Component

Mouse creatine kinase B / Ckb

Mouse creatine kinase B / Ckb. Species, exposure and limitations are retained in each linked claim.

6 recorded relationships. Experimental role, claim status and evidence remain attached to each record.

Read recorded mechanisms Open recursive mind map

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 it acts on

  1. CKB trafficked to adipocyte mitochondria through an internal mitochondrial targeting sequence and supported the futile creatine cycle.

    Mouse creatine kinase B / Ckb → Adipocyte futile creatine cycle source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/creatine-research/33597756.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "90b9ec2286a126569876b65a77450dec9f600bf04cb6f3e8c4aeb43edcc34c4b", "start_char": 0, "end_char": 942, "text_sha256": "90b9ec2286a126569876b65a77450dec9f600bf04cb6f3e8c4aeb43edcc34c4b"}
    experimental_model
    Adipocyte biochemical experiments and conditional gene deletion
    exposure
    Thermogenic stimulation and adipocyte Ckb loss
    limitations
    Human cell induction and mouse causal phenotypes are separately scoped; no human weight-loss intervention was tested.
    nutrient_topic
    Creatine research collection; topical membership is not evidence of a direct dietary effect. · Creatine
    organism
    Mouse adipocyte mechanistic experiments
    plain_language
    In fat cells, CKB can move to mitochondria and help run an energy-consuming creatine cycle.
    primary_references
    [creatine-p33597756] Creatine kinase B controls futile creatine cycling in thermogenic fat. (2021). https://pubmed.ncbi.nlm.nih.gov/33597756/ DOI: 10.1038/s41586-021-03221-y
    tissue_or_cell_type
    Thermogenic adipose tissue

    Creatine: synthesis, transport, phosphocreatine energetics and nutrient interactions (2026-09-17) · lines 477–488

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Adipocyte biochemical experiments and conditional gene deletion · source_derived_draft · unverified_draft

    ### creatine-ckb-mitochondrial-trafficking CKB trafficked to adipocyte mitochondria through an internal mitochondrial targeting sequence and supported the futile creatine cycle. Condition category: normal nutrient_topic: Creatine research collection; topical membership is not evidence of a direct dietary effect. plain_language: In fat cells, CKB can move to mitochondria and help run an energy-consuming creatine cycle. organism: Mouse adipocyte mechanistic experiments tissue_or_cell_type: Thermogenic adipose tissue experimental_model: Adipocyte biochemical experiments and conditional gene deletion limitations: Human cell induction and mouse causal phenotypes are separately scoped; no human weight-loss intervention was tested. exposure: Thermogenic stimulation and adipocyte Ckb loss evidence_span: {"source_cache": "artifacts/creatine-research/33597756.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "90b9ec2286a126569876b65a77450dec9f600bf04cb6f3e8c4aeb43edcc34c4b", "start_char": 0, "end_char": 942, "text_sha256": "90b9ec2286a126569876b65a77450dec9f600bf04cb6f3e8c4aeb43edcc34c4b"} [creatine-p33597756] Creatine kinase B controls futile creatine cycling in thermogenic fat. (2021). https://pubmed.ncbi.nlm.nih.gov/33597756/ DOI: 10.1038/s41586-021-03221-y
    Complete structured claim and evidence

  2. Adipocyte Ckb deletion reduced thermogenic capacity and predisposed mice to obesity and disturbed glucose handling.

    Mouse creatine kinase B / Ckb → Heat production and energy expenditure by thermogenic adipocytes source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/creatine-research/33597756.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "90b9ec2286a126569876b65a77450dec9f600bf04cb6f3e8c4aeb43edcc34c4b", "start_char": 0, "end_char": 942, "text_sha256": "90b9ec2286a126569876b65a77450dec9f600bf04cb6f3e8c4aeb43edcc34c4b"}
    experimental_model
    Adipocyte biochemical experiments and conditional gene deletion
    exposure
    Thermogenic stimulation and adipocyte Ckb loss
    limitations
    Human cell induction and mouse causal phenotypes are separately scoped; no human weight-loss intervention was tested.
    nutrient_topic
    Creatine research collection; topical membership is not evidence of a direct dietary effect. · Creatine
    organism
    Mice
    plain_language
    Removing this enzyme weakened the heat-producing pathway in mice.
    primary_references
    [creatine-p33597756] Creatine kinase B controls futile creatine cycling in thermogenic fat. (2021). https://pubmed.ncbi.nlm.nih.gov/33597756/ DOI: 10.1038/s41586-021-03221-y
    tissue_or_cell_type
    Thermogenic adipose tissue
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Creatine: synthesis, transport, phosphocreatine energetics and nutrient interactions (2026-09-17) · lines 490–501

