Title:Regulation of Ion Channels, Cellular Carriers and Na(+)/K(+)/ATPase by Janus Kinase 3
Volume: 24
Issue: 21
Author(s): Mentor Sopjani*, Shpëtim Thaçi, Berat Krasniqi, Miranda Selmonaj, Mark Rinnerthaler and Miribane Dërmaku-Sopjani*
Affiliation:
- 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
Keywords:
JAK3, JAK-STAT, cellular transport, ion channels, membrane carriers, Na+/K+-ATPase.
Abstract: Janus kinase-3 (JAK3), a tyrosine kinase, is expressed in a variety of tissues, including
the brain and is involved in the signaling of cytokine receptors. JAK3 participates in numerous
functions, such as cell survival and proliferation, neuroprotection, apoptosis and the
cellular response to hypoxia and ischemia-reperfusion. This kinase further contributes to the
signaling of hematopoietic cell cytokine receptors, activation of dendritic cells, maturation,
and immune suppression as well as to cell volume regulation. Recently, JAK3 has been demonstrated
to be an important regulator of transport processes across the plasma membrane. Either
directly or indirectly JAK3 affects the expression of transport proteins, including various
ion channels, a number of cellular carriers and the Na+/K+ pump. More specifically, JAK3 is
involved in the regulation of various potassium, sodium, and chloride ion channels, a wide
variety of Na+-coupled cellular carriers including the high-affinity Na+ coupled glucose transporter
SGLT1, the excitatory amino acid transporters EAAT1, EAAT2, EAAT3 and EAAT4,
the peptide transporters PepT1 and PepT2, CreaT1 and theNa+/K+-ATPase. Via these transporters
this kinase plays a role in various physiological and pathophysiological processes. Additional
research is needed to investigate the effects of JAK3 on other cellular transporters and
the underlying mechanisms.
