Investigators demonstrated that the loss of DOC-2/DAB2 interacting protein (DAB2IP) was responsible for temozolomide (TMZ)-resistance in glioblastoma multiforme (GBM) through ATG9B. DAB2IP sensitized GBM to TMZ and suppressed TMZ-induced autophagy by negatively regulating ATG9B expression.
[Cell Death & Disease]
Human neural stem cells and IMR-32 neuroblastoma cells were differentiated into neuronal cells for this study. Although the neuronal cells were permissive to EV-A71 infection, EV-A71 infection did not induce an obvious cytopathic effect on the neuronal cells.
The authors showed that glia could be reprogrammed to promote morphological and functional regeneration after central nervous system injury in Drosophila via increased glycolysis.
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Li, F., Sami, A., Noristani, H. N., Slattery, K., Qiu, J., Groves, T., Wang, S., Veerasammy, K., Chen, Y. X., Morales, J., Haynes, P., Sehgal, A., He, Y., Li, S., & Song, Y. (2020). Glial Metabolic Rewiring Promotes Axon Regeneration and Functional Recovery in the Central Nervous System. Cell Metabolism, 0(0). https://doi.org/10.1016/j.cmet.2020.08.015 Cite
CuraSen Therapeutics, Inc. announced that it has dosed its first subjects in a multi-part, Phase 1 clinical study with CST-2032, the company’s first proprietary compound intended for the treatment of neurodegenerative disease.
[CuraSen Therapeutics, Inc.]
Brainstorm Cell Therapeutics Inc. announced that the Japanese Patent Office has granted Brainstorm’s Japanese Patent, number: 6,753,887, titled: ‘Methods of Generating Mesenchymal Stem Cells which Secrete Neurotrophic Factors’.
[Brainstorm Cell Therapeutics Inc.]
The authors describe how glial cells play a role in adult hippocampal neurogenesis in both health and disease, especially focusing on glia‐derived factors.
[European Journal of Neuroscience]
Cerebellar granule neurons were plated on poly-L-lysine overnight, and neurite length was determined after one hour treatment with L1 cell adhesion molecule (L1) alone or L1 and bilirubin.
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Researchers investigated a novel hypoxia inducible factor 2α inhibitor, PT2385, both in vitro, with low-passage patient-derived cell lines, and in vivo, using orthotopic models of glioblastoma.
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Renfrow, J. J., Soike, M. H., West, J. L., Ramkissoon, S. H., Metheny-Barlow, L., Mott, R. T., Kittel, C. A., D’Agostino, R. B., Tatter, S. B., Laxton, A. W., Frenkel, M. B., Hawkins, G. A., Herpai, D., Sanders, S., Sarkaria, J. N., Lesser, G. J., Debinski, W., & Strowd, R. E. (2020). Attenuating hypoxia driven malignant behavior in glioblastoma with a novel hypoxia-inducible factor 2 alpha inhibitor. Scientific Reports, 10(1), 15195. https://doi.org/10.1038/s41598-020-72290-2 Cite
The authors developed a three-dimensional hBORG model containing major cell types important for HIV-1 neuropathogenesis; neurons and astrocytes along with incorporation of HIV-infected microglia.
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Researchers found that the chemokines CXCL1 and CCL2 were induced in the brain following HSV-1 infection. Ccr2-deficient mice had reduced monocyte recruitment, uncontrolled viral replication, and increased morbidity.
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Michael, B. D., Bricio-Moreno, L., Sorensen, E. W., Miyabe, Y., Lian, J., Solomon, T., Kurt-Jones, E. A., & Luster, A. D. (2020). Astrocyte- and Neuron-Derived CXCL1 Drives Neutrophil Transmigration and Blood-Brain Barrier Permeability in Viral Encephalitis. Cell Reports, 32(11). https://doi.org/10.1016/j.celrep.2020.108150 Cite
Researchers demonstrated across different metabolic stress conditions that modulate malonyl-CoA levels in cortical neurons that carnitine palmitoyltransferase 1C (CPT1C) regulated the trafficking of the major AMPA receptor subunit, GluA1, through the phosphatidyl-inositol-4-phosphate (PI(4)P) phosphatase SAC1.
[Journal of Cell Biology]
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Casas, M., Fadó, R., Domínguez, J. L., Roig, A., Kaku, M., Chohnan, S., Solé, M., Unzeta, M., Miñano-Molina, A. J., Rodríguez-Álvarez, J., Dickson, E. J., & Casals, N. (2020). Sensing of nutrients by CPT1C controls SAC1 activity to regulate AMPA receptor trafficking. Journal of Cell Biology, 219(10). https://doi.org/10.1083/jcb.201912045 Cite