Component
Rat GLT-1b transporter isoform
GLT-1b splice variant of rat Slc1a2, distinct from an assay of total GLT-1.
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 acts on it
NF-kappa-B inhibition attenuated GLT-1b loss in astrocytes exposed to the thiamine-disruption protocol.
Experimental context and source evidence
- availability_state
- nutrient_deficiency Imported condition classification; unverified.
- evidence_location
- Abstract; NF-kappa-B inhibitor experiment
- evidence_span
- ameliorated the decrease in GLT-1b
- experimental_model
- Newborn-rat astrocytes differentiated with dibutyryl cAMP; thiamine-free DMEM with 5% horse serum plus 10 micromolar pyrithiamine; conditioned-medium transfer and inflammatory-pathway inhibitors.
- exposure
- Thiamine-free medium plus pyrithiamine in cultured newborn-rat astrocytes
- limitations
- Pharmacological inhibition is not isoform-specific genetic proof; the accessible record does not establish efficacy in intact human brain.
- nutrient_topic
- Thiamine research collection; topical membership is not evidence of a direct dietary effect. · Thiamine (vitamin B1)
- organism
- Rattus norvegicus
- plain_language
- Suppressing the inflammatory pathway helped preserve this particular glutamate-transporter isoform.
- primary_references
- [jhala-2014-astrocyte-inflammatory-signaling] Thiamine deficiency results in release of soluble factors that disrupt mitochondrial membrane potential and downregulate the glutamate transporter splice-variant GLT-1b in cultured astrocytes. (2014). https://www.sciencedirect.com/science/article/abs/pii/S0006291X14006482 DOI: 10.1016/j.bbrc.2014.04.017
- tissue_or_cell_type
- Cultured astrocytes
- trigger_kind
- nutrient_deficiency Imported condition classification; unverified.
Thiamine: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1325–1337
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Newborn-rat astrocytes differentiated with dibutyryl cAMP; thiamine-free DMEM with 5% horse serum plus 10 micromolar pyrithiamine; conditioned-medium transfer and inflammatory-pathway inhibitors. · source_derived_draft · unverified_draft
### thiamine-def-nfkb-inhibition-glt1b NF-kappa-B inhibition attenuated GLT-1b loss in astrocytes exposed to the thiamine-disruption protocol. Condition category: nutrient_deficiency nutrient_topic: Thiamine research collection; topical membership is not evidence of a direct dietary effect. plain_language: Suppressing the inflammatory pathway helped preserve this particular glutamate-transporter isoform. organism: Rattus norvegicus tissue_or_cell_type: Cultured astrocytes experimental_model: Newborn-rat astrocytes differentiated with dibutyryl cAMP; thiamine-free DMEM with 5% horse serum plus 10 micromolar pyrithiamine; conditioned-medium transfer and inflammatory-pathway inhibitors. limitations: Pharmacological inhibition is not isoform-specific genetic proof; the accessible record does not establish efficacy in intact human brain. evidence_location: Abstract; NF-kappa-B inhibitor experiment evidence_span: ameliorated the decrease in GLT-1b exposure: Thiamine-free medium plus pyrithiamine in cultured newborn-rat astrocytes [jhala-2014-astrocyte-inflammatory-signaling] Thiamine deficiency results in release of soluble factors that disrupt mitochondrial membrane potential and downregulate the glutamate transporter splice-variant GLT-1b in cultured astrocytes. (2014). https://www.sciencedirect.com/science/article/abs/pii/S0006291X14006482 DOI: 10.1016/j.bbrc.2014.04.017
Complete structured claim and evidence
Where it participates (unsigned role)
Medium from depleted astrocytes reduced glutamate uptake in naive recipient astrocytes by over 70% after 24 hours.
Experimental context and source evidence
- availability_state
- nutrient_deficiency Imported condition classification; unverified.
- evidence_location
- Results snippet: Effects of TD conditioned media on glutamate transport; Figure 1A
- evidence_span
- reduced by over 70% after 24 h
- experimental_model
- Newborn-rat astrocytes differentiated with dibutyryl cAMP; thiamine-free DMEM with 5% horse serum plus 10 micromolar pyrithiamine; conditioned-medium transfer and inflammatory-pathway inhibitors.
- exposure
- Thiamine-free medium plus pyrithiamine in cultured newborn-rat astrocytes
- limitations
- Conditioned medium is a mixture; this comparison alone cannot identify a secreted mediator or exclude carried-over medium components.
- nutrient_topic
- Thiamine research collection; topical membership is not evidence of a direct dietary effect. · Thiamine (vitamin B1)
- organism
- Rattus norvegicus
- plain_language
- The culture environment from depleted cells transferred a defect in glutamate removal.
- primary_references
- [jhala-2014-astrocyte-inflammatory-signaling] Thiamine deficiency results in release of soluble factors that disrupt mitochondrial membrane potential and downregulate the glutamate transporter splice-variant GLT-1b in cultured astrocytes. (2014). https://www.sciencedirect.com/science/article/abs/pii/S0006291X14006482 DOI: 10.1016/j.bbrc.2014.04.017
- tissue_or_cell_type
- Cultured astrocytes
- trigger_kind
- nutrient_deficiency Imported condition classification; unverified.
Thiamine: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1297–1309
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Newborn-rat astrocytes differentiated with dibutyryl cAMP; thiamine-free DMEM with 5% horse serum plus 10 micromolar pyrithiamine; conditioned-medium transfer and inflammatory-pathway inhibitors. · source_derived_draft · unverified_draft
### thiamine-def-conditioned-medium-uptake Medium from depleted astrocytes reduced glutamate uptake in naive recipient astrocytes by over 70% after 24 hours. Condition category: nutrient_deficiency nutrient_topic: Thiamine research collection; topical membership is not evidence of a direct dietary effect. plain_language: The culture environment from depleted cells transferred a defect in glutamate removal. organism: Rattus norvegicus tissue_or_cell_type: Cultured astrocytes experimental_model: Newborn-rat astrocytes differentiated with dibutyryl cAMP; thiamine-free DMEM with 5% horse serum plus 10 micromolar pyrithiamine; conditioned-medium transfer and inflammatory-pathway inhibitors. limitations: Conditioned medium is a mixture; this comparison alone cannot identify a secreted mediator or exclude carried-over medium components. evidence_location: Results snippet: Effects of TD conditioned media on glutamate transport; Figure 1A evidence_span: reduced by over 70% after 24 h exposure: Thiamine-free medium plus pyrithiamine in cultured newborn-rat astrocytes [jhala-2014-astrocyte-inflammatory-signaling] Thiamine deficiency results in release of soluble factors that disrupt mitochondrial membrane potential and downregulate the glutamate transporter splice-variant GLT-1b in cultured astrocytes. (2014). https://www.sciencedirect.com/science/article/abs/pii/S0006291X14006482 DOI: 10.1016/j.bbrc.2014.04.017
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.