{"gene":"ZNF554","run_date":"2026-06-11T09:02:07","timeline":{"discoveries":[{"year":2018,"finding":"DNA hypermethylation in the regulatory region of ZNF554 leads to ZNF554 gene down-regulation, which impairs trophoblast invasion — established as a hub transcription factor in placental gene modules associated with preterm preeclampsia.","method":"Placental transcriptomics, placental 'virtual' liquid biopsy, in vitro experiments on trophoblast cells with ZNF554 modulation","journal":"Frontiers in immunology","confidence":"Medium","confidence_rationale":"Tier 2 / Moderate — in vitro functional experiments with defined cellular phenotype (trophoblast invasion), methylation-linked transcriptional regulation, single lab but multiple orthogonal methods (transcriptomics + in vitro functional assay)","pmids":["30135684"],"is_preprint":false},{"year":2023,"finding":"ZNF554 knockdown in trophoblast cells (HTR8/SVneo and JEG3) increases apoptosis, inhibits migration and invasion, decreases antioxidant capacity, and elevates ROS. ZNF554 activates the NRF2 signaling pathway (via p62-Keap1-Nrf2) to exert antioxidant effects; knockdown also promotes autophagy by suppressing p62 and enhancing LC3-II/LC3-I expression. The antioxidant NAC partially rescued the mitochondrial ROS increase and downstream autophagy/apoptosis effects caused by ZNF554 knockdown.","method":"siRNA knockdown and overexpression plasmids in HTR8/SVneo and JEG3 trophoblast cells; ROS measurement; apoptosis assays; migration/invasion assays; Western blot for NRF2 pathway components (p62, Keap1, NRF2, LC3-II/LC3-I); NAC rescue experiment","journal":"Placenta","confidence":"Medium","confidence_rationale":"Tier 2 / Moderate — loss-of-function and gain-of-function with defined cellular phenotypes, pathway rescue with NAC, multiple orthogonal readouts; single lab","pmids":["37804692"],"is_preprint":false},{"year":2020,"finding":"Overexpression of ZNF554 in U87 glioblastoma cells causes differential expression (mostly downregulation) of 899 genes, arrests cell cycle, and decreases cell proliferation; the PI3K-Akt signaling pathway is the most impacted among 116 dysregulated pathways, suggesting ZNF554 acts as a transcriptional repressor suppressing oncogenic signaling.","method":"Transient overexpression in U87 glioblastoma cells, genome-wide transcriptomics, cell proliferation assay, cell cycle analysis","journal":"International journal of molecular sciences","confidence":"Medium","confidence_rationale":"Tier 2 / Moderate — gain-of-function with genome-wide transcriptomic readout and cell-cycle phenotype; single lab, multiple orthogonal methods","pmids":["32796700"],"is_preprint":false},{"year":2024,"finding":"ZNF554 transcriptionally activates RBM5 (shown by chromatin immunoprecipitation and luciferase reporter assay), and through RBM5 inactivates the WNT/β-catenin signaling pathway (reducing β-catenin and p-GSK-3β levels). Rescue experiments showed that RBM5 knockdown negated the anti-proliferative and anti-migratory effects of ZNF554 overexpression, while RBM5 overexpression counteracted the pro-proliferative effects of ZNF554 knockdown, placing ZNF554 upstream of RBM5 in this pathway.","method":"Chromatin immunoprecipitation (ChIP), luciferase reporter assay, lentiviral overexpression and knockdown in endometrial cancer cell lines, CCK-8 proliferation assay, wound healing and Transwell invasion assays, Western blot for β-catenin and p-GSK-3β, rescue experiments with RBM5 modulation","journal":"Current medical science","confidence":"Medium","confidence_rationale":"Tier 2 / Moderate — direct transcriptional regulation shown by ChIP and luciferase assay, pathway placement by epistasis rescue; single lab, multiple orthogonal methods","pmids":["38619681"],"is_preprint":false}],"current_model":"ZNF554 is a KRAB-domain zinc finger transcription factor that suppresses cell proliferation, promotes migration/invasion, and exerts antioxidant protection in trophoblasts and cancer cells by: (1) transcriptionally activating RBM5 to inactivate WNT/β-catenin signaling; (2) activating the p62-Keap1-NRF2 antioxidant pathway to limit ROS-induced apoptosis and autophagy; and (3) broadly repressing oncogenic gene expression including the PI3K-Akt pathway, with its own expression regulated by promoter DNA methylation."