Component
Mouse PERK / Eif2ak3
Mouse PERK / Eif2ak3. Species, exposure and limitations are retained in each linked claim.
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
Boric acid induced eIF2α Ser51 phosphorylation in wild-type mouse fibroblasts at one hour, but not in Perk-null cells tested for up to six hours.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_span
- {"source_cache": "artifacts/boron-research/30196486.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e220df5fb0f9b8653035f7a144259ce66778467a7a72acbf7cd7d113f8b6030a", "start_char": 0, "end_char": 2006, "text_sha256": "e220df5fb0f9b8653035f7a144259ce66778467a7a72acbf7cd7d113f8b6030a"}
- experimental_model
- PERK knockout comparison, immunofluorescence and quantitative PCR
- exposure
- 10 µM boric acid; 1–6 hour comparisons
- limitations
- Knockout dependence in mouse fibroblasts is separate from human tumor-cell transcription. Increased GCLC mRNA is not a measured increase in glutathione synthesis or clinical antioxidant benefit.
- nutrient_topic
- Boron research collection; topical membership is not evidence of a direct dietary effect. · Boron
- organism
- Mouse embryonic fibroblasts and human DU-145 cells
- plain_language
- Removing PERK blocked this step of the boric-acid response.
- primary_references
- [boron-p30196486] Boric Acid Activation of eIF2α and Nrf2 Is PERK Dependent: a Mechanism that Explains How Boron Prevents DNA Damage and Enhances Antioxidant Status. (2019). https://pubmed.ncbi.nlm.nih.gov/30196486/ DOI: 10.1007/s12011-018-1498-4
- tissue_or_cell_type
- Cell culture
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Boron: chemistry, nutrient interactions, low-intake studies and mechanistic uncertainties (2026-09-17) · lines 495–506
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · PERK knockout comparison, immunofluorescence and quantitative PCR · source_derived_draft · unverified_draft
### boron-perk-eif2alpha-dependence Boric acid induced eIF2α Ser51 phosphorylation in wild-type mouse fibroblasts at one hour, but not in Perk-null cells tested for up to six hours. Condition category: machinery_impairment nutrient_topic: Boron research collection; topical membership is not evidence of a direct dietary effect. plain_language: Removing PERK blocked this step of the boric-acid response. organism: Mouse embryonic fibroblasts and human DU-145 cells tissue_or_cell_type: Cell culture experimental_model: PERK knockout comparison, immunofluorescence and quantitative PCR limitations: Knockout dependence in mouse fibroblasts is separate from human tumor-cell transcription. Increased GCLC mRNA is not a measured increase in glutathione synthesis or clinical antioxidant benefit. exposure: 10 µM boric acid; 1–6 hour comparisons evidence_span: {"source_cache": "artifacts/boron-research/30196486.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e220df5fb0f9b8653035f7a144259ce66778467a7a72acbf7cd7d113f8b6030a", "start_char": 0, "end_char": 2006, "text_sha256": "e220df5fb0f9b8653035f7a144259ce66778467a7a72acbf7cd7d113f8b6030a"} [boron-p30196486] Boric Acid Activation of eIF2α and Nrf2 Is PERK Dependent: a Mechanism that Explains How Boron Prevents DNA Damage and Enhances Antioxidant Status. (2019). https://pubmed.ncbi.nlm.nih.gov/30196486/ DOI: 10.1007/s12011-018-1498-4
Complete structured claim and evidenceBoric acid induced Nrf2 nuclear translocation in wild-type mouse fibroblasts but not in Perk-null cells.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_span
- {"source_cache": "artifacts/boron-research/30196486.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e220df5fb0f9b8653035f7a144259ce66778467a7a72acbf7cd7d113f8b6030a", "start_char": 0, "end_char": 2006, "text_sha256": "e220df5fb0f9b8653035f7a144259ce66778467a7a72acbf7cd7d113f8b6030a"}
- experimental_model
- PERK knockout comparison, immunofluorescence and quantitative PCR
- exposure
- 10 µM boric acid; 1–6 hour comparisons
- limitations
- Knockout dependence in mouse fibroblasts is separate from human tumor-cell transcription. Increased GCLC mRNA is not a measured increase in glutathione synthesis or clinical antioxidant benefit.
