Component

Serum and glucocorticoid-regulated kinase 1

Canonical protein; experimental species, state, expression context and nutritional dependence are specified per claim.

8 recorded relationships. Experimental role, claim status and evidence remain attached to each record.

Read recorded mechanisms Open recursive mind map

How nutrients influence it

Every nutrient with a recorded effect on this component, credited to the nutrient that acted rather than the chapter that recorded it. Open a nutrient to see the findings and the conditions they were measured under.

How nutrients reach it in more than one step

Chains of two or more recorded steps that end here, grouped by the nutrient they start from. Each step is a separate finding, so a chain is a route a mechanism could take, not proof that it does.

Tracing routes…

What it does

Every recorded relationship this component is part of, grouped by its role. Plain wording comes first; the technical statement follows.

Recorded relationships

What it acts on

  1. Coexpression of mouse sgk with the three ENaC subunits increased sodium current in Xenopus oocytes.

    Serum and glucocorticoid-regulated kinase 1 → ENaC-mediated sodium current source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/sodium-research/10358046.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7d53e3e8ce41bb21d5cac2a5bfe6a6abdc702d0870add9c0a002e58ac374a97b", "start_char": 0, "end_char": 1343, "text_sha256": "7d53e3e8ce41bb21d5cac2a5bfe6a6abdc702d0870add9c0a002e58ac374a97b"}
    experimental_model
    Immediate-early gene induction and channel coexpression
    exposure
    Aldosterone exposure; receptor dependence and protein-synthesis tests
    limitations
    Cell and oocyte mechanism; the study does not imply that dietary sodium directly activates SGK1 in every tissue.
    nutrient_topic
    Sodium research collection; topical membership is not evidence of a direct dietary effect. · Sodium
    organism
    Rabbit/mouse collecting-duct preparations; mouse SGK in Xenopus oocytes
    plain_language
    The kinase can increase sodium flow through ENaC.
    primary_references
    [sodium-p10358046] sgk is an aldosterone-induced kinase in the renal collecting duct. Effects on epithelial na+ channels. (1999). https://pubmed.ncbi.nlm.nih.gov/10358046/ DOI: 10.1074/jbc.274.24.16973
    tissue_or_cell_type
    Cortical collecting duct and expression system

    Sodium: gradients, nutrient transport, fluid regulation and loss states (2026-09-17) · lines 408–419

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Immediate-early gene induction and channel coexpression · source_derived_draft · unverified_draft

    ### sodium-sgk-enac Coexpression of mouse sgk with the three ENaC subunits increased sodium current in Xenopus oocytes. Condition category: normal nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The kinase can increase sodium flow through ENaC. organism: Rabbit/mouse collecting-duct preparations; mouse SGK in Xenopus oocytes tissue_or_cell_type: Cortical collecting duct and expression system experimental_model: Immediate-early gene induction and channel coexpression limitations: Cell and oocyte mechanism; the study does not imply that dietary sodium directly activates SGK1 in every tissue. exposure: Aldosterone exposure; receptor dependence and protein-synthesis tests evidence_span: {"source_cache": "artifacts/sodium-research/10358046.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7d53e3e8ce41bb21d5cac2a5bfe6a6abdc702d0870add9c0a002e58ac374a97b", "start_char": 0, "end_char": 1343, "text_sha256": "7d53e3e8ce41bb21d5cac2a5bfe6a6abdc702d0870add9c0a002e58ac374a97b"} [sodium-p10358046] sgk is an aldosterone-induced kinase in the renal collecting duct. Effects on epithelial na+ channels. (1999). https://pubmed.ncbi.nlm.nih.gov/10358046/ DOI: 10.1074/jbc.274.24.16973
    Complete structured claim and evidence

