ACTR5 is a component of the INO80 chromatin remodeling complex that functions as a dependency for hepatocellular carcinoma proliferation PMID:36563143. Its loss-of-function activates CDKN2A expression and ablates CDK/E2F-driven cell cycle signaling, thereby attenuating tumor growth PMID:36563143. ACTR5 acts together with its partner IES6 through a mechanism distinct from the canonical INO80 complex, since high-density CRISPR tiling profiles of ACTR5 and IES6 diverge from those of other INO80 subunits PMID:36563143. Beyond this chromatin-associated cell cycle role, no further biochemical mechanism (substrate specificity, recruitment, or structural basis of CDKN2A repression) has been characterized in the available corpus.
| Year | Confidence | Finding | PMIDs | Journal |
|---|---|---|---|---|
| 2022 | Medium | ACTR5, a component of the INO80 chromatin remodeling complex, is essential for hepatocellular carcinoma (HCC) tumor progression; its suppression activates CDKN2A expression and ablates CDK/E2F-driven cell cycle signaling, attenuating HCC tumor growth. | PMID:36563143 | Science advances |
| 2022 | Medium | ACTR5 and its interacting partner IES6 operate via an INO80-independent mechanism to support HCC cell proliferation, as revealed by differential CRISPR tiling profiles compared to other INO80 complex members. | PMID:36563143 | Science advances |
| 2025 | Low | A de novo variant in ACTR5 enhanced type I interferon (IFN-β) signaling, placing ACTR5 as a positive regulator of type I IFN signaling. | PMID:40386946 | Arthritis & rheumatology (Hoboken, N.J.) |