Abstract
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.
Keywords: Carrier, cellular transport, hormones, ion channel, JAK2, Na+/K+ pump.
Current Medicinal Chemistry
Title:The Relevance of JAK2 in the Regulation of Cellular Transport
Volume: 23 Issue: 6
Author(s): Mentor Sopjani, Vjollca Konjufca, Mark Rinnerthaler, Rexhep Rexhepaj and Miribane Dërmaku-Sopjani
Affiliation:
Keywords: Carrier, cellular transport, hormones, ion channel, JAK2, Na+/K+ pump.
Abstract: 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.
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Sopjani Mentor, Konjufca Vjollca, Rinnerthaler Mark, Rexhepaj Rexhep and Dërmaku-Sopjani Miribane, The Relevance of JAK2 in the Regulation of Cellular Transport, Current Medicinal Chemistry 2016; 23 (6) . https://dx.doi.org/10.2174/0929867323666151207111707
DOI https://dx.doi.org/10.2174/0929867323666151207111707 |
Print ISSN 0929-8673 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-533X |
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