  2. The study identified SGK1-dependent deactivation of Foxo1 in the TH17 program.

    Serum and glucocorticoid-regulated kinase 1 → Mouse forkhead transcription factor Foxo1 source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/sodium-research/23467085.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "25fdc34faa9d6f0b84dfc9daf98ecc8e09f2486853b9e99bdae552e5ca8c5b2e", "start_char": 0, "end_char": 1656, "text_sha256": "25fdc34faa9d6f0b84dfc9daf98ecc8e09f2486853b9e99bdae552e5ca8c5b2e"}
    experimental_model
    T-cell transcriptional profiling, kinase loss and experimental autoimmune assays
    exposure
    NaCl elevation and Sgk1 perturbation
    limitations
    The SGK1–Foxo1–IL23R pathway is scoped to this immune-cell program, not universal sodium action.
    nutrient_topic
    Sodium research collection; topical membership is not evidence of a direct dietary effect. · Sodium
    organism
    Mouse
    plain_language
    The same kinase family used in kidney salt handling has another role in immune cells.
    primary_references
    [sodium-p23467085] Induction of pathogenic TH17 cells by inducible salt-sensing kinase SGK1. (2013). https://pubmed.ncbi.nlm.nih.gov/23467085/ DOI: 10.1038/nature11984
    tissue_or_cell_type
    IL-23-responsive TH17 cells

    Sodium: gradients, nutrient transport, fluid regulation and loss states (2026-09-17) · lines 551–562

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · T-cell transcriptional profiling, kinase loss and experimental autoimmune assays · source_derived_draft · unverified_draft

    ### sodium-sgk-foxo The study identified SGK1-dependent deactivation of Foxo1 in the TH17 program. Condition category: normal nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The same kinase family used in kidney salt handling has another role in immune cells. organism: Mouse tissue_or_cell_type: IL-23-responsive TH17 cells experimental_model: T-cell transcriptional profiling, kinase loss and experimental autoimmune assays limitations: The SGK1–Foxo1–IL23R pathway is scoped to this immune-cell program, not universal sodium action. exposure: NaCl elevation and Sgk1 perturbation evidence_span: {"source_cache": "artifacts/sodium-research/23467085.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "25fdc34faa9d6f0b84dfc9daf98ecc8e09f2486853b9e99bdae552e5ca8c5b2e", "start_char": 0, "end_char": 1656, "text_sha256": "25fdc34faa9d6f0b84dfc9daf98ecc8e09f2486853b9e99bdae552e5ca8c5b2e"} [sodium-p23467085] Induction of pathogenic TH17 cells by inducible salt-sensing kinase SGK1. (2013). https://pubmed.ncbi.nlm.nih.gov/23467085/ DOI: 10.1038/nature11984
    Complete structured claim and evidence

  3. Silencing or chemical inhibition of SGK1 blocked the high-salt enhancement of TH17 differentiation in the study.

    Serum and glucocorticoid-regulated kinase 1 → Th17 differentiation source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/sodium-research/23467095.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "d16bb4b4becde85238492e01054f360aeaf57ea90015cba99459cd155fa4251f", "start_char": 0, "end_char": 1913, "text_sha256": "d16bb4b4becde85238492e01054f360aeaf57ea90015cba99459cd155fa4251f"}
    experimental_model
    Cytokine-driven T-cell culture, gene silencing/inhibition and experimental autoimmune encephalomyelitis
    exposure
    Increased NaCl in culture or high-salt mouse diet
    limitations
    NaCl exposure includes both ions and osmotic context. Mouse EAE and cultured T cells do not establish that salt causes human multiple sclerosis.
    nutrient_topic
    Sodium research collection; topical membership is not evidence of a direct dietary effect. · Sodium
    organism
    Human and mouse T cells; mouse disease model
    plain_language
    Blocking SGK1 interrupted this particular salt-sensitive immune response.
    primary_references
    [sodium-p23467095] Sodium chloride drives autoimmune disease by the induction of pathogenic TH17 cells. (2013). https://pubmed.ncbi.nlm.nih.gov/23467095/ DOI: 10.1038/nature11868
    tissue_or_cell_type
    T-helper cells and experimental CNS autoimmunity

    Sodium: gradients, nutrient transport, fluid regulation and loss states (2026-09-17) · lines 525–536

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cytokine-driven T-cell culture, gene silencing/inhibition and experimental autoimmune encephalomyelitis · source_derived_draft · unverified_draft

