Scientists demonstrated that salinomycin displayed potent anti-fibrotic activity in cardiac fibroblasts obtained from heart failure patients. In pre-clinical studies, salinomycin prevented cardiac fibrosis and functional decline in mouse models of ischemic and non-ischemic heart disease.
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Burke Ryan M, Dirkx, Jr. R. A., Quijada Pearl, Lighthouse Janet K, Mohan Amy, O’Brien Meghann, Wojciechowski Wojciech, Woeller Collynn, Phipps Richard P, Alexis Jeffrey D, Ashton John, & Small Eric M. (n.d.). Prevention of Fibrosis and Pathological Cardiac Remodeling by Salinomycin. Circulation Research, 0(0). https://doi.org/10.1161/CIRCRESAHA.120.317791 Cite
Investigators revealed a role for myeloid-derived cells-derived hypochlorous acid (HOCl) as a small-molecule paracrine signaling factor that trans-inhibited inhibited IκB kinase (IKK) in melanoma tumor cells, mediating antitumor responses during early tumor progression.
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Scientists demonstrated that ZIP8 was specifically upregulated in CD4+ T cells that infiltrated the inflamed joint and that ZIP8 deficiency in CD4+ T cells abrogated collagen-induced arthritis.
[Experimental & Molecular Medicine]
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To elucidate the interplay between epidermal growth factor signaling and extracellular-regulated kinase activation in tumors, scientists used patient-derived organoids from KRAS and BRAF mutant colorectal cancer.
[Nature Cell Biology]
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Ponsioen, B., Post, J. B., Buissant des Amorie, J. R., Laskaris, D., van Ineveld, R. L., Kersten, S., Bertotti, A., Sassi, F., Sipieter, F., Cappe, B., Mertens, S., Verlaan-Klink, I., Boj, S. F., Vries, R. G. J., Rehmann, H., Vandenabeele, P., Riquet, F. B., Trusolino, L., Bos, J. L., & Snippert, H. J. G. (2021). Quantifying single-cell ERK dynamics in colorectal cancer organoids reveals EGFR as an amplifier of oncogenic MAPK pathway signalling. Nature Cell Biology, 1–14. https://doi.org/10.1038/s41556-021-00654-5 Cite
Myelin alterations are accompanied by higher oligodendrocyte progenitor cell (OPC) density and proliferation during the first weeks of life, consistent with a transient alteration of mechanisms regulating OPC self-renewal and differentiation.
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Lorenzati, M., Boda, E., Parolisi, R., Bonato, M., Borsello, T., Herdegen, T., Buffo, A., & Vercelli, A. (2021). c-Jun N-terminal kinase 1 (JNK1) modulates oligodendrocyte progenitor cell architecture, proliferation and myelination. Scientific Reports, 11(1), 7264. https://doi.org/10.1038/s41598-021-86673-6 Cite
An analogous truncated mouse prolactin receptor (mPRLr) was found to be oncogenic when co-expressed with wild-type mPRLr. The authors determined if a similar transforming event occurs with the hPRLr in human breast epithelial cells.
[npj Breast Cancer]
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Tumor necrosis factor‐α‐induced protein 8‐like 2 suppressed nonalcoholic fatty liver disease (NAFLD) advancement by blocking transforming growth factor‐beta‐activated kinase 1‐c‐Jun NH2‐terminal kinase/p38 pathway and was a promising target molecule for NAFLD therapy.
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Liu, Y., Song, J., Yang, J., Zheng, J., Yang, L., Gao, J., Tian, S., Liu, Z., Meng, X., Wang, J.-C., Dai, Z., & Tang, Y.-D. (n.d.). Tumor necrosis factor-α-induced protein 8-like 2 alleviates nonalcoholic fatty liver disease via suppressing TAK1 activation. Hepatology, n/a(n/a). https://doi.org/https://doi.org/10.1002/hep.31832 Cite
Scientists compared PANC-1 and MIA PaCa-2 pancreatic cancer cells which are, respectively, resistant and sensitive to MEK- and PI3K-targeted therapy.
[Biochemical and Biophysical Research Communications]
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Aguilar-Valdés, A., Noriega, L. G., Tovar, A. R., Ibarra-Sánchez, M. de J., Sosa-Hernández, V. A., Maravillas-Montero, J. L., & Martínez-Aguilar, J. (2021). SWATH-MS proteomics of PANC-1 and MIA PaCa-2 pancreatic cancer cells allows identification of drug targets alternative to MEK and PI3K inhibition. Biochemical and Biophysical Research Communications, 552, 23–29. https://doi.org/10.1016/j.bbrc.2021.03.018 Cite
Researchers showed that, dasatinib in melanoma stimulated its proper mechanism of resistance, independently of MAPK and PI3K/AKT pathway reactivation commonly associated to secondary c-Kit mutations, but through CRTC3/MITF/Bcl-2 pathway activation at clinically relevant doses.
[Molecular Cancer Research]
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Researchers showed that exposure of endothelial cells to exosome-enriched airway basal cell extracellular vesicles (EVs) promoted the survival of these cells and that this effect also involved VEGFR2 activation and is, at least in part, mediated by VEGFA present in the EVs.
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Saxena, A., Walters, M. S., Shieh, J.-H., Shen, L.-B., Gomi, K., Downey, R. J., Crystal, R. G., & Moore, M. A. S. (2021). Extracellular vesicles from human airway basal cells respond to cigarette smoke extract and affect vascular endothelial cells. Scientific Reports, 11(1), 6104. https://doi.org/10.1038/s41598-021-85534-6 Cite
Colon cancer cell lines were treated with different doses of tectoridin, Then, CCK8 and clone formation experiments were performed to detect cell proliferation.
[Molecular and Cellular Biochemistry]
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