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Long noncoding RNA inflammatory and mucous response associated, antisense to ICAM1 (LIMASI, also called LASI or AC011511.2), is a nuclear/perinuclear-expressed lncRNA transcribed from the antisense strand of the ICAM-1 gene locus. It is upregulated in human airway epithelial cells in response to inflammatory stimuli such as lipopolysaccharide (LPS) and interleukin-13 (IL-13). Increased LASI expression is observed in asthma, particularly in goblet cells producing mucus (MUC5AC-positive). Functionally, LASI modulates both inflammatory mediator (IL-6, CXCL8) and mucin (MUC5AC) gene expression in airway epithelial cells. Knockdown of LASI impairs the LPS- and IL-13-induced upregulation of these genes, indicating its role in coordinating inflammatory and mucous hypersecretory responses in the airway epithelium. No drugs are reported to target LIMASI/LASI directly; however, it is a potential biomarker and regulator of pathological airway inflammation and mucus production.
Not applicable (no drugs target this lncRNA directly; its modulation affects ICAM1, IL-6, CXCL8, MUC5AC at the transcriptional level)
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