Publications by authors named "N J Carruthers"
In recent years, methamphetamine (METH) misuse in the US has been rapidly increasing, and there is no FDA-approved pharmacotherapy for METH use disorder (MUD). In addition to being dependent on the drug, people with MUD develop a variety of neurological problems related to the toxicity of this drug. A variety of molecular mechanisms underlying METH neurotoxicity has been identified, including the dysfunction of the neuroprotective protein parkin.
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- Methamphetamine misuse is rapidly increasing in the US, and there is currently no FDA-approved treatment for meth use disorder (MUD), leading to neurological issues from the drug's toxicity.
- This study explores the role of the protein parkin and its relationship with CDCrel-1 and VMAT2 in the neurotoxic effects of methamphetamine in male rats, demonstrating that binge METH alters CDCrel-1 levels and its interaction with VMAT2.
- Findings indicate significant individual differences in responses to meth's neurotoxicity, suggesting that understanding these genetic and molecular variations can help improve treatments for humans affected by MUD and associated neurological damage.
Metaplastic breast carcinomas (mBrCA) are a highly aggressive subtype of triple-negative breast cancer with histologic evidence of epithelial-to-mesenchymal transition and aberrant differentiation. Inactivation of the tumor suppressor gene cellular communication network factor 6 (CCN6; also known as Wnt1-induced secreted protein 3) is a feature of mBrCAs, and mice with conditional inactivation of Ccn6 in mammary epithelium (Ccn6-KO) develop spindle mBrCAs with epithelial-to-mesenchymal transition. Elucidation of the precise mechanistic details of how CCN6 acts as a tumor suppressor in mBrCA could help identify improved treatment strategies.
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- Inhibiting emopamil binding protein (EBP) may aid in treating multiple sclerosis by promoting oligodendrocyte formation through targeting a key enzyme in cholesterol biosynthesis.
- Researchers utilized structure-based drug design to discover hydantoin-based inhibitors of EBP, optimizing them for better safety, potency, and brain penetration.
- The resulting EBP inhibitor showed strong effectiveness in the brain and increased oligodendrocyte formation in human cortical organoids, supporting its potential as a therapeutic option.
We have shown previously that expression of R345W-Fibulin-3 induces epithelial-mesenchymal transition (EMT) in retinal pigment epithelial (RPE) cells. The purpose of the current study was to determine if extracellular vesicles (EVs) derived from RPE cells expressing R345W-Fibulin-3 mutation are sufficient to induce EMT in recipient cells. ARPE-19 cells were infected with luciferase-tagged wild-type (WT)- Fibulin-3 or luciferase-tagged R345W-Fibulin-3 (R345W) using lentiviruses.
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