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(2016). https://pubmed.ncbi.nlm.nih.gov/27729528/ DOI: 10.1073/pnas.1608679113","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"tissue_or_cell_type","value_text":"Cell-free","comparator":null,"unit":null,"notes":"","entity":null}],"evidence":[{"id":"c6376ece-268a-5fe2-80de-3e2c27d4ecf9","evidence_kind":"source_excerpt","locator":"Lines 1033-1045","start_line":1033,"end_line":1045,"excerpt":"### c-reg-tet-sufficient-ferrous-iron\nAt pH 6.8 with sufficient Fe(II), murine TET1-CD remained active without ascorbate and adding ascorbate did not increase the measured activity; substrate-free preincubation also did not rapidly destroy activity.\nCondition category: normal\nnutrient_topic: Vitamin C research collection; topical membership is not evidence of a direct dietary effect.\nplain_language: With usable iron maintained in this assay, the enzyme did not require extra vitamin C to keep working.\norganism: Mus musculus protein expressed in Escherichia coli\ntissue_or_cell_type: Cell-free\nexperimental_model: Recombinant murine TET1 catalytic domain expressed in E. coli; methylated 86-mer DNA ELISA assay\nlimitations: A conditional biochemical null result; it does not negate ascorbate enhancement in cells or more oxidizing buffers.\nexposure: 1.5 µM TET1-CD, 0.5 µM DNA, 1 mM 2-oxoglutarate, 10 or 100 µM iron; sodium L-ascorbate 1 mM; pH 6.8 versus pH 8.0. Substrate-free preincubation up to 30 min.\ncross_nutrient: true\nevidence_location: Figure 1D; Figure S1B–D\n[c-reg-hore] Retinol and ascorbate drive erasure of epigenetic memory and enhance reprogramming to naïve pluripotency by complementary mechanisms. (2016). https://pubmed.ncbi.nlm.nih.gov/27729528/ DOI: 10.1073/pnas.1608679113","model_system":"Recombinant murine TET1 catalytic domain expressed in E. coli; methylated 86-mer DNA ELISA assay","directness":"author_interpretation","verification_status":"source_derived_draft","notes":"Exact curation-document quotation, not publisher quotation. Study references: [c-reg-hore] Retinol and ascorbate drive erasure of epigenetic memory and enhance reprogramming to naïve pluripotency by complementary mechanisms. 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