Component

Human AMN double FXNPXF-signal mutant

Engineered human AMN construct with both cytosolic internalization motifs disrupted, designated I-II- by Pedersen 2010.

1 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.

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. Disruption of both human AMN FXNPXF motifs impaired IF-B12 internalization and degradation in CHO-K1 cells despite preserved cubam surface expression.

    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    false
    experimental_model
    Human AMN double-signal mutant plus rat cubilin 1-1389 in CHO-K1 cells
    exposure
    Both cytoplasmic motifs disrupted; wild-type and single-motif mutants as comparators
    limitations
    Engineered trafficking defect, not a patient genotype. Surface binding and intracellular entry are separate readouts.
    nutrient_topic
    Vitamin B12 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin B12 (cobalamins)
    organism
    Human AMN; rat cubilin; Chinese hamster host cells; human/porcine IF reagents
    plain_language
    A receptor can reach the surface yet fail to internalize its cargo.
    primary_references
    [pedersen-2010-amn-endocytosis] AMN directs endocytosis of the intrinsic factor-vitamin B(12) receptor cubam by engaging ARH or Dab2. (2010). https://pubmed.ncbi.nlm.nih.gov/20088845/ DOI: 10.1111/j.1600-0854.2010.01042.x
    tissue_or_cell_type
    Engineered receptor internalization model
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Vitamin B12: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 491–502

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human AMN double-signal mutant plus rat cubilin 1-1389 in CHO-K1 cells · source_derived_draft · unverified_draft

    ### b12-abs-amn-endocytic-signal-loss Disruption of both human AMN FXNPXF motifs impaired IF-B12 internalization and degradation in CHO-K1 cells despite preserved cubam surface expression. Condition category: machinery_impairment nutrient_topic: Vitamin B12 research collection; topical membership is not evidence of a direct dietary effect. plain_language: A receptor can reach the surface yet fail to internalize its cargo. organism: Human AMN; rat cubilin; Chinese hamster host cells; human/porcine IF reagents tissue_or_cell_type: Engineered receptor internalization model experimental_model: Human AMN double-signal mutant plus rat cubilin 1-1389 in CHO-K1 cells limitations: Engineered trafficking defect, not a patient genotype. Surface binding and intracellular entry are separate readouts. exposure: Both cytoplasmic motifs disrupted; wild-type and single-motif mutants as comparators cross_nutrient: false [pedersen-2010-amn-endocytosis] AMN directs endocytosis of the intrinsic factor-vitamin B(12) receptor cubam by engaging ARH or Dab2. (2010). https://pubmed.ncbi.nlm.nih.gov/20088845/ DOI: 10.1111/j.1600-0854.2010.01042.x
    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.

    Evidence, AI assistance and curation standards