{"gene":"MRPL9","run_date":"2026-06-10T02:59:51","timeline":{"discoveries":[{"year":2022,"finding":"MRPL9 physically interacts with GGCT (γ-glutamylcyclotransferase), as demonstrated by co-immunoprecipitation and immunofluorescence. This interaction activates the MAPK/ERK signaling pathway, promoting proliferation and migration of papillary thyroid cancer cells. Knockdown of either MRPL9 or GGCT inhibited subcutaneous xenograft growth and lung metastasis formation in nude mice.","method":"Co-immunoprecipitation, immunofluorescence, lentivirus-mediated overexpression/knockdown, in vivo xenograft and metastasis assays","journal":"International journal of molecular sciences","confidence":"Medium","confidence_rationale":"Tier 2 / Moderate — reciprocal Co-IP plus functional in vivo validation, single lab","pmids":["36233293"],"is_preprint":false},{"year":2023,"finding":"Knockdown of MRPL9 in lung cancer cells inhibited proliferation, sphere-formation, and migration. MRPL9 was found to be associated with the c-MYC signaling pathway, and c-MYC was confirmed experimentally to regulate the EMT regulator ZEB1; interference with c-MYC expression altered ZEB1 levels, placing MRPL9 upstream of c-MYC/ZEB1-driven EMT.","method":"siRNA knockdown, proliferation/migration assays, c-MYC interference with ZEB1 readout by Western blot/expression analysis","journal":"Pathology, research and practice","confidence":"Low","confidence_rationale":"Tier 3 / Weak — single lab, pathway placement inferred from knockdown + expression correlation without direct biochemical interaction assay for MRPL9-cMYC","pmids":["37343379"],"is_preprint":false},{"year":2023,"finding":"Overexpression of MRPL9 in HCC cells enhanced aggressiveness and facilitated G1/S cell cycle progression. Serum MRPL9 protein was elevated in HCC patients relative to healthy controls and benign liver disease patients, as measured by ELISA. Cell Counting Kit-8 proliferation assays, flow cytometry for cell cycle, and Transwell migration/invasion assays confirmed pro-tumorigenic functions of MRPL9 in HCC cell lines.","method":"MRPL9 overexpression in HCC cell lines, flow cytometry (cell cycle), CCK-8 proliferation assay, Transwell migration/invasion assay, ELISA of serum MRPL9","journal":"Frontiers in surgery","confidence":"Low","confidence_rationale":"Tier 3 / Weak — single lab, gain-of-function with cellular phenotype but no direct pathway mechanism established for MRPL9","pmids":["36684217"],"is_preprint":false},{"year":2025,"finding":"In vivo CRISPRa activation of Mrpl9 in mouse livers drove hepatocellular carcinoma tumorigenesis and decreased survival. RNA sequencing of Mrpl9-activated tumors revealed that Mrpl9 alters expression of genes functionally related to mitochondrial function, promoting cellular proliferation. This placed Mrpl9 as a bona fide HCC driver gene on chromosome 1q.","method":"In vivo CRISPRa screening in mouse liver, RNA sequencing of tumors, validation by separate CRISPRa activation cohorts with survival analysis","journal":"Cellular and molecular gastroenterology and hepatology","confidence":"Medium","confidence_rationale":"Tier 2 / Moderate — in vivo functional screen with transcriptomic mechanism, independently validated in separate mice, single lab","pmids":["39761726"],"is_preprint":false},{"year":2021,"finding":"Loss-of-function of MRPL9 (siRNA knockdown) in TNBC cell lines MDA-MB-231 and BT-549 inhibited colony-forming unit potential and enhanced sensitivity to paclitaxel, establishing a functional role for MRPL9 in TNBC cell survival and chemoresistance.","method":"siRNA knockdown, colony-forming unit assay, paclitaxel sensitivity assay in TNBC cell lines","journal":"Molecular therapy oncolytics","confidence":"Low","confidence_rationale":"Tier 3 / Weak — single lab, single method per readout, no direct molecular mechanism or pathway placement for MRPL9","pmids":["34703883"],"is_preprint":false}],"current_model":"MRPL9 is a mitochondrial ribosomal large subunit protein that, beyond its ribosomal role, physically interacts with GGCT to activate the MAPK/ERK pathway promoting cancer cell proliferation and migration; in vivo CRISPRa evidence establishes it as a chromosome 1q HCC driver gene whose activation perturbs mitochondrial function-related gene expression, and its knockdown suppresses proliferation, migration, and chemoresistance across multiple cancer types including lung, thyroid, and breast cancer."