Members of the ezrin-radixin-moesin (ERM) protein family serve as regulated microfilament-membrane crosslinking proteins that, upon activation, bind the scaffolding protein ERM-phosphoprotein of 50 kDa (EBP50). Here we report a 3.5 A resolution diffraction analysis of a complex between the active moesin N-terminal FERM domain and a 38 residue peptide from the C terminus of EBP50. This crystallographic result, combined with sequence and structural comparisons, suggests that the C-terminal 11 residues of EBP50 binds as an alpha-helix at the same site occupied in the dormant monomer by the last 11 residues of the inhibitory moesin C-terminal tail. Biochemical support for this interpretation derives from in vitro studies showing that appropriate mutations in both the EBP50 tail peptide and the FERM domain reduce binding, and that a peptide representing just the C-terminal 14 residues of EBP50 also binds to moesin. Combined with the recent identification of the I-CAM-2 binding site on the ERM FERM domain (Hamada, K., Shimizu, T., Yonemura, S., Tsukita, S., and Hakoshima, T. (2003) EMBO J. 22, 502-514), this study reveals that the FERM domain contains two distinct binding sites for membrane-associated proteins. The contribution of each ligand to ERM function can now be dissected by making structure-based mutations that specifically affect the binding of each ligand.
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http://dx.doi.org/10.1242/jcs.01038 | DOI Listing |
FASEB J
December 2024
Department of Laboratory Medicine, Shanghai Chest Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, People's Republic of China.
Metastasis is the leading cause of mortality from esophageal squamous cell carcinoma (ESCC). By the time of diagnosis, most ESCC tumors have already invaded the lymph nodes or distant organs; however, it has been challenging to identify and confirm genes with a crucial role in ESCC metastasis. The microfibrillar-associated protein 2 (MFAP2) is upregulated in human ESCC, and its expression level was positively associated with poor overall and disease-free survival.
View Article and Find Full Text PDFNat Commun
November 2024
Roy J. Carver Department of Biochemistry, Biophysics & Molecular Biology, Iowa State University, 2437 Pammel Drive, Ames, IA, 50011, USA.
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View Article and Find Full Text PDFJ Virol
December 2024
Guangdong Key Laboratory of Animal Conservation and Resource Utilization, Institute of Zoology, Guangdong Academy of Sciences, Guangzhou, Guangdong, China.
Viral nervous necrosis caused by the nervous necrosis virus (NNV) poses a significant threat to the global aquaculture industry. Developing preventive methods to minimize economic losses due to NNV infections is crucial. This study explored the role of the sorting nexin 27 () gene, encoded by the orange-spotted grouper () and referred to as , as an immune regulator affecting red-spotted grouper nervous necrosis virus (RGNNV) infection .
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UCD Diabetes Complications Research Centre, Conway Institute, UCD School of Medicine, University College Dublin, Dublin 4, Ireland.
Int J Mol Sci
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Laboratory of Neurogenetics and Molecular Medicine, Center for Genomic Sciences in Medicine, Institut de Recerca Sant Joan de Déu, 08950 Barcelona, Spain.
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