},"narrative":{"mechanistic_narrative":"ZNF554 is a transcription factor that functions predominantly as a repressor of oncogenic gene programs while exerting antioxidant cytoprotection, with roles documented in trophoblast biology and in glioblastoma and endometrial cancer cells [PMID:30135684, PMID:32796700]. As a regulator of placental gene modules, loss of ZNF554 through promoter-region DNA hypermethylation impairs trophoblast invasion and is associated with preterm preeclampsia [PMID:30135684]. In trophoblasts, ZNF554 sustains antioxidant capacity by activating the p62-Keap1-NRF2 pathway; its loss elevates mitochondrial ROS, increases apoptosis, and promotes autophagy through suppression of p62 and accumulation of LC3-II, effects partially reversed by the antioxidant NAC [PMID:37804692]. ZNF554 directly activates transcription of RBM5, and through RBM5 inactivates WNT/β-catenin signaling, reducing β-catenin and p-GSK-3β and thereby constraining proliferation and migration [PMID:38619681]. More broadly, ZNF554 overexpression downregulates hundreds of genes, arrests the cell cycle, and suppresses proliferation, with the PI3K-Akt pathway most strongly affected, consistent with its role as a transcriptional repressor of oncogenic signaling [PMID:32796700].","teleology":[{"year":2018,"claim":"Establishing that ZNF554 is an epigenetically silenced hub transcription factor answered how its dysregulation links to a disease phenotype, identifying methylation-driven down-regulation as the trigger for impaired trophoblast invasion in preterm preeclampsia.","evidence":"Placental transcriptomics and in vitro ZNF554 modulation in trophoblast cells","pmids":["30135684"],"confidence":"Medium","gaps":["Direct transcriptional targets in trophoblasts not yet identified","Which enzymes set the regulatory-region methylation is unknown","No structural or DNA-binding-site characterization"]},{"year":2020,"claim":"Genome-wide overexpression profiling answered whether ZNF554 acts as an activator or repressor, showing it predominantly downregulates genes, arrests the cell cycle, and most strongly impacts PI3K-Akt signaling, establishing it as a transcriptional repressor of oncogenic programs.","evidence":"Transient overexpression in U87 glioblastoma cells with transcriptomics, proliferation, and cell-cycle assays","pmids":["32796700"],"confidence":"Medium","gaps":["Direct vs indirect targets not distinguished by transcriptomics alone","No ChIP evidence for direct binding to the affected loci","Repression mechanism (cofactors, KRAB corepressors) not defined"]},{"year":2023,"claim":"Loss- and gain-of-function in trophoblasts answered how ZNF554 protects cells from oxidative stress, linking it to the p62-Keap1-NRF2 axis and showing its loss raises ROS and shifts cells toward apoptosis and autophagy.","evidence":"siRNA knockdown/overexpression in HTR8/SVneo and JEG3 cells, ROS and apoptosis assays, NRF2-pathway Western blots, NAC rescue","pmids":["37804692"],"confidence":"Medium","gaps":["Whether ZNF554 regulates p62/NRF2 components transcriptionally and directly is unresolved","Mechanism connecting ZNF554 to mitochondrial ROS is indirect","NAC only partially rescued the phenotype"]},{"year":2024,"claim":"ChIP and reporter assays with epistasis rescue answered which direct target mediates ZNF554's anti-proliferative effect, placing ZNF554 upstream of RBM5, which in turn inactivates WNT/β-catenin signaling.","evidence":"ChIP, luciferase reporter, lentiviral over/knockdown in endometrial cancer cells, proliferation/invasion