Wei J - Search Results

1

Disrupted Timing of MET Signaling Derails the Developmental Maturation of Cortical Circuits and Leads to Altered Behavior in Mice.

Ma X, Wei J, Cui Y, Xia B, Zhang L, Nehme A, Zuo Y, Ferguson D, Levitt P, Qiu S. Ma X, et al. Among authors: wei j. Cereb Cortex. 2022 Apr 5;32(8):1769-1786. doi: 10.1093/cercor/bhab323. Cereb Cortex. 2022. PMID: 34470051 Free PMC article.

2

Time-delimited signaling of MET receptor tyrosine kinase regulates cortical circuit development and critical period plasticity.

Chen K, Ma X, Nehme A, Wei J, Cui Y, Cui Y, Yao D, Wu J, Anderson T, Ferguson D, Levitt P, Qiu S. Chen K, et al. Among authors: wei j. Mol Psychiatry. 2021 Aug;26(8):3723-3736. doi: 10.1038/s41380-019-0635-6. Epub 2020 Jan 3. Mol Psychiatry. 2021. PMID: 31900430 Free PMC article.

3

Depletion of microglia in developing cortical circuits reveals its critical role in glutamatergic synapse development, functional connectivity, and critical period plasticity.

Ma X, Chen K, Cui Y, Huang G, Nehme A, Zhang L, Li H, Wei J, Liong K, Liu Q, Shi L, Wu J, Qiu S. Ma X, et al. Among authors: wei j. J Neurosci Res. 2020 Oct;98(10):1968-1986. doi: 10.1002/jnr.24641. Epub 2020 Jun 28. J Neurosci Res. 2020. PMID: 32594561

4

Conditional knockout of MET receptor tyrosine kinase in cortical excitatory neurons leads to enhanced learning and memory in young adult mice but early cognitive decline in older adult mice.

Xia B, Wei J, Ma X, Nehme A, Liong K, Cui Y, Chen C, Gallitano A, Ferguson D, Qiu S. Xia B, et al. Among authors: wei j. Neurobiol Learn Mem. 2021 Mar;179:107397. doi: 10.1016/j.nlm.2021.107397. Epub 2021 Jan 29. Neurobiol Learn Mem. 2021. PMID: 33524570 Free PMC article.

5

Shisa6 mediates cell-type specific regulation of depression in the nucleus accumbens.

Kim HD, Wei J, Call T, Quintus NT, Summers AJ, Carotenuto S, Johnson R, Ma X, Xu C, Park JG, Qiu S, Ferguson D. Kim HD, et al. Among authors: wei j. Mol Psychiatry. 2021 Dec;26(12):7316-7327. doi: 10.1038/s41380-021-01217-8. Epub 2021 Jul 12. Mol Psychiatry. 2021. PMID: 34253865 Free PMC article.

6

Reduced HGF/MET Signaling May Contribute to the Synaptic Pathology in an Alzheimer's Disease Mouse Model.

Wei J, Ma X, Nehme A, Cui Y, Zhang L, Qiu S. Wei J, et al. Front Aging Neurosci. 2022 Jul 12;14:954266. doi: 10.3389/fnagi.2022.954266. eCollection 2022. Front Aging Neurosci. 2022. PMID: 35903536 Free PMC article.

7

Early impairment of cortical circuit plasticity and connectivity in the 5XFAD Alzheimer's disease mouse model.

Chen C, Ma X, Wei J, Shakir N, Zhang JK, Zhang L, Nehme A, Cui Y, Ferguson D, Bai F, Qiu S. Chen C, et al. Among authors: wei j. Transl Psychiatry. 2022 Sep 8;12(1):371. doi: 10.1038/s41398-022-02132-4. Transl Psychiatry. 2022. PMID: 36075886 Free PMC article.

8

Disrupted Maturation of Prefrontal Layer 5 Neuronal Circuits in an Alzheimer's Mouse Model of Amyloid Deposition.

Chen C, Wei J, Ma X, Xia B, Shakir N, Zhang JK, Zhang L, Cui Y, Ferguson D, Qiu S, Bai F. Chen C, et al. Among authors: wei j. Neurosci Bull. 2023 Jun;39(6):881-892. doi: 10.1007/s12264-022-00951-5. Epub 2022 Sep 24. Neurosci Bull. 2023. PMID: 36152121 Free PMC article.

9

Loss-of-function mutation in PRMT9 causes abnormal synapse development by dysregulation of RNA alternative splicing.

Shen L, Ma X, Wang Y, Wang Z, Zhang Y, Pham HQH, Tao X, Cui Y, Wei J, Lin D, Abeywanada T, Hardikar S, Halabelian L, Smith N, Chen T, Barsyte-Lovejoy D, Qiu S, Xing Y, Yang Y. Shen L, et al. Among authors: wei j. Nat Commun. 2024 Apr 1;15(1):2809. doi: 10.1038/s41467-024-47107-9. Nat Commun. 2024. PMID: 38561334 Free PMC article.

10

SIRT1 Coordinates Transcriptional Regulation of Neural Activity and Modulates Depression-Like Behaviors in the Nucleus Accumbens.

Kim HD, Wei J, Call T, Ma X, Quintus NT, Summers AJ, Carotenuto S, Johnson R, Nguyen A, Cui Y, Park JG, Qiu S, Ferguson D. Kim HD, et al. Among authors: wei j. Biol Psychiatry. 2024 Sep 15;96(6):495-505. doi: 10.1016/j.biopsych.2024.03.017. Epub 2024 Apr 3. Biol Psychiatry. 2024. PMID: 38575105 Free article.

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