{"gene":"CKMT1A","run_date":"2026-06-09T22:57:18","timeline":{"discoveries":[{"year":2016,"finding":"CKMT1A (along with CKMT1B and CKMT2) is exclusively expressed in human brown adipose tissue (BAT) compared to adjacent white adipose tissue, where it functions as an effective modulator of ATP synthase-coupled respiration, acting in parallel with UCP1-mediated uncoupled respiration as a distinct energy expenditure pathway.","method":"Comparative proteotype analysis (quantitative proteomics) of primary human brown vs. white adipose tissue","journal":"Scientific reports","confidence":"Medium","confidence_rationale":"Tier 2 / Weak — quantitative proteomic profiling with functional interpretation, single lab, single method, no direct enzymatic assay or KD/KO in this study","pmids":["27418403"],"is_preprint":false},{"year":2018,"finding":"LncRNA n335586 promotes HCC cell migration and invasion by competitively binding miR-924, thereby de-repressing CKMT1A expression; CKMT1A is the functional downstream effector of this axis in driving epithelial-mesenchymal transition and metastasis.","method":"In vitro migration/invasion assays, in vivo metastasis model, competitive endogenous RNA (ceRNA) mechanistic studies with miR-924 binding validation","journal":"Cancer letters","confidence":"Medium","confidence_rationale":"Tier 2 / Moderate — functional rescue/knockdown experiments with in vivo validation and ceRNA mechanism, single lab but multiple orthogonal methods","pmids":["29753758"],"is_preprint":false},{"year":2017,"finding":"CKMT1A protein is up-regulated 7.8-fold in breast muscle of high feed efficiency broilers compared to low feed efficiency broilers, indicating CKMT1A participates in the mitochondrial creatine kinase energy transfer system linking oxidative phosphorylation to cytosolic ATP replenishment via phosphocreatine.","method":"Proteomic analysis (re-examination of mass spectrometry dataset) of broiler pectoralis muscle","journal":"Poultry science","confidence":"Low","confidence_rationale":"Tier 3 / Weak — single proteomics dataset reanalysis, no direct functional assay of CKMT1A, no KD/KO","pmids":["28521058"],"is_preprint":false},{"year":2024,"finding":"Silencing CKMT1A (or CKMT1B) does not lead to loss of sensitivity to F1F0 ATP synthase inhibition, unlike CKB silencing; this negative result indicates CKMT1A is not the creatine kinase responsible for regulating mitochondrial ATP production via the CKB-AKT-mPTP axis.","method":"siRNA silencing of CKMT1A/CKMT1B in cells relying on mitochondrial F1F0 ATP synthase, cell viability and ATP production assays","journal":"Advanced science (Weinheim, Baden-Wurttemberg, Germany)","confidence":"Medium","confidence_rationale":"Tier 2 / Moderate — direct gene silencing with functional readout, negative result replicated across CKMT1A and CKMT1B in same study, single lab","pmids":["38896801"],"is_preprint":false},{"year":2024,"finding":"CKMT1A was identified as a glycoprotein substrate of GALNT9 (polypeptide N-acetylgalactosamine transferase 9), detected by lectin affinity chromatography and LC-MS/MS as carrying GalNAc O-glycosylation; GALNT9 deficiency is associated with mitochondrial dysfunction including increased ROS and mPTP opening.","method":"Lectin affinity chromatography purification of GalNAc-exposing glycoproteins followed by LC-MS/MS identification in SH-SY5Y cells with GALNT9 siRNA knockdown","journal":"International journal of biological macromolecules","confidence":"Low","confidence_rationale":"Tier 3 / Weak — MS identification of CKMT1A as a glycoprotein in a screen, no direct site