- nutrient_topic
- Boron research collection; topical membership is not evidence of a direct dietary effect. · Boron
- organism
- Mouse embryonic fibroblasts and human DU-145 cells
- plain_language
- PERK was also needed for the measured movement of Nrf2 into the nucleus.
- primary_references
- [boron-p30196486] Boric Acid Activation of eIF2α and Nrf2 Is PERK Dependent: a Mechanism that Explains How Boron Prevents DNA Damage and Enhances Antioxidant Status. (2019). https://pubmed.ncbi.nlm.nih.gov/30196486/ DOI: 10.1007/s12011-018-1498-4
- tissue_or_cell_type
- Cell culture
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Boron: chemistry, nutrient interactions, low-intake studies and mechanistic uncertainties (2026-09-17) · lines 508–519
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · PERK knockout comparison, immunofluorescence and quantitative PCR · source_derived_draft · unverified_draft
### boron-perk-nrf2-dependence Boric acid induced Nrf2 nuclear translocation in wild-type mouse fibroblasts but not in Perk-null cells. Condition category: machinery_impairment nutrient_topic: Boron research collection; topical membership is not evidence of a direct dietary effect. plain_language: PERK was also needed for the measured movement of Nrf2 into the nucleus. organism: Mouse embryonic fibroblasts and human DU-145 cells tissue_or_cell_type: Cell culture experimental_model: PERK knockout comparison, immunofluorescence and quantitative PCR limitations: Knockout dependence in mouse fibroblasts is separate from human tumor-cell transcription. Increased GCLC mRNA is not a measured increase in glutathione synthesis or clinical antioxidant benefit. exposure: 10 µM boric acid; 1–6 hour comparisons evidence_span: {"source_cache": "artifacts/boron-research/30196486.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e220df5fb0f9b8653035f7a144259ce66778467a7a72acbf7cd7d113f8b6030a", "start_char": 0, "end_char": 2006, "text_sha256": "e220df5fb0f9b8653035f7a144259ce66778467a7a72acbf7cd7d113f8b6030a"} [boron-p30196486] Boric Acid Activation of eIF2α and Nrf2 Is PERK Dependent: a Mechanism that Explains How Boron Prevents DNA Damage and Enhances Antioxidant Status. (2019). https://pubmed.ncbi.nlm.nih.gov/30196486/ DOI: 10.1007/s12011-018-1498-4
Complete structured claim and evidence
What acts on it
Methionine restriction activated hepatic PERK and an antioxidant/ISR program in wild-type and Gcn2-null mice, without the measured ER-stress pattern.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Mouse liver signaling and dietary experiments.
- limitations
- The proposed glutathione-sensing mechanism is not evidence of direct methionine binding to PERK.
- nutrient_topic
- L-Methionine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Methionine
- plain_language
- Dietary sulfur status engaged an alternative stress-response route.
- primary_references
- Role of GCN2-Independent Signaling Through a Noncanonical PERK/NRF2 Pathway in the Physiological Responses to Dietary Methionine Restriction. · 2016 · https://pubmed.ncbi.nlm.nih.gov/26936965/ · DOI 10.2337/db15-1324
L-Methionine: transport, methylation, sulfur metabolism and cross-nutrient mechanisms (2026-09-19) · lines 388–394
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse liver signaling and dietary experiments. · source_derived_draft · unverified_draft
## methionine-perk-redox-response Dietary sulfur status engaged an alternative stress-response route. Methionine restriction activated hepatic PERK and an antioxidant/ISR program in wild-type and Gcn2-null mice, without the measured ER-stress pattern. Model: Mouse liver signaling and dietary experiments. Limitations: The proposed glutathione-sensing mechanism is not evidence of direct methionine binding to PERK. Evidence access: Primary abstract Role of GCN2-Independent Signaling Through a Noncanonical PERK/NRF2 Pathway in the Physiological Responses to Dietary Methionine Restriction. · 2016 · https://pubmed.ncbi.nlm.nih.gov/26936965/ · DOI 10.2337/db15-1324
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.