Component
Golgi protein glycosylation
Golgi protein glycosylation. Read the linked claim for experimental scope.
1 recorded relationships. Experimental role, claim status and evidence remain attached to each record.
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.
Other things that act on it
Enzymes, hormones, genes, and other components with a recorded effect. These are not nutrients, so they do not count toward the arrows above. Each finding names the chapter that recorded it.
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.
What acts on it
Manganese supplementation restored glycosylation in the TMEM165-depleted mammalian-cell experiments.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- cross_nutrient
- TMEM165 Golgi cation-homeostasis protein (affected_protein); Golgi apparatus (affected_compartment)
- evidence_span
- {"source_cache": "artifacts/manganese-glycosylation-sources/potelle2016.abstract.txt", "locator": "Indexed primary abstract", "file_sha256": "e1845bfbdbb15370fd1375534464f61aa6e5674cc4129b6f0992d9a022882cc3", "start_char": 0, "end_char": 1190, "text_sha256": "e1845bfbdbb15370fd1375534464f61aa6e5674cc4129b6f0992d9a022882cc3", "text_characters": 1190}
- experimental_model
- TMEM165-depleted mammalian cells and separate yeast Gdt1 loss experiments
- exposure
- Mn2+ supplementation of depleted cells.
- limitations
- These records describe the mammalian-cell arm. The indexed abstract does not specify every line, dose or treatment duration; rescue supports a homeostasis role rather than establishing a transport stoichiometry.
- nutrient_topic
- Manganese research collection; topical membership is not evidence of a direct dietary effect. · Manganese
- organism
- Mammalian cell model; yeast comparison
- plain_language
- More available manganese could compensate for this Golgi-handling defect in cells.
- primary_references
- [mn-gly-potelle2016] Glycosylation abnormalities in Gdt1p/TMEM165 deficient cells result from a defect in Golgi manganese homeostasis. (2016). https://pubmed.ncbi.nlm.nih.gov/27008884/ DOI: 10.1093/hmg/ddw026
- tissue_or_cell_type
- Golgi glycosylation
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Manganese: enzyme cofactors, glycosylation, transport and nutrient interactions (2026-09-17) · lines 740–752
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · TMEM165-depleted mammalian cells and separate yeast Gdt1 loss experiments · source_derived_draft · unverified_draft
### mn-gly-tmem165-mn-rescue Manganese supplementation restored glycosylation in the TMEM165-depleted mammalian-cell experiments. Condition category: machinery_impairment nutrient_topic: Manganese research collection; topical membership is not evidence of a direct dietary effect. plain_language: More available manganese could compensate for this Golgi-handling defect in cells. organism: Mammalian cell model; yeast comparison tissue_or_cell_type: Golgi glycosylation experimental_model: TMEM165-depleted mammalian cells and separate yeast Gdt1 loss experiments limitations: These records describe the mammalian-cell arm. The indexed abstract does not specify every line, dose or treatment duration; rescue supports a homeostasis role rather than establishing a transport stoichiometry. exposure: Mn2+ supplementation of depleted cells. cross_nutrient: TMEM165 Golgi cation-homeostasis protein (affected_protein); Golgi apparatus (affected_compartment) evidence_span: {"source_cache": "artifacts/manganese-glycosylation-sources/potelle2016.abstract.txt", "locator": "Indexed primary abstract", "file_sha256": "e1845bfbdbb15370fd1375534464f61aa6e5674cc4129b6f0992d9a022882cc3", "start_char": 0, "end_char": 1190, "text_sha256": "e1845bfbdbb15370fd1375534464f61aa6e5674cc4129b6f0992d9a022882cc3", "text_characters": 1190} [mn-gly-potelle2016] Glycosylation abnormalities in Gdt1p/TMEM165 deficient cells result from a defect in Golgi manganese homeostasis. (2016). https://pubmed.ncbi.nlm.nih.gov/27008884/ DOI: 10.1093/hmg/ddw026
Complete structured claim and evidence
The events it takes part in
A mechanism often involves more than two components. These are the full events, with every participant and its role.
Situations it appears in
Low-supply and faulty-machinery situations recorded in the chapters where this component plays a part.
In the sources
Preserved passages that mention this component, quoted exactly. Open one to read it in context.
Open hypotheses
Proposed ideas that involve this component. They are labeled as hypotheses and do not change any recorded statement.
This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.