assays, RBM5 rescue","pmids":["38619681"],"confidence":"Medium","gaps":["ZNF554 binding motif on the RBM5 promoter not mapped","Whether RBM5 fully accounts for the broader repressive program is unknown","Single cancer-type context for the RBM5-WNT link"]},{"year":null,"claim":"Whether the distinct ZNF554 activities — RBM5/WNT repression, NRF2 antioxidant activation, and PI3K-Akt suppression — reflect one unified DNA-binding program or context-specific target sets remains unresolved.","evidence":"","pmids":[],"confidence":"Medium","gaps":["No genome-wide DNA-binding map (ChIP-seq) across cell types","No structural characterization of the zinc-finger array or KRAB-mediated repression","Direct vs indirect status of most regulated genes undetermined"]}],"mechanism_profile":{"molecular_activity":[{"term_id":"GO:0140110","term_label":"transcription regulator activity","supporting_discovery_ids":[0,2,3]},{"term_id":"GO:0003677","term_label":"DNA binding","supporting_discovery_ids":[3]}],"localization":[{"term_id":"GO:0005634","term_label":"nucleus","supporting_discovery_ids":[3]}],"pathway":[{"term_id":"R-HSA-74160","term_label":"Gene expression (Transcription)","supporting_discovery_ids":[2,3]},{"term_id":"R-HSA-162582","term_label":"Signal Transduction","supporting_discovery_ids":[2,3]},{"term_id":"R-HSA-8953897","term_label":"Cellular responses to stimuli","supporting_discovery_ids":[1]}],"complexes":[],"partners":[],"other_free_text":[]}},"prefetch_data":{"uniprot":{"accession":"Q86TJ5","full_name":"Zinc finger protein 554","aliases":[],"length_aa":538,"mass_kda":60.6,"function":"May be involved in transcriptional regulation","subcellular_location":"Nucleus","url":"https://www.uniprot.org/uniprotkb/Q86TJ5/entry"},"depmap":{"release":"DepMap","has_data":true,"is_common_essential":false,"resolved_as":"","url":"https://depmap.org/portal/gene/ZNF554","classification":"Not Classified","n_dependent_lines":0,"n_total_lines":1208,"dependency_fraction":0.0},"opencell":{"profiled":false,"resolved_as":"","ensg_id":"","cell_line_id":"","localizations":[],"interactors":[{"gene":"MVD","stoichiometry":0.2}],"url":"https://opencell.sf.czbiohub.org/search/ZNF554","total_profiled":1310},"omim":[],"hpa":{"profiled":true,"resolved_as":"","reliability":"Enhanced","locations":[{"location":"Nucleoplasm","reliability":"Enhanced"},{"location":"Nucleoli","reliability":"Additional"}],"tissue_specificity":"Low tissue specificity","tissue_distribution":"Detected in many","driving_tissues":[],"url":"https://www.proteinatlas.org/search/ZNF554"},"hgnc":{"alias_symbol":["FLJ34817"],"prev_symbol":[]},"alphafold":{"accession":"Q86TJ5","domains":[{"cath_id":"3.30.160.60","chopping":"325-364","consensus_level":"medium","plddt":84.34,"start":325,"end":364},{"cath_id":"3.30.160.60","chopping":"463-538","consensus_level":"medium","plddt":78.0713,"start":463,"end":538},{"cath_id":"1.10.287","chopping":"46-85","consensus_level":"medium","plddt":81.4085,"start":46,"end":85}],"viewer_url":"https://alphafold.ebi.ac.uk/entry/Q86TJ5","model_url":"https://alphafold.ebi.ac.uk/files/AF-Q86TJ5-F1-model_v6.cif","pae_url":"https://alphafold.ebi.ac.uk/files/AF-Q86TJ5-F1-predicted_aligned_error_v6.png","plddt_mean":55.5},"mouse_models":{"mgi_url":"https://www.informatics.jax.org/marker/summary?nomen=ZNF554","jax_strain_url":"https://www.jax.org/strain/search?query=ZNF554"},"sequence":{"accession":"Q86TJ5","fasta_url":"https://rest.uniprot.org/uniprotkb/Q86TJ5.fasta","uniprot_url":"https://www.uniprot.org/uniprotkb/Q86TJ5/entry","alphafold_viewer_url":"https://alphafold.ebi.ac.uk/entry/Q86TJ5"}},"corpus_meta":[{"pmid":"30135684","id":"PMC_30135684","title":"Integrated Systems Biology Approach Identifies Novel Maternal and Placental Pathways of Preeclampsia.","date":"2018","source":"Frontiers in immunology","url":"https://pubmed.ncbi.nlm.nih.gov/30135684","citation_count":153,"is_preprint":false},{"pmid":"37804692","id":"PMC_37804692","title":"Dysfunction