Component

Riboflavin transporter 1 / SLC52A1

Human RFVT1; older literature calls this RFT1 or GPR172B.

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. Expression of human RFVT1 increased cellular riboflavin uptake in HEK293 and Caco-2 experiments.

    Riboflavin transporter 1 / SLC52A1 → Riboflavin (vitamin B2) source_derived_draftungraded
    Experimental context and source evidence
    evidence_location
    Functional characterization of hRFT1
    experimental_model
    Human transporter expression and radiotracer uptake
    exposure
    Wild-type transporter expression and radiolabeled riboflavin.
    limitations
    Expression-system kinetics do not establish whole-body absorption capacity.
    nutrient_topic
    Riboflavin research collection; topical membership is not evidence of a direct dietary effect. · Riboflavin (vitamin B2)
    organism
    Homo sapiens
    plain_language
    RFVT1 carries free riboflavin into cells.
    primary_references
    [transport-rfvt1-2008] Identification and functional characterization of a novel human and rat riboflavin transporter, RFT1. (2008). https://doi.org/10.1152/ajpcell.00019.2008 DOI: 10.1152/ajpcell.00019.2008
    tissue_or_cell_type
    HEK293 and Caco-2 cells
    transport_effect
    raises Expression increased cellular riboflavin uptake.
    transport_pool
    the expressing cell Expression increased cellular riboflavin uptake.

    Riboflavin: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 137–148

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human transporter expression and radiotracer uptake · source_derived_draft · unverified_draft

    ### transport-rfvt1-influx Expression of human RFVT1 increased cellular riboflavin uptake in HEK293 and Caco-2 experiments. Condition category: normal nutrient_topic: Riboflavin research collection; topical membership is not evidence of a direct dietary effect. plain_language: RFVT1 carries free riboflavin into cells. organism: Homo sapiens tissue_or_cell_type: HEK293 and Caco-2 cells experimental_model: Human transporter expression and radiotracer uptake limitations: Expression-system kinetics do not establish whole-body absorption capacity. exposure: Wild-type transporter expression and radiolabeled riboflavin. evidence_location: Functional characterization of hRFT1 [transport-rfvt1-2008] Identification and functional characterization of a novel human and rat riboflavin transporter, RFT1. (2008). https://doi.org/10.1152/ajpcell.00019.2008 DOI: 10.1152/ajpcell.00019.2008
    Complete structured claim and evidence

  2. Tagged human Riboflavin transporter 1 / SLC52A1 localized mainly at the basolateral membrane in polarized Caco-2 and MDCK imaging experiments.

    Riboflavin transporter 1 / SLC52A1 → Intestinal epithelial basolateral membrane source_derived_draftungraded
    Experimental context and source evidence
    evidence_location
    Live-cell imaging; historical RFT1/2/3 correspond to RFVT1/3/2
    experimental_model
    Live-cell confocal imaging of tagged transporter constructs
    exposure
    Expression of fluorescent transporter constructs.
    limitations
    Tagged overexpression in epithelial models; not a universal localization map across tissues.
    nutrient_topic
    Riboflavin research collection; topical membership is not evidence of a direct dietary effect. · Riboflavin (vitamin B2)
    organism
    Human proteins in human and canine cells
    plain_language
    The riboflavin transporters occupy different parts of polarized epithelial cells.
    primary_references
    [transport-localization-2011] Differential expression of human riboflavin transporters -1, -2, and -3 in polarized epithelia: a key role for hRFT-2 in intestinal riboflavin uptake. (2011). https://pubmed.ncbi.nlm.nih.gov/21854757/ DOI: 10.1016/j.bbamem.2011.08.004
    tissue_or_cell_type
    Polarized Caco-2 and MDCK cells

    Riboflavin: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 176–187

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Live-cell confocal imaging of tagged transporter constructs · source_derived_draft · unverified_draft

    ### transport-slc52a1-localization Tagged human Riboflavin transporter 1 / SLC52A1 localized mainly at the basolateral membrane in polarized Caco-2 and MDCK imaging experiments. Condition category: normal nutrient_topic: Riboflavin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The riboflavin transporters occupy different parts of polarized epithelial cells. organism: Human proteins in human and canine cells tissue_or_cell_type: Polarized Caco-2 and MDCK cells experimental_model: Live-cell confocal imaging of tagged transporter constructs limitations: Tagged overexpression in epithelial models; not a universal localization map across tissues. exposure: Expression of fluorescent transporter constructs. evidence_location: Live-cell imaging; historical RFT1/2/3 correspond to RFVT1/3/2 [transport-localization-2011] Differential expression of human riboflavin transporters -1, -2, and -3 in polarized epithelia: a key role for hRFT-2 in intestinal riboflavin uptake. (2011). https://pubmed.ncbi.nlm.nih.gov/21854757/ DOI: 10.1016/j.bbamem.2011.08.004
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. SLC52A1 c.1134+11G>A created a binding site for splice-inhibitory hnRNP A1 and promoted exon 4 skipping.

    SLC52A1 c.1134+11G>A variant → SLC52A1 exon 4 skipping source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_location
    Abstract; variant splicing mechanism
    experimental_model
    Variant functional splicing studies accompanying a clinical case
    exposure
    Variant versus reference SLC52A1 splicing context.
    limitations
    Clinical severity may depend on maternal nutritional context; mechanism should not be generalized to all intronic variants.
    nutrient_topic
    Riboflavin research collection; topical membership is not evidence of a direct dietary effect. · Riboflavin (vitamin B2)
    organism
    Homo sapiens
    plain_language
    An intronic change can disrupt production of the riboflavin transporter.
    primary_references
    [transport-slc52a1-splicing-2017] An intronic variation in SLC52A1 causes exon skipping and transient riboflavin-responsive multiple acyl-CoA dehydrogenation deficiency. (2017). https://pubmed.ncbi.nlm.nih.gov/29122468/ DOI: 10.1016/j.ymgme.2017.10.014
    tissue_or_cell_type
    Human SLC52A1 transcript in functional assays
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Riboflavin: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 477–488

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Variant functional splicing studies accompanying a clinical case · source_derived_draft · unverified_draft

    ### transport-slc52a1-splice-silencer SLC52A1 c.1134+11G>A created a binding site for splice-inhibitory hnRNP A1 and promoted exon 4 skipping. Condition category: machinery_impairment nutrient_topic: Riboflavin research collection; topical membership is not evidence of a direct dietary effect. plain_language: An intronic change can disrupt production of the riboflavin transporter. organism: Homo sapiens tissue_or_cell_type: Human SLC52A1 transcript in functional assays experimental_model: Variant functional splicing studies accompanying a clinical case limitations: Clinical severity may depend on maternal nutritional context; mechanism should not be generalized to all intronic variants. exposure: Variant versus reference SLC52A1 splicing context. evidence_location: Abstract; variant splicing mechanism [transport-slc52a1-splicing-2017] An intronic variation in SLC52A1 causes exon skipping and transient riboflavin-responsive multiple acyl-CoA dehydrogenation deficiency. (2017). https://pubmed.ncbi.nlm.nih.gov/29122468/ DOI: 10.1016/j.ymgme.2017.10.014
    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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