Component
Mouse cGMP-inhibited phosphodiesterase Pde3b
Mouse cGMP-inhibited phosphodiesterase Pde3b. 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
Copper-dependent PDE3B inhibition increased cAMP signaling and promoted lipolysis in 3T3-L1 adipocytes.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/copper-research/27272565.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "f8b7e13cc6ef608ddb589779fa85430ca530508013e710f380f4020c3f2632c7", "start_char": 0, "end_char": 1018, "text_sha256": "f8b7e13cc6ef608ddb589779fa85430ca530508013e710f380f4020c3f2632c7"}
- experimental_model
- Copper manipulation, purified Pde3b assays and adipocyte signaling
- exposure
- Copper perturbation and Pde3b cysteine mutations
- limitations
- This cellular signaling result is not a human weight-loss trial. Copper toxicity and systemic distribution are not captured by increasing one cell-culture signal.
- nutrient_topic
- Copper research collection; topical membership is not evidence of a direct dietary effect. · Copper
- organism
- Mouse proteins and 3T3-L1 adipocytes; Atp7b mutant mouse context
- plain_language
- The prolonged signal encouraged fat breakdown in these cells.
- primary_references
- [copper-p27272565] Copper regulates cyclic-AMP-dependent lipolysis. (2016). https://pubmed.ncbi.nlm.nih.gov/27272565/ DOI: 10.1038/nchembio.2098
- tissue_or_cell_type
- Adipocytes and purified enzyme
Copper: transport, cuproenzymes, deficiency, excess and nutrient interactions (2026-09-17) · lines 1209–1220
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Copper manipulation, purified Pde3b assays and adipocyte signaling · source_derived_draft · unverified_draft
### copper-pde3b-camp-lipolysis Copper-dependent PDE3B inhibition increased cAMP signaling and promoted lipolysis in 3T3-L1 adipocytes. Condition category: normal nutrient_topic: Copper research collection; topical membership is not evidence of a direct dietary effect. plain_language: The prolonged signal encouraged fat breakdown in these cells. organism: Mouse proteins and 3T3-L1 adipocytes; Atp7b mutant mouse context tissue_or_cell_type: Adipocytes and purified enzyme experimental_model: Copper manipulation, purified Pde3b assays and adipocyte signaling limitations: This cellular signaling result is not a human weight-loss trial. Copper toxicity and systemic distribution are not captured by increasing one cell-culture signal. exposure: Copper perturbation and Pde3b cysteine mutations evidence_span: {"source_cache": "artifacts/copper-research/27272565.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "f8b7e13cc6ef608ddb589779fa85430ca530508013e710f380f4020c3f2632c7", "start_char": 0, "end_char": 1018, "text_sha256": "f8b7e13cc6ef608ddb589779fa85430ca530508013e710f380f4020c3f2632c7"} [copper-p27272565] Copper regulates cyclic-AMP-dependent lipolysis. (2016). https://pubmed.ncbi.nlm.nih.gov/27272565/ DOI: 10.1038/nchembio.2098
Complete structured claim and evidence
What acts on it
Copper inhibited mouse PDE3B activity in the biochemical and adipocyte study.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/copper-research/27272565.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "f8b7e13cc6ef608ddb589779fa85430ca530508013e710f380f4020c3f2632c7", "start_char": 0, "end_char": 1018, "text_sha256": "f8b7e13cc6ef608ddb589779fa85430ca530508013e710f380f4020c3f2632c7"}
- experimental_model
- Copper manipulation, purified Pde3b assays and adipocyte signaling
- exposure
- Copper perturbation and Pde3b cysteine mutations
- limitations
- This cellular signaling result is not a human weight-loss trial. Copper toxicity and systemic distribution are not captured by increasing one cell-culture signal.
- nutrient_topic
- Copper research collection; topical membership is not evidence of a direct dietary effect. · Copper
- organism
- Mouse proteins and 3T3-L1 adipocytes; Atp7b mutant mouse context
- plain_language
- Copper slowed an enzyme that normally clears the cAMP signal.
- primary_references
- [copper-p27272565] Copper regulates cyclic-AMP-dependent lipolysis. (2016). https://pubmed.ncbi.nlm.nih.gov/27272565/ DOI: 10.1038/nchembio.2098
- tissue_or_cell_type
- Adipocytes and purified enzyme
Copper: transport, cuproenzymes, deficiency, excess and nutrient interactions (2026-09-17) · lines 1196–1207
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Copper manipulation, purified Pde3b assays and adipocyte signaling · source_derived_draft · unverified_draft
### copper-copper-pde3b Copper inhibited mouse PDE3B activity in the biochemical and adipocyte study. Condition category: normal nutrient_topic: Copper research collection; topical membership is not evidence of a direct dietary effect. plain_language: Copper slowed an enzyme that normally clears the cAMP signal. organism: Mouse proteins and 3T3-L1 adipocytes; Atp7b mutant mouse context tissue_or_cell_type: Adipocytes and purified enzyme experimental_model: Copper manipulation, purified Pde3b assays and adipocyte signaling limitations: This cellular signaling result is not a human weight-loss trial. Copper toxicity and systemic distribution are not captured by increasing one cell-culture signal. exposure: Copper perturbation and Pde3b cysteine mutations evidence_span: {"source_cache": "artifacts/copper-research/27272565.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "f8b7e13cc6ef608ddb589779fa85430ca530508013e710f380f4020c3f2632c7", "start_char": 0, "end_char": 1018, "text_sha256": "f8b7e13cc6ef608ddb589779fa85430ca530508013e710f380f4020c3f2632c7"} [copper-p27272565] Copper regulates cyclic-AMP-dependent lipolysis. (2016). https://pubmed.ncbi.nlm.nih.gov/27272565/ DOI: 10.1038/nchembio.2098
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.