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Topical Collection "Emerging Genetic and Genomic Mechanisms in Cell Death and Cell Proliferation "

Editors

Prof. Dr. Muralidhar L. Hegde
E-Mail Website1 Website2
Collection Editor
1. Associate Professor, Houston Methodist Research Institute, Houston, TX 77030, USA
2. Adjunct Associate Professor of Neurology, Weill Medical College of Cornell University, New York, NY, USA
3. Adjunct Faculty, INDICASAT, Panama
Adjunct Faculty, Texas A & M University Graduate Program, College Station, TX, USA
Houston Methodist Hospital, 6550 Fannin, Smith 8-05,Houston, TX 77030, USA
Interests: DNA damage responses; neurodegenerative diseases; DNA repair defects; RNA binding proteins in DNA repair; genome instability in cell death and proliferation
Special Issues and Collections in MDPI journals
Prof. Dr. George Perry
E-Mail Website
Collection Editor
College of Sciences, University of Texas at San Antonio, San Antonio, TX 79249, USA
Interests: mechanism of formation and physiological consequences of the cytopathology of Alzheimer disease; the mechanism for RNA-based redox metal binding; the consequences of RNA oxidation on protein synthesis rate and fidelity; the role of redox active metals in mediating prooxidant and antioxidant properties; the signal transduction pathways altered in Alzheimer disease that allow neurons to evade apoptosis; mechanism of phosphorylation control of oxidative damage to neurofilament proteins
Special Issues and Collections in MDPI journals
Prof. Istvan Boldogh
E-Mail Website
Collection Editor
Professor, Department of Microbiology & Immunology, Director of Cell Biology Core Laboratory, Department of Microbiology, NIEHS Center and Sealy Center for Environmental Health & Medicine, Sealy Center for Molecular Medicine, UTMB, Galveston, TX, USA
Interests: targeting inducible epigenetic reprogramming pathways
Prof. Dr. Chong Li
E-Mail Website
Co-Guest Editor
1: Director of Medical Immunodiagnostic Research Center, Institute of Biophysics, Chinese Academy of Sciences, Beijing, China
2: Adjunct Faculty, INDICASAT AIP, Panama
Interests: Cancer; Tumor Immunology and Antibody Drugs; Immunotherapy
Prof. Dr. K.S Jagannatha Rao
E-Mail Website
Co-Guest Editor
Director and Distinguished Professor, INDICASAT AIP, Building 208, City of Knowledge, Republic of Panama
Interests: Genome instability; aging; neurodegeneration

Topical Collection Information

Dear Colleagues,

Despite an enormous upsurge in our understanding of the cellular and molecular pathways associated with cell death and proliferation, the key molecular determinants to modulate these processes in human diseases is still not revealed completely, hindering the development of effective treatments and prevention avenues for aging, neurodegeneration, and cancer. Growing evidence suggests that neurodegenerative diseases occur less frequently in cancer survivors, and vice versa; however, the mechanistic basis for such an inverse comorbidity relation is unclear. While it is known that cancer and neurodegeneration share many common pathways, the implications/responses for these pathways in proliferating and quiescent cells are obviously different. Recent high-throughput genetic and genomic technologies have enabled genome-scale, multidimensional investigations to facilitate a better understanding of the underlying shared mechanisms and the identification of novel targets. Molecular insights gained through such systems genomics and gene network modeling approaches have provided an opportunity to compare the similarities and differences in cell death and cell proliferation. One area of research, which received great attention in this decade, is altered DNA damage responses (DDR), which play a central role in both neurodegenerative diseases. Persistent genome damage and DDR signaling has diverse cellular implications in both cycling and post-mitotic cells. Notably, several factors linked to genome maintenance are at a crossroads between neurodegeneration and cancer, underscoring their overlapping biology. A number of recent studies have highlighted link between defects in DNA repair pathways in nuclear and mitochondrial genomes, to both inherited and sporadic forms neurodegenerative diseases and cancers. It is important to note that while cells invoke DDR pathways for survival, paradoxical effects of sustained DDR in promoting senescence include inflammatory signaling as well as apoptosis/ferroptosis, all of which are linked to both cell death and abnormal proliferation. Senescence may have opposing implications in neurodegeneration vs. cancer.

