Component

Mouse TMEM165

Mouse TMEM165. Experimental scope belongs to each linked claim.

5 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

Where it participates (unsigned role)

  1. D-galactose did not rescue the decorin glycosaminoglycan defect in the tested mouse Tmem165-knockout ATDC5 cells.

    D-Galactose → Decorin glycosaminoglycan modification source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    Mouse TMEM165 (affected_protein)
    evidence_span
    {"source_cache": "artifacts/manganese-glycosylation-sources/morelle2022.txt", "locator": "Results and Figure 5; decorin", "file_sha256": "91d05677c6d7bb4224f71742888e39533e3f130d59e6b2ffcae3e2b2c058e9aa", "start_char": 25939, "end_char": 27086, "text_sha256": "d94138936b018635104317fedba6c1298f0d54c6cd7b3f578b60000cea925bf5", "text_characters": 1147}
    experimental_model
    Tmem165-knockout mouse ATDC5 chondrogenic cells
    exposure
    Decorin-transfected ATDC5 cells: 1 micromolar MnCl2, 1 millimolar galactose or 1 millimolar xylose for 36 hours.
    limitations
    Decorin chondroitin-sulfate elongation in mouse chondrogenic cells. This is a separate model from the human HEK N/O-glycosylation assays and does not establish clinical cartilage rescue.
    nutrient_topic
    Manganese research collection; topical membership is not evidence of a direct dietary effect. · Manganese
    organism
    Mus musculus
    plain_language
    Improved N-glycosylation did not mean the proteoglycan defect was corrected.
    primary_references
    [mn-gly-morelle2022] Differential Effects of D-Galactose Supplementation on Golgi Glycosylation Defects in TMEM165 Deficiency. (2022). https://pubmed.ncbi.nlm.nih.gov/35693943/ DOI: 10.3389/fcell.2022.903953
    tissue_or_cell_type
    Mouse chondrogenic ATDC5 cells and secreted decorin
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Manganese: enzyme cofactors, glycosylation, transport and nutrient interactions (2026-09-17) · lines 824–836

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Tmem165-knockout mouse ATDC5 chondrogenic cells · source_derived_draft · unverified_draft

    ### mn-gly-gal-gag-null D-galactose did not rescue the decorin glycosaminoglycan defect in the tested mouse Tmem165-knockout ATDC5 cells. Condition category: machinery_impairment nutrient_topic: Manganese research collection; topical membership is not evidence of a direct dietary effect. plain_language: Improved N-glycosylation did not mean the proteoglycan defect was corrected. organism: Mus musculus tissue_or_cell_type: Mouse chondrogenic ATDC5 cells and secreted decorin experimental_model: Tmem165-knockout mouse ATDC5 chondrogenic cells limitations: Decorin chondroitin-sulfate elongation in mouse chondrogenic cells. This is a separate model from the human HEK N/O-glycosylation assays and does not establish clinical cartilage rescue. exposure: Decorin-transfected ATDC5 cells: 1 micromolar MnCl2, 1 millimolar galactose or 1 millimolar xylose for 36 hours. cross_nutrient: Mouse TMEM165 (affected_protein) evidence_span: {"source_cache": "artifacts/manganese-glycosylation-sources/morelle2022.txt", "locator": "Results and Figure 5; decorin", "file_sha256": "91d05677c6d7bb4224f71742888e39533e3f130d59e6b2ffcae3e2b2c058e9aa", "start_char": 25939, "end_char": 27086, "text_sha256": "d94138936b018635104317fedba6c1298f0d54c6cd7b3f578b60000cea925bf5", "text_characters": 1147} [mn-gly-morelle2022] Differential Effects of D-Galactose Supplementation on Golgi Glycosylation Defects in TMEM165 Deficiency. (2022). https://pubmed.ncbi.nlm.nih.gov/35693943/ DOI: 10.3389/fcell.2022.903953
    Complete structured claim and evidence

