| Category | Key points | Key evidence/citations | Publication (first author year) | URL |
|---|---|---|---|---|
| Identity/isoforms/domains | Verified target is human ACIN1 or Acinus (UniProt Q9UKV3), a nuclear RNA-binding protein. Three main isoforms are described: Acinus-L, Acinus-S′, and Acinus-S. All share an RRM and C-terminal RS-like domain; Acinus-L additionally contains an N-terminal SAP domain. ASAP structural work identifies an RSB motif in Acinus that binds RNPS1 and SAP18. | Isoforms and domain architecture are explicitly described in peer-reviewed sources; figure evidence shows SAP, RRM, and RS-like organization (pqac-00000001, pqac-00000002, pqac-00000006, pqac-00000016, pqac-00000028) | Deka 2017; Rodor 2016 | https://doi.org/10.7150/ijbs.18649 ; https://doi.org/10.1261/rna.057158.116 |
| Complexes/partners | ACIN1 is a core component of the ASAP complex with RNPS1 and SAP18; related work indicates an alternative PSAP complex with PNN. ACIN1 is a peripheral or auxiliary EJC component associated with core EJC proteins including eIF4A3, Y14, MAGOH, and MLN51 or CASC3. An additional experimentally supported partner is API5, which binds ACIN1 and modulates apoptotic cleavage. | Mass spectrometry, structural, iCLIP, and yeast-two-hybrid evidence support ASAP, PSAP, and EJC associations and API5 binding (pqac-00000014, pqac-00000015, pqac-00000016, pqac-00000018, pqac-00000020, pqac-00000021) | Rodor 2016; Deka 2017; Abbas 2024 | https://doi.org/10.1261/rna.057158.116 ; https://doi.org/10.7150/ijbs.18649 ; https://doi.org/10.3390/biom14010136 |
| Molecular functions | ACIN1 is not an enzyme or transporter; its primary function is as a nuclear RNA-binding scaffold or regulator that helps coordinate pre-mRNA splicing, exon and intron definition, and EJC-linked post-transcriptional regulation. It binds pre-mRNAs and spliced mRNAs, especially suboptimal introns, promotes inclusion of selected cassette exons, and supports faithful splicing of certain introns, including DFFA or ICAD. In apoptosis, caspase-processed ACIN1 promotes chromatin condensation and contributes to DNA fragmentation pathways. | iCLIP, RNA-seq, siRNA depletion, and apoptosis studies support splicing and apoptotic functions (pqac-00000012, pqac-00000014, pqac-00000019, pqac-00000021) | Rodor 2016; Deka 2017 | https://doi.org/10.1261/rna.057158.116 ; https://doi.org/10.7150/ijbs.18649 |
| Cellular localization | ACIN1 acts mainly in the nucleus, including nuclear speck, nucleoplasm, and chromatin-associated contexts. The SAP motif contributes to chromatin targeting via binding to AT-rich SARs or MARs and influences isoform-specific subcellular localization. ACIN1 also shows EJC-related RNA association and has been discussed in mRNP or export contexts, but its principal annotated site of action is nuclear. | Nuclear localization and chromatin targeting are described across ASAP and EJC studies and reviews; HCC enrichment also places ACIN1-associated genes in nuclear speck and spliceosomal compartments (pqac-00000001, pqac-00000002, pqac-00000016, pqac-00000020, pqac-00000022) | Deka 2017; Rodor 2016; Tang 2024 | https://doi.org/10.7150/ijbs.18649 ; https://doi.org/10.1261/rna.057158.116 ; https://doi.org/10.5152/tjg.2024.23454 |
