Component

Human melatonin receptor 1B / MT2 / MTNR1B

Human melatonin receptor 1B / MT2 / MTNR1B. 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. Human MT2 expression supported melatonin-receptor-mediated inhibition of adenylyl cyclase.

    Human melatonin receptor 1B / MT2 / MTNR1B → Adenylyl cyclase catalytic activity, model specified source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/melatonin-research/7568007.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1873168e5fa570a1dec0bc112045a3bcffda494e92b52f3349c8b1afebbb505f", "start_char": 0, "end_char": 1269, "text_sha256": "1873168e5fa570a1dec0bc112045a3bcffda494e92b52f3349c8b1afebbb505f"}
    experimental_model
    Human receptor cloning and functional expression
    exposure
    Radioligand binding and adenylyl cyclase measurements
    limitations
    Receptor overexpression system; no claim a given oral dose produces the same occupancy in every human tissue.
    nutrient_topic
    Melatonin research collection; topical membership is not evidence of a direct dietary effect. · Melatonin
    organism
    Human MT2 expressed in COS-1 and NIH3T3 cells
    plain_language
    The second receptor can also reduce the signal that generates cAMP.
    primary_references
    [melatonin-p7568007] Molecular characterization of a second melatonin receptor expressed in human retina and brain: the Mel1b melatonin receptor. (1995). https://pubmed.ncbi.nlm.nih.gov/7568007/ DOI: 10.1073/pnas.92.19.8734
    tissue_or_cell_type
    Second melatonin receptor subtype

    Melatonin: synthesis, receptors, circadian timing and nutrient interactions (2026-09-17) · lines 383–394

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human receptor cloning and functional expression · source_derived_draft · unverified_draft

    ### melatonin-mt2-cyclase Human MT2 expression supported melatonin-receptor-mediated inhibition of adenylyl cyclase. Condition category: normal nutrient_topic: Melatonin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The second receptor can also reduce the signal that generates cAMP. organism: Human MT2 expressed in COS-1 and NIH3T3 cells tissue_or_cell_type: Second melatonin receptor subtype experimental_model: Human receptor cloning and functional expression limitations: Receptor overexpression system; no claim a given oral dose produces the same occupancy in every human tissue. exposure: Radioligand binding and adenylyl cyclase measurements evidence_span: {"source_cache": "artifacts/melatonin-research/7568007.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1873168e5fa570a1dec0bc112045a3bcffda494e92b52f3349c8b1afebbb505f", "start_char": 0, "end_char": 1269, "text_sha256": "1873168e5fa570a1dec0bc112045a3bcffda494e92b52f3349c8b1afebbb505f"} [melatonin-p7568007] Molecular characterization of a second melatonin receptor expressed in human retina and brain: the Mel1b melatonin receptor. (1995). https://pubmed.ncbi.nlm.nih.gov/7568007/ DOI: 10.1073/pnas.92.19.8734
    Complete structured claim and evidence

  2. Agonist-bound human MT2 was structurally resolved in a Gi signaling complex.

    Human melatonin receptor 1B / MT2 / MTNR1B → Inhibitory heterotrimeric G protein / Gi, assay-specified subunits source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/melatonin-research/35075127.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "08af0c72228d7c72723f238e83eeabef1ca9196833c7e385ed0c75577c97024b", "start_char": 0, "end_char": 1239, "text_sha256": "08af0c72228d7c72723f238e83eeabef1ca9196833c7e385ed0c75577c97024b"}
    experimental_model
    Cryo-EM structures and functional receptor assays
    exposure
    2-iodomelatonin/ramelteon for MT1; ramelteon for MT2
    limitations
    Structures used agonists, not native melatonin in every complex. Receptor structure does not itself prove clinical effects or subtype-selective supplement actions.
    nutrient_topic
    Melatonin research collection; topical membership is not evidence of a direct dietary effect. · Melatonin
    organism
    Human MT1 and MT2 signaling complexes
    plain_language
    The receptor and its signaling partner are separate searchable components.
    primary_references
    [melatonin-p35075127] Structural basis of the ligand binding and signaling mechanism of melatonin receptors. (2022). https://pubmed.ncbi.nlm.nih.gov/35075127/ DOI: 10.1038/s41467-022-28111-3
    tissue_or_cell_type
    Agonist-bound receptor-Gi coupling