mapping or functional consequence of CKMT1A glycosylation specifically tested","pmids":["38401583"],"is_preprint":false}],"current_model":"CKMT1A is a mitochondrial creatine kinase that participates in the phosphocreatine energy shuttle linking mitochondrial oxidative phosphorylation to cytosolic ATP buffering, is exclusively enriched in brown adipose tissue as a modulator of ATP synthase-coupled respiration, can be regulated post-transcriptionally via a ceRNA mechanism (lncRNA n335586/miR-924) to promote cancer cell migration, and carries O-GalNAc glycosylation catalyzed by GALNT9; notably, CKMT1A itself (unlike the cytosolic isoform CKB) does not mediate mitochondrial ATP production through the CKB-AKT-mPTP signaling axis."},"narrative":{"mechanistic_narrative":"CKMT1A is a mitochondrial creatine kinase that participates in the phosphocreatine energy-transfer shuttle linking mitochondrial oxidative phosphorylation to cytosolic ATP replenishment [PMID:28521058]. In human brown adipose tissue it is selectively enriched relative to white adipose tissue, where it functions as a modulator of ATP synthase-coupled respiration acting in parallel with UCP1-mediated uncoupled respiration as a distinct energy-expenditure pathway [PMID:27418403]. Despite this role in mitochondrial energetics, CKMT1A is not the creatine kinase that governs mitochondrial ATP production through the CKB-AKT-mPTP axis: silencing CKMT1A does not alter sensitivity to F1F0 ATP synthase inhibition, distinguishing it functionally from the cytosolic isoform CKB [PMID:38896801]. In hepatocellular carcinoma, CKMT1A acts as the downstream effector of an lncRNA n335586/miR-924 ceRNA circuit, where de-repression of CKMT1A promotes epithelial-mesenchymal transition, migration, and metastasis [PMID:29753758]. Beyond these contexts, the enzymatic and structural biology of CKMT1A has not been directly characterized in the available corpus.","teleology":[{"year":2016,"claim":"Established a tissue-specific physiological role by showing CKMT1A is selectively enriched in brown adipose tissue, positioning it within an ATP synthase-coupled energy-expenditure pathway parallel to UCP1.","evidence":"Comparative quantitative proteomics of primary human brown vs. white adipose tissue","pmids":["27418403"],"confidence":"Medium","gaps":["No direct enzymatic assay or knockdown/knockout in this study","Causal contribution to thermogenic energy expenditure not functionally tested"]},{"year":2017,"claim":"Linked CKMT1A abundance to oxidative-phosphorylation-coupled energy transfer in muscle, supporting its placement in the phosphocreatine shuttle connecting mitochondrial ATP synthesis to cytosolic demand.","evidence":"Reanalysis of proteomic mass spectrometry dataset from broiler pectoralis muscle (high vs. low feed efficiency)","pmids":["28521058"],"confidence":"Low","gaps":["Correlative abundance only, no functional assay of CKMT1A","No knockdown or rescue to establish causality"]},{"year":2018,"claim":"Defined a post-transcriptional regulatory circuit and a disease role, identifying CKMT1A as the functional effector of an lncRNA/miRNA ceRNA axis driving cancer cell migration and metastasis.","evidence":"In vitro migration/invasion assays, in vivo metastasis model, and miR-924 binding validation in HCC","pmids":["29753758"],"confidence":"Medium","gaps":["Mechanism by which CKMT1A promotes EMT not resolved","Whether its creatine kinase activity is required for the pro-metastatic effect unknown"]},{"year":2024,"claim":"Resolved which creatine kinase isoform controls mitochondrial ATP production, showing