},"narrative":{"mechanistic_narrative":"MRPL9 functions as an oncogenic driver across multiple epithelial cancers, where its activation promotes proliferation, migration, and survival [PMID:36233293, PMID:39761726]. In vivo CRISPRa activation of Mrpl9 in mouse liver drives hepatocellular carcinoma and shortens survival, and transcriptomic profiling of the resulting tumors links Mrpl9 to altered expression of mitochondrial function-related genes, establishing it as a bona fide chromosome 1q HCC driver [PMID:39761726]. At the molecular level, MRPL9 physically interacts with GGCT (γ-glutamylcyclotransferase), and this interaction activates MAPK/ERK signaling to promote proliferation and migration, with knockdown of either partner suppressing xenograft growth and lung metastasis [PMID:36233293]. Beyond these findings, the mechanism by which MRPL9 connects to the oncogenic signaling pathways it influences has not been further characterized in the available corpus.","teleology":[{"year":2021,"claim":"Whether MRPL9 contributes functionally to cancer cell survival was untested; knockdown established it as a determinant of clonogenic potential and chemosensitivity in triple-negative breast cancer.","evidence":"siRNA knockdown with colony-forming and paclitaxel sensitivity assays in TNBC cell lines","pmids":["34703883"],"confidence":"Low","gaps":["No molecular mechanism or pathway placement for MRPL9","Single method per readout from one lab","No in vivo validation"]},{"year":2022,"claim":"The first direct molecular partner and signaling consequence of MRPL9 was defined: it binds GGCT and activates MAPK/ERK to drive proliferation and migration.","evidence":"Reciprocal co-immunoprecipitation, immunofluorescence, lentiviral overexpression/knockdown, and xenograft/metastasis assays in papillary thyroid cancer","pmids":["36233293"],"confidence":"Medium","gaps":["Mechanism by which MRPL9-GGCT activates ERK not resolved","Single lab","Relationship to MRPL9's mitochondrial ribosomal role unaddressed"]},{"year":2023,"claim":"MRPL9's pro-tumorigenic activity was extended to lung cancer and the HCC, linking it to c-MYC/ZEB1-driven EMT and to G1/S cell cycle progression with elevated serum levels in patients.","evidence":"siRNA knockdown and overexpression with proliferation/migration assays, c-MYC interference with ZEB1 readout, flow cytometry cell cycle analysis, and ELISA of serum MRPL9","pmids":["37343379","36684217"],"confidence":"Low","gaps":["MRPL9-cMYC link inferred from expression correlation without direct biochemical assay","No mechanism establishing how MRPL9 acts upstream of c-MYC","Serum elevation is associative"]},{"year":2025,"claim":"Whether MRPL9 is a causal cancer driver rather than a correlate was resolved by in vivo gain-of-function, establishing it as a chromosome 1q HCC driver that perturbs mitochondrial function-related gene expression.","evidence":"In vivo CRISPRa activation in mouse liver with survival analysis and RNA sequencing of tumors, validated in independent cohorts","pmids":["39761726"],"confidence":"Medium","gaps":["How MRPL9 activation alters mitochondrial gene expression is undefined","Connection between transcriptomic changes and proliferation not mechanistically dissected","Single lab"]},{"year":null,"claim":"How MRPL9's canonical mitochondrial ribosomal role mechanistically connects to its GGCT/MAPK-ERK and c-MYC-linked oncogenic signaling remains unresolved.","evidence":"","pmids":[],"confidence":"Low","gaps":["No structural or biochemical basis for MRPL9-GGCT-ERK activation","No direct evidence linking ribosomal function to signaling outputs","Mechanism of c-MYC regulation not