| Regulation/PTMs | A key regulatory event is caspase-3 cleavage of ACIN1, generating the active p17 fragment that promotes apoptotic chromatin condensation. API5 binding protects ACIN1 from caspase-3 cleavage and blocks ACIN1-mediated DNA fragmentation. Prior work summarized in reviews also notes Akt phosphorylation can inhibit ACIN1 proteolysis and chromatin condensation, and SRPK2 phosphorylation links ACIN1 to growth-related splicing regulation. | Cleavage and protection by API5 are summarized in a 2024 review; phosphorylation and PTM links are summarized in review literature (pqac-00000011, pqac-00000017, pqac-00000018, pqac-00000019) | Abbas 2024; Deka 2017 | https://doi.org/10.3390/biom14010136 ; https://doi.org/10.7150/ijbs.18649 |
| Recent 2024 developments | 2024 literature adds translational and systems-level context. In HCC, ACIN1 is reported as upregulated and embedded in a network enriched for EJC, spliceosome, and nuclear speck biology, with predicted regulation by miR-674-5p and related ceRNA components. A 2024 review highlights API5 and ACIN1 as a direct anti-apoptotic mechanism. A 2024 proteomics and apoptosis study in A549 lung adenocarcinoma identifies increased ACIN1 in the context of TRAIL-DR5 and caspase activation. | Recent developments come from 2024 primary and review papers (pqac-00000009, pqac-00000010, pqac-00000011, pqac-00000018, pqac-00000022) | Tang 2024; Abbas 2024; Tian 2024 | https://doi.org/10.5152/tjg.2024.23454 ; https://doi.org/10.3390/biom14010136 ; https://doi.org/10.3390/molecules29040877 |
| Disease/translational evidence | ACIN1 has emerging biomarker or association value rather than established direct therapeutic targeting. Evidence links ACIN1 to hepatocellular carcinoma overexpression and ceRNA or miRNA regulation, cervical cancer through METTL3 and IGF2BP3-mediated mRNA stabilization, and prior reports of elevated platelet ACIN1 mRNA in lung cancer. Open Targets shows disease associations including HCC, acute lymphoblastic leukemia, and neurodegenerative disease, but evidence strength is currently modest for most indications. No direct ACIN1-targeted clinical trials were identified in the registry search. | Translational associations are from HCC, cervical cancer, and Open Targets evidence synthesis (pqac-00000022, pqac-00000023, pqac-00000025, pqac-00000027, pqac-00000000) | Tang 2024; Su 2022; Open Targets 2025 platform query | https://doi.org/10.5152/tjg.2024.23454 ; https://doi.org/10.1080/21655979.2022.2044261 |
| Quantitative stats | HCC data show ACIN1 significantly upregulated in tumor versus paracancerous and healthy tissue with P less than .001; differential-expression thresholds were absolute log2 FPKM ratio greater than 1 and Q less than .05. PPI analysis identified 37 closely related proteins; the top 10 were Slc3a2, Wiz, Srrm2, Akt1, Hnrnpu, Sap18b, Pabpn1, Ddx39b, Eif4a3, and Rnps1. The ceRNA network size was 2 lncRNAs, 50 miRNAs, and 49 mRNAs; negatively correlated miRNAs included miR-6395, miR-674-5p, and miR-7067-5p. In cervical cancer, METTL3 showed AUC 0.9681 and P less than 0.0001 in the study that positioned ACIN1 downstream of METTL3 and IGF2BP3. Open Targets disease-target scores in the retrieved query were about 0.062 for HCC and 0.549 for neurodegenerative disease. | Quantitative values extracted directly from gathered evidence (pqac-00000022, pqac-00000024, pqac-00000025, pqac-00000027) | Tang 2024; Su 2022; Open Targets 2025 platform query | https://doi.org/10.5152/tjg.2024.23454 ; https://doi.org/10.1080/21655979.2022.2044261 |


*Table: This table summarizes verified identity, domains, complexes, molecular functions, localization, regulation, recent 2024 developments, and translational evidence for human ACIN1 or Acinus (UniProt Q9UKV3). It provides a compact evidence map linking functional annotation to specific cited sources and quantitative findings.*