    Melatonin: synthesis, receptors, circadian timing and nutrient interactions (2026-09-17) · lines 409–420

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cryo-EM structures and functional receptor assays · source_derived_draft · unverified_draft

    ### melatonin-mt2-gi-structure Agonist-bound human MT2 was structurally resolved in a Gi signaling complex. Condition category: normal nutrient_topic: Melatonin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The receptor and its signaling partner are separate searchable components. organism: Human MT1 and MT2 signaling complexes tissue_or_cell_type: Agonist-bound receptor-Gi coupling experimental_model: Cryo-EM structures and functional receptor assays limitations: Structures used agonists, not native melatonin in every complex. Receptor structure does not itself prove clinical effects or subtype-selective supplement actions. exposure: 2-iodomelatonin/ramelteon for MT1; ramelteon for MT2 evidence_span: {"source_cache": "artifacts/melatonin-research/35075127.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "08af0c72228d7c72723f238e83eeabef1ca9196833c7e385ed0c75577c97024b", "start_char": 0, "end_char": 1239, "text_sha256": "08af0c72228d7c72723f238e83eeabef1ca9196833c7e385ed0c75577c97024b"} [melatonin-p35075127] Structural basis of the ligand binding and signaling mechanism of melatonin receptors. (2022). https://pubmed.ncbi.nlm.nih.gov/35075127/ DOI: 10.1038/s41467-022-28111-3
    Complete structured claim and evidence

What acts on it

  1. GPR50 formed heterodimers with MT2 in the same study.

    Human melatonin-related orphan receptor / GPR50 → Human melatonin receptor 1B / MT2 / MTNR1B source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/melatonin-research/16778767.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "19c9ae903fb7926bb21cc3bda0a610612b16a899f850b8e787581b72ac434135", "start_char": 0, "end_char": 1204, "text_sha256": "19c9ae903fb7926bb21cc3bda0a610612b16a899f850b8e787581b72ac434135"}
    experimental_model
    Biochemical and biophysical receptor heteromer experiments
    exposure
    Full-length versus C-terminally truncated GPR50
    limitations
    Cell-system regulation; does not establish that a person with poor sleep has excess GPR50 or that more melatonin overcomes it.
    nutrient_topic
    Melatonin research collection; topical membership is not evidence of a direct dietary effect. · Melatonin
    organism
    Human receptors in cultured cells
    plain_language
    Physical partnership alone does not establish functional inhibition.
    primary_references
    [melatonin-p16778767] The orphan GPR50 receptor specifically inhibits MT1 melatonin receptor function through heterodimerization. (2006). https://pubmed.ncbi.nlm.nih.gov/16778767/ DOI: 10.1038/sj.emboj.7601193
    tissue_or_cell_type
    GPR50-MT1/MT2 interactions

    Melatonin: synthesis, receptors, circadian timing and nutrient interactions (2026-09-17) · lines 435–446

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Biochemical and biophysical receptor heteromer experiments · source_derived_draft · unverified_draft

    ### melatonin-gpr50-mt2-heteromer GPR50 formed heterodimers with MT2 in the same study. Condition category: normal nutrient_topic: Melatonin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Physical partnership alone does not establish functional inhibition. organism: Human receptors in cultured cells tissue_or_cell_type: GPR50-MT1/MT2 interactions experimental_model: Biochemical and biophysical receptor heteromer experiments limitations: Cell-system regulation; does not establish that a person with poor sleep has excess GPR50 or that more melatonin overcomes it. exposure: Full-length versus C-terminally truncated GPR50 evidence_span: {"source_cache": "artifacts/melatonin-research/16778767.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "19c9ae903fb7926bb21cc3bda0a610612b16a899f850b8e787581b72ac434135", "start_char": 0, "end_char": 1204, "text_sha256": "19c9ae903fb7926bb21cc3bda0a610612b16a899f850b8e787581b72ac434135"} [melatonin-p16778767] The orphan GPR50 receptor specifically inhibits MT1 melatonin receptor function through heterodimerization. (2006). https://pubmed.ncbi.nlm.nih.gov/16778767/ DOI: 10.1038/sj.emboj.7601193
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Association with GPR50 did not modify MT2 function in the experiment.