established"]}],"mechanism_profile":{"molecular_activity":[],"localization":[],"pathway":[],"complexes":[],"partners":["GGCT"],"other_free_text":[]}},"prefetch_data":{"uniprot":{"accession":"Q9BYD2","full_name":"Large ribosomal subunit protein bL9m","aliases":["39S ribosomal protein L9, mitochondrial","L9mt","MRP-L9"],"length_aa":267,"mass_kda":30.2,"function":"","subcellular_location":"Mitochondrion","url":"https://www.uniprot.org/uniprotkb/Q9BYD2/entry"},"depmap":{"release":"DepMap","has_data":true,"is_common_essential":true,"resolved_as":"","url":"https://depmap.org/portal/gene/MRPL9","classification":"Common Essential","n_dependent_lines":567,"n_total_lines":1208,"dependency_fraction":0.4693708609271523},"opencell":{"profiled":false,"resolved_as":"","ensg_id":"","cell_line_id":"","localizations":[],"interactors":[{"gene":"RANBP1","stoichiometry":0.2}],"url":"https://opencell.sf.czbiohub.org/search/MRPL9","total_profiled":1310},"omim":[{"mim_id":"620646","title":"COMBINED OXIDATIVE PHOSPHORYLATION DEFICIENCY 59; COXPD59","url":"https://www.omim.org/entry/620646"},{"mim_id":"611845","title":"MITOCHONDRIAL RIBOSOMAL PROTEIN L39; MRPL39","url":"https://www.omim.org/entry/611845"},{"mim_id":"611824","title":"MITOCHONDRIAL RIBOSOMAL PROTEIN L9; MRPL9","url":"https://www.omim.org/entry/611824"}],"hpa":{"profiled":true,"resolved_as":"","reliability":"Enhanced","locations":[{"location":"Mitochondria","reliability":"Enhanced"}],"tissue_specificity":"Low tissue specificity","tissue_distribution":"Detected in all","driving_tissues":[],"url":"https://www.proteinatlas.org/search/MRPL9"},"hgnc":{"alias_symbol":["bL9m"],"prev_symbol":[]},"alphafold":{"accession":"Q9BYD2","domains":[{"cath_id":"3.40.5.10","chopping":"94-150","consensus_level":"high","plddt":94.8995,"start":94,"end":150},{"cath_id":"3.10.430.100","chopping":"160-240","consensus_level":"high","plddt":94.2431,"start":160,"end":240}],"viewer_url":"https://alphafold.ebi.ac.uk/entry/Q9BYD2","model_url":"https://alphafold.ebi.ac.uk/files/AF-Q9BYD2-F1-model_v6.cif","pae_url":"https://alphafold.ebi.ac.uk/files/AF-Q9BYD2-F1-predicted_aligned_error_v6.png","plddt_mean":81.69},"mouse_models":{"mgi_url":"https://www.informatics.jax.org/marker/summary?nomen=MRPL9","jax_strain_url":"https://www.jax.org/strain/search?query=MRPL9"},"sequence":{"accession":"Q9BYD2","fasta_url":"https://rest.uniprot.org/uniprotkb/Q9BYD2.fasta","uniprot_url":"https://www.uniprot.org/uniprotkb/Q9BYD2/entry","alphafold_viewer_url":"https://alphafold.ebi.ac.uk/entry/Q9BYD2"}},"corpus_meta":[{"pmid":"25296918","id":"PMC_25296918","title":"Potentiation of neurotoxicity in double-mutant mice with Pink1 ablation and A53T-SNCA overexpression.","date":"2014","source":"Human molecular genetics","url":"https://pubmed.ncbi.nlm.nih.gov/25296918","citation_count":54,"is_preprint":false},{"pmid":"34703883","id":"PMC_34703883","title":"Transcriptional landscape associated with TNBC resistance to neoadjuvant chemotherapy revealed by single-cell RNA-seq.","date":"2021","source":"Molecular therapy oncolytics","url":"https://pubmed.ncbi.nlm.nih.gov/34703883","citation_count":27,"is_preprint":false},{"pmid":"36233293","id":"PMC_36233293","title":"Interaction of MRPL9 and GGCT Promotes Cell Proliferation and Migration by Activating the MAPK/ERK Pathway in Papillary Thyroid Cancer.","date":"2022","source":"International journal of molecular sciences","url":"https://pubmed.ncbi.nlm.nih.gov/36233293","citation_count":20,"is_preprint":false},{"pmid":"34129020","id":"PMC_34129020","title":"Genome analysis of Candida subhashii reveals its hybrid nature and dual mitochondrial genome conformations.","date":"2021","source":"DNA research : an international journal for rapid publication of reports on genes and genomes","url":"https://pubmed.ncbi.nlm.nih.gov/34129020","citation_count":14,"is_preprint":false},{"pmid":"36684217","id":"PMC_36684217","title":"Classification of the mitochondrial ribosomal protein-associated molecular subtypes and identified a serological diagnostic biomarker in hepatocellular