| Functional aspect | Key claim (1 sentence) | Experimental system/approach | Notes on mechanism (domains/interactions) | Reference (with year) and URL |
|---|---|---|---|---|
| Post-mitotic NPC assembly seeding via chromatin binding and Y-complex recruitment | Human AHCTF1/ELYS is a chromatin-binding nucleoporin that seeds post-mitotic nuclear pore complex (NPC) reassembly by recruiting the Nup107–160/Y-complex to decondensing chromosomes, after which transmembrane nucleoporins such as POM121 and NDC1 are recruited. (pqac-00000007, pqac-00000008) | Review synthesis of vertebrate/cell-biology studies; microscopy and depletion-based NPC assembly assays summarized in the review. (pqac-00000007, pqac-00000008) | N-terminal β-propeller and α-helical regions associate with the Y-complex; the C-terminal chromatin-binding region with an AT-hook mediates chromatin capture during mitotic exit. (pqac-00000007, pqac-00000008) | Shevelyov 2020 — https://doi.org/10.3390/ijms21249475 |
| Nucleosome acidic patch binding via RRK stretch and AT-hook | The C-terminal region of ELYS binds nucleosomes directly, with an RRK basic stretch being essential for engagement of the nucleosome acidic patch and the AT-hook contributing DNA binding. (pqac-00000005, pqac-00000009) | Structural biology and biochemistry: cryo-EM, crosslinking mass spectrometry, mutational/deletion analysis, nucleosome/H2A-H2B binding assays. (pqac-00000005, pqac-00000009) | The critical basic cluster includes Arg2404, Arg2405, Lys2406 and nearby Arg2408; the ELYS C-terminus docks onto the H2A-H2B acidic patch while the AT-hook supports chromatin association. (pqac-00000005, pqac-00000009) | Kobayashi et al. 2019 — https://doi.org/10.1038/s42003-019-0385-7 |
| Interphase chromatin anchoring at NPCs | NPC-linked ELYS contributes to anchoring peripheral chromatin to the nuclear envelope in interphase, and ELYS depletion displaces peripheral chromatin and derepresses genes in those regions. (pqac-00000002) | Drosophila late embryos and S2 cells; DamID-seq, knockdown, chromatin compaction and nuclear-periphery analyses. (pqac-00000002) | The study distinguishes nucleoplasmic ELYS from NPC-linked ELYS, with the latter acting together with the nuclear lamina to maintain peripheral chromatin attachment. (pqac-00000002) | Doronin et al. 2024 — https://doi.org/10.1038/s42003-024-06495-w |
| Mitotic phosphorylation and VAPB interaction | During mitosis, phosphorylated ELYS binds the ER/NE membrane protein VAPB through a phospho-regulated FFAT motif, helping coordinate events at decondensing chromosomes and the forming non-core nuclear envelope. (pqac-00000003) | Human-cell biochemical and cell-biology assays including peptide/recombinant binding, co-immunoprecipitation, phosphoproteomics, and mitotic colocalization analysis. (pqac-00000003) | A predicted FFAT motif in ELYS mediates phosphorylation-dependent interaction with the MSP domain of VAPB; ELYS and VAPB colocalize in anaphase at the non-core region. (pqac-00000003) | James et al. 2024 — https://doi.org/10.1038/s44319-024-00125-6 |
| Nuclear size regulation via NPC density and nuclear import | ELYS positively regulates mammalian nuclear size by controlling NPC number/density and thereby nuclear import capacity. (pqac-00000001) | High-throughput imaging RNAi screen and follow-up functional assays in mammalian cells, including ELYS knockdown/overexpression and nuclear import perturbation. (pqac-00000001) | Reduced ELYS lowers NPC density and import capacity and alters lamin organization; increased importin-α can rescue import defects and nuclear size, linking ELYS function to transport-dependent size control. (pqac-00000001) | Jevtić et al. 2019 — https://doi.org/10.15252/embr.201847283 |
| Oncogenic stress interaction with kras and selinexor combinatorial effect | Partial loss of ahctf1/ELYS increases oncogenic stress in kras-driven liver cancer models, and combining ahctf1 reduction with ranbp2 heterozygosity or Selinexor can completely block krasG12V-driven hepatocyte hyperplasia. (pqac-00000006) | Zebrafish larval/adult hepatocellular carcinoma models, genetics, imaging, and transcriptomic/phenotypic analyses; patient survival association analysis in TCGA LIHC. (pqac-00000006) | Reduced ELYS dosage impairs nuclear pore formation, spindle assembly, and chromosome segregation, causing DNA damage and Tp53-dependent cell-cycle arrest/death; this supports nucleocytoplasmic transport/NPC vulnerability as a therapeutic angle. (pqac-00000006) | Morgan et al. 2023 — https://doi.org/10.7554/elife.73407 |
| WNT/β-catenin-driven MYC gene gating | In colon cancer cells, WNT/β-catenin-dependent trafficking of an oncogenic MYC super-enhancer to the nuclear pore requires recruitment of AHCTF1, enabling pathological MYC activation/export and growth advantage. (pqac-00000000) | Cancer-cell genome architecture and gene-regulation study using chromatin trafficking analyses and functional perturbation of the WNT/CTCF/AHCTF1 circuit. (pqac-00000000) | AHCTF1 is recruited to a distal CTCF binding site within the MYC oncogenic super-enhancer, where it participates in stepwise movement of the locus to the nuclear pore. (pqac-00000000) | Chachoua et al. 2022 — https://doi.org/10.1038/s41467-021-27868-3 |


*Table: This table summarizes the main experimentally supported functions of human AHCTF1/ELYS, emphasizing nuclear pore assembly, chromatin binding, mitotic regulation, and disease-relevant contexts. It is useful as a compact evidence map linking each functional claim to the underlying methods, mechanisms, and source.*