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Cells
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Cell Surface Receptors
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Cell Surface Receptors

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Biophysics".

Deadline for manuscript submissions: closed (3 June 2022) | Viewed by 5916

Special Issue Editor

Prof. Dr. Ichiro Maruyama

E-Mail Website
Guest Editor
Okinawa Institute of Science and Technology Graduate University, 1919-1 Tancha, Onna, Kunigami, Okinawa 904-0495, Japan
Interests: cell surface receptors; transmembrane signaling; receptor tyrosine kinases; learning and memory; decision-making; animal behavior
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Single-pass transmembrane cell surface receptors transfer extracellular information into the cytoplasm, and vice versa, across the plasma membrane. Cell–cell communication in a multicellular organism is also achieved through interaction between cell surface receptors and their ligands. More than 1000 such cell surface receptors are found in the human genome and represent the most functionally diverse membrane proteins, which comprise receptor tyrosine kinases, cytokine receptors, immune receptors, Toll-like receptors, receptor tyrosine phosphatases, receptor guanylyl (guanylate) cyclases, receptor serine/threonine kinases, cell adhesion receptors, C-type lectin receptors, etc.

These cell surface receptors consist of an extracellular ligand-binding (sensor) domain and an intracellular signaling domain separated by a transmembrane a-helix. These receptors take part in cell proliferation, differentiation, migration, apoptosis, cell–cell communication, immune response, and neuronal sensation, etc. Hence, malfunctions of the receptors cause diverse diseases, including developmental disease, cancer, diabetes, hematologic disease, autoimmune disease, immunodeficiencies, allergy, infectious disease, dwarfism, hypertension, schizophrenia, inflammation, etc.

This Special Issue will cover all aspects related to cell surface receptors. Both original research articles, reviews, minireviews, or shorter perspective articles are welcome.

Prof. Dr. Ichiro Maruyama
Guest Editor

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.

Keywords

  • activation
  • bitopic membrane protein
  • BMP
  • cadherin
  • cell adhesion
  • c-type lectin-like receptor
  • dephosphorylation
  • development
  • evolution
  • Fc receptor
  • function
  • integrin
  • interferon
  • interleukin
  • intracellular trafficking
  • leptin
  • mechanism
  • phosphorylation
  • protein kinase
  • serine/threonine kinase
  • structure
  • transmembrane signal transduction
  • TGF
  • tumor necrosis factor

Published Papers (2 papers)

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Research

25 pages, 8096 KiB  
Article
Constitutive Occurrence of E:N-cadherin Heterodimers in Adherens Junctions of Hepatocytes and Derived Tumors
by Tiemo Sven Gerber, Dirk Andreas Ridder, Mario Schindeldecker, Arndt Weinmann, Diane Duret, Kai Breuhahn, Peter R. Galle, Peter Schirmacher, Wilfried Roth, Hauke Lang and Beate Katharina Straub
Cells 2022, 11(16), 2507; https://doi.org/10.3390/cells11162507 - 12 Aug 2022
Cited by 4 | Viewed by 2138
Abstract
Cell–cell junctions are pivotal for embryogenesis and tissue homeostasis but also play a major role in tumorigenesis, tumor invasion, and metastasis. E-cadherin (CDH1) and N-cadherin (CDH2) are two adherens junction’s transmembrane glycoproteins with tissue-specific expression patterns in epithelial and [...] Read more.
Cell–cell junctions are pivotal for embryogenesis and tissue homeostasis but also play a major role in tumorigenesis, tumor invasion, and metastasis. E-cadherin (CDH1) and N-cadherin (CDH2) are two adherens junction’s transmembrane glycoproteins with tissue-specific expression patterns in epithelial and neural/mesenchymal cells. Aberrant expression has been implicated in the process of epithelial–mesenchymal transition (EMT) in malignant tumors. We could hitherto demonstrate cis-E:N-cadherin heterodimer in endoderm-derived cells. Using immunoprecipitation in cultured cells of the line PLC as well as in human hepatocellular carcinoma (HCC)-lysates, we isolated E-N-cadherin heterodimers in a complex with the plaque proteins α- and β-catenin, plakoglobin, and vinculin. In confocal laser scanning microscopy, E-cadherin co-localized with N-cadherin at the basolateral membrane of normal hepatocytes, hepatocellular adenoma (HCA), and in most cases of HCC. In addition, we analyzed E- and N-cadherin expression via immunohistochemistry in a large cohort of 868 HCCs from 570 patients, 25 HCA, and respective non-neoplastic liver tissue, and correlated our results with multiple prognostic markers. While E- or N-cadherin were similarly expressed in tumor sites with vascular invasion or HCC metastases, HCC with vascular encapsulated tumor clusters (VETC) displayed slightly reduced E-cadherin, and slightly increased N-cadherin expression. Analyzing The Cancer Genome Atlas patient cohort, we found that reduced mRNA levels of CDH1, but not CDH2 were significantly associated with unfavorable prognosis; however, in multivariate analysis, CDH1 did not correlate with prognosis. In summary, E- and N-cadherin are specific markers for hepatocytes and derived HCA and HCC. E:N-cadherin heterodimers are constitutively expressed in the hepatocytic lineage and only slightly altered in malignant progression, thereby not complying with the concept of EMT. Full article
(This article belongs to the Special Issue Cell Surface Receptors)
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14 pages, 2445 KiB  
Article
A Human In Vitro Model to Study Adenoviral Receptors and Virus Cell Interactions
by Raphael L. Tsoukas, Wolfram Volkwein, Jian Gao, Maren Schiwon, Nora Bahlmann, Thomas Dittmar, Claudia Hagedorn, Eric Ehrke-Schulz, Wenli Zhang, Armin Baiker and Anja Ehrhardt
Cells 2022, 11(5), 841; https://doi.org/10.3390/cells11050841 - 1 Mar 2022
Cited by 7 | Viewed by 2994
Abstract
To develop adenoviral cell- or tissue-specific gene delivery, understanding of the infection mechanisms of adenoviruses is crucial. Several adenoviral attachment proteins such as CD46, CAR and sialic acid have been identified and studied. However, most receptor studies were performed on non-human cells. Combining [...] Read more.
To develop adenoviral cell- or tissue-specific gene delivery, understanding of the infection mechanisms of adenoviruses is crucial. Several adenoviral attachment proteins such as CD46, CAR and sialic acid have been identified and studied. However, most receptor studies were performed on non-human cells. Combining our reporter gene-tagged adenovirus library with an in vitro human gene knockout model, we performed a systematic analysis of receptor usage comparing different adenoviruses side-by-side. The CRISPR/Cas9 system was used to knockout CD46 and CAR in the human lung epithelial carcinoma cell line A549. Knockout cells were infected with 22 luciferase-expressing adenoviruses derived from adenovirus species B, C, D and E. HAdV-B16, -B21 and -B50 from species B1 as well as HAdV-B34 and -B35 were found to be CD46-dependent. HAdV-C5 and HAdV-E4 from species E were found to be CAR-dependent. Regarding cell entry of HAdV-B3 and -B14 and all species D viruses, both CAR and CD46 play a role, and here, other receptors or attachment structures may also be important since transductions were reduced but not completely inhibited. The established human knockout cell model enables the identification of the most applicable adenovirus types for gene therapy and to further understand adenovirus infection biology. Full article
(This article belongs to the Special Issue Cell Surface Receptors)
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