ijms-logo

Journal Browser

Journal Browser

Special Issue "Gene Networks That Control Cell Proliferation and Differentiation"

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Genetics and Genomics".

Deadline for manuscript submissions: closed (31 December 2020).

Special Issue Editor

Prof. Dr. Bhagwati Gupta
Website1 Website2
Guest Editor
McMaster University, Faculty of Science, Hamilton, Canada
Interests: developmental genetics; molecular biology; molecular genetics; genomics; disease models; cell signaling; organ formation; neurobiology; gene networks; cell proliferation and differentiation; evolution of developmental mechanisms

Special Issue Information

Dear Colleagues,

Cell proliferation and differentiation are fundamental processes in multicellular eukaryotes. The regulation of these events is not only crucial to generate the desired number and diversity of cells during development, but also throughout life for processes such as tissue repair. Research in animal models has led to the discovery of a large number of genes that function to control cell division, and these cells ultimately differentiate to form different parts of the body. Many of the identified genes are shown to form regulatory networks and encode components of evolutionarily conserved signal transduction pathways. Functional studies have revealed that alterations in gene regulation and pathway activities can affect the ability of cells to divide and differentiate, which could cause diseases and lead to premature death of the animal. Hence, a comprehensive understanding of gene interactions and regulatory networks is needed to advance biomedical discoveries to treat illnesses. The Special Issue “Gene Networks That Control Cell Proliferation and Differentiation” of the International Journal of Molecular Sciences will include original research articles and reviews describing molecular mechanisms of processes in both normal and disease contexts. Studies using a wide range of genetic, cell biological, molecular, genome-wide, and bioinformatic approaches are encouraged.

Prof. Dr. Bhagwati Gupta
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 papers will be 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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • Cell proliferation
  • Cell differentiation
  • Gene function
  • Gene network
  • Signaling

Published Papers (2 papers)

Order results
Result details
Select all
Export citation of selected articles as:

Research

Open AccessArticle
Overexpression of miR-1306-5p, miR-3195, and miR-3914 Inhibits Ameloblast Differentiation through Suppression of Genes Associated with Human Amelogenesis Imperfecta
Int. J. Mol. Sci. 2021, 22(4), 2202; https://doi.org/10.3390/ijms22042202 (registering DOI) - 23 Feb 2021
Abstract
Amelogenesis imperfecta is a congenital form of enamel hypoplasia. Although a number of genetic mutations have been reported in humans, the regulatory network of these genes remains mostly unclear. To identify signatures of biological pathways in amelogenesis imperfecta, we conducted bioinformatic analyses on [...] Read more.
Amelogenesis imperfecta is a congenital form of enamel hypoplasia. Although a number of genetic mutations have been reported in humans, the regulatory network of these genes remains mostly unclear. To identify signatures of biological pathways in amelogenesis imperfecta, we conducted bioinformatic analyses on genes associated with the condition in humans. Through an extensive search of the main biomedical databases, we found 56 genes in which mutations and/or association/linkage were reported in individuals with amelogenesis imperfecta. These candidate genes were further grouped by function, pathway, protein–protein interaction, and tissue-specific expression patterns using various bioinformatic tools. The bioinformatic analyses highlighted a group of genes essential for extracellular matrix formation. Furthermore, advanced bioinformatic analyses for microRNAs (miRNAs), which are short non-coding RNAs that suppress target genes at the post-transcriptional level, predicted 37 candidates that may be involved in amelogenesis imperfecta. To validate the miRNA–gene regulation association, we analyzed the target gene expression of the top seven candidate miRNAs: miR-3195, miR-382-5p, miR-1306-5p, miR-4683, miR-6716-3p, miR-3914, and miR-3935. Among them, miR-1306-5p, miR-3195, and miR-3914 were confirmed to regulate ameloblast differentiation through the regulation of genes associated with amelogenesis imperfecta in AM-1 cells, a human ameloblastoma cell line. Taken together, our study suggests a potential role for miRNAs in amelogenesis imperfecta. Full article
(This article belongs to the Special Issue Gene Networks That Control Cell Proliferation and Differentiation)
Show Figures

Figure 1

Open AccessArticle
Developmental Roles of FUSE Binding Protein 1 (Fubp1) in Tooth Morphogenesis
Int. J. Mol. Sci. 2020, 21(21), 8079; https://doi.org/10.3390/ijms21218079 - 29 Oct 2020
Abstract
FUSE binding protein 1 (Fubp1), a regulator of the c-Myc transcription factor and a DNA/RNA-binding protein, plays important roles in the regulation of gene transcription and cellular physiology. In this study, to reveal the precise developmental function of Fubp1, we [...] Read more.
FUSE binding protein 1 (Fubp1), a regulator of the c-Myc transcription factor and a DNA/RNA-binding protein, plays important roles in the regulation of gene transcription and cellular physiology. In this study, to reveal the precise developmental function of Fubp1, we examined the detailed expression pattern and developmental function of Fubp1 during tooth morphogenesis by RT-qPCR, in situ hybridization, and knock-down study using in vitro organ cultivation methods. In embryogenesis, Fubp1 is obviously expressed in the enamel organ and condensed mesenchyme, known to be important for proper tooth formation. Knocking down Fubp1 at E14 for two days, showed the altered expression patterns of tooth development related signalling molecules, including Bmps and Fgf4. In addition, transient knock-down of Fubp1 at E14 revealed changes in the localization patterns of c-Myc and cell proliferation in epithelium and mesenchyme, related with altered tooth morphogenesis. These results also showed the decreased amelogenin and dentin sialophosphoprotein expressions and disrupted enamel rod and interrod formation in one- and three-week renal transplanted teeth respectively. Thus, our results suggested that Fubp1 plays a modulating role during dentinogenesis and amelogenesis by regulating the expression pattern of signalling molecules to achieve the proper structural formation of hard tissue matrices and crown morphogenesis in mice molar development. Full article
(This article belongs to the Special Issue Gene Networks That Control Cell Proliferation and Differentiation)
Show Figures

Figure 1

Back to TopTop