MicroRNA 502 (MIR502)

MicroRNA 502 (MIR502) is a non-coding RNA belonging to the microRNA family, encoded by the MIR502 gene on chromosome X (ENSG00000272080)[1][2]. MIR502 transcripts generate mature miR-502-3p, a regulatory RNA (20–24 nucleotides) that post-transcriptionally inhibits or destabilizes target mRNAs by imperfect base pairing within the RNA-induced silencing complex (RISC)[2]. MIR502 is expressed in many human tissues, including adipose, heart, brain, spinal cord, liver, and lung[1]. miR-502-3p has been implicated in diverse biological processes: it regulates synaptic function—especially GABAergic signaling—in the brain, modulates cell proliferation in pituitary adenoma by targeting KMT5A, suppresses immune responses in tuberculosis (by targeting ROCK1), and is associated with several human diseases such as Alzheimer’s disease, various cancers, diabetes, and osteoporosis[1][4]. In Alzheimer’s disease, miR-502-3p levels are upregulated in synapses and correlate with disease progression; experimental upregulation or inhibition modifies GABRA1 expression and synaptic function[1][4]. While miR-502-3p is considered a potential therapeutic target and biomarker, clinical applications are limited by challenges common to miRNA-based therapies, such as delivery and target specificity[1].

Other names

hsa-mir-502MIRN502hsa-miR-502mir-502MIR502microRNA-502-3pmiR-502-3p

miRNA mimics increase MIR502 activity to downregulate specific gene targets (e.g., GABRA1, ROCK1, KMT5A)[1][4]. miRNA inhibitors block MIR502 function to rescue target gene expression[1][4].