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Using shRNA to silence CD36 in LNCaP prostate cancer cells, the researchers found that treatment with SIM1-Me (10 nM) or ARV-110 (50 nM) led to: 5.6-fold and 19.6-fold reductions, respectively, in cellular drug uptake dramatically impaired target protein degradation markedly reduced cytotoxicity (up to 423-fold) Re-expression of CD36 restored activity, and loss of EEA1 also diminished SIM1-Me and ARV-110 cytotoxicity---confirming a dependence on the Rab5/EEA1 endocytic pathway

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used a kainic acid-induced TLE model to assess BBB disruption following SE and identified the optimal time window for intravenous infusion of dental pulp stem cells (DPSCs) and bone marrowderived mesenchymal stem cells (BM-MSCs) (Senthilkumar et al., 2023)

The following primers were used: mouse -actin, forward: 5-GGCTGTATTCCCCTCCATCG-3, reverse: 5-CCAGTTGGTAACAATGCCATGT-3