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Min-Yin Li

As seen in: Nature, BioRxiv, Cell Stem Cell, Cell Press
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Articles

Author Correction: Maturation and circuit integration of transplanted human cortical organoids

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By Omer Revah, Felicity Gore, Kevin Kelley, Jimena Andersen, Noriaki Sakai, Xiaoyu Chen, Min-Yin Li, Fikri Birey, Xiao Yang, Samuel Baker, Neal D. Amin, Rachana Mudipalli, Bianxiao Cui, Seiji Nishino, Gerald A. Grant, Juliet K. Knowles, Mehrdad Shamloo, John R. Huguenard, Karl Deisseroth, Sergiu Pasca, Shravanti Kulkarni
| Nature Verified
Correction to: Nature https://doi.org/10.1038/s41586-022-05277-w Published online 12 October 2022 In the version of this article initially published, due to a figure preparation error, the mPFC panel in Fig. 5a was an inadvertent duplicate of the Fig. 5a A1 panel. The figure is now revised in the HTML and PDF versions of the article.
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Human assembloids reveal the consequences of CACNA1G gene variants in the thalamocortical pathway

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By Ji-il Kim, Yuki Miura, Min-Yin Li, Omer Revah, Sridhar Selvaraj, Fikri Birey, Xiangling Meng, Mayuri Vijay Thete, Sergey Pavlov, Jimena Andersen, Matthew H. Porteus, John R. Huguenard
| Cell Press Verified
Keywords assembloids organoids thalamus thalamocortical disease Get full text access Log in, subscribe or purchase for full access. References 1. Sherman, S.M. ∙ Guillery, R.W. The role of the thalamus in the flow of information to the cortex Philos. Trans. R. Soc. Lond. B Biol. Sci. 2002; 357:1695-1708 2. Rikhye, R.V. ∙ Gilra, A. ∙ Halassa, M.M. Thalamic regulation of switching between cortical representations enables cognitive flexibility Nat. Neurosci. 2018; 21:1753-1763 3. Roy, D.S. ∙ Zhang, Y. ∙ Aida, T.
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Antisense oligonucleotide therapeutic approach for Timothy syndrome - Nature

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By Xiaoyu Chen, Fikri Birey, Min-Yin Li, Noah Reis, Jin Hao, Xiangling Meng
| Nature Verified
Abstract Timothy syndrome (TS) is a severe, multisystem disorder characterized by autism, epilepsy, long-QT syndrome and other neuropsychiatric conditions1. TS type 1 (TS1) is caused by a gain-of-function variant in the alternatively spliced and developmentally enriched CACNA1C exon 8A, as opposed to its counterpart exon 8.
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