Component
PiT-2 / SLC20A2
Type III sodium-dependent phosphate transporter; distinct from PiT-1/SLC20A1.
2 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.
Other things that act on it
Enzymes, hormones, genes, and other components with a recorded effect. These are not nutrients, so they do not count toward the arrows above. Each finding names the chapter that recorded it.
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.
What it acts on
PiT2 overexpression restored phosphate uptake and phosphate-induced calcification in human PiT1-deficient vascular smooth-muscle cells.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_span
- {"source_cache": "artifacts/phosphorus-research/23968976.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6704ac0400a286d5137384f4339dd6dffb0061a41a121b6c72a0b23353cbc6f9", "start_char": 0, "end_char": 1852, "text_sha256": "6704ac0400a286d5137384f4339dd6dffb0061a41a121b6c72a0b23353cbc6f9"}
- experimental_model
- Smooth-muscle-specific knockout and transporter compensation experiments
- exposure
- Mouse CKD plus dietary phosphate loading; PiT2 knockdown or expression rescue
- limitations
- Loss of one transporter can be masked by another. This refines a single-transporter model without proving every calcification pathway requires transport.
- nutrient_topic
- Phosphorus research collection; topical membership is not evidence of a direct dietary effect. · Phosphorus
- organism
- Human
- plain_language
- The human-cell rescue supported a backup role for PiT2.
- primary_references
- [phosphorus-p23968976] Sodium-dependent phosphate cotransporters and phosphate-induced calcification of vascular smooth muscle cells: redundant roles for PiT-1 and PiT-2. (2013). https://pubmed.ncbi.nlm.nih.gov/23968976/ DOI: 10.1161/atvbaha.113.302249
- tissue_or_cell_type
- Vascular smooth muscle
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Phosphorus: metabolism, signaling and nutrient connections (2026-09-17) · lines 854–865
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Smooth-muscle-specific knockout and transporter compensation experiments · source_derived_draft · unverified_draft
### phosphorus-human-pit2-rescue PiT2 overexpression restored phosphate uptake and phosphate-induced calcification in human PiT1-deficient vascular smooth-muscle cells. Condition category: machinery_impairment nutrient_topic: Phosphorus research collection; topical membership is not evidence of a direct dietary effect. plain_language: The human-cell rescue supported a backup role for PiT2. organism: Human tissue_or_cell_type: Vascular smooth muscle experimental_model: Smooth-muscle-specific knockout and transporter compensation experiments limitations: Loss of one transporter can be masked by another. This refines a single-transporter model without proving every calcification pathway requires transport. exposure: Mouse CKD plus dietary phosphate loading; PiT2 knockdown or expression rescue evidence_span: {"source_cache": "artifacts/phosphorus-research/23968976.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6704ac0400a286d5137384f4339dd6dffb0061a41a121b6c72a0b23353cbc6f9", "start_char": 0, "end_char": 1852, "text_sha256": "6704ac0400a286d5137384f4339dd6dffb0061a41a121b6c72a0b23353cbc6f9"} [phosphorus-p23968976] Sodium-dependent phosphate cotransporters and phosphate-induced calcification of vascular smooth muscle cells: redundant roles for PiT-1 and PiT-2. (2013). https://pubmed.ncbi.nlm.nih.gov/23968976/ DOI: 10.1161/atvbaha.113.302249
Complete structured claim and evidence
What acts on it
Dietary potassium deficiency decreased proximal-tubule brush-border PiT-2 abundance in rats and mice.
Experimental context and source evidence
- availability_state
- nutrient_deficiency Imported condition classification; unverified.
- cross_nutrient
- Potassium deficiency changes sodium-phosphate transport machinery in an isoform-specific manner.
- endpoint
- Dietary potassium deficiency decreased proximal-tubule brush-border PiT-2 abundance in rats and mice.
- experimental-exposure
- Potassium-deficient rats and mice; renal brush-border membrane protein, transcript, immunofluorescence and electron-microscopy analyses.
- experimental_model
- Potassium-deficient rats and mice; renal brush-border membrane protein, transcript, immunofluorescence and electron-microscopy analyses.
- limitations
- Isoform abundance and localization do not apportion total phosphate flux; transporter-specific contributions and initiating signal remain unresolved.
- nutrient_topic
- Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
- organism
- Rattus norvegicus; Mus musculus where specified
- plain_language
- A second, distinct sodium-phosphate transporter declined.
- primary_references
- [breusegem-2009-phosphate] Differential regulation of the renal sodium-phosphate cotransporters NaPi-IIa, NaPi-IIc, and PiT-2 in dietary potassium deficiency (2009). https://pubmed.ncbi.nlm.nih.gov/19493963/ DOI: 10.1152/ajprenal.90765.2008
- tissue_or_cell_type
- renal proximal-tubule brush border
- trigger_kind
- nutrient_deficiency Imported condition classification; unverified.
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1358–1370
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Potassium-deficient rats and mice; renal brush-border membrane protein, transcript, immunofluorescence and electron-microscopy analyses. · source_derived_draft · unverified_draft
### k-deficiency-pit2-abundance Dietary potassium deficiency decreased proximal-tubule brush-border PiT-2 abundance in rats and mice. Condition category: nutrient_deficiency nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: A second, distinct sodium-phosphate transporter declined. organism: Rattus norvegicus; Mus musculus where specified tissue_or_cell_type: renal proximal-tubule brush border experimental_model: Potassium-deficient rats and mice; renal brush-border membrane protein, transcript, immunofluorescence and electron-microscopy analyses. limitations: Isoform abundance and localization do not apportion total phosphate flux; transporter-specific contributions and initiating signal remain unresolved. cross_nutrient: Potassium deficiency changes sodium-phosphate transport machinery in an isoform-specific manner. experimental-exposure: Potassium-deficient rats and mice; renal brush-border membrane protein, transcript, immunofluorescence and electron-microscopy analyses. endpoint: Dietary potassium deficiency decreased proximal-tubule brush-border PiT-2 abundance in rats and mice. [breusegem-2009-phosphate] Differential regulation of the renal sodium-phosphate cotransporters NaPi-IIa, NaPi-IIc, and PiT-2 in dietary potassium deficiency (2009). https://pubmed.ncbi.nlm.nih.gov/19493963/ DOI: 10.1152/ajprenal.90765.2008
Complete structured claim and evidence
The events it takes part in
A mechanism often involves more than two components. These are the full events, with every participant and its role.
Situations it appears in
Low-supply and faulty-machinery situations recorded in the chapters where this component plays a part.
In the sources
Preserved passages that mention this component, quoted exactly. Open one to read it in context.
Open hypotheses
Proposed ideas that involve this component. They are labeled as hypotheses and do not change any recorded statement.
This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.