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Cells
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Nuclear Transport in Ageing and Diseases
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Nuclear Transport in Ageing and Diseases

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cell Nuclei: Function, Transport and Receptors".

Deadline for manuscript submissions: closed (30 April 2019) | Viewed by 54167

Special Issue Editor

Dr. Bor Luen Tang

E-Mail Website
Guest Editor
Department of Biochemistry, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore
Interests: membrane trafficking; neuronal death and regeneration; SIRT1 and aging
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The eukaryotic genome is physically and functionally partitioned from the rest of the cell by a nuclear envelope. A myriad of bidirectional RNA/protein transport and signalling processes between the plasma membrane-cytoplasm and the genetic blueprint-bearing nucleus occur through the nuclear pore complexes. Dynamic nuclear–cytoplasm communication underlies the physiological and homeostatic regulation of gene expression, as well as protein/organelle biogenesis in cells. Impairment of nuclear envelope integrity and nucleocytoplasmic transport processes have been implicated in a number of pathological conditions, such as aging, cardiovascular diseases, neurodegenerative disorders and cancer.

In this Special Issue of Cells, we invite your contributions, either in the form of original research articles, reviews, or shorter perspective articles on all aspects related to the theme of “Nuclear–Cytoplasmic Transport in Aging and Diseases”. Articles with mechanistic and functional insights from a cell and molecular biological perspective are especially welcome. Relevant topics include, but are not limited to

  • nuclear import and export transporters and mechanisms
  • nuclear pore complex and Nucleoporins
  • nucleocytoplasmic transport in cellular signalling
  • nucleocytoplasmic transport in aging
  • nuclear envelope and RNA/protein transport impairment in neurodegenerative disorders
  • nucleocytoplasmic transport in viral infection and diseases

Dr. Bor Luen Tang
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

  • importins/exportins
  • lamins
  • nuclear envelope
  • nuclear pore complex
  • nucleocytoplasmic transport
  • nucleoporins

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Published Papers (5 papers)

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Research

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15 pages, 2863 KiB  
Article
Novel Flavivirus Antiviral That Targets the Host Nuclear Transport Importin α/β1 Heterodimer
by Sundy N. Y. Yang, Sarah C. Atkinson, Johanna E. Fraser, Chunxiao Wang, Belinda Maher, Noelia Roman, Jade K. Forwood, Kylie M. Wagstaff, Natalie A. Borg and David A. Jans
Cells 2019, 8(3), 281; https://doi.org/10.3390/cells8030281 - 24 Mar 2019
Cited by 39 | Viewed by 8146
Abstract
Dengue virus (DENV) threatens almost 70% of the world’s population, with no effective vaccine or therapeutic currently available. A key contributor to infection is nuclear localisation in the infected cell of DENV nonstructural protein 5 (NS5) through the action of the host importin [...] Read more.
Dengue virus (DENV) threatens almost 70% of the world’s population, with no effective vaccine or therapeutic currently available. A key contributor to infection is nuclear localisation in the infected cell of DENV nonstructural protein 5 (NS5) through the action of the host importin (IMP) α/β1 proteins. Here, we used a range of microscopic, virological and biochemical/biophysical approaches to show for the first time that the small molecule GW5074 has anti-DENV action through its novel ability to inhibit NS5–IMPα/β1 interaction in vitro as well as NS5 nuclear localisation in infected cells. Strikingly, GW5074 not only inhibits IMPα binding to IMPβ1, but can dissociate preformed IMPα/β1 heterodimer, through targeting the IMPα armadillo (ARM) repeat domain to impact IMPα thermal stability and α-helicity, as shown using analytical ultracentrifugation, thermostability analysis and circular dichroism measurements. Importantly, GW5074 has strong antiviral activity at low µM concentrations against not only DENV-2, but also zika virus and West Nile virus. This work highlights DENV NS5 nuclear targeting as a viable target for anti-flaviviral therapeutics. Full article
(This article belongs to the Special Issue Nuclear Transport in Ageing and Diseases)
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Review

