Component

Mouse angiotensin-converting enzyme 2 / Ace2

Context-specific entity; species, compartment and exposure are stated on each claim.

6 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. Ace2 deletion removed intestinal B0AT1 expression and abolished sodium-dependent isoleucine uptake in mouse ileum segments.

    Mouse angiotensin-converting enzyme 2 / Ace2 → Isoleucine uptake in mouse ileum source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary full text
    experimental_model
    Ace2-null mouse intestine; expression, interaction and uptake assays.
    limitations
    Kidney accessory-protein dependence differs; not evidence that every change in ACE2 produces dietary isoleucine deficiency.
    nutrient_topic
    L-Isoleucine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Isoleucine
    plain_language
    A working transporter also needs its accessory protein in this tissue.
    primary_references
    Tissue-specific amino acid transporter partners ACE2 and collectrin differentially interact with hartnup mutations. · 2009 · https://pubmed.ncbi.nlm.nih.gov/19185582/ · DOI 10.1053/j.gastro.2008.10.055
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    L-Isoleucine: transport, translation, catabolism and cross-nutrient mechanisms (2026-09-19) · lines 26–32

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Ace2-null mouse intestine; expression, interaction and uptake assays. · source_derived_draft · unverified_draft

    ## isoleucine-intestinal-ace2 A working transporter also needs its accessory protein in this tissue. Ace2 deletion removed intestinal B0AT1 expression and abolished sodium-dependent isoleucine uptake in mouse ileum segments. Model: Ace2-null mouse intestine; expression, interaction and uptake assays. Limitations: Kidney accessory-protein dependence differs; not evidence that every change in ACE2 produces dietary isoleucine deficiency. Evidence access: Primary full text Tissue-specific amino acid transporter partners ACE2 and collectrin differentially interact with hartnup mutations. · 2009 · https://pubmed.ncbi.nlm.nih.gov/19185582/ · DOI 10.1053/j.gastro.2008.10.055
    Complete structured claim and evidence

  2. Ace2 loss removed intestinal B0AT1 expression in mice; kidney B0AT1 regulation differed and depended on collectrin.

    Mouse angiotensin-converting enzyme 2 / Ace2 → Mouse B0AT1 / Slc6a19 source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary full text, partner constructs and mouse tissue results
    experimental_model
    Mouse tissue expression and transporter-partner experiments.
    limitations
    Separate oocyte experiments combine human B0AT1 with mouse ACE2 or human collectrin; they are not an all-human ACE2 reconstruction.
    nutrient_topic
    Tryptophan collection; molecular form, preparation, species, exposure and manipulation remain explicit. · L-Tryptophan
    plain_language
    The same amino-acid transporter needs different support in intestine and kidney.
    primary_references
    Tissue-specific amino acid transporter partners ACE2 and collectrin differentially interact with hartnup mutations. · 2009 · https://pubmed.ncbi.nlm.nih.gov/19185582/ · DOI 10.1053/j.gastro.2008.10.055
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Tryptophan: transport, protein synthesis, neuroactive metabolites, NAD and microbial pathways (2026-09-19) · lines 66–72

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Mouse tissue expression and transporter-partner experiments. · source_derived_draft · unverified_draft

    ## tryptophan-ace2-transporter The same amino-acid transporter needs different support in intestine and kidney. Ace2 loss removed intestinal B0AT1 expression in mice; kidney B0AT1 regulation differed and depended on collectrin. Model: Mouse tissue expression and transporter-partner experiments. Limitations: Separate oocyte experiments combine human B0AT1 with mouse ACE2 or human collectrin; they are not an all-human ACE2 reconstruction. Evidence access: Primary full text, partner constructs and mouse tissue results Tissue-specific amino acid transporter partners ACE2 and collectrin differentially interact with hartnup mutations. · 2009 · https://pubmed.ncbi.nlm.nih.gov/19185582/ · DOI 10.1053/j.gastro.2008.10.055
    Complete structured claim and evidence

  3. Microbiota transfer from Ace2-mutant mice transmitted increased colitis susceptibility to germ-free wild-type recipients.

    Mouse angiotensin-converting enzyme 2 / Ace2 → Mouse susceptibility to chemically induced colitis in tryptophan experiments source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary full text, microbiota-transfer results
    experimental_model
    Mouse donor-to-recipient microbiota transfer.
    limitations
    Transfer does not isolate one bacterial species or one metabolite.
    nutrient_topic
    Tryptophan collection; molecular form, preparation, species, exposure and manipulation remain explicit. · L-Tryptophan
    plain_language
    The altered microbial community carried part of the susceptibility.
    primary_references
    ACE2 links amino acid malnutrition to microbial ecology and intestinal inflammation. · 2012 · https://pubmed.ncbi.nlm.nih.gov/22837003/ · DOI 10.1038/nature11228

    Tryptophan: transport, protein synthesis, neuroactive metabolites, NAD and microbial pathways (2026-09-19) · lines 106–112

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Mouse donor-to-recipient microbiota transfer. · source_derived_draft · unverified_draft

    ## tryptophan-microbiota-transfer The altered microbial community carried part of the susceptibility. Microbiota transfer from Ace2-mutant mice transmitted increased colitis susceptibility to germ-free wild-type recipients. Model: Mouse donor-to-recipient microbiota transfer. Limitations: Transfer does not isolate one bacterial species or one metabolite. Evidence access: Primary full text, microbiota-transfer results ACE2 links amino acid malnutrition to microbial ecology and intestinal inflammation. · 2012 · https://pubmed.ncbi.nlm.nih.gov/22837003/ · DOI 10.1038/nature11228
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Human B0AT1 D173N and P265L variants retained activation by coexpressed mouse ACE2 but not human collectrin; A69T and R240Q were not activated by either partner.