through a negative result that CKMT1A is dispensable for F1F0 ATP synthase inhibitor sensitivity unlike cytosolic CKB.","evidence":"siRNA silencing of CKMT1A/CKMT1B with cell viability and ATP production readouts","pmids":["38896801"],"confidence":"Medium","gaps":["Does not address CKMT1A's role in other energetic or signaling contexts","Single lab, single cell-model dependency"]},{"year":2024,"claim":"Added a candidate post-translational modification, identifying CKMT1A as an O-GalNAc glycoprotein substrate of GALNT9 in a glycoproteomic screen.","evidence":"Lectin affinity chromatography and LC-MS/MS in SH-SY5Y cells with GALNT9 knockdown","pmids":["38401583"],"confidence":"Low","gaps":["No glycosylation site mapping on CKMT1A","Functional consequence of CKMT1A glycosylation not tested specifically"]},{"year":null,"claim":"The direct enzymatic kinetics, structural organization, and the mechanism by which CKMT1A drives EMT remain unresolved.","evidence":"No direct biochemical or structural characterization present in the corpus","pmids":[],"confidence":"Low","gaps":["No reconstituted creatine kinase activity assay for CKMT1A","No structural model","Connection between energy-transfer role and pro-metastatic function unestablished"]}],"mechanism_profile":{"molecular_activity":[{"term_id":"GO:0016740","term_label":"transferase activity","supporting_discovery_ids":[0,2]}],"localization":[{"term_id":"GO:0005739","term_label":"mitochondrion","supporting_discovery_ids":[0,2]}],"pathway":[{"term_id":"R-HSA-1430728","term_label":"Metabolism","supporting_discovery_ids":[0,2]}],"complexes":[],"partners":[],"other_free_text":[]}},"prefetch_data":{"uniprot":{"accession":"P12532","full_name":"Creatine kinase U-type, mitochondrial","aliases":["Acidic-type mitochondrial creatine kinase","Mia-CK","Ubiquitous mitochondrial creatine kinase","U-MtCK"],"length_aa":417,"mass_kda":47.0,"function":"Reversibly catalyzes the transfer of phosphate between ATP and various phosphogens (e.g. creatine phosphate). Creatine kinase isoenzymes play a central role in energy transduction in tissues with large, fluctuating energy demands, such as skeletal muscle, heart, brain and spermatozoa","subcellular_location":"Mitochondrion inner membrane","url":"https://www.uniprot.org/uniprotkb/P12532/entry"},"depmap":{"release":"DepMap","has_data":false,"is_common_essential":false,"resolved_as":"","url":"https://depmap.org/portal/gene/CKMT1A"},"opencell":{"profiled":false,"resolved_as":"","ensg_id":"","cell_line_id":"","localizations":[],"interactors":[],"url":"https://opencell.sf.czbiohub.org/search/CKMT1A","total_profiled":1310},"omim":[{"mim_id":"614647","title":"COENZYME Q6, MONOOXYGENASE; COQ6","url":"https://www.omim.org/entry/614647"},{"mim_id":"613415","title":"CREATINE KINASE, MITOCHONDRIAL 1A; CKMT1A","url":"https://www.omim.org/entry/613415"},{"mim_id":"123290","title":"CREATINE KINASE, MITOCHONDRIAL 1B; CKMT1B","url":"https://www.omim.org/entry/123290"}],"hpa":{"profiled":true,"resolved_as":"","reliability":"","locations":[],"tissue_specificity":"Tissue enhanced","tissue_distribution":"Detected in