    ### sodium-th17-sgk1 Silencing or chemical inhibition of SGK1 blocked the high-salt enhancement of TH17 differentiation in the study. Condition category: normal nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Blocking SGK1 interrupted this particular salt-sensitive immune response. organism: Human and mouse T cells; mouse disease model tissue_or_cell_type: T-helper cells and experimental CNS autoimmunity experimental_model: Cytokine-driven T-cell culture, gene silencing/inhibition and experimental autoimmune encephalomyelitis limitations: NaCl exposure includes both ions and osmotic context. Mouse EAE and cultured T cells do not establish that salt causes human multiple sclerosis. exposure: Increased NaCl in culture or high-salt mouse diet evidence_span: {"source_cache": "artifacts/sodium-research/23467095.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "d16bb4b4becde85238492e01054f360aeaf57ea90015cba99459cd155fa4251f", "start_char": 0, "end_char": 1913, "text_sha256": "d16bb4b4becde85238492e01054f360aeaf57ea90015cba99459cd155fa4251f"} [sodium-p23467095] Sodium chloride drives autoimmune disease by the induction of pathogenic TH17 cells. (2013). https://pubmed.ncbi.nlm.nih.gov/23467095/ DOI: 10.1038/nature11868
    Complete structured claim and evidence

  4. Renal Sgk1 deletion blunted the early increase in urinary K excretion on high-K feeding, with hyperkalemia and reduced ENaC processing.

    Serum and glucocorticoid-regulated kinase 1 → Urinary potassium excretion source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    Impaired ENaC sodium-channel adaptation accompanies defective K clearance.
    evidence_location
    Results Figure 2; two-day versus five-day dietary comparison.
    experimental_model
    Inducible tubular deletion; two-day high-K citrate diet
    limitations
    Excretion approached controls after longer adaptation; ROMK apical localization increased rather than decreased.
    nutrient_topic
    Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
    organism
    Mus musculus
    plain_language
    Removing kidney SGK1 impairs the initial ability to clear a potassium load.
    primary_references
    [al-qusairi-2016-renal-sgk1] Renal tubular SGK1 deficiency causes impaired K+ excretion via loss of regulation of NEDD4-2/WNK1 and ENaC (2016). https://pmc.ncbi.nlm.nih.gov/articles/PMC5005279/ DOI: 10.1152/ajprenal.00002.2016
    tissue_or_cell_type
    Kidney tubules
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 434–445

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Inducible tubular deletion; two-day high-K citrate diet · source_derived_draft · unverified_draft

    ### renal-sgk1-loss-impairs-high-k-excretion Renal Sgk1 deletion blunted the early increase in urinary K excretion on high-K feeding, with hyperkalemia and reduced ENaC processing. Condition category: machinery_impairment nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Removing kidney SGK1 impairs the initial ability to clear a potassium load. organism: Mus musculus tissue_or_cell_type: Kidney tubules experimental_model: Inducible tubular deletion; two-day high-K citrate diet limitations: Excretion approached controls after longer adaptation; ROMK apical localization increased rather than decreased. cross_nutrient: Impaired ENaC sodium-channel adaptation accompanies defective K clearance. evidence_location: Results Figure 2; two-day versus five-day dietary comparison. [al-qusairi-2016-renal-sgk1] Renal tubular SGK1 deficiency causes impaired K+ excretion via loss of regulation of NEDD4-2/WNK1 and ENaC (2016). https://pmc.ncbi.nlm.nih.gov/articles/PMC5005279/ DOI: 10.1152/ajprenal.00002.2016
    Complete structured claim and evidence

  5. Sgk1 phosphorylated Nedd4-2 at Ser444 and less strongly Ser338 in Xenopus constructs.

    Serum and glucocorticoid-regulated kinase 1 → NEDD4-like E3 ubiquitin protein ligase source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    This biochemical sodium-channel pathway contributes to the machinery for K handling.
    evidence_location
    Figure 2.
    experimental_model
    Expression, kinase-dead and site-mutant experiments
    limitations
    Residue numbers are construct/species-specific; nutritional K sensing was not tested.
    nutrient_topic
    Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
    organism
    Xenopus laevis
    plain_language
    SGK1 modifies the protein that normally restrains sodium channels.
    primary_references
    [debonneville-2001-sgk-nedd4] Phosphorylation of Nedd4-2 by Sgk1 regulates epithelial Na(+) channel cell surface expression (2001). https://pubmed.ncbi.nlm.nih.gov/11742982/ DOI: 10.1093/emboj/20.24.7052
    tissue_or_cell_type
    Oocytes

    Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 408–419

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Expression, kinase-dead and site-mutant experiments · source_derived_draft · unverified_draft