This Special Issue will be a Topical Collection of original articles and focused thematic reviews on “Emerging Genetic and Genomic Mechanisms in Cell Death and Cell Proliferation” and is aimed at comprehensively summarizing recent advances in our understanding of genetic and genomic mechanisms during age-associated neurodegeneration and various cancers to stimulate an in-depth debate on what we can learn from the shared pathways in these two fields and challenges for DDR-targeted intervention strategies. We believe that this compendium of scholarly articles and reviews will not only push the current boundary of our understanding but also guide further research in this direction. Articles focusing on either cancer or neurodegeneration or on common pathways are welcome, with a focus on genetic and genomic pathways. 

Prof. Muralidhar L. Hegde
Prof. George Perry
Prof. Istvan Boldogh
Prof. Dr. K.S Jagannatha Rao
Prof. Dr. Chong Li
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 collection 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.

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Published Papers (2 papers)

2020

Jump to: 2019

Review
Emerging Roles of Estrogen-Regulated Enhancer and Long Non-Coding RNAs
Int. J. Mol. Sci. 2020, 21(10), 3711; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21103711 - 25 May 2020
Cited by 3 | Viewed by 1334
Abstract
Genome-wide RNA sequencing has shown that only a small fraction of the human genome is transcribed into protein-coding mRNAs. While once thought to be “junk” DNA, recent findings indicate that the rest of the genome encodes many types of non-coding RNA molecules with [...] Read more.
Genome-wide RNA sequencing has shown that only a small fraction of the human genome is transcribed into protein-coding mRNAs. While once thought to be “junk” DNA, recent findings indicate that the rest of the genome encodes many types of non-coding RNA molecules with a myriad of functions still being determined. Among the non-coding RNAs, long non-coding RNAs (lncRNA) and enhancer RNAs (eRNA) are found to be most copious. While their exact biological functions and mechanisms of action are currently unknown, technologies such as next-generation RNA sequencing (RNA-seq) and global nuclear run-on sequencing (GRO-seq) have begun deciphering their expression patterns and biological significance. In addition to their identification, it has been shown that the expression of long non-coding RNAs and enhancer RNAs can vary due to spatial, temporal, developmental, or hormonal variations. In this review, we explore newly reported information on estrogen-regulated eRNAs and lncRNAs and their associated biological functions to help outline their markedly prominent roles in estrogen-dependent signaling. Full article
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2019

Jump to: 2020

Article
Carotenoids as Novel Therapeutic Molecules Against Neurodegenerative Disorders: Chemistry and Molecular Docking Analysis
Int. J. Mol. Sci. 2019, 20(22), 5553; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms20225553 - 07 Nov 2019
Cited by 14 | Viewed by 1890
Abstract
Alzheimer’s disease (AD) is the most devastating neurodegenerative disorder that affects the aging population worldwide. Endogenous and exogenous factors are involved in triggering this complex and multifactorial disease, whose hallmark is Amyloid-β (Aβ), formed by cleavage of amyloid precursor protein by β- and [...] Read more.
Alzheimer’s disease (AD) is the most devastating neurodegenerative disorder that affects the aging population worldwide. Endogenous and exogenous factors are involved in triggering this complex and multifactorial disease, whose hallmark is Amyloid-β (Aβ), formed by cleavage of amyloid precursor protein by β- and γ-secretase. While there is no definitive cure for AD to date, many neuroprotective natural products, such as polyphenol and carotenoid compounds, have shown promising preventive activity, as well as helping in slowing down disease progression. In this article, we focus on the chemistry as well as structure of carotenoid compounds and their neuroprotective activity against Aβ aggregation using molecular docking analysis. In addition to examining the most prevalent anti-amyloidogenic carotenoid lutein, we studied cryptocapsin, astaxanthin, fucoxanthin, and the apocarotenoid bixin. Our computational structure-based drug design analysis and molecular docking simulation revealed important interactions between carotenoids and Aβ via hydrogen bonding and van der Waals interactions, and shows that carotenoids are powerful anti-amyloidogenic molecules with a potential role in preventing AD, especially since most of them can cross the blood-brain barrier and are considered nutraceutical compounds. Our studies thus illuminate mechanistic insights on how carotenoids inhibit Aβ aggregation. The potential role of carotenoids as novel therapeutic molecules in treating AD and other neurodegenerative disorders are discussed. Full article
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