Inflammatory MKL1 (megakaryoblastic leukemia 1) interacting long noncoding RNA (INKILN)

Inflammatory MKL1 interacting long noncoding RNA (INKILN) is a novel, human-specific long noncoding RNA that is upregulated during vascular inflammation, particularly in atherosclerosis and abdominal aortic aneurysm[1][2][3][6]. INKILN mainly resides in the cytoplasm of vascular smooth muscle cells (VSMCs), where it physically interacts with MKL1 (myocardin-related transcription factor A, also known as megakaryoblastic leukemia 1)[1][3]. This interaction stabilizes MKL1 by inhibiting its ubiquitination via the deubiquitinase USP10, thereby promoting the nuclear translocation and transcriptional activity of the MKL1/p65 (NF-κB) complex, which drives proinflammatory gene expression[1][2][3]. Experimental knockdown of INKILN decreases MKL1 stability, nuclear localization, and proinflammatory transcriptional activity, confirming its functional importance[1][3][6]. INKILN is proposed as a potential target for controlling pathological vascular inflammation and associated diseases, though no interacting drugs are currently known. Its expression correlates with disease states and can serve as a biomarker for vascular inflammation and injury[1][3][6].

Other names

INKILNInflammatory MKL1 interacting lncRNAInflammatory MKL1 (megakaryoblastic leukemia 1) interacting long noncoding RNAHuman-specific long noncoding RNA INKILN