Component

Transferrin glycosylation

Transferrin glycosylation. Experimental scope belongs to each linked claim.

3 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 acts on it

  1. Galactose plus uridine improved patient 2’s transferrin isoform pattern within 14 days.

    D-galactose and uridine coadministration → Transferrin glycosylation source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    D-Galactose (coadministered_substrate); Uridine (coadministered_substrate); Human ZIP8 (SLC39A8) (affected_protein)
    evidence_span
    {"source_cache": "artifacts/manganese-clinical-sources/riley2017.abstract.txt", "locator": "Indexed primary abstract", "file_sha256": "31e4e33ec5601d443fb2d469b2e2c7d1fd89c611db0f41938b43007952d0f005", "start_char": 0, "end_char": 1732, "text_sha256": "31e4e33ec5601d443fb2d469b2e2c7d1fd89c611db0f41938b43007952d0f005", "text_characters": 1732}
    experimental_model
    Two sisters with homozygous SLC39A8 p.Cys113Ser
    exposure
    Respiratory-chain tests in patient 1; manganese and transferrin measurements and galactose-plus-uridine response in patient 2.
    limitations
    Measurements were not performed in both sisters interchangeably. The proposed SOD2 explanation was not directly demonstrated; manganese had only recently been added and cannot explain the already observed 14-day galactose/uridine response.
    nutrient_topic
    Manganese research collection; topical membership is not evidence of a direct dietary effect. · Manganese
    organism
    Homo sapiens
    plain_language
    A combined substrate-support treatment improved the measured sugar pattern.
    primary_references
    [mn-clin-riley2017] A SLC39A8 variant causes manganese deficiency, and glycosylation and mitochondrial disorders. (2017). https://pubmed.ncbi.nlm.nih.gov/27995398/ DOI: 10.1007/s10545-016-0010-6
    tissue_or_cell_type
    Patient-specific liver, muscle and blood measurements
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Manganese: enzyme cofactors, glycosylation, transport and nutrient interactions (2026-09-17) · lines 1230–1242

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Two sisters with homozygous SLC39A8 p.Cys113Ser · source_derived_draft · unverified_draft

    ### mn-clin-zip8-gal-uridine Galactose plus uridine improved patient 2’s transferrin isoform pattern within 14 days. Condition category: machinery_impairment nutrient_topic: Manganese research collection; topical membership is not evidence of a direct dietary effect. plain_language: A combined substrate-support treatment improved the measured sugar pattern. organism: Homo sapiens tissue_or_cell_type: Patient-specific liver, muscle and blood measurements experimental_model: Two sisters with homozygous SLC39A8 p.Cys113Ser limitations: Measurements were not performed in both sisters interchangeably. The proposed SOD2 explanation was not directly demonstrated; manganese had only recently been added and cannot explain the already observed 14-day galactose/uridine response. exposure: Respiratory-chain tests in patient 1; manganese and transferrin measurements and galactose-plus-uridine response in patient 2. cross_nutrient: D-Galactose (coadministered_substrate); Uridine (coadministered_substrate); Human ZIP8 (SLC39A8) (affected_protein) evidence_span: {"source_cache": "artifacts/manganese-clinical-sources/riley2017.abstract.txt", "locator": "Indexed primary abstract", "file_sha256": "31e4e33ec5601d443fb2d469b2e2c7d1fd89c611db0f41938b43007952d0f005", "start_char": 0, "end_char": 1732, "text_sha256": "31e4e33ec5601d443fb2d469b2e2c7d1fd89c611db0f41938b43007952d0f005", "text_characters": 1732} [mn-clin-riley2017] A SLC39A8 variant causes manganese deficiency, and glycosylation and mitochondrial disorders. (2017). https://pubmed.ncbi.nlm.nih.gov/27995398/ DOI: 10.1007/s10545-016-0010-6
    Complete structured claim and evidence

  2. The genetic investigation linked SLC39A8 variants, very low blood manganese and type II glycosylation abnormalities.

    Human SLC39A8 transport deficiency → Transferrin glycosylation source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    Human ZIP8 (SLC39A8) (affected_protein); Blood manganese concentration (specimen not further specified) (low_marker); UDP-galactose (related_substrate)
    evidence_span
    {"source_cache": "artifacts/manganese-clinical-sources/park2015.abstract.txt", "locator": "Indexed primary abstract", "file_sha256": "c4e7009c947d1854370f8c9f62c206a8c2190b2e23099a5b991b01465321023d", "start_char": 0, "end_char": 1348, "text_sha256": "c4e7009c947d1854370f8c9f62c206a8c2190b2e23099a5b991b01465321023d", "text_characters": 1348}
    experimental_model
    Genetic investigation of two individuals with SLC39A8-CDG
    exposure
    Affected individuals with compound heterozygous SLC39A8 variants.
    limitations
    Inherited transport failure is distinct from dietary shortage. The study supports hypogalactosylation but does not directly measure activity of every manganese enzyme in every tissue.
    nutrient_topic
    Manganese research collection; topical membership is not evidence of a direct dietary effect. · Manganese
    organism
    Homo sapiens
    plain_language
    A transport defect can deprive sugar-building enzymes of manganese.
    primary_references
    [mn-clin-park2015] SLC39A8 Deficiency: A Disorder of Manganese Transport and Glycosylation. (2015). https://pubmed.ncbi.nlm.nih.gov/26637979/ DOI: 10.1016/j.ajhg.2015.11.003
    tissue_or_cell_type
    Blood manganese and serum glycoproteins
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Manganese: enzyme cofactors, glycosylation, transport and nutrient interactions (2026-09-17) · lines 1174–1186

