Special Issue "Nuclear Transport in Ageing and Diseases"
Deadline for manuscript submissions: 15 November 2018
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
Manuscript Submission Information
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- nuclear envelope
- nuclear pore complex
- nucleocytoplasmic transport
The below list represents only planned manuscripts. Some of these manuscripts have not been received by the Editorial Office yet. Papers submitted to MDPI journals are subject to peer-review.
Type of Paper: Review
Tentative Title: In and out: Therapeutic targeting of protein translocation
Authors: Friederike K. Kosyna, Reinhard Depping
Affiliations: University of Luebeck, Center for Structural and Cell Biology in Medicine, Institute of Physiology, Germany, Friederike.Kosyna@uni-luebeck.de
Abstract: Nuclear transport receptors of the Karyopherin superfamily of proteins transport macromolecules from the cytoplasm into the nucleus 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 discuss nuclear transport inhibitors and their clinical implications.
Tentative Title: Progeria HGPS -Current Knowledge and Prospects for Treatment
Authors: Katarzyna Grabowska*, Magdalena Machowska*, Katarzyna Piekarowicz*, Ryszard Rzepecki#
*- first joined author; # - corresponding author
Affiliations: Laboratory of Nuclear Proteins, Faculty of Biotechnology, University of Wroclaw, Fryderyka Joliot-Curie 14a, 50-383, Wroclaw, Poland
Abstract: Hutchison-Gilford Progeria Syndrome (HGPS) (OMIM 176670), is the most severe disorder characterized by the presence of aging-associated symptoms, including lack of subcutaneous fat, alopecia, swollen vein, growth retardation, age spot, joint contractures, osteoporosis, cardiovascular pathology, and death due to heart attacks and strokes in childhood. HGPS belongs to laminopathies, a heterogeneous group of disorders gathering genetic disorders with molecular background based on mutations in LMNA gene and genes coding for interacting proteins such as EMD. LMNA gene codes for two major alternatively spliced transcripts, giving rise to lamin A and lamin C proteins. Mutations in single LMNA gene, depending on nature and location, may result in expression of abnormal protein or loss of protein expression and cause different disease phenotypes such as EDMD2 (Emery-Dreifuss muscular dystrophy, OMIM 181350 , DCM (dilated cardiomyopathy, OMIM 115200), LGMD1B (limb girdle muscular dystrophy type 1B, OMIM 159001), FPLD (Dunnigan familial partial lipodystrophy, OMIM 151660), APL (acquired partial lipodystrophy, Barraquer-Simons syndrome, OMIM 608709), CMT2B1 (Charcot–Marie–Tooth disorder, type 2B1, OMIM 605588), ADLD (adult-onset autosomal dominant leukodystrophy, OMIM 169500), AWS (atypical Werner syndrome, OMIM 277700), MAD (mandibuloacral dysplasia, OMIM 248370), RD (restrictive dermopathy, OMIM 275210) and HGPS. In this review we discuss current knowledge on the molecular mechanisms underlying the development of the HGPS progeria disease and provide a critical analyses of current research trends in this field. We also discuss current status of treatment of the disease and future prospect for the development of efficient therapy including gene therapy for HGPS.