Component

RAF proto-oncogene serine/threonine-protein kinase / RAF1

RAF proto-oncogene serine/threonine-protein kinase / RAF1. 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

Where it participates (unsigned role)

  1. Mice lacking functional T and B lymphocytes are protected against reinfection with Candida albicans in a monocyte-dependent manner, C. albicans and fungal cell wall beta-glucans induced functional reprogramming of monocytes leading to enhanced cytokine production in vivo and in vitro, the training required the beta-glucan receptor dectin-1 and the noncanonical Raf-1 pathway, and monocyte training by beta-glucans was associated with stable changes in histone trimethylation at H3K4 which suggests the involvement of epigenetic mechanisms.

    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/glucan-research/22901542.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "75bc4bedb7017f3d94d8f7441862392ddca229ed16f93eb528d3f9df3da66408", "start_char": 0, "end_char": 1067, "text_sha256": "75bc4bedb7017f3d94d8f7441862392ddca229ed16f93eb528d3f9df3da66408"}
    experimental_model
    Reinfection protection in mice lacking functional T and B lymphocytes, with monocyte reprogramming in vitro and in vivo
    exposure
    Candida albicans and fungal cell wall beta-glucans as the training stimulus, with the first exposure resolved before rechallenge
    limitations
    The Raf-1 dependence belongs to this training protocol. It does not establish that every beta-glucan training protocol is independent of the canonical Syk route.
    nutrient_topic
    Beta-glucan research collection; topical membership is not evidence of a direct clinical effect, and each preparation is recorded as its own entity with no family link joining any pair. · Beta-glucan
    organism
    Mouse
    plain_language
    Animals with no adaptive immune system at all were still protected the second time, because their monocytes had been rewired.
    primary_references
    [bg-p22901542] Candida albicans infection affords protection against reinfection via functional reprogramming of monocytes. (2012). https://pubmed.ncbi.nlm.nih.gov/22901542/ DOI: 10.1016/j.chom.2012.06.006
    tissue_or_cell_type
    Monocyte

    Beta-glucan: a structural family rather than an agent, what decides whether a bound glucan actually signals, the complement route that a cereal and a yeast preparation share, and the unequal human evidence behind each (2026-09-22) · lines 424–435

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Reinfection protection in mice lacking functional T and B lymphocytes, with monocyte reprogramming in vitro and in vivo · source_derived_draft · unverified_draft

    ### bg-training-runs-through-raf1 Mice lacking functional T and B lymphocytes are protected against reinfection with Candida albicans in a monocyte-dependent manner, C. albicans and fungal cell wall beta-glucans induced functional reprogramming of monocytes leading to enhanced cytokine production in vivo and in vitro, the training required the beta-glucan receptor dectin-1 and the noncanonical Raf-1 pathway, and monocyte training by beta-glucans was associated with stable changes in histone trimethylation at H3K4 which suggests the involvement of epigenetic mechanisms. Condition category: normal nutrient_topic: Beta-glucan research collection; topical membership is not evidence of a direct clinical effect, and each preparation is recorded as its own entity with no family link joining any pair. plain_language: Animals with no adaptive immune system at all were still protected the second time, because their monocytes had been rewired. organism: Mouse tissue_or_cell_type: Monocyte experimental_model: Reinfection protection in mice lacking functional T and B lymphocytes, with monocyte reprogramming in vitro and in vivo limitations: The Raf-1 dependence belongs to this training protocol. It does not establish that every beta-glucan training protocol is independent of the canonical Syk route. exposure: Candida albicans and fungal cell wall beta-glucans as the training stimulus, with the first exposure resolved before rechallenge evidence_span: {"source_cache": "artifacts/glucan-research/22901542.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "75bc4bedb7017f3d94d8f7441862392ddca229ed16f93eb528d3f9df3da66408", "start_char": 0, "end_char": 1067, "text_sha256": "75bc4bedb7017f3d94d8f7441862392ddca229ed16f93eb528d3f9df3da66408"} [bg-p22901542] Candida albicans infection affords protection against reinfection via functional reprogramming of monocytes. (2012). https://pubmed.ncbi.nlm.nih.gov/22901542/ DOI: 10.1016/j.chom.2012.06.006
    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.

    Evidence, AI assistance and curation standards