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Adipocyte biochemical experiments and conditional gene deletion · source_derived_draft · unverified_draft

    ### creatine-fat-ckb-loss Adipocyte Ckb deletion reduced thermogenic capacity and predisposed mice to obesity and disturbed glucose handling. Condition category: machinery_impairment nutrient_topic: Creatine research collection; topical membership is not evidence of a direct dietary effect. plain_language: Removing this enzyme weakened the heat-producing pathway in mice. organism: Mice tissue_or_cell_type: Thermogenic adipose tissue experimental_model: Adipocyte biochemical experiments and conditional gene deletion limitations: Human cell induction and mouse causal phenotypes are separately scoped; no human weight-loss intervention was tested. exposure: Thermogenic stimulation and adipocyte Ckb loss evidence_span: {"source_cache": "artifacts/creatine-research/33597756.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "90b9ec2286a126569876b65a77450dec9f600bf04cb6f3e8c4aeb43edcc34c4b", "start_char": 0, "end_char": 942, "text_sha256": "90b9ec2286a126569876b65a77450dec9f600bf04cb6f3e8c4aeb43edcc34c4b"} [creatine-p33597756] Creatine kinase B controls futile creatine cycling in thermogenic fat. (2021). https://pubmed.ncbi.nlm.nih.gov/33597756/ DOI: 10.1038/s41586-021-03221-y
    Complete structured claim and evidence

  3. Ckb or Slc6a8 loss impaired T-cell function without changing global adenylate energy charge in the study.

    Mouse creatine kinase B / Ckb → T-cell adenylate energy charge source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/creatine-research/35235777.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a81515a03473f41d52c2e13de56ac9b13ea5cd813e288d166159d517f9855958", "start_char": 0, "end_char": 1025, "text_sha256": "a81515a03473f41d52c2e13de56ac9b13ea5cd813e288d166159d517f9855958"}
    experimental_model
    Transporter or kinase loss, T-cell homeostasis and infection experiments
    exposure
    Slc6a8 or Ckb deletion
    limitations
    The study distinguishes TCR–mTORC1 signaling from whole-cell adenylate energy charge; it does not demonstrate clinical immune benefits of supplements.
    nutrient_topic
    Creatine research collection; topical membership is not evidence of a direct dietary effect. · Creatine
    organism
    Mice
    plain_language
    The observed signaling defect could not be reduced to a simple fall in the cell-wide energy measurement.
    primary_references
    [creatine-p35235777] Creatine transport and creatine kinase activity is required for CD8+ T cell immunity. (2022). https://pubmed.ncbi.nlm.nih.gov/35235777/ DOI: 10.1016/j.celrep.2022.110446
    tissue_or_cell_type
    Naive and activated CD8 T cells
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Creatine: synthesis, transport, phosphocreatine energetics and nutrient interactions (2026-09-17) · lines 633–644

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Transporter or kinase loss, T-cell homeostasis and infection experiments · source_derived_draft · unverified_draft

    ### creatine-tcell-energy-charge Ckb or Slc6a8 loss impaired T-cell function without changing global adenylate energy charge in the study. Condition category: machinery_impairment nutrient_topic: Creatine research collection; topical membership is not evidence of a direct dietary effect. plain_language: The observed signaling defect could not be reduced to a simple fall in the cell-wide energy measurement. organism: Mice tissue_or_cell_type: Naive and activated CD8 T cells experimental_model: Transporter or kinase loss, T-cell homeostasis and infection experiments limitations: The study distinguishes TCR–mTORC1 signaling from whole-cell adenylate energy charge; it does not demonstrate clinical immune benefits of supplements. exposure: Slc6a8 or Ckb deletion evidence_span: {"source_cache": "artifacts/creatine-research/35235777.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a81515a03473f41d52c2e13de56ac9b13ea5cd813e288d166159d517f9855958", "start_char": 0, "end_char": 1025, "text_sha256": "a81515a03473f41d52c2e13de56ac9b13ea5cd813e288d166159d517f9855958"} [creatine-p35235777] Creatine transport and creatine kinase activity is required for CD8+ T cell immunity. (2022). https://pubmed.ncbi.nlm.nih.gov/35235777/ DOI: 10.1016/j.celrep.2022.110446
    Complete structured claim and evidence

