Component

Human APT2 knockdown in A375

4 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.

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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. APT2 knockdown did not significantly change GPX4 mRNA in the reported A375 and HT1080 RT-qPCR experiments.

    Human APT2 knockdown in A375 → GPX4 mRNA abundance in human cells source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_cache
    artifacts/discovery-research/round6-sources/gpx4-primary-passages.json; SHA256 384aaae29ec0e6fe9814782b3e5d885753751fa1b2bbd103e30e8ffa113df5dc
    experimental_model
    Human A375 and HT1080 cancer cells; lentiviral APT2 shRNA
    exposure
    RT-qPCR; three independent experiments; exposure timing unresolved.
    limitations
    These are separate experimental observations, not a demonstrated sulforaphane-GPX4-ZDHHC6 pathway. Sulforaphane-driven APT2 relocalization is not equivalent to genetic depletion or general catalytic inhibition. No dietary, clinical or selenium-repletion effect is inferred. Protein stability, palmitoylation and substrate output remain different measurements. The actor names the A375 arm; the parallel HT1080 observation is preserved in the context. No transcriptional effect is inferred.
    organism
    Human experimental cells; construct species unresolved where stated for discussion-only nulls
    primary_locator
    Figure 5f
    primary_references
    https://doi.org/10.1038/s41467-025-56344-5
    source_access
    Selected primary Results and Figure 5/6 legends reviewed. No supplement or raw-data reanalysis.
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    APT2: sulforaphane engagement, GPX4 stability and ZDHHC6 turnover · lines 129–137

    Targeted primary-literature curation from recursive ZDHHC6 exploration, 2026-09-20. · supports · Human A375 and HT1080 cancer cells; lentiviral APT2 shRNA · source_derived_draft · unverified_draft

    APT2 knockdown did not significantly change GPX4 mRNA in the reported A375 and HT1080 RT-qPCR experiments. primary_references: https://doi.org/10.1038/s41467-025-56344-5 primary_locator: Figure 5f source_access: Selected primary Results and Figure 5/6 legends reviewed. No supplement or raw-data reanalysis. evidence_cache: artifacts/discovery-research/round6-sources/gpx4-primary-passages.json; SHA256 384aaae29ec0e6fe9814782b3e5d885753751fa1b2bbd103e30e8ffa113df5dc experimental_model: Human A375 and HT1080 cancer cells; lentiviral APT2 shRNA organism: Human experimental cells; construct species unresolved where stated for discussion-only nulls exposure: RT-qPCR; three independent experiments; exposure timing unresolved. limitations: These are separate experimental observations, not a demonstrated sulforaphane-GPX4-ZDHHC6 pathway. Sulforaphane-driven APT2 relocalization is not equivalent to genetic depletion or general catalytic inhibition. No dietary, clinical or selenium-repletion effect is inferred. Protein stability, palmitoylation and substrate output remain different measurements. The actor names the A375 arm; the parallel HT1080 observation is preserved in the context. No transcriptional effect is inferred.
    Complete structured claim and evidence

  2. APT2 shRNA increased GPX4 palmitoylation measured by acyl-biotin exchange in A375 cells.

    Human APT2 knockdown in A375 → GPX4 palmitoylation in human cells source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_cache
    artifacts/discovery-research/round6-sources/gpx4-primary-passages.json; SHA256 384aaae29ec0e6fe9814782b3e5d885753751fa1b2bbd103e30e8ffa113df5dc
    experimental_model
    Human A375 melanoma; lentiviral APT2 shRNA; exogenous GPX4
    exposure
    ABE assay with and without hydroxylamine; representative of three independent experiments; exact shRNA exposure duration unresolved.
    limitations
    These are separate experimental observations, not a demonstrated sulforaphane-GPX4-ZDHHC6 pathway. Sulforaphane-driven APT2 relocalization is not equivalent to genetic depletion or general catalytic inhibition. No dietary, clinical or selenium-repletion effect is inferred. Protein stability, palmitoylation and substrate output remain different measurements. The Results prose calls this deletion, but Figure 5d specifies shRNA; record the figure-defined knockdown, not a knockout.
    organism
    Human experimental cells; construct species unresolved where stated for discussion-only nulls
    primary_locator
    Figure 5d and Results: APT2 mediates the depalmitoylation of GPX4
    primary_references
    https://doi.org/10.1038/s41467-025-56344-5
    source_access
    Selected primary Results and Figure 5/6 legends reviewed. No supplement or raw-data reanalysis.
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    APT2: sulforaphane engagement, GPX4 stability and ZDHHC6 turnover · lines 107–115

