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Bo Xiao

Researcher at Sichuan University

Publications -  59
Citations -  9667

Bo Xiao is an academic researcher from Sichuan University. The author has contributed to research in topics: Medicine & Metabotropic glutamate receptor. The author has an hindex of 29, co-authored 42 publications receiving 8745 citations. Previous affiliations of Bo Xiao include Johns Hopkins University & Central South University.

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The mTOR kinase differentially regulates effector and regulatory T cell lineage commitment.

TL;DR: Overall, the studies suggest that mTOR kinase signaling regulates decisions between effector and regulatory T cell lineage commitment.
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Coupling of mGluR/Homer and PSD-95 Complexes by the Shank Family of Postsynaptic Density Proteins

TL;DR: It is reported that Shank proteins also bind to Homer, and Shank may cross-link Homer and PSD-95 complexes in the PSD and play a role in the signaling mechanisms of both mGluRs and NMDA receptors.
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The kinase mTOR regulates the differentiation of helper T cells through the selective activation of signaling by mTORC1 and mTORC2

TL;DR: It is demonstrated that differentiation into the TH1 and TH17 subsets of helper T cells was selectively regulated by signaling from mTOR complex 1 (mTORC1) that was dependent on the small GTPase Rheb.
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Shank, a Novel Family of Postsynaptic Density Proteins that Binds to the NMDA Receptor/PSD-95/GKAP Complex and Cortactin

TL;DR: A novel family of postsynaptic density proteins, termed Shank, that binds via its PDZ domain to the C terminus of PSD-95-associated protein GKAP, and may function as a scaffold protein in the PSD, potentially cross-linking NMDA receptor/PSD- 95 complexes and coupling them to regulators of the actin cytoskeleton.
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Homer Binds a Novel Proline-Rich Motif and Links Group 1 Metabotropic Glutamate Receptors with IP3 Receptors

TL;DR: This work presents evidence that Homer proteins form a physical tether linking mGluRs with the inositol trisphosphate receptors (IP3R), and identifies a novel mechanism in calcium signaling and provides evidence that an IEG, whose expression is driven by synaptic activity, can directly modify a specific synaptic function.