Sopjani Mentor, Konjufca Vjollca, Rinnerthaler Mark, Rexhepaj Rexhep, Dërmaku-Sopjani Miribane
Faculty of Medicine of the University of Prishtina, Str. Bulevardi i Dëshmorëve, p.n. 10 000, Prishtina, Kosova.
Department of Chemistry, Faculty of Natural Sciences and Mathematics, University of Prishtina. Str. Mother Teresa, p.n. 10 000, Prishtina, Kosova.
Curr Med Chem. 2016;23(6):578-88. doi: 10.2174/0929867323666151207111707.
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.
Janus激酶2（JAK2）是一种非受体酪氨酸激酶信号分子，可介导多种激素和细胞因子的作用，包括干扰素、促红细胞生成素、瘦素和生长激素。它还促进肿瘤生长并改变几种营养转运蛋白的活性。JAK2有助于调节细胞体积，在能量消耗、增殖过程中保护细胞，并有助于肿瘤细胞的存活。最近，JAK2被确定为跨质膜转运过程的强大调节因子。JAK2可能直接或间接刺激或抑制转运蛋白，包括离子通道、载体和钠钾泵。作为跨细胞膜转运机制的强大调节因子，JAK2调节多种钾、钙、钠和氯离子通道，多种与钠偶联的细胞载体，包括EAAT1 - 4、NaPi - IIa、SGLT1、BoaT1、PepT1 - 2、CreaT1、SMIT1和BGT1以及钠钾ATP酶。这些细胞转运调节作用参与各种生理和病理生理过程，从而产生对JAK2敏感的效应。未来的研究对于确定JAK2是否调节其他转运蛋白的细胞表面表达以及进一步阐明JAK2作用的潜在机制至关重要。
