Investigators identified that the transcription factor 4-mediated cell death was essential for generating an appropriate number of oligodendrocyte progenitor cells and thereby oligodendrocytes in the olfactory bulb.
[Cell Death & Disease]
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Researchers showed that KDM4C knockdown significantly repressed proliferation and tumorigenesis of glioblastoma cells in vitro and in vivo that were rescued by overexpressing wild-type KDM4C but not a catalytic dead mutant.
[Cell Death & Disease]
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Lee, D. H., Kim, G. W., Yoo, J., Lee, S. W., Jeon, Y. H., Kim, S. Y., Kang, H. G., Kim, D.-H., Chun, K.-H., Choi, J., & Kwon, S. H. (2021). Histone demethylase KDM4C controls tumorigenesis of glioblastoma by epigenetically regulating p53 and c-Myc. Cell Death & Disease, 12(1), 1–14. https://doi.org/10.1038/s41419-020-03380-2 Cite
Researchers supplemented capsaicin in the diet of the animals to upregulate calcitonin gene-related peptide (CGRP) and reversed the downregulation of the neuropeptide in the dorsal root ganglion (DRG) neurons dissociated from the diabetic animals, via gene transfection and exogenous CGRP, to test disease-preventing and disease-limiting effects of CGRP.
Scientists unravelled the down-stream pathways associated with mitochondrial complex II (CII) inhibition and compared with CI inhibition and the Manganese neurotoxicity. Genome-wide transcriptomics of N27 neuronal cells exposed to 3-nitropropionic acid, compared with 1-methyl-4-phenylpyridinium and Mn revealed varied transcriptomic profile.
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Ranganayaki, S., Jamshidi, N., Aiyaz, M., Rashmi, S.-K., Gayathri, N., Harsha, P. K., Padmanabhan, B., & Srinivas Bharath, M. M. (2021). Inhibition of mitochondrial complex II in neuronal cells triggers unique pathways culminating in autophagy with implications for neurodegeneration. Scientific Reports, 11(1), 1483. https://doi.org/10.1038/s41598-020-79339-2 Cite
The authors report significant locomotor recovery of both hindlimbs after a complete spinal cord crush. This was achieved by the unilateral transduction of cortical motoneurons with an AAV expressing hyper-IL-6, a potent designer cytokine stimulating JAK/STAT3 signaling and axon regeneration.
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Transneuronal delivery of hyper-interleukin-6 enables functional recovery after severe spinal cord injury in mice | Nature Communications. (n.d.). Retrieved January 15, 2021, from https://www.nature.com/articles/s41467-020-20112-4 Cite
Investigators review the possible roles of stem cell marker- or stemness-related genes in axon regeneration to gain a better understanding of the regeneration mechanism and to identify targets that can enhance regenerative capacity.
[Experimental and Molecular Medicine]
Scientists analyzed Toll-like receptor 4 (TLR4) expression in different grades of astrocytoma, and observed increased expression in tumors, mainly in glioblastoma, compared to non-neoplastic brain tissue.
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Moretti, I. F., Lerario, A. M., Trombetta-Lima, M., Sola, P. R., da Silva Soares, R., Oba-Shinjo, S. M., & Marie, S. K. N. (2021). Late p65 nuclear translocation in glioblastoma cells indicates non-canonical TLR4 signaling and activation of DNA repair genes. Scientific Reports, 11(1), 1333. https://doi.org/10.1038/s41598-020-79356-1 Cite
The authors found that O-GlcNAcylation plays a protective role in Alzheimer’s disease by inhibiting necroptosis.
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Park, J., Ha, H.-J., Chung, E. S., Baek, S. H., Cho, Y., Kim, H. K., Han, J., Sul, J. H., Lee, J., Kim, E., Kim, J., Yang, Y. R., Park, M., Kim, S. H., Arumugam, T. V., Jang, H., Seo, S. W., Suh, P.-G., & Jo, D.-G. (2021). O-GlcNAcylation ameliorates the pathological manifestations of Alzheimer’s disease by inhibiting necroptosis. Science Advances, 7(3), eabd3207. https://doi.org/10.1126/sciadv.abd3207 Cite
Researchers showed that FMRpolyG interacts with pathogenic CGG repeat-derived RNA G-quadruplexes, propagates cell to cell, and induces neuronal dysfunction.
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Asamitsu, S., Yabuki, Y., Ikenoshita, S., Kawakubo, K., Kawasaki, M., Usuki, S., Nakayama, Y., Adachi, K., Kugoh, H., Ishii, K., Matsuura, T., Nanba, E., Sugiyama, H., Fukunaga, K., & Shioda, N. (2021). CGG repeat RNA G-quadruplexes interact with FMRpolyG to cause neuronal dysfunction in fragile X-related tremor/ataxia syndrome. Science Advances, 7(3), eabd9440. https://doi.org/10.1126/sciadv.abd9440 Cite
Scientists identified a subset of inhibitory interneurons in the spinal dorsal horn (SDH) operated by adeno-associated viral vectors incorporating a neuropeptide Y promoter (AAV-NpyP+) and showed that specific ablation or silencing of AAV-NpyP+ SDH interneurons converted touch-sensing Aβ fiber-derived signals to morphine-resistant pain-like behavioral responses.
[Proceedings of the National Academy of Sciences of the United States of America]
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Tashima, R., Koga, K., Yoshikawa, Y., Sekine, M., Watanabe, M., Tozaki-Saitoh, H., Furue, H., Yasaka, T., & Tsuda, M. (2021). A subset of spinal dorsal horn interneurons crucial for gating touch-evoked pain-like behavior. Proceedings of the National Academy of Sciences, 118(3). https://doi.org/10.1073/pnas.2021220118 Cite
Kintara Therapeutics, Inc. announced that patient recruitment has commenced in the Global Coalition for Adaptive Research registrational Phase II/III clinical trial for glioblastoma (GBM).
[Kintara Therapeutics, Inc.]
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