    Human neutral amino acid transporter B0AT1 / SLC6A19 → Accessory-protein response of human B0AT1 variants source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary full text
    experimental_model
    Human transporter variants in Xenopus oocytes with mouse ACE2 or human collectrin.
    limitations
    Mixed-species expression system; not a direct measurement of each patient intestine or kidney.
    nutrient_topic
    L-Isoleucine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Isoleucine
    plain_language
    The same transporter mutation can behave differently with different helper proteins.
    primary_references
    Tissue-specific amino acid transporter partners ACE2 and collectrin differentially interact with hartnup mutations. · 2009 · https://pubmed.ncbi.nlm.nih.gov/19185582/ · DOI 10.1053/j.gastro.2008.10.055
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    L-Isoleucine: transport, translation, catabolism and cross-nutrient mechanisms (2026-09-19) · lines 34–40

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human transporter variants in Xenopus oocytes with mouse ACE2 or human collectrin. · source_derived_draft · unverified_draft

    ## isoleucine-hartnup-partners The same transporter mutation can behave differently with different helper proteins. Human B0AT1 D173N and P265L variants retained activation by coexpressed mouse ACE2 but not human collectrin; A69T and R240Q were not activated by either partner. Model: Human transporter variants in Xenopus oocytes with mouse ACE2 or human collectrin. Limitations: Mixed-species expression system; not a direct measurement of each patient intestine or kidney. Evidence access: Primary full text Tissue-specific amino acid transporter partners ACE2 and collectrin differentially interact with hartnup mutations. · 2009 · https://pubmed.ncbi.nlm.nih.gov/19185582/ · DOI 10.1053/j.gastro.2008.10.055
    Complete structured claim and evidence

  2. Gly-Trp feeding restored serum tryptophan and reduced DSS-colitis susceptibility in Ace2-deficient mice, bypassing loss of single-amino-acid uptake.

    Glycyl-L-tryptophan / Gly-Trp dipeptide → Mouse susceptibility to chemically induced colitis in tryptophan experiments source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary full text, Figure 2 and rescue results
    experimental_model
    Ace2-mutant mouse dietary rescue.
    limitations
    Not a clinical Gly-Trp treatment recommendation or evidence that free tryptophan always bypasses transporter loss.
    nutrient_topic
    Tryptophan collection; molecular form, preparation, species, exposure and manipulation remain explicit. · L-Tryptophan
    plain_language
    A dipeptide delivery route bypassed missing transport support.
    primary_references
    ACE2 links amino acid malnutrition to microbial ecology and intestinal inflammation. · 2012 · https://pubmed.ncbi.nlm.nih.gov/22837003/ · DOI 10.1038/nature11228
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Tryptophan: transport, protein synthesis, neuroactive metabolites, NAD and microbial pathways (2026-09-19) · lines 74–80

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Ace2-mutant mouse dietary rescue. · source_derived_draft · unverified_draft

    ## tryptophan-glytrp-bypass A dipeptide delivery route bypassed missing transport support. Gly-Trp feeding restored serum tryptophan and reduced DSS-colitis susceptibility in Ace2-deficient mice, bypassing loss of single-amino-acid uptake. Model: Ace2-mutant mouse dietary rescue. Limitations: Not a clinical Gly-Trp treatment recommendation or evidence that free tryptophan always bypasses transporter loss. Evidence access: Primary full text, Figure 2 and rescue results ACE2 links amino acid malnutrition to microbial ecology and intestinal inflammation. · 2012 · https://pubmed.ncbi.nlm.nih.gov/22837003/ · DOI 10.1038/nature11228
    Complete structured claim and evidence

  3. Nicotinamide supplementation markedly alleviated colitis and diarrhea in Ace2-deficient mice.

    Nicotinamide → Mouse susceptibility to chemically induced colitis in tryptophan experiments source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary full text, Figure 2
    experimental_model
    Mouse Ace2 loss and DSS challenge.
    limitations
    Does not establish identical effects for nicotinic acid or human inflammatory bowel disease.
    nutrient_topic
    Tryptophan collection; molecular form, preparation, species, exposure and manipulation remain explicit. · L-Tryptophan
    plain_language
    A downstream vitamin B3 form bypassed part of the disturbed pathway.
    primary_references
    ACE2 links amino acid malnutrition to microbial ecology and intestinal inflammation. · 2012 · https://pubmed.ncbi.nlm.nih.gov/22837003/ · DOI 10.1038/nature11228
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Tryptophan: transport, protein synthesis, neuroactive metabolites, NAD and microbial pathways (2026-09-19) · lines 90–96

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Mouse Ace2 loss and DSS challenge. · source_derived_draft · unverified_draft

    ## tryptophan-nam-rescue A downstream vitamin B3 form bypassed part of the disturbed pathway. Nicotinamide supplementation markedly alleviated colitis and diarrhea in Ace2-deficient mice. Model: Mouse Ace2 loss and DSS challenge. Limitations: Does not establish identical effects for nicotinic acid or human inflammatory bowel disease. Evidence access: Primary full text, Figure 2 ACE2 links amino acid malnutrition to microbial ecology and intestinal inflammation. · 2012 · https://pubmed.ncbi.nlm.nih.gov/22837003/ · DOI 10.1038/nature11228
    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.

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