    Human melatonin-related orphan receptor / GPR50 → MT2 agonist binding and signaling in heteromer experiments source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/melatonin-research/16778767.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "19c9ae903fb7926bb21cc3bda0a610612b16a899f850b8e787581b72ac434135", "start_char": 0, "end_char": 1204, "text_sha256": "19c9ae903fb7926bb21cc3bda0a610612b16a899f850b8e787581b72ac434135"}
    experimental_model
    Biochemical and biophysical receptor heteromer experiments
    exposure
    Full-length versus C-terminally truncated GPR50
    limitations
    Cell-system regulation; does not establish that a person with poor sleep has excess GPR50 or that more melatonin overcomes it.
    nutrient_topic
    Melatonin research collection; topical membership is not evidence of a direct dietary effect. · Melatonin
    organism
    Human receptors in cultured cells
    plain_language
    The inhibition was receptor-subtype-specific.
    primary_references
    [melatonin-p16778767] The orphan GPR50 receptor specifically inhibits MT1 melatonin receptor function through heterodimerization. (2006). https://pubmed.ncbi.nlm.nih.gov/16778767/ DOI: 10.1038/sj.emboj.7601193
    tissue_or_cell_type
    GPR50-MT1/MT2 interactions

    Melatonin: synthesis, receptors, circadian timing and nutrient interactions (2026-09-17) · lines 474–485

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Biochemical and biophysical receptor heteromer experiments · source_derived_draft · unverified_draft

    ### melatonin-gpr50-mt2-null Association with GPR50 did not modify MT2 function in the experiment. Condition category: normal nutrient_topic: Melatonin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The inhibition was receptor-subtype-specific. organism: Human receptors in cultured cells tissue_or_cell_type: GPR50-MT1/MT2 interactions experimental_model: Biochemical and biophysical receptor heteromer experiments limitations: Cell-system regulation; does not establish that a person with poor sleep has excess GPR50 or that more melatonin overcomes it. exposure: Full-length versus C-terminally truncated GPR50 evidence_span: {"source_cache": "artifacts/melatonin-research/16778767.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "19c9ae903fb7926bb21cc3bda0a610612b16a899f850b8e787581b72ac434135", "start_char": 0, "end_char": 1204, "text_sha256": "19c9ae903fb7926bb21cc3bda0a610612b16a899f850b8e787581b72ac434135"} [melatonin-p16778767] The orphan GPR50 receptor specifically inhibits MT1 melatonin receptor function through heterodimerization. (2006). https://pubmed.ncbi.nlm.nih.gov/16778767/ DOI: 10.1038/sj.emboj.7601193
    Complete structured claim and evidence

  2. Melatonin lowered cAMP in the insulin-secreting cells in the study.

    Melatonin → Intracellular cyclic AMP content source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/melatonin-research/27185156.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "61fcf7c730c1349e5b306e5c9cfcabcb2905290d7f8762cbfba06f2b5fccaded", "start_char": 0, "end_char": 1043, "text_sha256": "61fcf7c730c1349e5b306e5c9cfcabcb2905290d7f8762cbfba06f2b5fccaded"}
    experimental_model
    Human islet genetics, cell experiments and recall-by-genotype intervention
    exposure
    Risk G allele, receptor overexpression and melatonin exposure
    limitations
    Genotype associations, cultured-cell manipulation and human intervention are separate evidence types. Do not generalize islet signaling to every tissue.
    nutrient_topic
    Melatonin research collection; topical membership is not evidence of a direct dietary effect. · Melatonin
    organism
    Human islets and volunteers; separate insulin-cell and mouse experiments
    plain_language
    The receptor signal meets a messenger involved in insulin release.
    primary_references
    [melatonin-p27185156] Increased Melatonin Signaling Is a Risk Factor for Type 2 Diabetes. (2016). https://pubmed.ncbi.nlm.nih.gov/27185156/ DOI: 10.1016/j.cmet.2016.04.009
    tissue_or_cell_type
    MTNR1B signaling and insulin secretion

    Melatonin: synthesis, receptors, circadian timing and nutrient interactions (2026-09-17) · lines 1111–1122

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human islet genetics, cell experiments and recall-by-genotype intervention · source_derived_draft · unverified_draft

