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The human genome has 15 genes that code for potassium channels with a two-pore domain (K2P-channels). Four transmembrane domains (M1–M4), two pore domains (P1 and P2), and two helical cap domains (C1 and C2) make up the K2P-channel subunits. Of the five K2P-channel subfamilies, the acid-sensitive potassium channels TASK-1, TASK-3, and TASK-5 are one. The three TASK channels share more than 50% of their amino acids. The heart, the adrenal gland, the central and peripheral neurological systems, as well as many other tissues, depend on TASK-1 and TASK-3 for proper function. The other member of the TASK subfamily, TASK-5, lacks any known functional features.

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Overview of TASK

  • TASK channels in oncology

Potassium channels play a significant role in the signaling pathways that control cell growth and death. Human lymphocytes, embryonic stem cells, melanoma, hepatocarcinoma, glioma, small cell lung, breast, and prostate cancer cells have all showed decreased cell growth when these channels are inhibited. One K2P family member, TASK3, was discovered to be a novel proto-oncogene in breast cancer when it was demonstrated that it was amplified 3–10-fold in 10% of human breast cancer samples. In addition, it was discovered that 10% to 50% of breast cancer, lung cancer, and colorectal cancer cells overexpressed TASK3.

  • TASK channels and ischemia

In clinical practice, neuronal damage brought on by ischemia or inflammatory events is a significant contributor to death and permanent impairment. The function of K2P channels during cellular stress is unknown and controversially addressed. When potassium channels are activated, the resulting membrane hyperpolarization has significant effects on how neurons function and survive. For example, reduced metabolic requirement due to decreased neural activity may improve neuronal survival in stressful situations. The focus of study to date has been on the alleged neuroprotective function of TREK and TASK channels. When the intracellular pH value is reduced, as in ischemia or inflammation, the open probability of TREK1 and TREK2 channels is significantly increased.

  • TASK channels in inflammation

Key participants in the pathophysiology of autoimmune illnesses like MS, rheumatoid arthritis (RA), and type I diabetes mellitus are human T cells. Although the underlying pathophysiological mechanisms of these disorders are still not fully known, it has been proposed that ion channels play a significant role in T lymphocyte activities. In the context of T cell activation, three members of the K2P family—TASK1, TASK2, and TASK3—could be identified and functionally defined. As TASK1, TASK2, and TASK3 are expressed constitutively in human, rat, and mouse T cells, pharmacological inhibition reduces the production of cytokines and the proliferation of T cell-stimulated lymphocytes.

  • TASK channels in epilepsy

A typical feature of the chronic neurological illness epilepsy is the development of localized or generalized bouts of neuronal discharges on their own. Alterations in synaptic transmission, regulation of transmembrane K+ gradients, and activity-dependent changes in extracellular pH levels have all been linked to certain forms of frontal, generalized, and infantile seizure disorders. Numerous K2P subtypes in neurons and glia cells have been researched in relation to their potential involvement in the development of and adaptation to epilepsy because K2P channels are highly regulated by pH.


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