many","driving_tissues":[{"tissue":"brain","ntpm":73.9},{"tissue":"esophagus","ntpm":82.6},{"tissue":"intestine","ntpm":70.3}],"url":"https://www.proteinatlas.org/search/CKMT1A"},"hgnc":{"alias_symbol":[],"prev_symbol":["CKMT1"]},"alphafold":{"accession":"P12532","domains":[{"cath_id":"1.10.135.10","chopping":"50-129","consensus_level":"medium","plddt":96.5146,"start":50,"end":129}],"viewer_url":"https://alphafold.ebi.ac.uk/entry/P12532","model_url":"https://alphafold.ebi.ac.uk/files/AF-P12532-F1-model_v6.cif","pae_url":"https://alphafold.ebi.ac.uk/files/AF-P12532-F1-predicted_aligned_error_v6.png","plddt_mean":89.31},"mouse_models":{"mgi_url":"https://www.informatics.jax.org/marker/summary?nomen=CKMT1A","jax_strain_url":"https://www.jax.org/strain/search?query=CKMT1A"},"sequence":{"accession":"P12532","fasta_url":"https://rest.uniprot.org/uniprotkb/P12532.fasta","uniprot_url":"https://www.uniprot.org/uniprotkb/P12532/entry","alphafold_viewer_url":"https://alphafold.ebi.ac.uk/entry/P12532"}},"corpus_meta":[{"pmid":"29753758","id":"PMC_29753758","title":"LncRNA n335586/miR-924/CKMT1A axis contributes to cell migration and invasion in hepatocellular carcinoma cells.","date":"2018","source":"Cancer letters","url":"https://pubmed.ncbi.nlm.nih.gov/29753758","citation_count":62,"is_preprint":false},{"pmid":"27418403","id":"PMC_27418403","title":"Proteomic Analysis of Human Brown Adipose Tissue Reveals Utilization of Coupled and Uncoupled Energy Expenditure Pathways.","date":"2016","source":"Scientific reports","url":"https://pubmed.ncbi.nlm.nih.gov/27418403","citation_count":61,"is_preprint":false},{"pmid":"28235404","id":"PMC_28235404","title":"Progesterone signalling in broiler skeletal muscle is associated with divergent feed efficiency.","date":"2017","source":"BMC systems biology","url":"https://pubmed.ncbi.nlm.nih.gov/28235404","citation_count":29,"is_preprint":false},{"pmid":"31991880","id":"PMC_31991880","title":"The Effects of Early-Onset Pre-Eclampsia on Placental Creatine Metabolism in the Third Trimester.","date":"2020","source":"International journal of molecular sciences","url":"https://pubmed.ncbi.nlm.nih.gov/31991880","citation_count":15,"is_preprint":false},{"pmid":"28521058","id":"PMC_28521058","title":"Enhanced expression of proteins involved in energy production and transfer in breast muscle of pedigree male broilers exhibiting high feed efficiency.","date":"2017","source":"Poultry science","url":"https://pubmed.ncbi.nlm.nih.gov/28521058","citation_count":14,"is_preprint":false},{"pmid":"38896801","id":"PMC_38896801","title":"CKB Promotes Mitochondrial ATP Production by Suppressing Permeability Transition Pore.","date":"2024","source":"Advanced science (Weinheim, Baden-Wurttemberg, Germany)","url":"https://pubmed.ncbi.nlm.nih.gov/38896801","citation_count":13,"is_preprint":false},{"pmid":"35705641","id":"PMC_35705641","title":"An integrative pan-cancer analysis of molecular characteristics and oncogenic role of mitochondrial creatine kinase 1A (CKMT1A) in human tumors.","date":"2022","source":"Scientific reports","url":"https://pubmed.ncbi.nlm.nih.gov/35705641","citation_count":6,"is_preprint":false},{"pmid":"34884994","id":"PMC_34884994","title":"Detection of VAR2CSA-Captured Colorectal Cancer Cells from Blood Samples by Real-Time Reverse Transcription PCR.","date":"2021","source":"Cancers","url":"https://pubmed.ncbi.nlm.nih.gov/34884994","citation_count":6,"is_preprint":false},{"pmid":"38401583","id":"PMC_38401583","title":"Deficiency of polypeptide N-acetylgalactosamine transferase 9 contributes to a risk for Parkinson's disease via mitochondrial dysfunctions.","date":"2024","source":"International journal of biological macromolecules","url":"https://pubmed.ncbi.nlm.nih.gov/38401583","citation_count":6,"is_preprint":false},{"pmid":"40341240","id":"PMC_40341240","title":"Refining the detection of complex rearrangements in 15q15.3 region involving the STRC gene in hereditary hearing loss patients.","date":"2025","source":"Journal of human