of ZNF554 promotes ROS-induced apoptosis and autophagy in Fetal Growth Restriction via the p62-Keap1-Nrf2 pathway.","date":"2023","source":"Placenta","url":"https://pubmed.ncbi.nlm.nih.gov/37804692","citation_count":9,"is_preprint":false},{"pmid":"32796700","id":"PMC_32796700","title":"Decreased Expression of ZNF554 in Gliomas is Associated with the Activation of Tumor Pathways and Shorter Patient Survival.","date":"2020","source":"International journal of molecular sciences","url":"https://pubmed.ncbi.nlm.nih.gov/32796700","citation_count":6,"is_preprint":false},{"pmid":"38619681","id":"PMC_38619681","title":"ZNF554 Inhibits Endometrial Cancer Progression via Regulating RBM5 and Inactivating WNT/β-Catenin Signaling Pathway.","date":"2024","source":"Current medical science","url":"https://pubmed.ncbi.nlm.nih.gov/38619681","citation_count":2,"is_preprint":false}],"cost":{"stage1":{"model":"claude-sonnet-4-6","input_tokens":4864,"output_tokens":1363,"usd":0.017518,"stage1_stop_reason":"end_turn"},"stage2":{"model":"claude-opus-4-8","input_tokens":8045,"output_tokens":2168,"usd":0.047212,"stage2_stop_reason":"end_turn"},"total_usd":0.06473,"stage1_batch_id":"msgbatch_01UT1AahFPCAyn2uVweS7A9z","stage2_batch_id":"msgbatch_01HuKWtKNT4Pqj1bc8eEP5RV","note":"batch pricing = 50% of standard"},"stage1_raw":"```json\n{\n  \"discoveries\": [\n    {\n      \"year\": 2018,\n      \"finding\": \"DNA hypermethylation in the regulatory region of ZNF554 leads to ZNF554 gene down-regulation, which impairs trophoblast invasion — established as a hub transcription factor in placental gene modules associated with preterm preeclampsia.\",\n      \"method\": \"Placental transcriptomics, placental 'virtual' liquid biopsy, in vitro experiments on trophoblast cells with ZNF554 modulation\",\n      \"journal\": \"Frontiers in immunology\",\n      \"confidence\": \"Medium\",\n      \"confidence_rationale\": \"Tier 2 / Moderate — in vitro functional experiments with defined cellular phenotype (trophoblast invasion), methylation-linked transcriptional regulation, single lab but multiple orthogonal methods (transcriptomics + in vitro functional assay)\",\n      \"pmids\": [\"30135684\"],\n      \"is_preprint\": false\n    },\n    {\n      \"year\": 2023,\n      \"finding\": \"ZNF554 knockdown in trophoblast cells (HTR8/SVneo and JEG3) increases apoptosis, inhibits migration and invasion, decreases antioxidant capacity, and elevates ROS. ZNF554 activates the NRF2 signaling pathway (via p62-Keap1-Nrf2) to exert antioxidant effects; knockdown also promotes autophagy by suppressing p62 and enhancing LC3-II/LC3-I expression. The antioxidant NAC partially rescued the mitochondrial ROS increase and downstream autophagy/apoptosis effects caused by ZNF554 knockdown.\",\n      \"method\": \"siRNA knockdown and overexpression plasmids in HTR8/SVneo and JEG3 trophoblast cells; ROS measurement; apoptosis assays; migration/invasion assays; Western blot for NRF2 pathway components (p62, Keap1, NRF2, LC3-II/LC3-I); NAC rescue experiment\",\n      \"journal\": \"Placenta\",\n      \"confidence\": \"Medium\",\n      \"confidence_rationale\": \"Tier 2 / Moderate — loss-of-function and gain-of-function with defined cellular phenotypes, pathway rescue with NAC, multiple orthogonal readouts; single lab\",\n      \"pmids\": [\"37804692\"],\n      \"is_preprint\": false\n    },\n    {\n      \"year\": 2020,\n      \"finding\": \"Overexpression of ZNF554 in U87 glioblastoma cells causes differential expression (mostly downregulation) of 899 genes, arrests cell cycle, and decreases cell proliferation; the PI3K-Akt signaling pathway is the most impacted among 116 dysregulated pathways, suggesting ZNF554 acts as a transcriptional repressor suppressing oncogenic signaling.