The authors found that p65 was activated during cellular senescence and inflammatory activation in human umbilical cord-derived MSCs.
[International Journal of Molecular Sciences]
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Mato-Basalo, R., Morente-López, M., Arntz, O. J., van de Loo, F. A. J., Fafián-Labora, J., & Arufe, M. C. (2021). Therapeutic Potential for Regulation of the Nuclear Factor Kappa-B Transcription Factor p65 to Prevent Cellular Senescence and Activation of Pro-Inflammatory in Mesenchymal Stem Cells. International Journal of Molecular Sciences, 22(7), 3367. https://doi.org/10.3390/ijms22073367 Cite
Researchers performed loss and gain of function experiments for the expression of miR-499 in lung cancer cells exposed to irradiation to determine the effect of miR-499 expression on cell viability and apoptosis as well as tumor growth.
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Human umbilical cord (HUC)-MSCs were separated from the umbilical cord using the adherence method. Surface markers of HUC-MSCs were detected by flow cytometry for MSC identification.
[Cancer Biotherapy and Radiopharmaceuticals]
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The authors hypothesized that cAMP response element-binding protein (CREB) associated with KMT5A to modulate PTP1B expression, thus contributing to high glucose-mediated glomerular endothelial inflammation.
[Cell Death & Disease]
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The therapeutic effects of MMP-1 decorated polymersomes (MMPsomes), compared to matrix metalloproteinase-1 (MMP-1), were evaluated in vivo in carbon-tetrachloride-induced early liver fibrosis mouse model. MMPsomes exhibited favorable physicochemical properties, MMP-1 surface localization and improved therapeutic efficacy in TGFβ-activated human hepatic stellate cells in vitro.
[Journal of Controlled Release]
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Researchers determined whether recombinant Islet NeoGenesis Associated Protein (rINGAP) and its active core, a pentadecapeptide INGAP104–118, protected β cells against cytokine-induced death.
[Cell Death Discovery]
The authors showed that mesenchymal stem cells differentiated into cancer-associated fibroblasts, induced by the exosomes derived from gastric cancer cells.
[Cell Death & Disease]
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Gu, J., Li, X., Zhao, L., Yang, Y., Xue, C., Gao, Y., Li, J., Han, Q., Sun, Z., Bai, C., & Zhao, R. C. (2021). The role of PKM2 nuclear translocation in the constant activation of the NF-κB signaling pathway in cancer-associated fibroblasts. Cell Death & Disease, 12(4), 1–13. https://doi.org/10.1038/s41419-021-03579-x Cite
miR-410 expression was determined using qRT-PCR in both mouse models of atherosclerosis and HUVECs treated with ox-LDL.
[Molecular Therapy-Nucleic Acids]
Investigators demonstrated a mechanistic link between connective tissue growth factor (CTGF) and enhanced aerobic glycolysis in TNBC.
β-arrestin 1 (ARRB1) ablation ameliorated whereas ARRB2 knockout aggravated, the pathological features of Parkinson’s disease, including dopaminergic neuron loss, neuroinflammation and microglia activation in vivo, and microglia-mediated neuron damage in vitro.
[Cell Death & Differentiation]
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Fang, Y., Jiang, Q., Li, S., Zhu, H., Xu, R., Song, N., Ding, X., Liu, J., Chen, M., Song, M., Ding, J., Lu, M., Wu, G., & Hu, G. (2021). Opposing functions of β-arrestin 1 and 2 in Parkinson’s disease via microglia inflammation and Nprl3. Cell Death & Differentiation, 1–15. https://doi.org/10.1038/s41418-020-00704-9 Cite
The biological roles of Pentraxin 3 in NSCLC progression and NSCLC cell resistance to cisplatin were evaluated using enzyme-linked immunosorbent assay, cell count kit-8, colony formation assay, flow cytometry, as well as xenograft tumor assay.
[Archives of Biochemistry and Biophysics]
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