Component

A frameshift arising from retention of an unprocessed intron

A frameshift arising from retention of an unprocessed intron. Species, exposure and limitations are retained in each linked claim.

1 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.

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.

Recorded relationships

What acts on it

  1. The 98 base pair intron 1 of the cyclooxygenase-1 gene remains unprocessed in rat COX-1b messenger RNA, causing a frameshift mutation and a 127 amino acid open reading frame with no sequence similarity with known cyclooxygenases, and transfection of COS-7 cells produced a protein of the expected size which was also detected in rat tissues with highest expression in heart, kidney and neuronal tissue, but rat COX-1b does not have cyclooxygenase activity and does not have any effect on the inhibition of prostaglandin production by acetaminophen, leading the authors to propose the name cyclooxygenase variant protein instead.

    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/paracetamol-research/15650114.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1661f4d2b21244e0fc16b9a3b947cf4d09d39be35367ed263cce441f43a60563", "start_char": 0, "end_char": 1473, "text_sha256": "1661f4d2b21244e0fc16b9a3b947cf4d09d39be35367ed263cce441f43a60563"}
    experimental_model
    Cloning and sequencing of rat COX-1b from cerebral endothelial cells with transfection and antibody generation
    exposure
    Rat COX-1b complementary DNA transfected into COS-7 cells, assayed for activity and for effect on acetaminophen inhibition
    limitations
    Tests the proposal in a second species by building the protein and asking whether it works. The protein is detected in rat tissue, so the finding is that it exists and is not a cyclooxygenase.
    nutrient_topic
    Paracetamol research collection; topical membership is not evidence of a direct clinical effect, and the drug is recorded separately from the metabolites NAPQI and AM404. · Paracetamol
    organism
    Rat
    plain_language
    In the rat the retained intron shifts the reading frame, so what is made is a different protein altogether and not an enzyme.
    primary_references
    [apap-p15650114] Cloning and characterization of cyclooxygenase-1b (putative cyclooxygenase-3) in rat. (2005). https://pubmed.ncbi.nlm.nih.gov/15650114/ DOI: 10.1124/jpet.104.079533
    tissue_or_cell_type
    Cerebral endothelial cells

    Paracetamol: the enzyme it reduces rather than blocks, the isoform that turned out not to exist, the metabolite that carries the analgesia, and the metabolite that destroys the liver (2026-09-22) · lines 220–231

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cloning and sequencing of rat COX-1b from cerebral endothelial cells with transfection and antibody generation · source_derived_draft · unverified_draft

    ### apap-frameshift-makes-a-different-protein The 98 base pair intron 1 of the cyclooxygenase-1 gene remains unprocessed in rat COX-1b messenger RNA, causing a frameshift mutation and a 127 amino acid open reading frame with no sequence similarity with known cyclooxygenases, and transfection of COS-7 cells produced a protein of the expected size which was also detected in rat tissues with highest expression in heart, kidney and neuronal tissue, but rat COX-1b does not have cyclooxygenase activity and does not have any effect on the inhibition of prostaglandin production by acetaminophen, leading the authors to propose the name cyclooxygenase variant protein instead. Condition category: normal nutrient_topic: Paracetamol research collection; topical membership is not evidence of a direct clinical effect, and the drug is recorded separately from the metabolites NAPQI and AM404. plain_language: In the rat the retained intron shifts the reading frame, so what is made is a different protein altogether and not an enzyme. organism: Rat tissue_or_cell_type: Cerebral endothelial cells experimental_model: Cloning and sequencing of rat COX-1b from cerebral endothelial cells with transfection and antibody generation limitations: Tests the proposal in a second species by building the protein and asking whether it works. The protein is detected in rat tissue, so the finding is that it exists and is not a cyclooxygenase. exposure: Rat COX-1b complementary DNA transfected into COS-7 cells, assayed for activity and for effect on acetaminophen inhibition evidence_span: {"source_cache": "artifacts/paracetamol-research/15650114.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1661f4d2b21244e0fc16b9a3b947cf4d09d39be35367ed263cce441f43a60563", "start_char": 0, "end_char": 1473, "text_sha256": "1661f4d2b21244e0fc16b9a3b947cf4d09d39be35367ed263cce441f43a60563"} [apap-p15650114] Cloning and characterization of cyclooxygenase-1b (putative cyclooxygenase-3) in rat. (2005). https://pubmed.ncbi.nlm.nih.gov/15650114/ DOI: 10.1124/jpet.104.079533
    Complete structured claim and evidence

In the sources

Preserved passages that mention this component, quoted exactly. Open one to read it in context.

    This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.

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