Component

Human MID1 interacting protein 1 / MID1IP1

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 it acts on

  1. MID1IP1 siRNA depletion increased AMPK phosphorylation in HepG2 cells.

    Human MID1 interacting protein 1 / MID1IP1 → Human HepG2 AMPK phosphorylation source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary full text retrieved; relevant methods/results/figures reviewed. Selective extraction, not raw-data reanalysis or exhaustive supplemental extraction.
    experimental_contrast
    {"intervention": "MID1IP1 siRNA depletion", "comparator": "Control transfection", "endpoint": "MID1IP1 siRNA depletion increased AMPK phosphorylation in HepG2 cells.", "effect_direction": "increase", "combination": "single", "conditions": []} Explicit extracted experimental comparison; source-derived draft.
    experimental_model
    Human HepG2 genetic perturbation.
    interpretation_status
    Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
    limitations
    The subject is depleted, not added; this is not an ordinary positive effect of MID1IP1 abundance.
    plain_language
    MID1IP1 siRNA depletion increased AMPK phosphorylation in HepG2 cells.
    primary_references
    Hypolipogenic Effect of Shikimic Acid Via Inhibition of MID1IP1 and Phosphorylation of AMPK/ACC. | 2019 | DOI 10.3390/ijms20030582 | PMID 30700011 | https://pubmed.ncbi.nlm.nih.gov/30700011/ | https://doi.org/10.3390/ijms20030582 | https://pmc.ncbi.nlm.nih.gov/articles/PMC6387373/
    source_locator
    Reviewed reference lines 81-81; exact primary location described in quoted passage where extracted.
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Shikimic acid: detailed mechanisms of action (reviewed 5 October 2026) · lines 81–81

    Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Human HepG2 genetic perturbation. · source_derived_draft · unverified_draft

    **The lipid study contains a useful null result.** Depleting MID1IP1 by siRNA in HepG2 cells reduced SREBP-1c and FAS expression and increased AMPK/ACC phosphorylation. In mouse AML-12 cells, MID1IP1 overexpression attenuated AMPK phosphorylation associated with 80 µM shikimic acid. Conversely, compound C did not alter MID1IP1 expression in the tested HepG2 comparison. This limits a simple claim that AMPK inhibition must reverse every MID1IP1 response. The source tested 10–160 µM SA in viability assays; MTT could fall to about 70% of control at the highest concentration, so reduced lipid staining must not be interpreted without viability context. [Hypolipogenic Effect of Shikimic Acid Via Inhibition of MID1IP1 and Phosphorylation of AMPK/ACC.](https://pubmed.ncbi.nlm.nih.gov/30700011/)
    Complete structured claim and evidence

What acts on it

  1. Compound C did not alter MID1IP1 expression in the tested HepG2 comparison.

    Compound C AMPK inhibitor → Human MID1 interacting protein 1 / MID1IP1 source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary full text retrieved; relevant methods/results/figures reviewed. Selective extraction, not raw-data reanalysis or exhaustive supplemental extraction.
    experimental_contrast
    {"intervention": "Compound C in the recorded comparison", "comparator": "Matched comparison without compound C", "endpoint": "Compound C did not alter MID1IP1 expression in the tested HepG2 comparison.", "effect_direction": "no_detected_change", "combination": "single", "conditions": []} Explicit extracted experimental comparison; source-derived draft.
    experimental_model
    Human HepG2 pharmacological signaling experiment.
    interpretation_status
    Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
    limitations
    Assay-specific null, not proof of perfect AMPK specificity or absence of all AMPK involvement.
    plain_language
    Compound C did not alter MID1IP1 expression in the tested HepG2 comparison.
    primary_references
    Hypolipogenic Effect of Shikimic Acid Via Inhibition of MID1IP1 and Phosphorylation of AMPK/ACC. | 2019 | DOI 10.3390/ijms20030582 | PMID 30700011 | https://pubmed.ncbi.nlm.nih.gov/30700011/ | https://doi.org/10.3390/ijms20030582 | https://pmc.ncbi.nlm.nih.gov/articles/PMC6387373/
    source_locator
    Reviewed reference lines 81-81; exact primary location described in quoted passage where extracted.

    Shikimic acid: detailed mechanisms of action (reviewed 5 October 2026) · lines 81–81

    Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Human HepG2 pharmacological signaling experiment. · source_derived_draft · unverified_draft

    **The lipid study contains a useful null result.** Depleting MID1IP1 by siRNA in HepG2 cells reduced SREBP-1c and FAS expression and increased AMPK/ACC phosphorylation. In mouse AML-12 cells, MID1IP1 overexpression attenuated AMPK phosphorylation associated with 80 µM shikimic acid. Conversely, compound C did not alter MID1IP1 expression in the tested HepG2 comparison. This limits a simple claim that AMPK inhibition must reverse every MID1IP1 response. The source tested 10–160 µM SA in viability assays; MTT could fall to about 70% of control at the highest concentration, so reduced lipid staining must not be interpreted without viability context. [Hypolipogenic Effect of Shikimic Acid Via Inhibition of MID1IP1 and Phosphorylation of AMPK/ACC.](https://pubmed.ncbi.nlm.nih.gov/30700011/)
    Complete structured claim and evidence

  2. SA lowered MID1IP1 expression in the tested human hepatoma cells.

    Shikimic acid → Human MID1 interacting protein 1 / MID1IP1 source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary full text retrieved; relevant methods/results/figures reviewed. Selective extraction, not raw-data reanalysis or exhaustive supplemental extraction.
    experimental_contrast
    {"intervention": "SA treatment", "comparator": "Matched untreated cells", "endpoint": "SA lowered MID1IP1 expression in the tested human hepatoma cells.", "effect_direction": "decrease", "combination": "single", "conditions": []} Explicit extracted experimental comparison; source-derived draft.
    experimental_model
    HepG2/Huh7 24-hour expression assays.
    interpretation_status
    Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
    limitations
    Expression response, not direct binding or purified-enzyme inhibition.
    plain_language
    SA lowered MID1IP1 expression in the tested human hepatoma cells.
    primary_references
    Hypolipogenic Effect of Shikimic Acid Via Inhibition of MID1IP1 and Phosphorylation of AMPK/ACC. | 2019 | DOI 10.3390/ijms20030582 | PMID 30700011 | https://pubmed.ncbi.nlm.nih.gov/30700011/ | https://doi.org/10.3390/ijms20030582 | https://pmc.ncbi.nlm.nih.gov/articles/PMC6387373/
    source_locator
    Reviewed reference lines 77-77; exact primary location described in quoted passage where extracted.

    Shikimic acid: detailed mechanisms of action (reviewed 5 October 2026) · lines 77–77

    Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · HepG2/Huh7 24-hour expression assays. · source_derived_draft · unverified_draft

    **Lipid accumulation studies identify responses, not direct inhibition.** In HepG2/Huh7 and 3T3-L1 experiments, shikimic acid was associated with lower lipid staining and altered lipogenic proteins, including lower MID1IP1, LXRα and SREBP-1c; AMPKα and ACC phosphorylation increased in the reported cell contexts. Genetic manipulation of MID1IP1 and compound-C experiments probed pathway involvement. These cultured-cell observations do not prove direct binding to MID1IP1, human fatty-liver efficacy, or that AMPK causes the triglyceride change in the separate mouse-feeding study. Individual cell-dose details remain in the original paper rather than being guessed. [Hypolipogenic Effect of Shikimic Acid Via Inhibition of MID1IP1 and Phosphorylation of AMPK/ACC.](https://pubmed.ncbi.nlm.nih.gov/30700011/)
    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.