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Genetic investigation of two individuals with SLC39A8-CDG · source_derived_draft · unverified_draft

    ### mn-clin-zip8-glycosylation The genetic investigation linked SLC39A8 variants, very low blood manganese and type II glycosylation abnormalities. Condition category: machinery_impairment nutrient_topic: Manganese research collection; topical membership is not evidence of a direct dietary effect. plain_language: A transport defect can deprive sugar-building enzymes of manganese. organism: Homo sapiens tissue_or_cell_type: Blood manganese and serum glycoproteins experimental_model: Genetic investigation of two individuals with SLC39A8-CDG limitations: Inherited transport failure is distinct from dietary shortage. The study supports hypogalactosylation but does not directly measure activity of every manganese enzyme in every tissue. exposure: Affected individuals with compound heterozygous SLC39A8 variants. cross_nutrient: Human ZIP8 (SLC39A8) (affected_protein); Blood manganese concentration (specimen not further specified) (low_marker); UDP-galactose (related_substrate) evidence_span: {"source_cache": "artifacts/manganese-clinical-sources/park2015.abstract.txt", "locator": "Indexed primary abstract", "file_sha256": "c4e7009c947d1854370f8c9f62c206a8c2190b2e23099a5b991b01465321023d", "start_char": 0, "end_char": 1348, "text_sha256": "c4e7009c947d1854370f8c9f62c206a8c2190b2e23099a5b991b01465321023d", "text_characters": 1348} [mn-clin-park2015] SLC39A8 Deficiency: A Disorder of Manganese Transport and Glycosylation. (2015). https://pubmed.ncbi.nlm.nih.gov/26637979/ DOI: 10.1016/j.ajhg.2015.11.003
    Complete structured claim and evidence

  3. Manganese sulfate treatment corrected the measured biochemical dysfunctions, including glycosylation, in the two SLC39A8-deficient patients.

    Manganese(II) sulfate → Transferrin glycosylation source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    Human ZIP8 (SLC39A8) (affected_protein); Manganese (administered_element)
    evidence_span
    {"source_cache": "artifacts/manganese-clinical-sources/park2018.abstract.txt", "locator": "Indexed primary abstract", "file_sha256": "30cd68e96efec971f2e431d24f5b2a45c680ce0b5efe572e30d76aee758563f5", "start_char": 0, "end_char": 1522, "text_sha256": "30cd68e96efec971f2e431d24f5b2a45c680ce0b5efe572e30d76aee758563f5", "text_characters": 1522}
    experimental_model
    Manganese treatment report in two patients with SLC39A8 deficiency
    exposure
    15 and 20 mg MnSO4/kg body weight/day as reported in the indexed abstract, with blood manganese, glycosylation and MRI monitoring.
    limitations
    Amounts describe manganese sulfate mass, not elemental manganese. Hydration state is not verified from this abstract, so no elemental conversion is made. Small uncontrolled rare-disease series; follow-up of previously described disease, not a general supplementation trial.
    nutrient_topic
    Manganese research collection; topical membership is not evidence of a direct dietary effect. · Manganese
    organism
    Homo sapiens
    plain_language
    Supplying manganese improved the measured biochemical abnormalities in these patients.
    primary_references
    [mn-clin-park2018] SLC39A8 deficiency: biochemical correction and major clinical improvement by manganese therapy. (2018). https://pubmed.ncbi.nlm.nih.gov/28749473/ DOI: 10.1038/gim.2017.106
    tissue_or_cell_type
    Biochemical and neurological outcomes
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Manganese: enzyme cofactors, glycosylation, transport and nutrient interactions (2026-09-17) · lines 1188–1200

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Manganese treatment report in two patients with SLC39A8 deficiency · source_derived_draft · unverified_draft

    ### mn-clin-zip8-manganese-biochemical Manganese sulfate treatment corrected the measured biochemical dysfunctions, including glycosylation, in the two SLC39A8-deficient patients. Condition category: machinery_impairment nutrient_topic: Manganese research collection; topical membership is not evidence of a direct dietary effect. plain_language: Supplying manganese improved the measured biochemical abnormalities in these patients. organism: Homo sapiens tissue_or_cell_type: Biochemical and neurological outcomes experimental_model: Manganese treatment report in two patients with SLC39A8 deficiency limitations: Amounts describe manganese sulfate mass, not elemental manganese. Hydration state is not verified from this abstract, so no elemental conversion is made. Small uncontrolled rare-disease series; follow-up of previously described disease, not a general supplementation trial. exposure: 15 and 20 mg MnSO4/kg body weight/day as reported in the indexed abstract, with blood manganese, glycosylation and MRI monitoring. cross_nutrient: Human ZIP8 (SLC39A8) (affected_protein); Manganese (administered_element) evidence_span: {"source_cache": "artifacts/manganese-clinical-sources/park2018.abstract.txt", "locator": "Indexed primary abstract", "file_sha256": "30cd68e96efec971f2e431d24f5b2a45c680ce0b5efe572e30d76aee758563f5", "start_char": 0, "end_char": 1522, "text_sha256": "30cd68e96efec971f2e431d24f5b2a45c680ce0b5efe572e30d76aee758563f5", "text_characters": 1522} [mn-clin-park2018] SLC39A8 deficiency: biochemical correction and major clinical improvement by manganese therapy. (2018). https://pubmed.ncbi.nlm.nih.gov/28749473/ DOI: 10.1038/gim.2017.106
    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