carcinoma.","date":"2023","source":"Frontiers in surgery","url":"https://pubmed.ncbi.nlm.nih.gov/36684217","citation_count":8,"is_preprint":false},{"pmid":"8701610","id":"PMC_8701610","title":"Sequence analysis of the 43 kb CRM1-YLM9-PET54-DIE2-SMI1-PHO81-YHB4-PFK1 region from the right arm of Saccharomyces cerevisiae chromosome VII.","date":"1996","source":"Yeast (Chichester, England)","url":"https://pubmed.ncbi.nlm.nih.gov/8701610","citation_count":8,"is_preprint":false},{"pmid":"37343379","id":"PMC_37343379","title":"Identification of a novel therapeutic target for lung cancer: Mitochondrial ribosome protein L9.","date":"2023","source":"Pathology, research and practice","url":"https://pubmed.ncbi.nlm.nih.gov/37343379","citation_count":7,"is_preprint":false},{"pmid":"39761726","id":"PMC_39761726","title":"In Vivo CRISPR Activation Screening Reveals Chromosome 1q Genes VPS72, GBA1, and MRPL9 Drive Hepatocellular Carcinoma.","date":"2025","source":"Cellular and molecular gastroenterology and hepatology","url":"https://pubmed.ncbi.nlm.nih.gov/39761726","citation_count":6,"is_preprint":false},{"pmid":"40406416","id":"PMC_40406416","title":"Genetic mechanisms of hemispheric functional connectivity in diabetic retinopathy: a joint neuroimaging and transcriptomic study.","date":"2025","source":"Frontiers in cell and developmental biology","url":"https://pubmed.ncbi.nlm.nih.gov/40406416","citation_count":3,"is_preprint":false},{"pmid":"37895191","id":"PMC_37895191","title":"Identification of Missense Variants Affecting Carcass Traits for Hanwoo Precision Breeding.","date":"2023","source":"Genes","url":"https://pubmed.ncbi.nlm.nih.gov/37895191","citation_count":2,"is_preprint":false},{"pmid":"35674862","id":"PMC_35674862","title":"Long Non-coding RNA and mRNA Co-expression Network Reveals Novel Players in Pleomorphic Xanthoastrocytoma.","date":"2022","source":"Molecular neurobiology","url":"https://pubmed.ncbi.nlm.nih.gov/35674862","citation_count":1,"is_preprint":false},{"pmid":"41630109","id":"PMC_41630109","title":"MRPL13 deficiency triggers trophoblast mitochondrial unfolded protein response in early-onset preeclampsia.","date":"2026","source":"Reproduction (Cambridge, England)","url":"https://pubmed.ncbi.nlm.nih.gov/41630109","citation_count":0,"is_preprint":false}],"cost":{"stage1":{"model":"claude-sonnet-4-6","input_tokens":8570,"output_tokens":1382,"usd":0.02322,"stage1_stop_reason":"end_turn"},"stage2":{"model":"claude-opus-4-8","input_tokens":8108,"output_tokens":1635,"usd":0.040708,"stage2_stop_reason":"end_turn"},"total_usd":0.063928,"stage1_batch_id":"msgbatch_01BbTCMyrRPyhtEq6b1MdwCN","stage2_batch_id":"msgbatch_011dEed5bbxYvTAaQWKJevxu","note":"batch pricing = 50% of standard"},"stage1_raw":"```json\n{\n  \"discoveries\": [\n    {\n      \"year\": 2022,\n      \"finding\": \"MRPL9 physically interacts with GGCT (γ-glutamylcyclotransferase), as demonstrated by co-immunoprecipitation and immunofluorescence. This interaction activates the MAPK/ERK signaling pathway, promoting proliferation and migration of papillary thyroid cancer cells. Knockdown of either MRPL9 or GGCT inhibited subcutaneous xenograft growth and lung metastasis formation in nude mice.\",\n      \"method\": \"Co-immunoprecipitation, immunofluorescence, lentivirus-mediated overexpression/knockdown, in vivo xenograft and metastasis assays\",\n      \"journal\": \"International journal of molecular sciences\",\n      \"confidence\": \"Medium\",\n      \"confidence_rationale\": \"Tier 2 / Moderate — reciprocal Co-IP plus functional in vivo validation, single lab\",\n      \"pmids\": [\"36233293\"],\n      \"is_preprint\": false\n    },\n    {\n      \"year\": 2023,\n      \"finding\": \"Knockdown of MRPL9 in lung cancer cells inhibited proliferation, sphere-formation, and migration. MRPL9 was found to be associated with the c-MYC signaling pathway, and c-MYC was confirmed experimentally to regulate the EMT regulator ZEB1; interference with c-MYC expression altered ZEB1 levels, placing MRPL9 upstream of c-MYC/ZEB1-driven EMT.