Component

Human heterogeneous nuclear ribonucleoprotein A2/B1 / HNRNPA2B1

Human heterogeneous nuclear ribonucleoprotein A2/B1 / HNRNPA2B1

5 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 acts on it

  1. Apigenin bound the glycine-rich C-terminal region of hnRNPA2 and inhibited its homodimerization in the reported biochemical experiments.

    Apigenin → Human heterogeneous nuclear ribonucleoprotein A2/B1 / HNRNPA2B1 Recorded from sourceungraded
    Experimental context and source evidence
    evidence_access
    Primary indexed abstract plus PMC full-text Results retrieved through web; no claim that every screening hit is functionally validated.
    experimental_model
    Human protein fragments, affinity pull-down and follow-up assays.
    interpretation_status
    Recorded from source with stated access limits; ungraded, not independent replication.
    limitations
    Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
    nutrient_topic
    Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin
    plain_language
    Apigenin bound the glycine-rich C-terminal region of hnRNPA2 and inhibited its homodimerization in the reported biochemical experiments.
    primary_references
    Molecular basis for the action of a dietary flavonoid revealed by the comprehensive identification of apigenin human targets. | https://pubmed.ncbi.nlm.nih.gov/23697369/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC3683737/ | https://doi.org/10.1073/pnas.1303726110
    source_locator
    Reviewed reference api-hnrnpa2-binding; The screen nominated 160 candidate proteins; only selected targets received functional follow-up. Do not label all 160 validated causal targets or dietary target engagement.

    Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 644–650

    AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · Human protein fragments, affinity pull-down and follow-up assays. · Recorded from source · Recorded from source

    ### api-hnrnpa2-binding Apigenin bound the glycine-rich C-terminal region of hnRNPA2 and inhibited its homodimerization in the reported biochemical experiments. The screen nominated 160 candidate proteins; only selected targets received functional follow-up. Do not label all 160 validated causal targets or dietary target engagement. Model and exposure: Human protein fragments, affinity pull-down and follow-up assays. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Molecular basis for the action of a dietary flavonoid revealed by the comprehensive identification of apigenin human targets. | 2013 | https://pubmed.ncbi.nlm.nih.gov/23697369/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC3683737/ | https://doi.org/10.1073/pnas.1303726110 | Access: Primary indexed abstract plus PMC full-text Results retrieved through web; no claim that every screening hit is functionally validated.
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Apigenin increased the relative abundance of Human BAXL transcript in MDA-MB-231 breast-cancer cells.

    Apigenin → Human BAXL transcript Recorded from sourceungraded
    Experimental context and source evidence
    evidence_access
    Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
    experimental_contrast
    {"intervention": "Apigenin", "comparator": "DMSO", "endpoint": "Apigenin increased the relative abundance of Human BAXL transcript in MDA-MB-231 breast-cancer cells.", "effect_direction": "increase", "combination": "single", "conditions": []} Explicit extracted experimental comparison; recorded from source.
    experimental_model
    50 micromolar apigenin for 48 hours; RNA-seq and isoform-specific PCR.
    interpretation_status
    Recorded from source with stated access limits; ungraded, not independent replication.
    limitations
    Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
    nutrient_topic
    Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin
    plain_language
    Apigenin increased the relative abundance of Human BAXL transcript in MDA-MB-231 breast-cancer cells.
    primary_references
    Transcriptome reprogramming through alternative splicing triggered by apigenin drives cell death in triple-negative breast cancer. | https://pubmed.ncbi.nlm.nih.gov/38092740/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC10719380/ | https://doi.org/10.1038/s41419-023-06342-6
    source_locator
    Reviewed reference api-splice-baxl; Figure 4. RNA isoform abundance is not automatically protein amount or proof that one isoform alone causes apoptosis.

    Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 668–674

    AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · 50 micromolar apigenin for 48 hours; RNA-seq and isoform-specific PCR. · Recorded from source · Recorded from source

    ### api-splice-baxl Apigenin increased the relative abundance of Human BAXL transcript in MDA-MB-231 breast-cancer cells. Figure 4. RNA isoform abundance is not automatically protein amount or proof that one isoform alone causes apoptosis. Model and exposure: 50 micromolar apigenin for 48 hours; RNA-seq and isoform-specific PCR. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Transcriptome reprogramming through alternative splicing triggered by apigenin drives cell death in triple-negative breast cancer. | 2023 | https://pubmed.ncbi.nlm.nih.gov/38092740/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC10719380/ | https://doi.org/10.1038/s41419-023-06342-6 | Access: Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
    Complete structured claim and evidence

  2. Apigenin increased the relative abundance of Human translation-competent CCNL2 transcripts in MDA-MB-231 breast-cancer cells.

    Apigenin → Human translation-competent CCNL2 transcripts Recorded from sourceungraded
    Experimental context and source evidence
    evidence_access
    Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
    experimental_contrast
    {"intervention": "Apigenin", "comparator": "DMSO", "endpoint": "Apigenin increased the relative abundance of Human translation-competent CCNL2 transcripts in MDA-MB-231 breast-cancer cells.", "effect_direction": "increase", "combination": "single", "conditions": []} Explicit extracted experimental comparison; recorded from source.
    experimental_model
    50 micromolar apigenin for 48 hours; RNA-seq and isoform-specific PCR.
    interpretation_status
    Recorded from source with stated access limits; ungraded, not independent replication.
    limitations
    Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
    nutrient_topic
    Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin
    plain_language
    Apigenin increased the relative abundance of Human translation-competent CCNL2 transcripts in MDA-MB-231 breast-cancer cells.
    primary_references
    Transcriptome reprogramming through alternative splicing triggered by apigenin drives cell death in triple-negative breast cancer. | https://pubmed.ncbi.nlm.nih.gov/38092740/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC10719380/ | https://doi.org/10.1038/s41419-023-06342-6
    source_locator
    Reviewed reference api-splice-ccnl2; Figure 4. RNA isoform abundance is not automatically protein amount or proof that one isoform alone causes apoptosis.

    Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 676–682

    AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · 50 micromolar apigenin for 48 hours; RNA-seq and isoform-specific PCR. · Recorded from source · Recorded from source

    ### api-splice-ccnl2 Apigenin increased the relative abundance of Human translation-competent CCNL2 transcripts in MDA-MB-231 breast-cancer cells. Figure 4. RNA isoform abundance is not automatically protein amount or proof that one isoform alone causes apoptosis. Model and exposure: 50 micromolar apigenin for 48 hours; RNA-seq and isoform-specific PCR. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Transcriptome reprogramming through alternative splicing triggered by apigenin drives cell death in triple-negative breast cancer. | 2023 | https://pubmed.ncbi.nlm.nih.gov/38092740/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC10719380/ | https://doi.org/10.1038/s41419-023-06342-6 | Access: Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
    Complete structured claim and evidence

  3. Apigenin decreased the relative abundance of Human CFLAR short transcript / CFLAR-S in MDA-MB-231 breast-cancer cells.

    Apigenin → Human CFLAR short transcript / CFLAR-S Recorded from sourceungraded
    Experimental context and source evidence
    evidence_access
    Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
    experimental_contrast
    {"intervention": "Apigenin", "comparator": "DMSO", "endpoint": "Apigenin decreased the relative abundance of Human CFLAR short transcript / CFLAR-S in MDA-MB-231 breast-cancer cells.", "effect_direction": "decrease", "combination": "single", "conditions": []} Explicit extracted experimental comparison; recorded from source.
    experimental_model
    50 micromolar apigenin for 48 hours; RNA-seq and isoform-specific PCR.
    interpretation_status
    Recorded from source with stated access limits; ungraded, not independent replication.
    limitations
    Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
    nutrient_topic
    Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin
    plain_language
    Apigenin decreased the relative abundance of Human CFLAR short transcript / CFLAR-S in MDA-MB-231 breast-cancer cells.
    primary_references
    Transcriptome reprogramming through alternative splicing triggered by apigenin drives cell death in triple-negative breast cancer. | https://pubmed.ncbi.nlm.nih.gov/38092740/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC10719380/ | https://doi.org/10.1038/s41419-023-06342-6
    source_locator
    Reviewed reference api-splice-cflar; Figure 4. RNA isoform abundance is not automatically protein amount or proof that one isoform alone causes apoptosis.

    Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 652–658

    AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · 50 micromolar apigenin for 48 hours; RNA-seq and isoform-specific PCR. · Recorded from source · Recorded from source

    ### api-splice-cflar Apigenin decreased the relative abundance of Human CFLAR short transcript / CFLAR-S in MDA-MB-231 breast-cancer cells. Figure 4. RNA isoform abundance is not automatically protein amount or proof that one isoform alone causes apoptosis. Model and exposure: 50 micromolar apigenin for 48 hours; RNA-seq and isoform-specific PCR. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Transcriptome reprogramming through alternative splicing triggered by apigenin drives cell death in triple-negative breast cancer. | 2023 | https://pubmed.ncbi.nlm.nih.gov/38092740/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC10719380/ | https://doi.org/10.1038/s41419-023-06342-6 | Access: Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
    Complete structured claim and evidence

  4. Apigenin decreased the relative abundance of Human MAP3K7-A transcript lacking exon 12 in MDA-MB-231 breast-cancer cells.

    Apigenin → Human MAP3K7-A transcript lacking exon 12 Recorded from sourceungraded
    Experimental context and source evidence
    evidence_access
    Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
    experimental_contrast
    {"intervention": "Apigenin", "comparator": "DMSO", "endpoint": "Apigenin decreased the relative abundance of Human MAP3K7-A transcript lacking exon 12 in MDA-MB-231 breast-cancer cells.", "effect_direction": "decrease", "combination": "single", "conditions": []} Explicit extracted experimental comparison; recorded from source.
    experimental_model
    50 micromolar apigenin for 48 hours; RNA-seq and isoform-specific PCR.
    interpretation_status
    Recorded from source with stated access limits; ungraded, not independent replication.
    limitations
    Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
    nutrient_topic
    Apigenin collection; exact intervention and molecular form govern interpretation. · Apigenin
    plain_language
    Apigenin decreased the relative abundance of Human MAP3K7-A transcript lacking exon 12 in MDA-MB-231 breast-cancer cells.
    primary_references
    Transcriptome reprogramming through alternative splicing triggered by apigenin drives cell death in triple-negative breast cancer. | https://pubmed.ncbi.nlm.nih.gov/38092740/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC10719380/ | https://doi.org/10.1038/s41419-023-06342-6
    source_locator
    Reviewed reference api-splice-map3k7a; Figure 4. RNA isoform abundance is not automatically protein amount or proof that one isoform alone causes apoptosis.

    Apigenin: detailed mechanisms of action (reviewed 10 October 2026) · lines 660–666

    AI-assisted original curation of primary studies; claim-local access and experimental limitations stated. Includes original-draft correction history. No independent replication claimed. · supports · 50 micromolar apigenin for 48 hours; RNA-seq and isoform-specific PCR. · Recorded from source · Recorded from source

    ### api-splice-map3k7a Apigenin decreased the relative abundance of Human MAP3K7-A transcript lacking exon 12 in MDA-MB-231 breast-cancer cells. Figure 4. RNA isoform abundance is not automatically protein amount or proof that one isoform alone causes apoptosis. Model and exposure: 50 micromolar apigenin for 48 hours; RNA-seq and isoform-specific PCR. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Transcriptome reprogramming through alternative splicing triggered by apigenin drives cell death in triple-negative breast cancer. | 2023 | https://pubmed.ncbi.nlm.nih.gov/38092740/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC10719380/ | https://doi.org/10.1038/s41419-023-06342-6 | Access: Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
    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.