Journal Menu► ▼ Journal Menu
Journal Browser► ▼ Journal Browser
Special Issue "Insulin and Insulin Receptor in Diseases"
A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".
Deadline for manuscript submissions: closed (1 August 2018).
Department of Medicine, Georgetown University, Washington, DC 20007, USA
Interests: renal physiology; renal sodium transport; insulin in the kidney; blood pressure regulation; metabolic syndrome; diabetic nephropathy; sex differences in the kidney; renal gluconeogenesis
Endocrinology Section, Department of Clinical and Experimental Medicine, Garibaldi-Nesima Medical Center, University of Catania, Catania, Italy
Interests: insulin receptor isoforms; insulin analogs; intracellular signal transduction of insulin receptor; diabetes and cancer; pregestational diabetes; gestational diabetes; type 1 diabetes
Reduced insulin receptor (Insr) signaling, especially in key metabolic tissues, i.e., the liver, skeletal muscle, and adipose, is associated with type 2 diabetes mellitus due to impaired glucose uptake in cells. However, the Insr may have important roles in other tissues, e.g., vasculature, heart, and kidney with less-defined effects. The human Insr cDNA was first cloned in 1985. The receptor is composed of two subunits: alpha and beta—both derived by the proteolytic processing of a 1382-amino acid pre-proreceptor. Insr signaling proceeds primarily through autophosphorylation on key tyrosine residues with the eventual activation of Akt kinase. On the other hand, phosphorylation of Insr on several serine residues is associated with reduced activation of this signaling cascade.
In addition, the insulin receptor exists in two isoforms (InsrA and InsrB) generated by alternative splicing of the exon 11. The two isoforms may have different tissue expression with different biological effects in several diseases. Dysregulation of the InsrA: InsrB ratio is associated with insulin resistance and increased proliferative activity of normal and neoplastic tissues.
This Special Issue focuses on Insr modifications with disease (expression, post-translational modifications, and downstream signaling), as well as hypothetical, experimental, and tested therapies to restore, alter, or enhance signaling.
We welcome submissions, including original papers and reviews, on this widely-discussed topic.
Assoc. Prof. Carolyn M. Ecelbarger
Assoc. Prof. Laura Sciacca
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.
- metabolic syndrome
- insulin resistance
- type 2 diabetes
- tyrosine-kinase receptor