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Homo sapiens (human) PKIA antisense RNA 1 (PKIA-AS1) URS00007E4AE0_9606

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PKIA-AS1: PKIA-AS1 is a long non-coding RNA (lncRNA) that has been found to play a role in neuropathic pain (NP) [PMC7225849]. Studies have shown that the silencing of PKIA-AS1 can attenuate NP by downregulating the expression of cyclin-dependent kinase 6 (CDK6) in the spinal cord tissues of a rat model of spinal nerve ligation (SNL) [PMC6815541]. PKIA-AS1 has been found to be highly expressed in the SNL rat model, along with other lncRNAs such as SNHG4, STAC3, and CIRBP-AS1 [PMC8722684]. Overexpression of PKIA-AS1 can induce NP-like symptoms in uninjured rats, while knockdown of PKIA-AS1 can attenuate SNL-induced NP progression [PMC8733285]. PKIA-AS1 has been shown to regulate CDK6 expression and function, which is essential for neuroinflammation and NP [PMC6401634]. Inhibition of PKIA-AS1 decreases CDK6 expression and alleviates SNL-induced NP [PMC9668864]. Furthermore, knockdown of PKIA-AS1 inhibits the activation of astrocytes and microglia as well as the expression of proinflammatory cytokines associated with neuroinflammation and NP [PMC6401634][PMC9823062]. Overall, these findings suggest that PKIA-AS1 is a potential therapeutic target for neuroinflammation associated with NP.

Genome locations

Gene Ontology annotations

Sequence

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AUCGUCUCUUGCCGCUGCCAUGAAAGGAGUGCUUUUUGCCUCCCACCAUGAUUCUGAGGCCUCCCCAGCCAUGUAGAAUUAGCCAGCCUGUUUUUGAUGAAGAGCAACUGUACUGGAGAGAAAGCCUGUAUUCAUAUUCAUCGUCAUCAGGCAAAUCGAGGAGCUGACUUGCUUAGGAUCAUCUGCUGGUUGAAUCCAUGGAUGCAGAACCCCAGAUUCGGAGGGCUGAAUGUACUUUCGAUAGGUUCCUGAGCAGCAGUGAUUAUAGUCACAGCAGACUGGACAGUUUGGUGAGCAAGUUCAGGGGCUGGCUUAGUGAUUCAUAGUUCUUUCUUCCUCCUCCCCCAGCAGUUUUGUUUCAGCAGUGAUUUGGUCAAAUGUGAACCACAAACCAGCAGCAAAAGCAUUUUCUAGGAACUUGUUAAAACUGGAAGGCCCAAGGUUGCACUCAGGCUUACUGAGUCAGUCACUCCAAGUGGACCCCAUCCCUAAACCUUGAGACUCACUGCUCCUCUUUUGAUCUGGGAGAGAAACAGAAAAAAGAAGGAAAAAAAAUCCCCAAUGUGAGUAUGCUGGAAAGUAAAUUUGAAUAGCUUUUUAUAUUGGGUACUUACUGUGGGUAAUUUACAAACUAUUGGAAGGAACCACAAAUUCAAACACAGCCAAAUUUAAGGUCUCUUUAGCAGAAAUCAAUCUUACAUCAUGGCAGUUCUCCCAUUCUCCAGUCUUUCACUUGAUAGAUCACUUCCUCAUUAGGAUGACCUACAGCAAUUCUACAUGAACUGCUCUUUACAUUUAAACAGUGCUUUCUGUCCUAACAUGUCAAAAUGCUUGACAAGCAAUCAAAAGGUAGCUCACUAAUUUUUUCAACUCAUGGCAGUAAAUAGCCUGCAUCUACCAUCACUGCUGUUUACUGGUGAUUUCUUGGCAGGGAAACUUUAAAUGCCUUAGCAAUGUCUAGAAAGUCAAUGACUAAAGAAAAUAUUCAUUUUGGCUUCCAUAGGGCUGUAUUUGAUGAACUGCUCACUAACUUCUAUUAUUACGUCUCAAGAAUAGAUAAUGAUACUCAGCAAGGGCAAAUCCCAAAGAAUAGUCUAUGCUUUCCUUGAUUGAAUCUGAUUUUUGAGAAAUUACAUGGCCCAAUCUACAUUUAAUAUGAUACAAAUGCUACUUAACUCCCUGUUAUUUCUGGUUGCAUAUAAUUGAUACUACUUGAAGAGUAAGAAGCAGAGUCUCACUACACUGGGGACCCUUUGAGAGCCAAGUCUGUGUCUUAGUCAUCUUUGAUGCCUUAGUGACCAGUACCAUACCUGGAAUAGUAUAUGUGAUCAGUAACUCAAAUGUAUGUAUUUCUUGAAUGUAUGGUGCAUGAAUGAGUCAAGAUACCUUUAGCGUUGGAAGCAAUCUGUCAUGGAGUAGGAGGAGAAAAAGUAGUGAAAAAACUUCUAAAUUCUCAAAACCUAGUGCUGAACUGAAUGCUGAUAAUAACUUGACAACGUCCUUUGGCAUUGCAGAUGUUGAGAUACCAACAUCUAAUCCGCCAAGAAAGAAUUUCAGAAUUAAAAUUUGGGUGUGUUCUUGCGCUGGGGAUUUCUCUGACCUACCUUCUGAUAGAACUUUGAACCCGAGUCAAUAGUCAAUAUACUAGUUUUUUACUUAAAACUGUAACAUUUUAAUCUAAUUUUGGAGACGUGAAAUAAAACUGAUGGGAAACUCUUGAAAUUUUUAUCACUGGAAUAACCUAAUUUUGAAAACACUGAUGGUUAGUUUCUUGAAAUAUUAAUAUUACUACAAGUCAUAAGUAAAAGCAUUCUAUCUUAAGUGAGAAACUAUAAAGUUGGAUAAUUACUAUUUGAGUUUGUGGCUUGGUUUGAAUAAACACUUGCUUGUUUUAAGUAAAAGUUCAGCUGAAGUGACAAUCAACCUUUAAUCUUGUAAAGCUUCUGUGUUAGAUAUUUUCUAUCUCUAACAUGCCAAACAUGCAUAUUAAACUGAGUUUUUUUGCAUGCAAAAAAAAAAAAAAAAAAAA

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Publications