  4. Loss of either Ckb or Slc6a8 compromised CD8 T-cell expansion in response to infection.

    Mouse creatine kinase B / Ckb → CD8 T-cell expansion in response to infection source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/creatine-research/35235777.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a81515a03473f41d52c2e13de56ac9b13ea5cd813e288d166159d517f9855958", "start_char": 0, "end_char": 1025, "text_sha256": "a81515a03473f41d52c2e13de56ac9b13ea5cd813e288d166159d517f9855958"}
    experimental_model
    Transporter or kinase loss, T-cell homeostasis and infection experiments
    exposure
    Slc6a8 or Ckb deletion
    limitations
    The study distinguishes TCR–mTORC1 signaling from whole-cell adenylate energy charge; it does not demonstrate clinical immune benefits of supplements.
    nutrient_topic
    Creatine research collection; topical membership is not evidence of a direct dietary effect. · Creatine
    organism
    Mice
    plain_language
    Both the transporter and the phosphate-transfer enzyme mattered for the immune response.
    primary_references
    [creatine-p35235777] Creatine transport and creatine kinase activity is required for CD8+ T cell immunity. (2022). https://pubmed.ncbi.nlm.nih.gov/35235777/ DOI: 10.1016/j.celrep.2022.110446
    tissue_or_cell_type
    Naive and activated CD8 T cells
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Creatine: synthesis, transport, phosphocreatine energetics and nutrient interactions (2026-09-17) · lines 607–618

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Transporter or kinase loss, T-cell homeostasis and infection experiments · source_derived_draft · unverified_draft

    ### creatine-tcell-expansion-loss Loss of either Ckb or Slc6a8 compromised CD8 T-cell expansion in response to infection. Condition category: machinery_impairment nutrient_topic: Creatine research collection; topical membership is not evidence of a direct dietary effect. plain_language: Both the transporter and the phosphate-transfer enzyme mattered for the immune response. organism: Mice tissue_or_cell_type: Naive and activated CD8 T cells experimental_model: Transporter or kinase loss, T-cell homeostasis and infection experiments limitations: The study distinguishes TCR–mTORC1 signaling from whole-cell adenylate energy charge; it does not demonstrate clinical immune benefits of supplements. exposure: Slc6a8 or Ckb deletion evidence_span: {"source_cache": "artifacts/creatine-research/35235777.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a81515a03473f41d52c2e13de56ac9b13ea5cd813e288d166159d517f9855958", "start_char": 0, "end_char": 1025, "text_sha256": "a81515a03473f41d52c2e13de56ac9b13ea5cd813e288d166159d517f9855958"} [creatine-p35235777] Creatine transport and creatine kinase activity is required for CD8+ T cell immunity. (2022). https://pubmed.ncbi.nlm.nih.gov/35235777/ DOI: 10.1016/j.celrep.2022.110446
    Complete structured claim and evidence

  5. Ckb or Slc6a8 loss weakened TCR-mediated mTORC1 activation required for CD8 T-cell expansion.

    Mouse creatine kinase B / Ckb → Mechanistic target of rapamycin complex 1 source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/creatine-research/35235777.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a81515a03473f41d52c2e13de56ac9b13ea5cd813e288d166159d517f9855958", "start_char": 0, "end_char": 1025, "text_sha256": "a81515a03473f41d52c2e13de56ac9b13ea5cd813e288d166159d517f9855958"}
    experimental_model
    Transporter or kinase loss, T-cell homeostasis and infection experiments
    exposure
    Slc6a8 or Ckb deletion
    limitations
    The study distinguishes TCR–mTORC1 signaling from whole-cell adenylate energy charge; it does not demonstrate clinical immune benefits of supplements.
    nutrient_topic
    Creatine research collection; topical membership is not evidence of a direct dietary effect. · Creatine
    organism
    Mice
    plain_language
    The pathway also affected the signal telling T cells to expand.
    primary_references
    [creatine-p35235777] Creatine transport and creatine kinase activity is required for CD8+ T cell immunity. (2022). https://pubmed.ncbi.nlm.nih.gov/35235777/ DOI: 10.1016/j.celrep.2022.110446
    tissue_or_cell_type
    Naive and activated CD8 T cells
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Creatine: synthesis, transport, phosphocreatine energetics and nutrient interactions (2026-09-17) · lines 620–631