\",\n      \"method\": \"siRNA knockdown, proliferation/migration assays, c-MYC interference with ZEB1 readout by Western blot/expression analysis\",\n      \"journal\": \"Pathology, research and practice\",\n      \"confidence\": \"Low\",\n      \"confidence_rationale\": \"Tier 3 / Weak — single lab, pathway placement inferred from knockdown + expression correlation without direct biochemical interaction assay for MRPL9-cMYC\",\n      \"pmids\": [\"37343379\"],\n      \"is_preprint\": false\n    },\n    {\n      \"year\": 2023,\n      \"finding\": \"Overexpression of MRPL9 in HCC cells enhanced aggressiveness and facilitated G1/S cell cycle progression. Serum MRPL9 protein was elevated in HCC patients relative to healthy controls and benign liver disease patients, as measured by ELISA. Cell Counting Kit-8 proliferation assays, flow cytometry for cell cycle, and Transwell migration/invasion assays confirmed pro-tumorigenic functions of MRPL9 in HCC cell lines.\",\n      \"method\": \"MRPL9 overexpression in HCC cell lines, flow cytometry (cell cycle), CCK-8 proliferation assay, Transwell migration/invasion assay, ELISA of serum MRPL9\",\n      \"journal\": \"Frontiers in surgery\",\n      \"confidence\": \"Low\",\n      \"confidence_rationale\": \"Tier 3 / Weak — single lab, gain-of-function with cellular phenotype but no direct pathway mechanism established for MRPL9\",\n      \"pmids\": [\"36684217\"],\n      \"is_preprint\": false\n    },\n    {\n      \"year\": 2025,\n      \"finding\": \"In vivo CRISPRa activation of Mrpl9 in mouse livers drove hepatocellular carcinoma tumorigenesis and decreased survival. RNA sequencing of Mrpl9-activated tumors revealed that Mrpl9 alters expression of genes functionally related to mitochondrial function, promoting cellular proliferation. This placed Mrpl9 as a bona fide HCC driver gene on chromosome 1q.\",\n      \"method\": \"In vivo CRISPRa screening in mouse liver, RNA sequencing of tumors, validation by separate CRISPRa activation cohorts with survival analysis\",\n      \"journal\": \"Cellular and molecular gastroenterology and hepatology\",\n      \"confidence\": \"Medium\",\n      \"confidence_rationale\": \"Tier 2 / Moderate — in vivo functional screen with transcriptomic mechanism, independently validated in separate mice, single lab\",\n      \"pmids\": [\"39761726\"],\n      \"is_preprint\": false\n    },\n    {\n      \"year\": 2021,\n      \"finding\": \"Loss-of-function of MRPL9 (siRNA knockdown) in TNBC cell lines MDA-MB-231 and BT-549 inhibited colony-forming unit potential and enhanced sensitivity to paclitaxel, establishing a functional role for MRPL9 in TNBC cell survival and chemoresistance.\",\n      \"method\": \"siRNA knockdown, colony-forming unit assay, paclitaxel sensitivity assay in TNBC cell lines\",\n      \"journal\": \"Molecular therapy oncolytics\",\n      \"confidence\": \"Low\",\n      \"confidence_rationale\": \"Tier 3 / Weak — single lab, single method per readout, no direct molecular mechanism or pathway placement for MRPL9\",\n      \"pmids\": [\"34703883\"],\n      \"is_preprint\": false\n    }\n  ],\n  \"current_model\": \"MRPL9 is a mitochondrial ribosomal large subunit protein that, beyond its ribosomal role, physically interacts with GGCT to activate the MAPK/ERK pathway promoting cancer cell proliferation and migration; in vivo CRISPRa evidence establishes it as a chromosome 1q HCC driver gene whose activation perturbs mitochondrial function-related gene expression, and its knockdown suppresses proliferation, migration, and chemoresistance across multiple cancer types including lung, thyroid, and breast cancer.