    Targeted primary-literature curation from recursive ZDHHC6 exploration, 2026-09-20. · supports · Human A375 melanoma; lentiviral APT2 shRNA; exogenous GPX4 · source_derived_draft · unverified_draft

    APT2 shRNA increased GPX4 palmitoylation measured by acyl-biotin exchange in A375 cells. primary_references: https://doi.org/10.1038/s41467-025-56344-5 primary_locator: Figure 5d and Results: APT2 mediates the depalmitoylation of GPX4 source_access: Selected primary Results and Figure 5/6 legends reviewed. No supplement or raw-data reanalysis. evidence_cache: artifacts/discovery-research/round6-sources/gpx4-primary-passages.json; SHA256 384aaae29ec0e6fe9814782b3e5d885753751fa1b2bbd103e30e8ffa113df5dc experimental_model: Human A375 melanoma; lentiviral APT2 shRNA; exogenous GPX4 organism: Human experimental cells; construct species unresolved where stated for discussion-only nulls exposure: ABE assay with and without hydroxylamine; representative of three independent experiments; exact shRNA exposure duration unresolved. limitations: These are separate experimental observations, not a demonstrated sulforaphane-GPX4-ZDHHC6 pathway. Sulforaphane-driven APT2 relocalization is not equivalent to genetic depletion or general catalytic inhibition. No dietary, clinical or selenium-repletion effect is inferred. Protein stability, palmitoylation and substrate output remain different measurements. The Results prose calls this deletion, but Figure 5d specifies shRNA; record the figure-defined knockdown, not a knockout.
    Complete structured claim and evidence

  3. APT2 knockdown increased GPX4 protein stability in A375 cycloheximide-chase experiments.

    Human APT2 knockdown in A375 → GPX4 protein stability in human cells source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_cache
    artifacts/discovery-research/round6-sources/gpx4-primary-passages.json; SHA256 384aaae29ec0e6fe9814782b3e5d885753751fa1b2bbd103e30e8ffa113df5dc
    experimental_model
    Human A375 melanoma; lentiviral APT2 shRNA
    exposure
    Cycloheximide chase; three independent experiments; exact CHX concentration and time series not resolved from reviewed legend.
    limitations
    These are separate experimental observations, not a demonstrated sulforaphane-GPX4-ZDHHC6 pathway. Sulforaphane-driven APT2 relocalization is not equivalent to genetic depletion or general catalytic inhibition. No dietary, clinical or selenium-repletion effect is inferred. Protein stability, palmitoylation and substrate output remain different measurements.
    organism
    Human experimental cells; construct species unresolved where stated for discussion-only nulls
    primary_locator
    Figure 5i,j
    primary_references
    https://doi.org/10.1038/s41467-025-56344-5
    source_access
    Selected primary Results and Figure 5/6 legends reviewed. No supplement or raw-data reanalysis.
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    APT2: sulforaphane engagement, GPX4 stability and ZDHHC6 turnover · lines 118–126

    Targeted primary-literature curation from recursive ZDHHC6 exploration, 2026-09-20. · supports · Human A375 melanoma; lentiviral APT2 shRNA · source_derived_draft · unverified_draft