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Transporter or kinase loss, T-cell homeostasis and infection experiments · source_derived_draft · unverified_draft

    ### creatine-tcell-mtor-loss Ckb or Slc6a8 loss weakened TCR-mediated mTORC1 activation required for CD8 T-cell expansion. Condition category: machinery_impairment nutrient_topic: Creatine research collection; topical membership is not evidence of a direct dietary effect. plain_language: The pathway also affected the signal telling T cells to expand. organism: Mice tissue_or_cell_type: Naive and activated CD8 T cells experimental_model: Transporter or kinase loss, T-cell homeostasis and infection experiments limitations: The study distinguishes TCR–mTORC1 signaling from whole-cell adenylate energy charge; it does not demonstrate clinical immune benefits of supplements. exposure: Slc6a8 or Ckb deletion evidence_span: {"source_cache": "artifacts/creatine-research/35235777.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a81515a03473f41d52c2e13de56ac9b13ea5cd813e288d166159d517f9855958", "start_char": 0, "end_char": 1025, "text_sha256": "a81515a03473f41d52c2e13de56ac9b13ea5cd813e288d166159d517f9855958"} [creatine-p35235777] Creatine transport and creatine kinase activity is required for CD8+ T cell immunity. (2022). https://pubmed.ncbi.nlm.nih.gov/35235777/ DOI: 10.1016/j.celrep.2022.110446
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Thermogenic stimulation induced CKB expression in human and mouse adipocytes in the study.

    Human creatine kinase B / CKB → Adipocyte futile creatine cycle source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/creatine-research/33597756.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "90b9ec2286a126569876b65a77450dec9f600bf04cb6f3e8c4aeb43edcc34c4b", "start_char": 0, "end_char": 942, "text_sha256": "90b9ec2286a126569876b65a77450dec9f600bf04cb6f3e8c4aeb43edcc34c4b"}
    experimental_model
    Adipocyte biochemical experiments and conditional gene deletion
    exposure
    Thermogenic stimulation and adipocyte Ckb loss
    limitations
    Human cell induction and mouse causal phenotypes are separately scoped; no human weight-loss intervention was tested.
    nutrient_topic
    Creatine research collection; topical membership is not evidence of a direct dietary effect. · Creatine
    organism
    Human and mouse adipocytes; mice for gene deletion
    plain_language
    The enzyme commonly called brain-type creatine kinase also participates in thermogenic fat.
    primary_references
    [creatine-p33597756] Creatine kinase B controls futile creatine cycling in thermogenic fat. (2021). https://pubmed.ncbi.nlm.nih.gov/33597756/ DOI: 10.1038/s41586-021-03221-y
    tissue_or_cell_type
    Thermogenic adipose tissue

    Creatine: synthesis, transport, phosphocreatine energetics and nutrient interactions (2026-09-17) · lines 464–475

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Adipocyte biochemical experiments and conditional gene deletion · source_derived_draft · unverified_draft

    ### creatine-ckb-thermogenic-induction Thermogenic stimulation induced CKB expression in human and mouse adipocytes in the study. Condition category: normal nutrient_topic: Creatine research collection; topical membership is not evidence of a direct dietary effect. plain_language: The enzyme commonly called brain-type creatine kinase also participates in thermogenic fat. organism: Human and mouse adipocytes; mice for gene deletion tissue_or_cell_type: Thermogenic adipose tissue experimental_model: Adipocyte biochemical experiments and conditional gene deletion limitations: Human cell induction and mouse causal phenotypes are separately scoped; no human weight-loss intervention was tested. exposure: Thermogenic stimulation and adipocyte Ckb loss evidence_span: {"source_cache": "artifacts/creatine-research/33597756.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "90b9ec2286a126569876b65a77450dec9f600bf04cb6f3e8c4aeb43edcc34c4b", "start_char": 0, "end_char": 942, "text_sha256": "90b9ec2286a126569876b65a77450dec9f600bf04cb6f3e8c4aeb43edcc34c4b"} [creatine-p33597756] Creatine kinase B controls futile creatine cycling in thermogenic fat. (2021). https://pubmed.ncbi.nlm.nih.gov/33597756/ DOI: 10.1038/s41586-021-03221-y
    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