genetics","url":"https://pubmed.ncbi.nlm.nih.gov/40341240","citation_count":2,"is_preprint":false},{"pmid":"41899633","id":"PMC_41899633","title":"A Mitochondrial Plasma Proteomic Signature Identifies Metastatic Chromophobe Renal Cell Carcinoma.","date":"2026","source":"Cancers","url":"https://pubmed.ncbi.nlm.nih.gov/41899633","citation_count":0,"is_preprint":false}],"cost":{"stage1":{"model":"claude-sonnet-4-6","input_tokens":7929,"output_tokens":1380,"usd":0.022243,"stage1_stop_reason":"end_turn"},"stage2":{"model":"claude-opus-4-8","input_tokens":8053,"output_tokens":1950,"usd":0.044507,"stage2_stop_reason":"end_turn"},"total_usd":0.06675,"stage1_batch_id":"msgbatch_01ACAxJQabDsht39JXeWG22d","stage2_batch_id":"msgbatch_01QEU22A9U5sbPTgsMzTmvSf","note":"batch pricing = 50% of standard"},"stage1_raw":"```json\n{\n  \"discoveries\": [\n    {\n      \"year\": 2016,\n      \"finding\": \"CKMT1A (along with CKMT1B and CKMT2) is exclusively expressed in human brown adipose tissue (BAT) compared to adjacent white adipose tissue, where it functions as an effective modulator of ATP synthase-coupled respiration, acting in parallel with UCP1-mediated uncoupled respiration as a distinct energy expenditure pathway.\",\n      \"method\": \"Comparative proteotype analysis (quantitative proteomics) of primary human brown vs. white adipose tissue\",\n      \"journal\": \"Scientific reports\",\n      \"confidence\": \"Medium\",\n      \"confidence_rationale\": \"Tier 2 / Weak — quantitative proteomic profiling with functional interpretation, single lab, single method, no direct enzymatic assay or KD/KO in this study\",\n      \"pmids\": [\"27418403\"],\n      \"is_preprint\": false\n    },\n    {\n      \"year\": 2018,\n      \"finding\": \"LncRNA n335586 promotes HCC cell migration and invasion by competitively binding miR-924, thereby de-repressing CKMT1A expression; CKMT1A is the functional downstream effector of this axis in driving epithelial-mesenchymal transition and metastasis.\",\n      \"method\": \"In vitro migration/invasion assays, in vivo metastasis model, competitive endogenous RNA (ceRNA) mechanistic studies with miR-924 binding validation\",\n      \"journal\": \"Cancer letters\",\n      \"confidence\": \"Medium\",\n      \"confidence_rationale\": \"Tier 2 / Moderate — functional rescue/knockdown experiments with in vivo validation and ceRNA mechanism, single lab but multiple orthogonal methods\",\n      \"pmids\": [\"29753758\"],\n      \"is_preprint\": false\n    },\n    {\n      \"year\": 2017,\n      \"finding\": \"CKMT1A protein is up-regulated 7.8-fold in breast muscle of high feed efficiency broilers compared to low feed efficiency broilers, indicating CKMT1A participates in the mitochondrial creatine kinase energy transfer system linking oxidative phosphorylation to cytosolic ATP replenishment via phosphocreatine.\",\n      \"method\": \"Proteomic analysis (re-examination of mass spectrometry dataset) of broiler pectoralis muscle\",\n      \"journal\": \"Poultry science\",\n      \"confidence\": \"Low\",\n      \"confidence_rationale\": \"Tier 3 / Weak — single proteomics dataset reanalysis, no direct functional assay of CKMT1A, no KD/KO\",\n      \"pmids\": [\"28521058\"],\n      \"is_preprint\": false\n    },\n    {\n      \"year\": 2024,\n      \"finding\": \"Silencing CKMT1A (or CKMT1B) does not lead to loss of sensitivity to F1F0 ATP synthase inhibition, unlike CKB silencing; this negative result indicates CKMT1A is not the creatine kinase responsible for regulating mitochondrial ATP production via the CKB-AKT-mPTP axis.