\",\n      \"method\": \"Transient overexpression in U87 glioblastoma cells, genome-wide transcriptomics, cell proliferation assay, cell cycle analysis\",\n      \"journal\": \"International journal of molecular sciences\",\n      \"confidence\": \"Medium\",\n      \"confidence_rationale\": \"Tier 2 / Moderate — gain-of-function with genome-wide transcriptomic readout and cell-cycle phenotype; single lab, multiple orthogonal methods\",\n      \"pmids\": [\"32796700\"],\n      \"is_preprint\": false\n    },\n    {\n      \"year\": 2024,\n      \"finding\": \"ZNF554 transcriptionally activates RBM5 (shown by chromatin immunoprecipitation and luciferase reporter assay), and through RBM5 inactivates the WNT/β-catenin signaling pathway (reducing β-catenin and p-GSK-3β levels). Rescue experiments showed that RBM5 knockdown negated the anti-proliferative and anti-migratory effects of ZNF554 overexpression, while RBM5 overexpression counteracted the pro-proliferative effects of ZNF554 knockdown, placing ZNF554 upstream of RBM5 in this pathway.\",\n      \"method\": \"Chromatin immunoprecipitation (ChIP), luciferase reporter assay, lentiviral overexpression and knockdown in endometrial cancer cell lines, CCK-8 proliferation assay, wound healing and Transwell invasion assays, Western blot for β-catenin and p-GSK-3β, rescue experiments with RBM5 modulation\",\n      \"journal\": \"Current medical science\",\n      \"confidence\": \"Medium\",\n      \"confidence_rationale\": \"Tier 2 / Moderate — direct transcriptional regulation shown by ChIP and luciferase assay, pathway placement by epistasis rescue; single lab, multiple orthogonal methods\",\n      \"pmids\": [\"38619681\"],\n      \"is_preprint\": false\n    }\n  ],\n  \"current_model\": \"ZNF554 is a KRAB-domain zinc finger transcription factor that suppresses cell proliferation, promotes migration/invasion, and exerts antioxidant protection in trophoblasts and cancer cells by: (1) transcriptionally activating RBM5 to inactivate WNT/β-catenin signaling; (2) activating the p62-Keap1-NRF2 antioxidant pathway to limit ROS-induced apoptosis and autophagy; and (3) broadly repressing oncogenic gene expression including the PI3K-Akt pathway, with its own expression regulated by promoter DNA methylation.\"\n}\n```","stage2_raw":"{\n  \"mechanistic_narrative\": \"ZNF554 is a transcription factor that functions predominantly as a repressor of oncogenic gene programs while exerting antioxidant cytoprotection, with roles documented in trophoblast biology and in glioblastoma and endometrial cancer cells [#0, #2]. As a regulator of placental gene modules, loss of ZNF554 through promoter-region DNA hypermethylation impairs trophoblast invasion and is associated with preterm preeclampsia [#0]. In trophoblasts, ZNF554 sustains antioxidant capacity by activating the p62-Keap1-NRF2 pathway; its loss elevates mitochondrial ROS, increases apoptosis, and promotes autophagy through suppression of p62 and accumulation of LC3-II, effects partially reversed by the antioxidant NAC [#1]. ZNF554 directly activates transcription of RBM5, and through RBM5 inactivates WNT/\\u03b2-catenin signaling, reducing \\u03b2-catenin and p-GSK-3\\u03b2 and thereby constraining proliferation and migration [#3]. More broadly, ZNF554 overexpression downregulates hundreds of genes, arrests the cell cycle, and suppresses proliferation, with the PI3K-Akt pathway most strongly affected, consistent with its role as a transcriptional repressor of oncogenic signaling [#2].\",\n  \"teleology\": [\n    {\n      \"year\": 2018,\n      \"claim\": \"Establishing that ZNF554 is an epigenetically silenced hub transcription factor answered how its dysregulation links to a disease phenotype, identifying methylation-driven down-regulation as the trigger for impaired trophoblast invasion in preterm preeclampsia.