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Biology subjects

Chen, L.-K.

Publications and source records attributed to Chen, L.-K..

2 recordsLinked to original sources

An On-Demand Nanodisc Platform for Reconstitution of Functional Membrane Proteins into Model and Living Membranes

Membrane proteins are central to transport, signaling, and pharmacological regulation, yet their direct functional reconstitution into defined membrane environments remains technically challenging. Detergent-based workflows have enabled major advances in membrane protein research, but some applications require complementary strategies that better preserve native-like lipid environments. Cell-based expression approaches, meanwhile, require long incubation times and suffer from cell-type-dependent variability. Here, we establish nanodiscs as modular carriers for the rapid delivery of both lipids and full-length membrane proteins into model and cellular membranes. Using supported lipid bilayers, we first show that membrane scaffold protein (MSP) nanodiscs mediate efficient lipid transfer within minutes, with fluorescence recovery after photobleaching confirming lateral mobility of the delivered lipids. We then extend this strategy to the bacterial calcium channel BsYetJ, achieving concentration-dependent protein incorporation and single-molecule diffusion within supported lipid bilayers. Importantly, BsYetJ-loaded nanodiscs enable direct reconstitution of functional channels into intact mammalian plasma membranes across multiple cell lines. Calcium imaging demonstrates robust BsYetJ-mediated calcium influx, confirming that the delivered channel retains ion-conductive activity after transfer into heterologous cellular membranes. Crucially, this nanodisc-mediated delivery bypasses the variable trafficking pathways inherent to different host systems, allowing for the direct reconstitution of membrane proteins into target membranes while preserving their functional activity. Furthermore, unlike MSP nanodiscs, styrene-maleic acid (SMA) nanodiscs can directly capture membrane proteins from native cell membranes. This capability makes them particularly well-suited for studying complex and challenging membrane proteins. Therefore, we further generalize this platform using SMA nanodiscs . We demonstrate that, similar to MSP nanodiscs, SMA nanodiscs can efficiently deliver lipid cargo to supported bilayers and mammalian cells. By directly capturing full-length dopamine D2 receptor from cellular membranes and transferring it into naive target cells, we achieve functional GPCR reconstitution, as validated by specific binding of a custom fluorescent agonist. Together, these results demonstrate that nanodiscs can serve not only as stabilizing membrane mimetics but also as active delivery vehicles for on-demand membrane protein reconstitution. This approach provides a rapid and broadly applicable platform for interrogating ion channels, GPCRs, and other challenging pharmacological targets in user-defined membrane environments.

biochemistry↗

Reduced glutamate decarboxylase 1 underlies morphine-promoted lung metastasis of triple-negative breast cancer in mice

IntroductionMorphine is commonly used for cancer-related pain management. Long-term morphine use is not only addictive but also has been associated with risk factor for cancer. MethodsWe intraperitoneally administered morphine to mice for 14 days and then implanted EO771 cells, triple negative breast cancer cells, into their mammary fat pad. After primary tumors were removed on 38th day, a subset of mice were continuously giving saline or morphine until the 68th day. Tumor size, organ metastasis, and tumor RNA expression were analyzed. ResultsOur results revealed that long-term morphine treatment increased lung metastasis in the triple-negative breast cancer mouse model. To determine cellular pathways responsible for morphine-mediated metastasis, we performed RNA sequencing analysis to compare transcriptional profiles during metastasis. Transcriptional analysis revealed a significant number of genes down-regulated by morphine treatment. Based on pathway analysis, we focused on the novel effect of morphine on down-regulating taurine/hypotaurine biosynthesis. Considering that morphine, droperidol (dopamine receptor antagonist), and naloxone (opioid receptor antagonist) may act through opioid receptor or dopamine receptor, we further demonstrated that taurine reduced EO771 cell invasion caused by morphine, but not by droperidol, or naloxone treatment. In addition, morphine treatment significantly reduced the expression of GAD1, one of the enzymes required for biosynthesis of taurine, whereas droperidol and naloxone did not. ConclusionThese novel findings of morphine reduces GAD1 level and taurine reverses invasion suggest that taurine could potentially be employed as a supplement for triple negative breast cancer patients using morphine as pain management. Key MessagesO_LIMorphine usage has been implicated in modulating immune system and affecting cancer progression. C_LIO_LILong-term usage of morphine promotes metastasis of triple negative breast cancer through reducing taurine biosynthesis. C_LIO_LIThese novel findings of morphine reduces GAD1 level and taurine reverses invasion suggest that taurine could potentially be employed as a supplement for triple negative breast cancer patients using morphine as pain management. C_LI

cancer biology↗