ELAV-like protein 1 (ELAVL1) (HuR)

ELAV-like protein 1 (ELAVL1), commonly known as HuR, is a ubiquitously expressed RNA-binding protein that plays a critical role in post-transcriptional gene regulation (UniProt Q15717) [1]. It primarily functions by binding to adenylate-uridylate-rich elements (AREs) in the 3' untranslated regions (UTRs) of target mRNAs, thereby increasing their stability and translation efficiency (PubMed: 23839033) [2]. These target mRNAs often encode proteins involved in cell proliferation, survival, angiogenesis, and inflammation, such as cyclins, VEGF, and TNF-alpha (PubMed: 25646012) [3]. In many cancers, HuR is overexpressed and translocates from the nucleus to the cytoplasm, where it promotes a pro-tumorigenic phenotype (PubMed: 23839033) [2]. Consequently, ELAVL1 is considered a promising therapeutic target, with drug development efforts focusing on small molecules that inhibit its RNA-binding domain or prevent its dimerization and cytoplasmic export (PubMed: 25646012) [3]. Additionally, nucleic acid-based therapies like siRNA are being explored to directly target ELAVL1 mRNA to reduce protein levels in diseased tissues (ClinicalTrials.gov) [4].

Other names

Hu-antigen RHuRELAV-like protein 1MelGELAV1

Inhibition of RNA-binding activity, disruption of protein dimerization, or antisense-mediated degradation of ELAVL1 mRNA to prevent the stabilization of pro-oncogenic and pro-inflammatory transcripts.