\",\n      \"evidence\": \"Placental transcriptomics and in vitro ZNF554 modulation in trophoblast cells\",\n      \"pmids\": [\"30135684\"],\n      \"confidence\": \"Medium\",\n      \"gaps\": [\n        \"Direct transcriptional targets in trophoblasts not yet identified\",\n        \"Which enzymes set the regulatory-region methylation is unknown\",\n        \"No structural or DNA-binding-site characterization\"\n      ]\n    },\n    {\n      \"year\": 2020,\n      \"claim\": \"Genome-wide overexpression profiling answered whether ZNF554 acts as an activator or repressor, showing it predominantly downregulates genes, arrests the cell cycle, and most strongly impacts PI3K-Akt signaling, establishing it as a transcriptional repressor of oncogenic programs.\",\n      \"evidence\": \"Transient overexpression in U87 glioblastoma cells with transcriptomics, proliferation, and cell-cycle assays\",\n      \"pmids\": [\"32796700\"],\n      \"confidence\": \"Medium\",\n      \"gaps\": [\n        \"Direct vs indirect targets not distinguished by transcriptomics alone\",\n        \"No ChIP evidence for direct binding to the affected loci\",\n        \"Repression mechanism (cofactors, KRAB corepressors) not defined\"\n      ]\n    },\n    {\n      \"year\": 2023,\n      \"claim\": \"Loss- and gain-of-function in trophoblasts answered how ZNF554 protects cells from oxidative stress, linking it to the p62-Keap1-NRF2 axis and showing its loss raises ROS and shifts cells toward apoptosis and autophagy.\",\n      \"evidence\": \"siRNA knockdown/overexpression in HTR8/SVneo and JEG3 cells, ROS and apoptosis assays, NRF2-pathway Western blots, NAC rescue\",\n      \"pmids\": [\"37804692\"],\n      \"confidence\": \"Medium\",\n      \"gaps\": [\n        \"Whether ZNF554 regulates p62/NRF2 components transcriptionally and directly is unresolved\",\n        \"Mechanism connecting ZNF554 to mitochondrial ROS is indirect\",\n        \"NAC only partially rescued the phenotype\"\n      ]\n    },\n    {\n      \"year\": 2024,\n      \"claim\": \"ChIP and reporter assays with epistasis rescue answered which direct target mediates ZNF554's anti-proliferative effect, placing ZNF554 upstream of RBM5, which in turn inactivates WNT/\\u03b2-catenin signaling.\",\n      \"evidence\": \"ChIP, luciferase reporter, lentiviral over/knockdown in endometrial cancer cells, proliferation/invasion assays, RBM5 rescue\",\n      \"pmids\": [\"38619681\"],\n      \"confidence\": \"Medium\",\n      \"gaps\": [\n        \"ZNF554 binding motif on the RBM5 promoter not mapped\",\n        \"Whether RBM5 fully accounts for the broader repressive program is unknown\",\n        \"Single cancer-type context for the RBM5-WNT link\"\n      ]\n    },\n    {\n      \"year\": null,\n      \"claim\": \"Whether the distinct ZNF554 activities — RBM5/WNT repression, NRF2 antioxidant activation, and PI3K-Akt suppression — reflect one unified DNA-binding program or context-specific target sets remains unresolved.\",\n      \"evidence\": \"\",\n      \"pmids\": [],\n      \"confidence\": \"Medium\",\n      \"gaps\": [\n        \"No genome-wide DNA-binding map (ChIP-seq) across cell types\",\n        \"No structural characterization of the zinc-finger array or KRAB-mediated repression\",\n        \"Direct vs indirect status of most regulated genes undetermined\"\n      ]\n    }\n  ],\n  \"mechanism_profile\": {\n    \"molecular_activity\": [\n      {\"term_id\": \"GO:0140110\", \"supporting_discovery_ids\": [0, 2, 3]},\n      {\"term_id\": \"GO:0003677\", \"supporting_discovery_ids\": [3]}\n    ],\n    \"localization\": [\n      {\"term_id\": \"GO:0005634\", \"supporting_discovery_ids\": [3]}\n    ],\n    \"pathway\": [\n      {\"term_id\": \"R-HSA-74160\", \"supporting_discovery_ids\": [2, 3]},\n      {\"term_id\": \"R-HSA-162582\", \"supporting_discovery_ids\": [2, 3]},\n      {\"term_id\": \"R-HSA-8953897\", \"supporting_discovery_ids\": [1]}\n    ],\n    \"complexes\": [],\n    \"partners\": [],\n    \"other_free_text\": []\n  }\n}","audit_flag":null,"evaluation":{"faith_supported":4,"faith_total":5,"faith_pct":80.0}}