v24

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Homo sapiens (human) B3GALT5 antisense RNA 1 (B3GALT5-AS1) URS000075B4E2_9606

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B3GALT5-AS1: B3GALT5-AS1 is a long non-coding RNA (lncRNA) that has been studied for its regulatory role in gene expression. Dual luciferase reporter assays and depletion mapping assays have shown that B3GALT5-AS1 inhibits the promoter activity of miR-203, and this inhibition is dependent on the interaction region [PMC6326654]. Furthermore, binding sites have been identified between the sequences of B3GALT5-AS1 and CSNK2A1 [PMC8281446]. B3GALT5-AS1 is a long non-coding RNA (lncRNA) that has been found to play a role in gene regulation. It has been shown to inhibit the promoter activity of miR-203, a microRNA involved in various cellular processes [PMC6326654]. This inhibition is dependent on the interaction region between B3GALT5-AS1 and miR-203 [PMC6326654]. Additionally, binding sites have been identified between B3GALT5-AS1 and CSNK2A1, a gene encoding for casein kinase 2 alpha 1 subunit [PMC8281446]. This suggests that B3GALT5-AS1 may interact with CSNK2A1 to regulate its expression or function. These findings highlight the regulatory role of B3GALT5-AS1 in gene expression. By inhibiting miR-203 promoter activity and potentially interacting with CSNK2A1, B3GALT5-AS1 may contribute to the fine-tuning of cellular processes controlled by these genes. Overall, these studies provide insights into the molecular mechanisms by which B3GALT5-AS1 regulates gene expression and suggest potential therapeutic targets for further investigation.

Genome locations

Gene Ontology annotations

Sequence

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GACGCGGCGGGCGGCUCCGGGAGGCGACGGGACCCCCAGGCCGGCAGCCGAGUGAAGAGGCAGGAACUGUCUACAAAUGCUCCGGCUCCGAAGCCCCGAGGGAAAGAGCAUCUUUCACGGAGCACCAGGAAUUGACGACGGUGGAAUUUGCUCAGAUCCCCUGAGGCCGGUUCUUUGAGUUUCUGUCUGGCCCUCCGGGAGAACCGUCCCAAAGUUAACUUUGAAAACACUCACAGGAGAGGGAAGGCUGUGGGGUCCUUCGCUUCUCAAACCCCAGAUGCCCCCGGAAAGAACACCGCCCCCGACCACCACCACAACCAGAUGUUUUUAAAAAGAGAUGCUAAGCAAAAGGCCUGAUUAUGAGGAAUGAGCCAAAGUCAUGCAAGGCGUGGGGCGCUAUGGGACUGCGCAGUGACGACCCAGUGAAGUAGAUGCCUUGACGAUUCCCAUUUCACGGAUGAGACGACUCCGGCACAGAGAAGUCAGAGGGCCUGUCCUGGGUCACACAGCCACAGGCGGCCCCCAGAACGGGACUUCAGGGUGCACCACUGCACCCCAGCAGAGACCUCCGCCUGGCACACAGGGAAUGCUGGAGCAAUACUUAAAUAGGGGAGGUCAGAAAUCUCACGGGCUCUGCUGGCUUCUGUGCUUCGUCUCUCAAGGCCAAAAUCAAGAUGUCAUCAGUGCUGAGCUCUGGUGCAGGAUCCACGUCCAGGCUCACUGGGGCUGCUGGCAGAAUUCAGCUGUGUGGGGUUGUAGGAAUGAAGUCCUUGUUUCCUUGCUGGCUGUUGGCCAGGGGCUGCCCUCAGCUUCUGGAGGCCGCCUGCCCUCCCUGGUUCAUGGCCCAUCUCAUCCUGACAGCCAGCACCCGCGGGAAGUCCCUCUUGCACUGUGACUCUCUCCCGCCUCUUCCAUUCUCUAUGGCUUGUCUGCCUCCCUCUUUCAUCUUUAAGAGUGCAUGUGAGUAUAUUGGACCUACCUGAAUCAGCCAGGCUAACCUCCCCAUUUUAAGGUCUGCAGCCUUAAUUCUACCUGCAAAGUCCCUUUUGCCAUGUAAUGUGCCAUAUUCACAGGUGUCAGGAAUCAGAGGGCAGGUAUAUUGGGGGACCAUUAUUCUGCCAACUACACAGGGCCUUAUAUGGUCUGGCUCUGUGUCCCCAUUCAAAUCUCAUCUUGAAUUGUAAUCCGAAUUGUAACCCCCACGUGUUGGGGGGAGGGACCUUGUGGGAGGUAAUUAAAUCAUGGGGGCGGUUACCCUCAUGCUGUUCUUGUGAUAGUGAGUGAGUUCUCACGAGAUCUGAAGGUUUUGCAAGGAGCUUUUCCCCCUUUUGCUCAGGACUCUCCUUCCUGCAGCCAAGUGAAGGACAAGUUUGCUUCCCCUUCCACAAUGAUUGUAAGUUUCUUGAGGCCUCUCCAGAACUAUGAGUCAAUUAAACCUCUUUCCUUUAUAAAAAAAAAAAAAAAAAAAA

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Publications