\",\n      \"method\": \"siRNA silencing of CKMT1A/CKMT1B in cells relying on mitochondrial F1F0 ATP synthase, cell viability and ATP production assays\",\n      \"journal\": \"Advanced science (Weinheim, Baden-Wurttemberg, Germany)\",\n      \"confidence\": \"Medium\",\n      \"confidence_rationale\": \"Tier 2 / Moderate — direct gene silencing with functional readout, negative result replicated across CKMT1A and CKMT1B in same study, single lab\",\n      \"pmids\": [\"38896801\"],\n      \"is_preprint\": false\n    },\n    {\n      \"year\": 2024,\n      \"finding\": \"CKMT1A was identified as a glycoprotein substrate of GALNT9 (polypeptide N-acetylgalactosamine transferase 9), detected by lectin affinity chromatography and LC-MS/MS as carrying GalNAc O-glycosylation; GALNT9 deficiency is associated with mitochondrial dysfunction including increased ROS and mPTP opening.\",\n      \"method\": \"Lectin affinity chromatography purification of GalNAc-exposing glycoproteins followed by LC-MS/MS identification in SH-SY5Y cells with GALNT9 siRNA knockdown\",\n      \"journal\": \"International journal of biological macromolecules\",\n      \"confidence\": \"Low\",\n      \"confidence_rationale\": \"Tier 3 / Weak — MS identification of CKMT1A as a glycoprotein in a screen, no direct site mapping or functional consequence of CKMT1A glycosylation specifically tested\",\n      \"pmids\": [\"38401583\"],\n      \"is_preprint\": false\n    }\n  ],\n  \"current_model\": \"CKMT1A is a mitochondrial creatine kinase that participates in the phosphocreatine energy shuttle linking mitochondrial oxidative phosphorylation to cytosolic ATP buffering, is exclusively enriched in brown adipose tissue as a modulator of ATP synthase-coupled respiration, can be regulated post-transcriptionally via a ceRNA mechanism (lncRNA n335586/miR-924) to promote cancer cell migration, and carries O-GalNAc glycosylation catalyzed by GALNT9; notably, CKMT1A itself (unlike the cytosolic isoform CKB) does not mediate mitochondrial ATP production through the CKB-AKT-mPTP signaling axis.\"\n}\n```","stage2_raw":"{\n  \"mechanistic_narrative\": \"CKMT1A is a mitochondrial creatine kinase that participates in the phosphocreatine energy-transfer shuttle linking mitochondrial oxidative phosphorylation to cytosolic ATP replenishment [#2]. In human brown adipose tissue it is selectively enriched relative to white adipose tissue, where it functions as a modulator of ATP synthase-coupled respiration acting in parallel with UCP1-mediated uncoupled respiration as a distinct energy-expenditure pathway [#0]. Despite this role in mitochondrial energetics, CKMT1A is not the creatine kinase that governs mitochondrial ATP production through the CKB-AKT-mPTP axis: silencing CKMT1A does not alter sensitivity to F1F0 ATP synthase inhibition, distinguishing it functionally from the cytosolic isoform CKB [#3]. In hepatocellular carcinoma, CKMT1A acts as the downstream effector of an lncRNA n335586/miR-924 ceRNA circuit, where de-repression of CKMT1A promotes epithelial-mesenchymal transition, migration, and metastasis [#1]. Beyond these contexts, the enzymatic and structural biology of CKMT1A has not been directly characterized in the available corpus.\",\n  \"teleology\": [\n    {\n      \"year\": 2016,\n      \"claim\": \"Established a tissue-specific physiological role by showing CKMT1A is selectively enriched in brown adipose tissue, positioning it within an ATP synthase-coupled energy-expenditure pathway parallel to UCP1.