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| http://dx.doi.org/10.1038/jid.2013.162 | DOI Listing |
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Sleep drive is coupled to tissue damage via shedding of Caenorhabditis elegans EGFR ligand SISS-1.
Nat Commun
December 2024
Department of Biology, California State University Northridge, Northridge, CA, USA.
The benefits of sleep extend beyond the nervous system. Peripheral tissues impact sleep regulation, and increased sleep is observed in response to damaging conditions, even those that selectively affect non-neuronal cells. However, the 'sleep need' signal released by stressed tissues is not known.
View Article and Find Full Text PDFLow-affinity ligands of the epidermal growth factor receptor are long-range signal transmitters in collective cell migration of epithelial cells.
Cell Rep
November 2024
Department of Pathology and Biology of Diseases, Graduate School of Medicine, Kyoto University, Yoshida-Konoe-Cho, Sakyo-ku, Kyoto 606-8501, Japan; Graduate School of Medicine, Tokushima University, Shinkura-cho, Tokushima 770-8501, Japan. Electronic address:
Article Synopsis
- The study explores how low-affinity EGFR ligands, specifically epiregulin (EREG), activate the EGFR in cells during processes like collective cell migration.
- It reveals that during this migration, certain patterns of signal activation occur that depend on the shedding of EGFR ligands and the structural integrity of cell junctions.
- The absence of EREG in mice leads to slower ERK wave propagation and less effective cell movement, suggesting that low-affinity ligands are crucial for quick signaling between cells.
Fully human monoclonal antibody targeting the cysteine-rich substrate-interacting region of ADAM17 on cancer cells.
Biomed Pharmacother
November 2024
Structural Biology Program, Memorial Sloan Kettering Cancer Center, New York, NY 10065, United States. Electronic address:
Article Synopsis
- * One selective antibody fragment, C12, was developed into a full IgG and was shown to bind effectively to ADAM17, preventing the activation of cancer cell pathways by inhibiting EGFR phosphorylation.
- * C12 demonstrated anti-tumor effects by reducing the viability of various EGFR-expressing cancer cells and inhibiting tumor growth in an ovarian cancer model, with imaging confirming its presence at tumor sites.
Heparin-binding EGF-like growth factor via miR-126 controls tumor formation/growth and the proteolytic niche in murine models of colorectal and colitis-associated cancers.
Cell Death Dis
October 2024
Division of Stem Cell Dynamics, Center for Stem Cell Biology and Regenerative Medicine, The Institute of Medical Science, The University of Tokyo, 4-6-1 Shirokanedai, Minato-ku, Tokyo, 108-8639, Japan.
MicroRNAs, including the tumor-suppressor miR-126 and the oncogene miR-221, regulate tumor formation and growth in colitis-associated cancer (CAC) and colorectal cancer (CRC). This study explores the impact of the epithelial cytokine heparin-binding epidermal growth factor (HB-EGF) and its receptor epidermal growth factor receptor (EGFR) on the pathogenesis of CAC and CRC, particularly in the regulation of microRNA-driven tumor growth and protease expression. In murine models of CRC and CAC, lack of miR-126 and elevated miR-221 expression in colonic tissues enhanced tumor formation and growth.
View Article and Find Full Text PDFEpidermal growth factor receptor ligands (EGFRLs) consist of seven proteins. In stark contrast to the amassed knowledge concerning the epidermal growth factor receptors themselves, the extracellular dynamics of individual EGFRLs remain elusive. Here, employing fluorescent probes and a tool for triggering ectodomain shedding of EGFRLs, we show that EREG, a low-affinity EGFRL, exhibits the most rapid and efficient activation of EGFR in confluent epithelial cells and mouse epidermis.
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