Component
NBCe1-A splice variant
Renal NBCe1-A sodium-bicarbonate cotransporter splice variant of SLC4A4; distinct from other NBCe1 variants.
3 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
Mutagenesis of NBCe1 residues E91 or R298 reduced transport function in the expression assay.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_span
- {"source_cache": "artifacts/sodium-research/18441326.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "3ca538a7ecb046a47f9246778b3dede99c503a45c6048f75541612c8db37448c", "start_char": 0, "end_char": 1213, "text_sha256": "3ca538a7ecb046a47f9246778b3dede99c503a45c6048f75541612c8db37448c"}
- experimental_model
- Homology modeling and site-directed mutagenesis with oocyte transport assays
- exposure
- E91 and R298 mutations and charge-reversal construct
- limitations
- Structure model plus functional assay; charge rescue does not establish clinical treatment or dietary sodium responsiveness.
- nutrient_topic
- Sodium research collection; topical membership is not evidence of a direct dietary effect. · Sodium
- organism
- Human kidney NBCe1 in Xenopus oocytes
- plain_language
- Acid–base regulation depends on the protein’s structure as well as available sodium.
- primary_references
- [sodium-p18441326] Entry to "formula tunnel" revealed by SLC4A4 human mutation and structural model. (2008). https://pubmed.ncbi.nlm.nih.gov/18441326/ DOI: 10.1074/jbc.m709819200
- tissue_or_cell_type
- Sodium/bicarbonate transporter N-terminal domain
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Sodium: gradients, nutrient transport, fluid regulation and loss states (2026-09-17) · lines 707–718
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Homology modeling and site-directed mutagenesis with oocyte transport assays · source_derived_draft · unverified_draft
### sodium-nbce1-mutation Mutagenesis of NBCe1 residues E91 or R298 reduced transport function in the expression assay. Condition category: machinery_impairment nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Acid–base regulation depends on the protein’s structure as well as available sodium. organism: Human kidney NBCe1 in Xenopus oocytes tissue_or_cell_type: Sodium/bicarbonate transporter N-terminal domain experimental_model: Homology modeling and site-directed mutagenesis with oocyte transport assays limitations: Structure model plus functional assay; charge rescue does not establish clinical treatment or dietary sodium responsiveness. exposure: E91 and R298 mutations and charge-reversal construct evidence_span: {"source_cache": "artifacts/sodium-research/18441326.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "3ca538a7ecb046a47f9246778b3dede99c503a45c6048f75541612c8db37448c", "start_char": 0, "end_char": 1213, "text_sha256": "3ca538a7ecb046a47f9246778b3dede99c503a45c6048f75541612c8db37448c"} [sodium-p18441326] Entry to "formula tunnel" revealed by SLC4A4 human mutation and structural model. (2008). https://pubmed.ncbi.nlm.nih.gov/18441326/ DOI: 10.1074/jbc.m709819200
Complete structured claim and evidenceNBCe1-A deletion blunted the urinary ammonia-excretion response to potassium-free feeding.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- cross_nutrient
- Sodium-bicarbonate transport machinery is required for the full potassium-responsive ammonia adaptation.
- endpoint
- NBCe1-A deletion blunted the urinary ammonia-excretion response to potassium-free feeding.
- experimental-exposure
- NBCe1-A-selective knockout mice and wild-type littermates on control or potassium-free diets; four-day response.
- experimental_model
- NBCe1-A-selective knockout mice and wild-type littermates on control or potassium-free diets; four-day response.
- limitations
- Assay reports total ammonia. Knockout also causes acidosis and outer-medullary compensation; the exact signal is unresolved.
- nutrient_topic
- Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
- organism
- Mus musculus
- plain_language
- A sodium-bicarbonate transporter was needed for the full kidney ammonia response to potassium deprivation.
