microRNA-101a-3p (miR-101a-3p)

miR-101a-3p (microRNA-101a-3p) is a mature non-coding RNA derived from the 3’ arm of pre-miR-101, encoded by genes in both human and mouse genomes[4]. It regulates expression of a large network of genes by binding to specific mRNA targets, resulting in transcript degradation or inhibition of translation. miR-101a-3p is implicated in critical cellular processes such as cell proliferation, apoptosis, and immune modulation. It acts in several disease contexts: as a tumor suppressor in many cancers (e.g., breast, prostate, glioblastoma), with loss leading to increased oncogenic activity; as a modulator in neurodegenerative and autoimmune diseases (e.g., Parkinson’s, SLE), where its expression correlates with disease activity; and as a mediator of cell survival in diabetes and degenerative diseases. Therapeutic targeting is under preclinical investigation, mainly using oligonucleotide agomirs and antagomirs to restore or inhibit miR-101a-3p function[4][5]. microRNA-101a-3p is a microRNA, broadly acting post-transcriptional regulator with established roles as both biomarker and therapeutic target in various diseases, especially cancer, neurodegeneration, autoimmunity, and metabolic disorders[2][3][4][5].

Other names

miR-101-3pmiRNA-101a-3phsa-miR-101-3p (human)mmu-miR-101a-3p (mouse)microRNA-101-3p

miR-101a-3p binds complementary sequences in target mRNAs, triggering mRNA degradation or translational repression[1][4]. Therapeutic targeting uses oligonucleotide mimics to increase activity or antagomirs to inhibit it[5].