    ### renal-sgk1-phosphorylates-nedd4l Sgk1 phosphorylated Nedd4-2 at Ser444 and less strongly Ser338 in Xenopus constructs. Condition category: normal nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: SGK1 modifies the protein that normally restrains sodium channels. organism: Xenopus laevis tissue_or_cell_type: Oocytes experimental_model: Expression, kinase-dead and site-mutant experiments limitations: Residue numbers are construct/species-specific; nutritional K sensing was not tested. cross_nutrient: This biochemical sodium-channel pathway contributes to the machinery for K handling. evidence_location: Figure 2. [debonneville-2001-sgk-nedd4] Phosphorylation of Nedd4-2 by Sgk1 regulates epithelial Na(+) channel cell surface expression (2001). https://pubmed.ncbi.nlm.nih.gov/11742982/ DOI: 10.1093/emboj/20.24.7052
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Aldosterone increased collecting-duct sgk mRNA within 30 minutes through mineralocorticoid receptors without requiring new protein synthesis.

    Aldosterone → SGK1 transcript and protein expression source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/sodium-research/10358046.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7d53e3e8ce41bb21d5cac2a5bfe6a6abdc702d0870add9c0a002e58ac374a97b", "start_char": 0, "end_char": 1343, "text_sha256": "7d53e3e8ce41bb21d5cac2a5bfe6a6abdc702d0870add9c0a002e58ac374a97b"}
    experimental_model
    Immediate-early gene induction and channel coexpression
    exposure
    Aldosterone exposure; receptor dependence and protein-synthesis tests
    limitations
    Cell and oocyte mechanism; the study does not imply that dietary sodium directly activates SGK1 in every tissue.
    nutrient_topic
    Sodium research collection; topical membership is not evidence of a direct dietary effect. · Sodium
    organism
    Rabbit/mouse collecting-duct preparations; mouse SGK in Xenopus oocytes
    plain_language
    A hormone can quickly increase the instructions for a kinase that regulates sodium transport.
    primary_references
    [sodium-p10358046] sgk is an aldosterone-induced kinase in the renal collecting duct. Effects on epithelial na+ channels. (1999). https://pubmed.ncbi.nlm.nih.gov/10358046/ DOI: 10.1074/jbc.274.24.16973
    tissue_or_cell_type
    Cortical collecting duct and expression system

    Sodium: gradients, nutrient transport, fluid regulation and loss states (2026-09-17) · lines 395–406

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Immediate-early gene induction and channel coexpression · source_derived_draft · unverified_draft

    ### sodium-aldosterone-sgk Aldosterone increased collecting-duct sgk mRNA within 30 minutes through mineralocorticoid receptors without requiring new protein synthesis. Condition category: normal nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: A hormone can quickly increase the instructions for a kinase that regulates sodium transport. organism: Rabbit/mouse collecting-duct preparations; mouse SGK in Xenopus oocytes tissue_or_cell_type: Cortical collecting duct and expression system experimental_model: Immediate-early gene induction and channel coexpression limitations: Cell and oocyte mechanism; the study does not imply that dietary sodium directly activates SGK1 in every tissue. exposure: Aldosterone exposure; receptor dependence and protein-synthesis tests evidence_span: {"source_cache": "artifacts/sodium-research/10358046.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7d53e3e8ce41bb21d5cac2a5bfe6a6abdc702d0870add9c0a002e58ac374a97b", "start_char": 0, "end_char": 1343, "text_sha256": "7d53e3e8ce41bb21d5cac2a5bfe6a6abdc702d0870add9c0a002e58ac374a97b"} [sodium-p10358046] sgk is an aldosterone-induced kinase in the renal collecting duct. Effects on epithelial na+ channels. (1999). https://pubmed.ncbi.nlm.nih.gov/10358046/ DOI: 10.1074/jbc.274.24.16973
    Complete structured claim and evidence

  2. Modestly increased NaCl induced SGK1 and promoted IL-23 receptor expression in the tested T-cell program.

    Sodium chloride → Mouse IL-23 receptor expression source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/sodium-research/23467085.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "25fdc34faa9d6f0b84dfc9daf98ecc8e09f2486853b9e99bdae552e5ca8c5b2e", "start_char": 0, "end_char": 1656, "text_sha256": "25fdc34faa9d6f0b84dfc9daf98ecc8e09f2486853b9e99bdae552e5ca8c5b2e"}
    experimental_model
    T-cell transcriptional profiling, kinase loss and experimental autoimmune assays
    exposure
    NaCl elevation and Sgk1 perturbation
    limitations
    The SGK1–Foxo1–IL23R pathway is scoped to this immune-cell program, not universal sodium action.
    nutrient_topic
    Sodium research collection; topical membership is not evidence of a direct dietary effect. · Sodium
    organism
    Mouse
    plain_language
    Salt exposure can reinforce responsiveness to an immune signal in this model.
    primary_references
    [sodium-p23467085] Induction of pathogenic TH17 cells by inducible salt-sensing kinase SGK1. (2013). https://pubmed.ncbi.nlm.nih.gov/23467085/ DOI: 10.1038/nature11984
    tissue_or_cell_type
    IL-23-responsive TH17 cells

