In yes-associated protein (YAP)S127A-induced tumorigenesis, a gradual replacement of liver sinusoidal endothelial cells by continuous endothelial cells was associated with dynamic changes in the expression of genes involved in paracrine communication.
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Thomann, S., Weiler, S. M. E., Marquard, S., Rose, F., Ball, C. R., Tóth, M., Wei, T., Sticht, C., Fritzsche, S., Roessler, S., Torre, C. D. L., Ryschich, E., Ermakova, O., Mogler, C., Kazdal, D., Gretz, N., Glimm, H., Rempel, E., Schirmacher, P., & Breuhahn, K. (2020). YAP orchestrates heterotypic endothelial cell communication via HGF/c-MET signaling in liver tumorigenesis. Cancer Research. https://doi.org/10.1158/0008-5472.CAN-20-0242 Cite
M2 macrophage-derived exosomal miR-590-3p reduced inflammatory signals and promoted epithelial regeneration by targeting LATS1 and subsequently activating YAP/β-catenin-regulated transcription
[Journal of Crohns & Colitis]
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M2 macrophage-derived exosomal-miR-590-3p attenuates DSS-induced mucosal damage and promotes epithelial repair via the LATS1/YAP/β-catenin signalling axis | Journal of Crohn’s and Colitis | Oxford Academic. (n.d.). Retrieved October 20, 2020, from https://academic.oup.com/ecco-jcc/advance-article-abstract/doi/10.1093/ecco-jcc/jjaa214/5930684?redirectedFrom=fulltext Cite
Progesterone supplementation enhanced cardiomyocyte proliferation in a progesterone receptor‐dependent manner. Progesterone up‐regulated YAP expression and knockdown of YAP by small interfering RNA reduced progesterone‐mediated cardiomyocyte proliferative effect.
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Lan, C., Cao, N., Chen, C., Qu, S., Fan, C., Luo, H., Zeng, A., Yu, C., Xue, Y., Ren, H., Li, L., Wang, H., Jose, P. A., Xu, Z., & Zeng, C. (n.d.). Progesterone, via yes-associated protein, promotes cardiomyocyte proliferation and cardiac repair. Cell Proliferation, n/a(n/a), e12910. https://doi.org/10.1111/cpr.12910 Cite
Overexpression of activated ERBB2 in cardiomyocytes presented an epithelial-mesenchymal transition-like regenerative response manifested by cytoskeletal remodeling, junction dissolution, migration and ECM turnover.
[Nature Cell Biology]
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Aharonov, A., Shakked, A., Umansky, K. B., Savidor, A., Genzelinakh, A., Kain, D., Lendengolts, D., Revach, O.-Y., Morikawa, Y., Dong, J., Levin, Y., Geiger, B., Martin, J. F., & Tzahor, E. (2020). ERBB2 drives YAP activation and EMT-like processes during cardiac regeneration. Nature Cell Biology, 1–11. https://doi.org/10.1038/s41556-020-00588-4 Cite
ATR-defective cells were defective in neuronal migration during development and in metastatic dissemination from circulating tumor cells.
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Kidiyoor, G. R., Li, Q., Bastianello, G., Bruhn, C., Giovannetti, I., Mohamood, A., Beznoussenko, G. V., Mironov, A., Raab, M., Piel, M., Restuccia, U., Matafora, V., Bachi, A., Barozzi, S., Parazzoli, D., Frittoli, E., Palamidessi, A., Panciera, T., Piccolo, S., … Foiani, M. (2020). ATR is essential for preservation of cell mechanics and nuclear integrity during interstitial migration. Nature Communications, 11(1), 4828. https://doi.org/10.1038/s41467-020-18580-9 Cite
The authors investigated the anti-tumor functions and the feasible molecular basis of nitidine chloride in NSCLC cells.
[Cell Death Discovery]
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The authors performed a dual-luciferase-based, genome-wide E3 ligase siRNA library screen and identified ASB13 as an E3 ubiquitin ligase that targeted SNAI2 for ubiquitination and degradation.
[Genes & Development]
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Scientists performed genetic manipulation of Yes-Associated Protein (YAP) in human-derived neuroblastoma cell lines to investigate YAP function in key aspects of the malignant phenotype, including mesenchymal properties, tumor growth, chemotherapy response, and MEK inhibitor response.
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Shim, J., Lee, J. Y., Jonus, H. C., Arnold, A., Schnepp, R. W., Janssen, K. M., Maximov, V., & Goldsmith, K. C. (2020). YAP-mediated repression of HRK regulates tumor growth, therapy response, and survival under tumor environmental stress in neuroblastoma. Cancer Research. https://doi.org/10.1158/0008-5472.CAN-20-0025 Cite
The authors clarify the unique consequences of YAP/TAZ activation in the ductal cell population of the pancreas by generating mice with pancreatic duct cell-specific, inducible knockouts of Lats1 and Lats2, the main kinases upstream of YAP/TAZ.
Researchers found that disturbance of the E-cadherin-based adherens junction triggered the nuclear translocation and activation of YAP-1/YAP in the gut of worms. Although YAP is a major downstream effector of the Hippo signaling, their study revealed that the activation of YAP-1/YAP was independent of the Hippo pathway during disruption of intestinal barrier.
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Adult cardiac fibroblasts were freshly isolated and cultured on ECM topographical mimetics for 72 hours. Aligned mimetics caused cardiac fibroblasts to elongate while randomly organized topographies induced circular morphology similar to the disparate myofibroblast morphologies measured in vivo.
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Bugg Darrian, Bretherton Ross C, Kim Peter, Olszewski Emily, Nagle Abigail, Schumacher Austin E, Chu Nickolas, Gunaje Jagadambika, DeForest Cole A, Stevens Kelly, Kim Deok-Ho, & Davis Jennifer M. (n.d.). Infarct Collagen Topography Regulates Fibroblast Fate Via p38-Yap-TEAD Signals. Circulation Research, 0(0). https://doi.org/10.1161/CIRCRESAHA.119.316162 Cite