- primary_references
- [lee-2020-nbce1a] NBCe1-A is required for the renal ammonia and K+ response to hypokalemia (2020). https://pubmed.ncbi.nlm.nih.gov/31841393/ DOI: 10.1152/ajprenal.00481.2019
- tissue_or_cell_type
- cortical proximal tubule and urinary ammonia output
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1082–1094
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · NBCe1-A-selective knockout mice and wild-type littermates on control or potassium-free diets; four-day response. · source_derived_draft · unverified_draft
### nbce1a-loss-blunts-k-ammonia-response NBCe1-A deletion blunted the urinary ammonia-excretion response to potassium-free feeding. Condition category: machinery_impairment nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: A sodium-bicarbonate transporter was needed for the full kidney ammonia response to potassium deprivation. organism: Mus musculus tissue_or_cell_type: cortical proximal tubule and urinary ammonia output experimental_model: NBCe1-A-selective knockout mice and wild-type littermates on control or potassium-free diets; four-day response. limitations: Assay reports total ammonia. Knockout also causes acidosis and outer-medullary compensation; the exact signal is unresolved. cross_nutrient: Sodium-bicarbonate transport machinery is required for the full potassium-responsive ammonia adaptation. experimental-exposure: NBCe1-A-selective knockout mice and wild-type littermates on control or potassium-free diets; four-day response. endpoint: NBCe1-A deletion blunted the urinary ammonia-excretion response to potassium-free feeding. [lee-2020-nbce1a] NBCe1-A is required for the renal ammonia and K+ response to hypokalemia (2020). https://pubmed.ncbi.nlm.nih.gov/31841393/ DOI: 10.1152/ajprenal.00481.2019
Complete structured claim and evidence
What acts on it
Four days of potassium-free diet increased cortical proximal-tubule NBCe1-A expression in wild-type mice.
Experimental context and source evidence
- availability_state
- nutrient_deficiency Imported condition classification; unverified.
- cross_nutrient
- Potassium deprivation regulates sodium-bicarbonate transport machinery.
- endpoint
- Four days of potassium-free diet increased cortical proximal-tubule NBCe1-A expression in wild-type mice.
- experimental-exposure
- NBCe1-A-selective knockout mice and wild-type littermates on control or potassium-free diets; four-day response.
- experimental_model
- NBCe1-A-selective knockout mice and wild-type littermates on control or potassium-free diets; four-day response.
- limitations
- Expression was measured; this record does not assign a bicarbonate transport stoichiometry or measure its flux.
- nutrient_topic
- Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
- organism
- Mus musculus
- plain_language
- A sodium-bicarbonate transporter adapted during potassium conservation.
- primary_references
- [lee-2020-nbce1a] NBCe1-A is required for the renal ammonia and K+ response to hypokalemia (2020). https://pubmed.ncbi.nlm.nih.gov/31841393/ DOI: 10.1152/ajprenal.00481.2019
- tissue_or_cell_type
- cortical proximal tubule
- trigger_kind
- nutrient_deficiency Imported condition classification; unverified.
Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1068–1080
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · NBCe1-A-selective knockout mice and wild-type littermates on control or potassium-free diets; four-day response. · source_derived_draft · unverified_draft
### k-free-diet-increases-nbce1a Four days of potassium-free diet increased cortical proximal-tubule NBCe1-A expression in wild-type mice. Condition category: nutrient_deficiency nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: A sodium-bicarbonate transporter adapted during potassium conservation. organism: Mus musculus tissue_or_cell_type: cortical proximal tubule experimental_model: NBCe1-A-selective knockout mice and wild-type littermates on control or potassium-free diets; four-day response. limitations: Expression was measured; this record does not assign a bicarbonate transport stoichiometry or measure its flux. cross_nutrient: Potassium deprivation regulates sodium-bicarbonate transport machinery. experimental-exposure: NBCe1-A-selective knockout mice and wild-type littermates on control or potassium-free diets; four-day response. endpoint: Four days of potassium-free diet increased cortical proximal-tubule NBCe1-A expression in wild-type mice. [lee-2020-nbce1a] NBCe1-A is required for the renal ammonia and K+ response to hypokalemia (2020). https://pubmed.ncbi.nlm.nih.gov/31841393/ DOI: 10.1152/ajprenal.00481.2019
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.