    ### melatonin-islet-camp Melatonin lowered cAMP in the insulin-secreting cells in the study. Condition category: normal nutrient_topic: Melatonin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The receptor signal meets a messenger involved in insulin release. organism: Human islets and volunteers; separate insulin-cell and mouse experiments tissue_or_cell_type: MTNR1B signaling and insulin secretion experimental_model: Human islet genetics, cell experiments and recall-by-genotype intervention limitations: Genotype associations, cultured-cell manipulation and human intervention are separate evidence types. Do not generalize islet signaling to every tissue. exposure: Risk G allele, receptor overexpression and melatonin exposure evidence_span: {"source_cache": "artifacts/melatonin-research/27185156.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "61fcf7c730c1349e5b306e5c9cfcabcb2905290d7f8762cbfba06f2b5fccaded", "start_char": 0, "end_char": 1043, "text_sha256": "61fcf7c730c1349e5b306e5c9cfcabcb2905290d7f8762cbfba06f2b5fccaded"} [melatonin-p27185156] Increased Melatonin Signaling Is a Risk Factor for Type 2 Diabetes. (2016). https://pubmed.ncbi.nlm.nih.gov/27185156/ DOI: 10.1016/j.cmet.2016.04.009
    Complete structured claim and evidence

  3. Risk G-allele carriers had increased MTNR1B expression in human islets.

    Human MTNR1B rs10830963 G risk allele → Human islet MTNR1B expression source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/melatonin-research/27185156.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "61fcf7c730c1349e5b306e5c9cfcabcb2905290d7f8762cbfba06f2b5fccaded", "start_char": 0, "end_char": 1043, "text_sha256": "61fcf7c730c1349e5b306e5c9cfcabcb2905290d7f8762cbfba06f2b5fccaded"}
    experimental_model
    Human islet genetics, cell experiments and recall-by-genotype intervention
    exposure
    Risk G allele, receptor overexpression and melatonin exposure
    limitations
    Genotype associations, cultured-cell manipulation and human intervention are separate evidence types. Do not generalize islet signaling to every tissue.
    nutrient_topic
    Melatonin research collection; topical membership is not evidence of a direct dietary effect. · Melatonin
    organism
    Human islets and volunteers; separate insulin-cell and mouse experiments
    plain_language
    A receptor-gene variant can change the strength of a hormone response.
    primary_references
    [melatonin-p27185156] Increased Melatonin Signaling Is a Risk Factor for Type 2 Diabetes. (2016). https://pubmed.ncbi.nlm.nih.gov/27185156/ DOI: 10.1016/j.cmet.2016.04.009
    tissue_or_cell_type
    MTNR1B signaling and insulin secretion

    Melatonin: synthesis, receptors, circadian timing and nutrient interactions (2026-09-17) · lines 1098–1109

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human islet genetics, cell experiments and recall-by-genotype intervention · source_derived_draft · unverified_draft

    ### melatonin-mtnr1b-risk-expression Risk G-allele carriers had increased MTNR1B expression in human islets. Condition category: normal nutrient_topic: Melatonin research collection; topical membership is not evidence of a direct dietary effect. plain_language: A receptor-gene variant can change the strength of a hormone response. organism: Human islets and volunteers; separate insulin-cell and mouse experiments tissue_or_cell_type: MTNR1B signaling and insulin secretion experimental_model: Human islet genetics, cell experiments and recall-by-genotype intervention limitations: Genotype associations, cultured-cell manipulation and human intervention are separate evidence types. Do not generalize islet signaling to every tissue. exposure: Risk G allele, receptor overexpression and melatonin exposure evidence_span: {"source_cache": "artifacts/melatonin-research/27185156.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "61fcf7c730c1349e5b306e5c9cfcabcb2905290d7f8762cbfba06f2b5fccaded", "start_char": 0, "end_char": 1043, "text_sha256": "61fcf7c730c1349e5b306e5c9cfcabcb2905290d7f8762cbfba06f2b5fccaded"} [melatonin-p27185156] Increased Melatonin Signaling Is a Risk Factor for Type 2 Diabetes. (2016). https://pubmed.ncbi.nlm.nih.gov/27185156/ DOI: 10.1016/j.cmet.2016.04.009
    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