in both bacterial compartments.

• Primidone Workflows for TRPM3 and RIPK1 Studies

  2026-09-01

  Primidone, also known as Mysoline, supports mechanism-specific studies spanning TRPM3 channel pharmacology, RIPK1 signaling, pain biology, and disease models. This workflow connects concentration selection and formulation controls with the adenomyosis findings that make Primidone especially useful for translational assay design.

• MK-0812 Workflow for CCR2 Monocyte Research

  2026-08-31

  Use MK-0812 to separate CCR2-dependent monocyte recruitment from broader gut–liver inflammatory effects in MASH models. This workflow combines whole-blood pharmacology, chemotaxis, flow cytometry, and intestinal–hepatic readouts for more defensible mechanism-of-action studies.

• CRISPR/Cas9 Targeting of ABCB1 Multidrug Resistance

  2026-08-31

  Yang and colleagues used CRISPR/Cas9 genome editing to disrupt ABCB1 in two multidrug-resistant cancer cell lines. ABCB1 loss increased intracellular doxorubicin and rhodamine 123 while sensitizing cells to ABCB1-substrate chemotherapeutics, providing a genetic strategy for studying transporter-driven resistance.

• ATF4–H2S Signaling in Doxorubicin Cardiotoxicity

  2026-08-30

  This preprint identifies a KLF16–ATF4–CSE–H2S pathway that limits oxidative stress and apoptosis during doxorubicin-induced cardiomyopathy. Using genetic mouse models, AAV9-mediated cardiac gene delivery, RNA sequencing, chromatin immunoprecipitation, and reporter assays, the study connects loss of ATF4 activity with impaired endogenous hydrogen sulfide production and cardiac dysfunction.

• DON Liver Injury: Mitophagy–Nrf2 Mechanisms

  2026-08-29

  The reference study proposes that deoxynivalenol-induced liver injury is driven by excessive PINK1/Parkin-mediated mitophagy together with suppression of the p62–Keap1–Nrf2 cytoprotective pathway. Its combined mouse, AML-12 cell, gene-silencing, inhibitor, and p62-rescue design provides a useful mechanistic framework, although the reported work is identified as a non-peer-reviewed preprint and requires independent validation.

• (S)-Mephenytoin: Translating CYP2C19

  2026-08-28

  A translational framework for using (S)-Mephenytoin as a CYP2C19 substrate across recombinant enzymes, microsomes, and human pluripotent stem cell-derived intestinal organoids. The article connects mechanistic cytochrome P450 metabolism with assay design, model selection, genetic variability, and pharmacokinetic decision-making while defining the limitations of extending CYP3A-focused organoid evidence to CYP2C19.

• Berberine Hydrochloride in Metabolic Assays

  2026-08-28

  Build reproducible metabolic, lipid, cancer, and exploratory cardiac assays with Berberine hydrochloride. This workflow emphasizes solvent control, pathway-matched readouts, and a practical translation of AMPK–mitochondrial findings from a cardiotoxicity study.

• Protease Inhibitor Cocktail: Assay Reliability

  2026-08-27

  Learn how Protease Inhibitor Cocktail (100X H₂O, EDTA Plus), SKU K4003, can reduce post-lysis protein degradation in viability, proliferation, cytotoxicity, and lipid-droplet workflows. This scenario-based guide covers compatibility, protocol parameters, EDTA limitations, interpretation, and practical vendor selection.

• CA-074 Me for Lysosomal Cathepsin B Studies

  2026-08-27

  CA-074 Me enables cell-based dissection of cathepsin B activity after lysosomal membrane permeabilization, with practical value in necroptosis, apoptosis assay design, and inflammation research. This guide translates MLKL–lysosome findings into an actionable workflow with controls, dosing logic, and troubleshooting safeguards.

• HIV-1 Signalling Remodels Nuclear Pores in Resting T Cells

  2026-08-26

  The reference study shows that HIV-1 cell–cell spread overcomes a nuclear import barrier in resting CD4+ T cells by activating CD4–LCK–CDK1 signalling and remodeling nuclear pore complexes. Its experimental strategy separates contact-dependent signalling from viral transfer, providing a mechanistic explanation for why virological synapses can infect resting T cells more efficiently than cell-free virions.

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