Ankib1, ankyrin repeat and IBR domain containing 1, is an E3 ligase. It plays a role in regulating innate immune responses by being involved in the retinoic acid-inducible gene-I-like receptor (RLR) signaling pathway [1]. This pathway is crucial for initiating innate immune responses upon sensing cytosolic viral RNA.

In terms of functional studies, deficiency of ANKIB1 in in vivo studies significantly increases RLR-mediated production of type I interferon (IFN) along with pro-inflammatory factors. This leads to a remarkable increase in antiviral immunity and a decrease in viral replication [1]. In osteosarcoma, circular RNA_ANKIB1 accelerates chemo-resistance by binding microRNA-26b-5p and modulating enhancer of zeste homolog 2 [2]. It also stabilizes the regulation of miR-19b on SOCS3/STAT3 pathway to promote osteosarcoma cell growth and invasion [3]. In addition, circular RNA ANKIB1 alleviates hypoxia-induced cardiomyocyte injury by modulating miR-452-5p/SLC7A11 axis [4]. A Schwann cell-enriched circular RNA circ-Ankib1 regulates Schwann cell proliferation following peripheral nerve injury [5]. LncRNA CCDC26 enhances myeloid leukemia cell proliferation and invasion via the circRNA_ANKIB1/miR-195-5p/PRR11 axis [6]. Deregulation of circ-Ankib1 is involved in neuropathic pain development [7]. Association analysis replicated ANKIB1 (rs2040498) in ambidexterity [8].

In conclusion, Ankib1, through its various circular RNA forms, is involved in multiple biological processes and disease conditions such as antiviral immune responses, osteosarcoma development, cardiomyocyte injury, nerve injury repair, myeloid leukemia progression, and neuropathic pain. The study of Ankib1 using gene knockout or other loss-of-function models has provided valuable insights into its role in these biological processes and diseases, contributing to a better understanding of the underlying mechanisms and potentially leading to new therapeutic strategies.