Component
Human HIOMT298 / ASMT 298-amino-acid splice isoform
Human HIOMT298 / ASMT 298-amino-acid splice isoform. Species, exposure and limitations are retained in each linked claim.
2 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 it acts on
Restoring HIOMT298 in A549 cells restored 5-methoxytryptophan production.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/melatonin-research/29794137.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "051e28814382bea96e610c4cc406e7bc1d4d705d245b43dea0bba61050ae341e", "start_char": 0, "end_char": 1575, "text_sha256": "051e28814382bea96e610c4cc406e7bc1d4d705d245b43dea0bba61050ae341e"}
- experimental_model
- Isoform expression, transfection and metabolic measurements
- exposure
- HIOMT298 expression versus pineal HIOMT345
- limitations
- The 298-aa isoform was studied for 5-MTP production. Do not assign its anti-tumor findings to melatonin or assume all ASMT isoforms have identical products.
- nutrient_topic
- Melatonin research collection; topical membership is not evidence of a direct dietary effect. · Melatonin
- organism
- Human fibroblasts, A549 cancer cells and mouse xenografts
- plain_language
- An alternatively spliced form connects to a different tryptophan product.
- primary_references
- [melatonin-p29794137] Restoration of hydroxyindole O-methyltransferase levels in human cancer cells induces a tryptophan-metabolic switch and attenuates cancer progression. (2018). https://pubmed.ncbi.nlm.nih.gov/29794137/ DOI: 10.1074/jbc.ra117.000597
- tissue_or_cell_type
- Alternative tryptophan metabolism
Melatonin: synthesis, receptors, circadian timing and nutrient interactions (2026-09-17) · lines 331–342
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Isoform expression, transfection and metabolic measurements · source_derived_draft · unverified_draft
### melatonin-asmt-isoform-5mtp Restoring HIOMT298 in A549 cells restored 5-methoxytryptophan production. Condition category: normal nutrient_topic: Melatonin research collection; topical membership is not evidence of a direct dietary effect. plain_language: An alternatively spliced form connects to a different tryptophan product. organism: Human fibroblasts, A549 cancer cells and mouse xenografts tissue_or_cell_type: Alternative tryptophan metabolism experimental_model: Isoform expression, transfection and metabolic measurements limitations: The 298-aa isoform was studied for 5-MTP production. Do not assign its anti-tumor findings to melatonin or assume all ASMT isoforms have identical products. exposure: HIOMT298 expression versus pineal HIOMT345 evidence_span: {"source_cache": "artifacts/melatonin-research/29794137.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "051e28814382bea96e610c4cc406e7bc1d4d705d245b43dea0bba61050ae341e", "start_char": 0, "end_char": 1575, "text_sha256": "051e28814382bea96e610c4cc406e7bc1d4d705d245b43dea0bba61050ae341e"} [melatonin-p29794137] Restoration of hydroxyindole O-methyltransferase levels in human cancer cells induces a tryptophan-metabolic switch and attenuates cancer progression. (2018). https://pubmed.ncbi.nlm.nih.gov/29794137/ DOI: 10.1074/jbc.ra117.000597
Complete structured claim and evidenceHIOMT298 expression shifted the measured tryptophan metabolism from serotonin toward 5-MTP production.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/melatonin-research/29794137.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "051e28814382bea96e610c4cc406e7bc1d4d705d245b43dea0bba61050ae341e", "start_char": 0, "end_char": 1575, "text_sha256": "051e28814382bea96e610c4cc406e7bc1d4d705d245b43dea0bba61050ae341e"}
- experimental_model
- Isoform expression, transfection and metabolic measurements
- exposure
- HIOMT298 expression versus pineal HIOMT345
- limitations
- The 298-aa isoform was studied for 5-MTP production. Do not assign its anti-tumor findings to melatonin or assume all ASMT isoforms have identical products.
- nutrient_topic
- Melatonin research collection; topical membership is not evidence of a direct dietary effect. · Melatonin
- organism
- Human fibroblasts, A549 cancer cells and mouse xenografts
- plain_language
- A shared enzyme name does not mean every isoform feeds the melatonin branch.
- primary_references
- [melatonin-p29794137] Restoration of hydroxyindole O-methyltransferase levels in human cancer cells induces a tryptophan-metabolic switch and attenuates cancer progression. (2018). https://pubmed.ncbi.nlm.nih.gov/29794137/ DOI: 10.1074/jbc.ra117.000597
- tissue_or_cell_type
- Alternative tryptophan metabolism
Melatonin: synthesis, receptors, circadian timing and nutrient interactions (2026-09-17) · lines 344–355
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Isoform expression, transfection and metabolic measurements · source_derived_draft · unverified_draft
### melatonin-asmt-isoform-serotonin-switch HIOMT298 expression shifted the measured tryptophan metabolism from serotonin toward 5-MTP production. Condition category: normal nutrient_topic: Melatonin research collection; topical membership is not evidence of a direct dietary effect. plain_language: A shared enzyme name does not mean every isoform feeds the melatonin branch. organism: Human fibroblasts, A549 cancer cells and mouse xenografts tissue_or_cell_type: Alternative tryptophan metabolism experimental_model: Isoform expression, transfection and metabolic measurements limitations: The 298-aa isoform was studied for 5-MTP production. Do not assign its anti-tumor findings to melatonin or assume all ASMT isoforms have identical products. exposure: HIOMT298 expression versus pineal HIOMT345 evidence_span: {"source_cache": "artifacts/melatonin-research/29794137.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "051e28814382bea96e610c4cc406e7bc1d4d705d245b43dea0bba61050ae341e", "start_char": 0, "end_char": 1575, "text_sha256": "051e28814382bea96e610c4cc406e7bc1d4d705d245b43dea0bba61050ae341e"} [melatonin-p29794137] Restoration of hydroxyindole O-methyltransferase levels in human cancer cells induces a tryptophan-metabolic switch and attenuates cancer progression. (2018). https://pubmed.ncbi.nlm.nih.gov/29794137/ DOI: 10.1074/jbc.ra117.000597
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.