    Sodium: gradients, nutrient transport, fluid regulation and loss states (2026-09-17) · lines 577–588

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · T-cell transcriptional profiling, kinase loss and experimental autoimmune assays · source_derived_draft · unverified_draft

    ### sodium-salt-il23r Modestly increased NaCl induced SGK1 and promoted IL-23 receptor expression in the tested T-cell program. Condition category: normal nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Salt exposure can reinforce responsiveness to an immune signal in this model. organism: Mouse tissue_or_cell_type: IL-23-responsive TH17 cells experimental_model: T-cell transcriptional profiling, kinase loss and experimental autoimmune assays limitations: The SGK1–Foxo1–IL23R pathway is scoped to this immune-cell program, not universal sodium action. exposure: NaCl elevation and Sgk1 perturbation evidence_span: {"source_cache": "artifacts/sodium-research/23467085.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "25fdc34faa9d6f0b84dfc9daf98ecc8e09f2486853b9e99bdae552e5ca8c5b2e", "start_char": 0, "end_char": 1656, "text_sha256": "25fdc34faa9d6f0b84dfc9daf98ecc8e09f2486853b9e99bdae552e5ca8c5b2e"} [sodium-p23467085] Induction of pathogenic TH17 cells by inducible salt-sensing kinase SGK1. (2013). https://pubmed.ncbi.nlm.nih.gov/23467085/ DOI: 10.1038/nature11984
    Complete structured claim and evidence

  3. SGK-dependent Nedd4-2 phosphorylation reduced its ENaC interaction and increased ENaC surface expression in oocytes.

    SGK-phosphorylated NEDD4L → ENaC surface abundance source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    Higher sodium-channel availability can support the secretory machinery used for K balance.
    evidence_location
    Figures 3-5; interaction and anti-FLAG surface-labeling experiments.
    experimental_model
    Oocyte binding, current and surface-labeling assays
    limitations
    Molecular sufficiency does not establish exclusive control in intact kidneys.
    nutrient_topic
    Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
    organism
    Xenopus laevis
    plain_language
    Phosphorylation weakens the sodium-channel removal signal, leaving more channels at the surface.
    primary_references
    [debonneville-2001-sgk-nedd4] Phosphorylation of Nedd4-2 by Sgk1 regulates epithelial Na(+) channel cell surface expression (2001). https://pubmed.ncbi.nlm.nih.gov/11742982/ DOI: 10.1093/emboj/20.24.7052
    tissue_or_cell_type
    Oocytes

    Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 421–432

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Oocyte binding, current and surface-labeling assays · source_derived_draft · unverified_draft

    ### renal-phospho-nedd4l-releases-enac SGK-dependent Nedd4-2 phosphorylation reduced its ENaC interaction and increased ENaC surface expression in oocytes. Condition category: normal nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Phosphorylation weakens the sodium-channel removal signal, leaving more channels at the surface. organism: Xenopus laevis tissue_or_cell_type: Oocytes experimental_model: Oocyte binding, current and surface-labeling assays limitations: Molecular sufficiency does not establish exclusive control in intact kidneys. cross_nutrient: Higher sodium-channel availability can support the secretory machinery used for K balance. evidence_location: Figures 3-5; interaction and anti-FLAG surface-labeling experiments. [debonneville-2001-sgk-nedd4] Phosphorylation of Nedd4-2 by Sgk1 regulates epithelial Na(+) channel cell surface expression (2001). https://pubmed.ncbi.nlm.nih.gov/11742982/ DOI: 10.1093/emboj/20.24.7052
    Complete structured claim and evidence

In the sources

Preserved passages that mention this component, quoted exactly. Open one to read it in context.

    This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.

    Evidence, AI assistance and curation standards