The Relevance of JAK2 in the Regulation of Cellular Transport.

Curr Med Chem

Department of Chemistry, Faculty of Natural Sciences and Mathematics, University of Prishtina. Str. Mother Teresa, p.n. 10 000, Prishtina, Kosova.

Published: November 2016

Janus kinase-2 (JAK2) is a non-receptor tyrosine kinase signaling molecule that mediates the effects of various hormones and cytokines, including interferon, erythropoietin, leptin, and growth hormone. It also fosters tumor growth and modifies the activity of several nutrient transporters. JAK2 contributes to the regulation of the cell volume, protectS cells during energy depletion, proliferation, and aids the survival of tumor cells. Recently, JAK2 was identified as a powerful regulator of transport processes across the plasma membrane. Either directly or indirectly JAK2 may stimulate or inhibit transporter proteins, including ion channels, carriers and Na(+)/K(+) pumps. As a powerful regulator of transport mechanisms across the cell membrane, JAK2 regulates a wide variety of potassium, calcium, sodium and chloride ion channels, multiple Na+-coupled cellular carriers including EAAT1-4, NaPi-IIa, SGLT1, BoaT1, PepT1-2, CreaT1, SMIT1, and BGT1 as well as Na(+)/K(+)-ATPase. These cellular transport regulations contribute to various physiological and pathophysiological processes and thus exerting JAK2-sensitive effects. Future investigations will be important to determine whether JAK2 regulates cell-surface expression of other transporters and further elucidate underlying mechanisms governing JAK2 actions.

Download full-text PDF

Source
http://dx.doi.org/10.2174/0929867323666151207111707DOI Listing

Publication Analysis

Top Keywords

cellular transport
8
powerful regulator
8
regulator transport
8
ion channels
8
jak2 regulates
8
jak2
7
relevance jak2
4
jak2 regulation
4
regulation cellular
4
transport
4

Similar Publications

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!