\"\n}\n```","stage2_raw":"{\n  \"mechanistic_narrative\": \"MRPL9 functions as an oncogenic driver across multiple epithelial cancers, where its activation promotes proliferation, migration, and survival [#0, #3]. In vivo CRISPRa activation of Mrpl9 in mouse liver drives hepatocellular carcinoma and shortens survival, and transcriptomic profiling of the resulting tumors links Mrpl9 to altered expression of mitochondrial function-related genes, establishing it as a bona fide chromosome 1q HCC driver [#3]. At the molecular level, MRPL9 physically interacts with GGCT (γ-glutamylcyclotransferase), and this interaction activates MAPK/ERK signaling to promote proliferation and migration, with knockdown of either partner suppressing xenograft growth and lung metastasis [#0]. Beyond these findings, the mechanism by which MRPL9 connects to the oncogenic signaling pathways it influences has not been further characterized in the available corpus.\"\n  ,\n  \"teleology\": [\n    {\n      \"year\": 2021,\n      \"claim\": \"Whether MRPL9 contributes functionally to cancer cell survival was untested; knockdown established it as a determinant of clonogenic potential and chemosensitivity in triple-negative breast cancer.\",\n      \"evidence\": \"siRNA knockdown with colony-forming and paclitaxel sensitivity assays in TNBC cell lines\",\n      \"pmids\": [\"34703883\"],\n      \"confidence\": \"Low\",\n      \"gaps\": [\"No molecular mechanism or pathway placement for MRPL9\", \"Single method per readout from one lab\", \"No in vivo validation\"]\n    },\n    {\n      \"year\": 2022,\n      \"claim\": \"The first direct molecular partner and signaling consequence of MRPL9 was defined: it binds GGCT and activates MAPK/ERK to drive proliferation and migration.\",\n      \"evidence\": \"Reciprocal co-immunoprecipitation, immunofluorescence, lentiviral overexpression/knockdown, and xenograft/metastasis assays in papillary thyroid cancer\",\n      \"pmids\": [\"36233293\"],\n      \"confidence\": \"Medium\",\n      \"gaps\": [\"Mechanism by which MRPL9-GGCT activates ERK not resolved\", \"Single lab\", \"Relationship to MRPL9's mitochondrial ribosomal role unaddressed\"]\n    },\n    {\n      \"year\": 2023,\n      \"claim\": \"MRPL9's pro-tumorigenic activity was extended to lung cancer and the HCC, linking it to c-MYC/ZEB1-driven EMT and to G1/S cell cycle progression with elevated serum levels in patients.\",\n      \"evidence\": \"siRNA knockdown and overexpression with proliferation/migration assays, c-MYC interference with ZEB1 readout, flow cytometry cell cycle analysis, and ELISA of serum MRPL9\",\n      \"pmids\": [\"37343379\", \"36684217\"],\n      \"confidence\": \"Low\",\n      \"gaps\": [\"MRPL9-cMYC link inferred from expression correlation without direct biochemical assay\", \"No mechanism establishing how MRPL9 acts upstream of c-MYC\", \"Serum elevation is associative\"]\n    },\n    {\n      \"year\": 2025,\n      \"claim\": \"Whether MRPL9 is a causal cancer driver rather than a correlate was resolved by in vivo gain-of-function, establishing it as a chromosome 1q HCC driver that perturbs mitochondrial function-related gene expression.\",\n      \"evidence\": \"In vivo CRISPRa activation in mouse liver with survival analysis and RNA sequencing of tumors, validated in independent cohorts\",\n      \"pmids\": [\"39761726\"],\n      \"confidence\": \"Medium\",\n      \"gaps\": [\"How MRPL9 activation alters mitochondrial gene expression is undefined\", \"Connection between transcriptomic changes and proliferation not mechanistically dissected\", \"Single lab\"]\n    },\n    {\n      \"year\": null,\n      \"claim\": \"How MRPL9's canonical mitochondrial ribosomal role mechanistically connects to its GGCT/MAPK-ERK and c-MYC-linked oncogenic signaling remains unresolved.\",\n      \"evidence\": \"\",\n      \"pmids\": [],\n      \"confidence\": \"Low\",\n      \"gaps\": [\"No structural or biochemical basis for MRPL9-GGCT-ERK activation\", \"No direct evidence linking ribosomal function to signaling outputs\", \"Mechanism of c-MYC regulation not established\"]\n    }\n  ],\n  \"mechanism_profile\": {\n    \"molecular_activity\": [],\n    \"localization\": [],\n    \"pathway\": [],\n    \"complexes\": [],\n    \"partners\": [\"GGCT\"],\n    \"other_free_text\": []\n  }\n}","audit_flag":null,"evaluation":{"faith_supported":2,"faith_total":3,"faith_pct":66.66666666666667}}