EGFR endocytosis: more than meets the eye

Sapmaz, Ayşegül; Erson-Bensan, Ayşe Elif

doi:10.18632/oncotarget.28400

Cited by 2 publications

References 33 publications

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Rme-6 integrates EGFR trafficking and signalling to regulate ERK1/2 signalosome dynamics

Smythe

Alshahrani

Zhu

et al. 2023

Preprint

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Epidermal growth factor receptor (EGFR) signalling results in a variety of cell behaviours, including cell proliferation, migration and apoptosis, which depend on cell context. Here we have explored how the Rab5GEF, Rme-6, regulates EGFR signalling by modulating endocytic flux. We demonstrate that Rme-6, which acts early in the endocytic pathway, regulates EGFR trafficking through an endocytic compartment that is competent for ERK1/2 signalling. While overexpression of Rme-6 results in enhanced ERK1/2 nuclear localisation and c-Fos activation, loss of Rme-6 results in aberrant ERK1/2 signalling with increased cytoplasmic ERK1/2 phosphorylation (Thr202/Tyr204) but decreased ERK1/2 nuclear translocation and c-Fos activation, the latter leading to decreased cell proliferation. Phosphorylation of ERK1/2 by protein kinase 2 (CK2) is required for its nuclear translocation and our data support a model whereby Rme-6 provides a scaffold for a population of CK2 which is required for efficient nuclear translocation of ERK1/2. Rme-6 is itself a substrate for CK2 on Thr642 and Ser996 and phosphorylation on these sites can activate its Rab5GEF activity and endocytic trafficking of EGFR. Together our results indicate that that Rme-6 co-ordinates EGFR trafficking and signalling to regulate the assembly and disassembly of an ERK1/2 signalosome.

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Rme-6 integrates EGFR trafficking and signalling to regulate ERK1/2 signalosome dynamics

Smythe

Alshahrani

Zhu

et al. 2023

Preprint

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Hepatitis B virus entry, assembly, and egress

Chuang,

2024

Microbiol Mol Biol Rev

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SUMMARY Hepatitis B virus (HBV) is an important human pathogen that chronically infects approximately 250 million people in the world, resulting in ~1 million deaths annually. This virus is a hepatotropic virus and can cause severe liver diseases including cirrhosis and hepatocellular carcinoma. The entry of HBV into hepatocytes is initiated by the interaction of its envelope proteins with its receptors. This is followed by the delivery of the viral nucleocapsid to the nucleus for the release of its genomic DNA and the transcription of viral RNAs. The assembly of the viral capsid particles may then take place in the nucleus or the cytoplasm and may involve cellular membranes. This is followed by the egress of the virus from infected cells. In recent years, significant research progresses had been made toward understanding the entry, the assembly, and the egress of HBV particles. In this review, we discuss the molecular pathways of these processes and compare them with those used by hepatitis delta virus and hepatitis C virus , two other hepatotropic viruses that are also enveloped. The understanding of these processes will help us to understand how HBV replicates and causes diseases, which will help to improve the treatments for HBV patients.

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EGFR endocytosis: more than meets the eye

Cited by 2 publications

References 33 publications

Rme-6 integrates EGFR trafficking and signalling to regulate ERK1/2 signalosome dynamics

Rme-6 integrates EGFR trafficking and signalling to regulate ERK1/2 signalosome dynamics

Hepatitis B virus entry, assembly, and egress

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