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These channels are insensitive to changes in membrane potential and are activated solely by rises in the intracellular Ca\n                    <jats:sup>2+<\/jats:sup>\n                    . According to the phylogenic research done on the K\n                    <jats:sub>Ca<\/jats:sub>\n                    2.x channels family, there are three channels' subtypes: K\n                    <jats:sub>Ca<\/jats:sub>\n                    2.1, K\n                    <jats:sub>Ca<\/jats:sub>\n                    2.2, and K\n                    <jats:sub>Ca<\/jats:sub>\n                    2.3, which are encoded by\n                    <jats:italic>KCNN1<\/jats:italic>\n                    ,\n                    <jats:italic>KCNN2<\/jats:italic>\n                    , and\n                    <jats:italic>KCNN3<\/jats:italic>\n                    genes, respectively. The K\n                    <jats:sub>Ca<\/jats:sub>\n                    2.x channels regulate neuronal excitability and responsiveness to synaptic input patterns. K\n                    <jats:sub>Ca<\/jats:sub>\n                    2.x channels inhibit excitatory postsynaptic potentials (EPSPs) in neuronal dendrites and contribute to the medium afterhyperpolarization (mAHP) that follows the action potential bursts. Multiple brain regions, including the hippocampus, express the K\n                    <jats:sub>Ca<\/jats:sub>\n                    2.2 channel encoded by the\n                    <jats:italic>KCNN<\/jats:italic>\n                    2 gene on chromosome 5. Of particular interest, rat cerebellar Purkinje cells express K\n                    <jats:sub>Ca<\/jats:sub>\n                    2.2 channels, which are crucial for various cellular processes during development and maturation. Patients with a loss\u2010of\u2010function of\n                    <jats:italic>KCNN2<\/jats:italic>\n                    mutations typically exhibit extrapyramidal symptoms, cerebellar ataxia, motor and language developmental delays, and intellectual disabilities. Studies have revealed that autosomal dominant neurodevelopmental movement disorders resembling rodent symptoms are caused by heterozygous loss\u2010of\u2010function mutations, which are most likely to induce\n                    <jats:italic>KCNN2<\/jats:italic>\n                    haploinsufficiency. The K\n                    <jats:sub>Ca<\/jats:sub>\n                    2.2 channel is a promising drug target for spinocerebellar ataxias (SCAs). SCAs exhibit the dysregulation of firing in cerebellar Purkinje cells which is one of the first signs of pathology. Thus, selective K\n                    <jats:sub>Ca<\/jats:sub>\n                    2.2 modulators are promising potential therapeutics for SCAs.\n                  <\/jats:p>","DOI":"10.1002\/jnr.25233","type":"journal-article","created":{"date-parts":[[2023,7,19]],"date-time":"2023-07-19T09:50:39Z","timestamp":1689760239000},"page":"1699-1710","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":13,"title":["<scp>\n                      K\n                      <sub>Ca<\/sub>\n                      2\n                    <\/scp>\n                    .2 (\n                    <scp>\n                      <i>KCNN2<\/i>\n                    <\/scp>\n                    ): A physiologically and therapeutically important potassium channel"],"prefix":"10.1002","volume":"101","author":[{"given":"Mohammad Asikur","family":"Rahman","sequence":"first","affiliation":[{"name":"Department of Biomedical and Pharmaceutical Sciences Chapman 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