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Cells
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Cell Biology: State-of-the-Art and Perspectives in Australia
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Cell Biology: State-of-the-Art and Perspectives in Australia

A special issue of Cells (ISSN 2073-4409).

Deadline for manuscript submissions: closed (1 July 2023) | Viewed by 5393

Special Issue Editors

Prof. Dr. David A. Jans

E-Mail Website
Guest Editor
1. Nuclear Signalling Lab, Infection and Immunity Program, Monash Biomedicine Discovery Institute, Clayton, Australia
2. Department of Biochemistry and Molecular Biology, Monash University, Clayton, Australia
Interests: regulation of nucleocytoplasmic transport; viral infection; stress biology
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Jeremy M. Crook

E-Mail Website
Guest Editor
1. Biomedical Innovation, Chris O`Brien Lifehouse, Camperdown, NSW 2050, Australia
2. School of Medical Sciences, Faculty of Medicine and Health, University of Sydney, Camperdown, NSW 2006, Australia
Interests: stem cell biology; cancer cell biology; neurobiology; biomaterials; electroceuticals; organoids; tissue engineering; bioprinting; regenerative medicine
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear colleagues,

This Special Issue aims to provide a comprehensive overview of the state-of-the-art of cell biology in Australia. We invite research papers that will consolidate our understanding in this area. The Special Issue will publish full research articles and comprehensive reviews. Potential topics include, but are not limited to, the following research areas:

  • OMICS: transcriptomics, genomics, proteomics, metabolomics, glycomics, lipidomics, interactomics, fluxomics, and biomics;
  • Cell structure: organelles, cytoskeleton, cell membrane, capsule, flagella, etc.;
  • Cell physiology: cell growth, metabolism, protein synthesis, division, movement of proteins, active/passive transport, intra- and extracellular signaling, adhesion, DNA repair, etc.;
  • Cell movement and motility;
  • Autophagy;
  • Apoptosis;
  • PANoptosis;
  • Cell aging;
  • Cell techniques: cell and tissue culture, isolation, and fractionation of cells, immunocytochemistry (ICC), in situ hybridization (ISH), transfection, and optogenetics;
  • Cell growth and differentiation;
  • Hematopoiesis and stem cells;
  • Cancer stem cells;
  • Genetic disorders;
  • CAR-T cell research.

Prof. Dr. David A. Jans
Prof. Dr. Jeremy M. Crook
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Published Papers (2 papers)

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Research

17 pages, 6509 KiB  
Article
Multifaceted Roles of Retromer in EGFR Trafficking and Signaling Activation
by Zhe Yang, Zhengyang Feng, Zebin Li and Rohan D. Teasdale
Cells 2022, 11(21), 3358; https://doi.org/10.3390/cells11213358 - 25 Oct 2022
Viewed by 1702
Abstract
Mammalian retromer complex contributes to multiple early endosome-associated trafficking pathways whose origins are dependent on which sorting nexin (SNX) they are complexed with. In an attempt to dissect out the contribution of individual retromer–SNX complexes, we examined the trafficking of EGFR in detail [...] Read more.
Mammalian retromer complex contributes to multiple early endosome-associated trafficking pathways whose origins are dependent on which sorting nexin (SNX) they are complexed with. In an attempt to dissect out the contribution of individual retromer–SNX complexes, we examined the trafficking of EGFR in detail within a series of KO cell line models. We demonstrated that the depletion of retromer subunit Vps35 leads to decreased EGFR protein levels in resting cells with enhanced association of EGFR with lysosomal compartments. Compared to control cells, the addition of EGF to Vps35 KO cells resulted in a reduced rate of EGFR degradation; AKT activation and cell prolferation rates were elevated, while ERK activation remained relatively unchanged. These observations are consistent with a prolonged temporal association of EGFR within early endosomes due to the inefficiency of early endosome-associated protein trafficking pathways or organelle maturation due to retromer absence. We did not fully delineate the discrete contributions from retromer-associated SNXs to the phenotypes observed from retromer Vps35 depletion. While each of the knock-outs of SNX1/2, SNX3, or SNX27 promotes the enhanced association of EGFR with early endosomal compartments, only the decreased EGF-mediated EGFR degradation was observed in SNX1/2 dKO cells, while the enhanced AKT activation was only increased in SNX3 KO or SNX27 KO cells. Despite this, each of the knock-outs showed increased EGF-stimulated cell proliferation rates. Full article
(This article belongs to the Special Issue Cell Biology: State-of-the-Art and Perspectives in Australia)
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27 pages, 9122 KiB  
Article
Hydrocephalus in Nfix−/− Mice Is Underpinned by Changes in Ependymal Cell Physiology
by Danyon Harkins, Tracey J. Harvey, Cooper Atterton, Ingrid Miller, Laura Currey, Sabrina Oishi, Maria Kasherman, Raul Ayala Davila, Lucy Harris, Kathryn Green, Hannah Piper, Robert G. Parton, Stefan Thor, Helen M. Cooper and Michael Piper
Cells 2022, 11(15), 2377; https://doi.org/10.3390/cells11152377 - 02 Aug 2022
Cited by 1 | Viewed by 3096
Abstract
Nuclear factor one X (NFIX) is a transcription factor required for normal ependymal development. Constitutive loss of Nfix in mice (Nfix−/−) is associated with hydrocephalus and sloughing of the dorsal ependyma within the lateral ventricles. Previous studies have implicated NFIX [...] Read more.
Nuclear factor one X (NFIX) is a transcription factor required for normal ependymal development. Constitutive loss of Nfix in mice (Nfix−/−) is associated with hydrocephalus and sloughing of the dorsal ependyma within the lateral ventricles. Previous studies have implicated NFIX in the transcriptional regulation of genes encoding for factors essential to ependymal development. However, the cellular and molecular mechanisms underpinning hydrocephalus in Nfix−/− mice are unknown. To investigate the role of NFIX in hydrocephalus, we examined ependymal cells in brains from postnatal Nfix−/− and control (Nfix+/+) mice using a combination of confocal and electron microscopy. This revealed that the ependymal cells in Nfix−/− mice exhibited abnormal cilia structure and disrupted localisation of adhesion proteins. Furthermore, we modelled ependymal cell adhesion using epithelial cell culture and revealed changes in extracellular matrix and adherens junction gene expression following knockdown of NFIX. Finally, the ablation of Nfix from ependymal cells in the adult brain using a conditional approach culminated in enlarged ventricles, sloughing of ependymal cells from the lateral ventricles and abnormal localisation of adhesion proteins, which are phenotypes observed during development. Collectively, these data demonstrate a pivotal role for NFIX in the regulation of cell adhesion within ependymal cells of the lateral ventricles. Full article
(This article belongs to the Special Issue Cell Biology: State-of-the-Art and Perspectives in Australia)
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