    APT2 knockdown increased GPX4 protein stability in A375 cycloheximide-chase experiments. primary_references: https://doi.org/10.1038/s41467-025-56344-5 primary_locator: Figure 5i,j source_access: Selected primary Results and Figure 5/6 legends reviewed. No supplement or raw-data reanalysis. evidence_cache: artifacts/discovery-research/round6-sources/gpx4-primary-passages.json; SHA256 384aaae29ec0e6fe9814782b3e5d885753751fa1b2bbd103e30e8ffa113df5dc experimental_model: Human A375 melanoma; lentiviral APT2 shRNA organism: Human experimental cells; construct species unresolved where stated for discussion-only nulls exposure: Cycloheximide chase; three independent experiments; exact CHX concentration and time series not resolved from reviewed legend. limitations: These are separate experimental observations, not a demonstrated sulforaphane-GPX4-ZDHHC6 pathway. Sulforaphane-driven APT2 relocalization is not equivalent to genetic depletion or general catalytic inhibition. No dietary, clinical or selenium-repletion effect is inferred. Protein stability, palmitoylation and substrate output remain different measurements.
    Complete structured claim and evidence

  4. APT2 knockdown reduced RSL3-induced cell death measured with SYTOX Green in A375 cells.

    Human APT2 knockdown in A375 → RSL3-induced cell death in A375 cells source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_cache
    artifacts/discovery-research/round6-sources/gpx4-primary-passages.json; SHA256 384aaae29ec0e6fe9814782b3e5d885753751fa1b2bbd103e30e8ffa113df5dc
    experimental_model
    Human A375 melanoma; lentiviral APT2 shRNA
    exposure
    4 micromolar RSL3 for 6 hours; SYTOX Green staining; three independent experiments.
    limitations
    These are separate experimental observations, not a demonstrated sulforaphane-GPX4-ZDHHC6 pathway. Sulforaphane-driven APT2 relocalization is not equivalent to genetic depletion or general catalytic inhibition. No dietary, clinical or selenium-repletion effect is inferred. Protein stability, palmitoylation and substrate output remain different measurements. This is a response to a GPX4 inhibitor in cancer cells. It does not establish an effect of sulforaphane or dietary selenium.
    organism
    Human experimental cells; construct species unresolved where stated for discussion-only nulls
    primary_locator
    Figure 6c,d
    primary_references
    https://doi.org/10.1038/s41467-025-56344-5
    source_access
    Selected primary Results and Figure 5/6 legends reviewed. No supplement or raw-data reanalysis.
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    APT2: sulforaphane engagement, GPX4 stability and ZDHHC6 turnover · lines 140–148

    Targeted primary-literature curation from recursive ZDHHC6 exploration, 2026-09-20. · supports · Human A375 melanoma; lentiviral APT2 shRNA · source_derived_draft · unverified_draft

    APT2 knockdown reduced RSL3-induced cell death measured with SYTOX Green in A375 cells. primary_references: https://doi.org/10.1038/s41467-025-56344-5 primary_locator: Figure 6c,d source_access: Selected primary Results and Figure 5/6 legends reviewed. No supplement or raw-data reanalysis. evidence_cache: artifacts/discovery-research/round6-sources/gpx4-primary-passages.json; SHA256 384aaae29ec0e6fe9814782b3e5d885753751fa1b2bbd103e30e8ffa113df5dc experimental_model: Human A375 melanoma; lentiviral APT2 shRNA organism: Human experimental cells; construct species unresolved where stated for discussion-only nulls exposure: 4 micromolar RSL3 for 6 hours; SYTOX Green staining; three independent experiments. limitations: These are separate experimental observations, not a demonstrated sulforaphane-GPX4-ZDHHC6 pathway. Sulforaphane-driven APT2 relocalization is not equivalent to genetic depletion or general catalytic inhibition. No dietary, clinical or selenium-repletion effect is inferred. Protein stability, palmitoylation and substrate output remain different measurements. This is a response to a GPX4 inhibitor in cancer cells. It does not establish an effect of sulforaphane or dietary selenium.
    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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