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| http://dx.doi.org/10.1038/cr.2011.122 | DOI Listing |
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Transient activation of YAP/TAZ confers resistance to morusin-induced apoptosis.
BMC Mol Cell Biol
January 2025
Department of Biological Sciences, Sungkyunkwan University, Suwon, 16419, Republic of Korea.
Background: The Hippo signaling pathway involves a kinase cascade that controls phosphorylation of the effector proteins YAP and TAZ, leading to regulation of cell growth, tissue homeostasis, and apoptosis. Morusin, a compound extracted from Morus alba, has shown potential in cancer therapy by targeting multiple signaling pathways, including the PI3K/Akt/mTOR, JAK/STAT, MAPK/ERK, and apoptosis pathways. This study explores the effects of morusin on YAP activation and its implications for apoptosis resistance.
View Article and Find Full Text PDFLive-cell FRET assay on the stoichiometry and affinity of the YAP complexes in MCF-7 cells.
Arch Biochem Biophys
January 2025
Department of Pain Management, the First Affiliated Hospital of Jinan University, Guangzhou, 510630, China. Electronic address:
Yes-associated protein (YAP), a focal point of current biological research, is involved in regulating various life processes. In this report, live-cell fluorescence resonance energy transfer (FRET) imaging was employed to unravel the YAP complexes in MCF-7 cells. Fluorescence imaging of living cells co-expressing CFP (cyan fluorescent protein)-YAP and YFP (yellow fluorescent protein)-LATS1 (large tumor suppressor 1) plasmids revealed that YAP promoted LATS1 oligomerization around mitochondria.
View Article and Find Full Text PDFDoublecortin-like kinase 1 promotes stem cell-like properties through the Hippo-YAP pathway in prostate cancer.
Int J Med Sci
January 2025
Department of Urology, Kidney and Urology Center, the Seventh Affiliated Hospital of Sun Yat-Sen University, Shenzhen, China.
Doublecortin-like kinase 1 (DCLK1) has been revealed to be involved in modulating cancer stemness and tumor progression, but its role in prostate cancer (PCa) remains obscure. Castration-resistant and metastatic PCa exhibit aggressive behaviors, and current therapeutic approaches have shown limited beneficial effects on the overall survival rate of patients with advanced PCa. This study aimed to investigate the biological role and potential molecular mechanism of DCLK1 in the progression of PCa.
View Article and Find Full Text PDFD-ribose-5-phosphate inactivates YAP and functions as a metabolic checkpoint.
J Hematol Oncol
January 2025
Department of Radiation Oncology, Henan Provincial Key Laboratory of Radiation Medicine, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, Henan, People's Republic of China.
Background: Targeting glucose uptake by glucose transporter (GLUT) inhibitors is a therapeutic opportunity, but efforts on GLUT inhibitors have not been successful in the clinic and the underlying mechanism remains unclear. We aim to identify the key metabolic changes responsible for cancer cell survival from glucose limitation and elucidate its mechanism.
Methods: The level of phosphorylated YAP was analyzed with Western blotting and Phos-tag immunoblotting.
CDK5 interacts with MST2 and modulates the Hippo signalling pathway.
FEBS Open Bio
December 2024
Center for Drug Research, Ludwig-Maximilians-University Munich, Germany.
MST2 (STK3) is a major upstream kinase in the Hippo signalling pathway, an evolutionary conserved pathway in regulation of organ size, self-renewal and tissue homeostasis. Its downstream effectors are the transcriptional regulators YAP and TAZ. This pathway is regulated by a variety of factors, such as substrate stiffness or cell-cell contacts.
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