Component
Rat cannabinoid receptor 1 / Cnr1
Rat cannabinoid receptor 1 / Cnr1. Species, exposure and limitations are retained in each linked claim.
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
The authors linked CB1 antagonism to ERK-dependent regulation of glutamine synthetase in rats, with different ERK responses in normal and stressed conditions.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/theanine-research/34037653.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c792377afacbf5a17e93e4675a4a28ee6849d0288bfc09ad53a2377a0bb982b1", "start_char": 0, "end_char": 1786, "text_sha256": "c792377afacbf5a17e93e4675a4a28ee6849d0288bfc09ad53a2377a0bb982b1"}
- experimental_model
- Receptor interaction and pathway assays
- exposure
- Theanine; normal versus experimental stress conditions
- limitations
- Preclinical CB1-binding claim requires independent confirmation at human exposures; signaling direction differed between normal and stressed rats. No equivalence to cannabinoid drugs inferred.
- nutrient_topic
- L-Theanine research collection; topical membership is not evidence of a direct dietary effect. · L-Theanine
- organism
- Normal and E44813-stressed rats
- plain_language
- Receptor signaling connects to the enzyme that makes glutamine; the direction depends on context.
- primary_references
- [theanine-p34037653] L-Theanine regulates glutamine metabolism and immune function by binding to cannabinoid receptor 1. (2021). https://pubmed.ncbi.nlm.nih.gov/34037653/ DOI: 10.1039/d1fo00505g
- tissue_or_cell_type
- CB1-associated immune and glutamine regulation
L-Theanine: metabolism, neural signaling, nutrient connections and human outcomes (2026-09-17) · lines 484–495
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Receptor interaction and pathway assays · source_derived_draft · unverified_draft
### theanine-cb1-gs The authors linked CB1 antagonism to ERK-dependent regulation of glutamine synthetase in rats, with different ERK responses in normal and stressed conditions. Condition category: normal nutrient_topic: L-Theanine research collection; topical membership is not evidence of a direct dietary effect. plain_language: Receptor signaling connects to the enzyme that makes glutamine; the direction depends on context. organism: Normal and E44813-stressed rats tissue_or_cell_type: CB1-associated immune and glutamine regulation experimental_model: Receptor interaction and pathway assays limitations: Preclinical CB1-binding claim requires independent confirmation at human exposures; signaling direction differed between normal and stressed rats. No equivalence to cannabinoid drugs inferred. exposure: Theanine; normal versus experimental stress conditions evidence_span: {"source_cache": "artifacts/theanine-research/34037653.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c792377afacbf5a17e93e4675a4a28ee6849d0288bfc09ad53a2377a0bb982b1", "start_char": 0, "end_char": 1786, "text_sha256": "c792377afacbf5a17e93e4675a4a28ee6849d0288bfc09ad53a2377a0bb982b1"} [theanine-p34037653] L-Theanine regulates glutamine metabolism and immune function by binding to cannabinoid receptor 1. (2021). https://pubmed.ncbi.nlm.nih.gov/34037653/ DOI: 10.1039/d1fo00505g
Complete structured claim and evidence
What acts on it
The study reported competitive binding and inhibition of rat cannabinoid receptor 1 by theanine.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/theanine-research/34037653.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c792377afacbf5a17e93e4675a4a28ee6849d0288bfc09ad53a2377a0bb982b1", "start_char": 0, "end_char": 1786, "text_sha256": "c792377afacbf5a17e93e4675a4a28ee6849d0288bfc09ad53a2377a0bb982b1"}
- experimental_model
- Receptor interaction and pathway assays
- exposure
- Theanine; normal versus experimental stress conditions
- limitations
- Preclinical CB1-binding claim requires independent confirmation at human exposures; signaling direction differed between normal and stressed rats. No equivalence to cannabinoid drugs inferred.
- nutrient_topic
- L-Theanine research collection; topical membership is not evidence of a direct dietary effect. · L-Theanine
- organism
- Normal and E44813-stressed rats
- plain_language
- A proposed receptor connection is preserved with its rat-model limits.
- primary_references
- [theanine-p34037653] L-Theanine regulates glutamine metabolism and immune function by binding to cannabinoid receptor 1. (2021). https://pubmed.ncbi.nlm.nih.gov/34037653/ DOI: 10.1039/d1fo00505g
- tissue_or_cell_type
- CB1-associated immune and glutamine regulation
L-Theanine: metabolism, neural signaling, nutrient connections and human outcomes (2026-09-17) · lines 471–482
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Receptor interaction and pathway assays · source_derived_draft · unverified_draft
### theanine-cb1 The study reported competitive binding and inhibition of rat cannabinoid receptor 1 by theanine. Condition category: normal nutrient_topic: L-Theanine research collection; topical membership is not evidence of a direct dietary effect. plain_language: A proposed receptor connection is preserved with its rat-model limits. organism: Normal and E44813-stressed rats tissue_or_cell_type: CB1-associated immune and glutamine regulation experimental_model: Receptor interaction and pathway assays limitations: Preclinical CB1-binding claim requires independent confirmation at human exposures; signaling direction differed between normal and stressed rats. No equivalence to cannabinoid drugs inferred. exposure: Theanine; normal versus experimental stress conditions evidence_span: {"source_cache": "artifacts/theanine-research/34037653.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c792377afacbf5a17e93e4675a4a28ee6849d0288bfc09ad53a2377a0bb982b1", "start_char": 0, "end_char": 1786, "text_sha256": "c792377afacbf5a17e93e4675a4a28ee6849d0288bfc09ad53a2377a0bb982b1"} [theanine-p34037653] L-Theanine regulates glutamine metabolism and immune function by binding to cannabinoid receptor 1. (2021). https://pubmed.ncbi.nlm.nih.gov/34037653/ DOI: 10.1039/d1fo00505g
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.