\",\n      \"evidence\": \"Comparative quantitative proteomics of primary human brown vs. white adipose tissue\",\n      \"pmids\": [\"27418403\"],\n      \"confidence\": \"Medium\",\n      \"gaps\": [\"No direct enzymatic assay or knockdown/knockout in this study\", \"Causal contribution to thermogenic energy expenditure not functionally tested\"]\n    },\n    {\n      \"year\": 2017,\n      \"claim\": \"Linked CKMT1A abundance to oxidative-phosphorylation-coupled energy transfer in muscle, supporting its placement in the phosphocreatine shuttle connecting mitochondrial ATP synthesis to cytosolic demand.\",\n      \"evidence\": \"Reanalysis of proteomic mass spectrometry dataset from broiler pectoralis muscle (high vs. low feed efficiency)\",\n      \"pmids\": [\"28521058\"],\n      \"confidence\": \"Low\",\n      \"gaps\": [\"Correlative abundance only, no functional assay of CKMT1A\", \"No knockdown or rescue to establish causality\"]\n    },\n    {\n      \"year\": 2018,\n      \"claim\": \"Defined a post-transcriptional regulatory circuit and a disease role, identifying CKMT1A as the functional effector of an lncRNA/miRNA ceRNA axis driving cancer cell migration and metastasis.\",\n      \"evidence\": \"In vitro migration/invasion assays, in vivo metastasis model, and miR-924 binding validation in HCC\",\n      \"pmids\": [\"29753758\"],\n      \"confidence\": \"Medium\",\n      \"gaps\": [\"Mechanism by which CKMT1A promotes EMT not resolved\", \"Whether its creatine kinase activity is required for the pro-metastatic effect unknown\"]\n    },\n    {\n      \"year\": 2024,\n      \"claim\": \"Resolved which creatine kinase isoform controls mitochondrial ATP production, showing through a negative result that CKMT1A is dispensable for F1F0 ATP synthase inhibitor sensitivity unlike cytosolic CKB.\",\n      \"evidence\": \"siRNA silencing of CKMT1A/CKMT1B with cell viability and ATP production readouts\",\n      \"pmids\": [\"38896801\"],\n      \"confidence\": \"Medium\",\n      \"gaps\": [\"Does not address CKMT1A's role in other energetic or signaling contexts\", \"Single lab, single cell-model dependency\"]\n    },\n    {\n      \"year\": 2024,\n      \"claim\": \"Added a candidate post-translational modification, identifying CKMT1A as an O-GalNAc glycoprotein substrate of GALNT9 in a glycoproteomic screen.\",\n      \"evidence\": \"Lectin affinity chromatography and LC-MS/MS in SH-SY5Y cells with GALNT9 knockdown\",\n      \"pmids\": [\"38401583\"],\n      \"confidence\": \"Low\",\n      \"gaps\": [\"No glycosylation site mapping on CKMT1A\", \"Functional consequence of CKMT1A glycosylation not tested specifically\"]\n    },\n    {\n      \"year\": null,\n      \"claim\": \"The direct enzymatic kinetics, structural organization, and the mechanism by which CKMT1A drives EMT remain unresolved.\",\n      \"evidence\": \"No direct biochemical or structural characterization present in the corpus\",\n      \"pmids\": [],\n      \"confidence\": \"Low\",\n      \"gaps\": [\"No reconstituted creatine kinase activity assay for CKMT1A\", \"No structural model\", \"Connection between energy-transfer role and pro-metastatic function unestablished\"]\n    }\n  ],\n  \"mechanism_profile\": {\n    \"molecular_activity\": [\n      {\"term_id\": \"GO:0016740\", \"supporting_discovery_ids\": [0, 2]}\n    ],\n    \"localization\": [\n      {\"term_id\": \"GO:0005739\", \"supporting_discovery_ids\": [0, 2]}\n    ],\n    \"pathway\": [\n      {\"term_id\": \"R-HSA-1430728\", \"supporting_discovery_ids\": [0, 2]}\n    ],\n    \"complexes\": [],\n    \"partners\": [],\n    \"other_free_text\": []\n  }\n}","audit_flag":null,"evaluation":{"pairwise":"win","faith_supported":4,"faith_total":4,"faith_pct":100.0}}