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23 pages, 1048 KiB  
Review
Viral Appropriation: Laying Claim to Host Nuclear Transport Machinery
by Tanner M. Tessier, Mackenzie J. Dodge, Martin A. Prusinkiewicz and Joe S. Mymryk
Cells 2019, 8(6), 559; https://doi.org/10.3390/cells8060559 - 8 Jun 2019
Cited by 20 | Viewed by 8203
Abstract
Protein nuclear transport is an integral process to many cellular pathways and often plays a critical role during viral infection. To overcome the barrier presented by the nuclear membrane and gain access to the nucleus, virally encoded proteins have evolved ways to appropriate [...] Read more.
Protein nuclear transport is an integral process to many cellular pathways and often plays a critical role during viral infection. To overcome the barrier presented by the nuclear membrane and gain access to the nucleus, virally encoded proteins have evolved ways to appropriate components of the nuclear transport machinery. By binding karyopherins, or the nuclear pore complex, viral proteins influence their own transport as well as the transport of key cellular regulatory proteins. This review covers how viral proteins can interact with different components of the nuclear import machinery and how this influences viral replicative cycles. We also highlight the effects that viral perturbation of nuclear transport has on the infected host and how we can exploit viruses as tools to study novel mechanisms of protein nuclear import. Finally, we discuss the possibility that drugs targeting these transport pathways could be repurposed for treating viral infections. Full article
(This article belongs to the Special Issue Nuclear Transport in Ageing and Diseases)
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22 pages, 915 KiB  
Review
Hutchinson-Gilford Progeria Syndrome—Current Status and Prospects for Gene Therapy Treatment
by Katarzyna Piekarowicz, Magdalena Machowska, Volha Dzianisava and Ryszard Rzepecki
Cells 2019, 8(2), 88; https://doi.org/10.3390/cells8020088 - 25 Jan 2019
Cited by 40 | Viewed by 16135
Abstract
Hutchinson-Gilford progeria syndrome (HGPS) is one of the most severe disorders among laminopathies—a heterogeneous group of genetic diseases with a molecular background based on mutations in the LMNA gene and genes coding for interacting proteins. HGPS is characterized by the presence of aging-associated [...] Read more.
Hutchinson-Gilford progeria syndrome (HGPS) is one of the most severe disorders among laminopathies—a heterogeneous group of genetic diseases with a molecular background based on mutations in the LMNA gene and genes coding for interacting proteins. HGPS is characterized by the presence of aging-associated symptoms, including lack of subcutaneous fat, alopecia, swollen veins, growth retardation, age spots, joint contractures, osteoporosis, cardiovascular pathology, and death due to heart attacks and strokes in childhood. LMNA codes for two major, alternatively spliced transcripts, give rise to lamin A and lamin C proteins. Mutations in the LMNA gene alone, depending on the nature and location, may result in the expression of abnormal protein or loss of protein expression and cause at least 11 disease phenotypes, differing in severity and affected tissue. LMNA gene-related HGPS is caused by a single mutation in the LMNA gene in exon 11. The mutation c.1824C > T results in activation of the cryptic donor splice site, which leads to the synthesis of progerin protein lacking 50 amino acids. The accumulation of progerin is the reason for appearance of the phenotype. In this review, we discuss current knowledge on the molecular mechanisms underlying the development of HGPS and provide a critical analysis of current research trends in this field. We also discuss the mouse models available so far, the current status of treatment of the disease, and future prospects for the development of efficient therapies, including gene therapy for HGPS. Full article
(This article belongs to the Special Issue Nuclear Transport in Ageing and Diseases)
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20 pages, 1910 KiB  
Review
NUP214 in Leukemia: It’s More than Transport
by Adélia Mendes and Birthe Fahrenkrog
Cells 2019, 8(1), 76; https://doi.org/10.3390/cells8010076 - 21 Jan 2019
Cited by 48 | Viewed by 9185
Abstract
NUP214 is a component of the nuclear pore complex (NPC) with a key role in protein and mRNA nuclear export. Chromosomal translocations involving the NUP214 locus are recurrent in acute leukemia and frequently fuse the C-terminal region of NUP214 with SET and DEK, [...] Read more.
NUP214 is a component of the nuclear pore complex (NPC) with a key role in protein and mRNA nuclear export. Chromosomal translocations involving the NUP214 locus are recurrent in acute leukemia and frequently fuse the C-terminal region of NUP214 with SET and DEK, two chromatin remodeling proteins with roles in transcription regulation. SET-NUP214 and DEK-NUP214 fusion proteins disrupt protein nuclear export by inhibition of the nuclear export receptor CRM1, which results in the aberrant accumulation of CRM1 protein cargoes in the nucleus. SET-NUP214 is primarily associated with acute lymphoblastic leukemia (ALL), whereas DEK-NUP214 exclusively results in acute myeloid leukemia (AML), indicating different leukemogenic driver mechanisms. Secondary mutations in leukemic blasts may contribute to the different leukemia outcomes. Additional layers of complexity arise from the respective functions of SET and DEK in transcription regulation and chromatin remodeling, which may drive malignant hematopoietic transformation more towards ALL or AML. Another, less frequent fusion protein involving the C terminus of NUP214 results in the sequestosome-1 (SQSTM1)-NUP214 chimera, which was detected in ALL. SQSTM1 is a ubiquitin-binding protein required for proper autophagy induction, linking the NUP214 fusion protein to yet another cellular mechanism. The scope of this review is to summarize the general features of NUP214-related leukemia and discuss how distinct chromosomal translocation partners can influence the cellular effects of NUP214 fusion proteins in leukemia. Full article
(This article belongs to the Special Issue Nuclear Transport in Ageing and Diseases)
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18 pages, 1743 KiB  
Review
Controlling the Gatekeeper: Therapeutic Targeting of Nuclear Transport
by Friederike K. Kosyna and Reinhard Depping
Cells 2018, 7(11), 221; https://doi.org/10.3390/cells7110221 - 21 Nov 2018
Cited by 61 | Viewed by 11193
Abstract
Nuclear transport receptors of the karyopherin superfamily of proteins transport macromolecules from one compartment to the other and are critical for both cell physiology and pathophysiology. The nuclear transport machinery is tightly regulated and essential to a number of key cellular processes since [...] Read more.
Nuclear transport receptors of the karyopherin superfamily of proteins transport macromolecules from one compartment to the other and are critical for both cell physiology and pathophysiology. The nuclear transport machinery is tightly regulated and essential to a number of key cellular processes since the spatiotemporally expression of many proteins and the nuclear transporters themselves is crucial for cellular activities. Dysregulation of the nuclear transport machinery results in localization shifts of specific cargo proteins and associates with the pathogenesis of disease states such as cancer, inflammation, viral illness and neurodegenerative diseases. Therefore, inhibition of the nuclear transport system has future potential for therapeutic intervention and could contribute to the elucidation of disease mechanisms. In this review, we recapitulate clue findings in the pathophysiological significance of nuclear transport processes and describe the development of nuclear transport inhibitors. Finally, clinical implications and results of the first clinical trials are discussed for the most promising nuclear transport inhibitors. Full article
(This article belongs to the Special Issue Nuclear Transport in Ageing and Diseases)
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