  2. Mammary epithelial Tmem165 deletion reduced lactose biosynthesis in lactating mice.

    Mouse mammary epithelial TMEM165 loss → Mammary lactose biosynthesis source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    Mouse TMEM165 (affected_protein); Lactose (affected_product)
    evidence_span
    {"source_cache": "artifacts/manganese-glycosylation-sources/milk2019.abstract.txt", "locator": "Indexed primary abstract", "file_sha256": "88bcb50ecdb918803c5950bcff8f48665dbd17148b365a4f9f3b463fe7edd2a4", "start_char": 0, "end_char": 1462, "text_sha256": "88bcb50ecdb918803c5950bcff8f48665dbd17148b365a4f9f3b463fe7edd2a4", "text_characters": 1462}
    experimental_model
    Conditional mammary epithelial Tmem165 deletion in mice
    exposure
    Tissue-specific deletion with milk composition and pup-growth measurements.
    limitations
    The primary abstract supports normalized milk minerals and reduced lactose; altered concentration can reflect less milk dilution. Proposed cation/H+ exchange is an interpretation, not a transport stoichiometry measured here.
    nutrient_topic
    Manganese research collection; topical membership is not evidence of a direct dietary effect. · Manganese
    organism
    Mus musculus
    plain_language
    Manganese-handling machinery in the milk-producing cell affected milk production.
    primary_references
    [mn-gly-milk2019] Milk biosynthesis requires the Golgi cation exchanger TMEM165. (2019). https://pubmed.ncbi.nlm.nih.gov/30622138/ DOI: 10.1074/jbc.ra118.006270
    tissue_or_cell_type
    Lactating mammary gland and milk
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Manganese: enzyme cofactors, glycosylation, transport and nutrient interactions (2026-09-17) · lines 880–892

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Conditional mammary epithelial Tmem165 deletion in mice · source_derived_draft · unverified_draft

    ### mn-gly-mammary-lactose Mammary epithelial Tmem165 deletion reduced lactose biosynthesis in lactating mice. Condition category: machinery_impairment nutrient_topic: Manganese research collection; topical membership is not evidence of a direct dietary effect. plain_language: Manganese-handling machinery in the milk-producing cell affected milk production. organism: Mus musculus tissue_or_cell_type: Lactating mammary gland and milk experimental_model: Conditional mammary epithelial Tmem165 deletion in mice limitations: The primary abstract supports normalized milk minerals and reduced lactose; altered concentration can reflect less milk dilution. Proposed cation/H+ exchange is an interpretation, not a transport stoichiometry measured here. exposure: Tissue-specific deletion with milk composition and pup-growth measurements. cross_nutrient: Mouse TMEM165 (affected_protein); Lactose (affected_product) evidence_span: {"source_cache": "artifacts/manganese-glycosylation-sources/milk2019.abstract.txt", "locator": "Indexed primary abstract", "file_sha256": "88bcb50ecdb918803c5950bcff8f48665dbd17148b365a4f9f3b463fe7edd2a4", "start_char": 0, "end_char": 1462, "text_sha256": "88bcb50ecdb918803c5950bcff8f48665dbd17148b365a4f9f3b463fe7edd2a4", "text_characters": 1462} [mn-gly-milk2019] Milk biosynthesis requires the Golgi cation exchanger TMEM165. (2019). https://pubmed.ncbi.nlm.nih.gov/30622138/ DOI: 10.1074/jbc.ra118.006270
    Complete structured claim and evidence

  3. After normalization to milk protein, calcium and manganese were lower in milk from Tmem165-deficient dams.

    Mouse mammary epithelial TMEM165 loss → Milk manganese normalized to protein source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    Mouse TMEM165 (affected_protein); Milk calcium normalized to protein (measured_endpoint); Calcium (affected_nutrient); Manganese (affected_nutrient)
    evidence_span
    {"source_cache": "artifacts/manganese-glycosylation-sources/milk2019.abstract.txt", "locator": "Indexed primary abstract", "file_sha256": "88bcb50ecdb918803c5950bcff8f48665dbd17148b365a4f9f3b463fe7edd2a4", "start_char": 0, "end_char": 1462, "text_sha256": "88bcb50ecdb918803c5950bcff8f48665dbd17148b365a4f9f3b463fe7edd2a4", "text_characters": 1462}
    experimental_model
    Conditional mammary epithelial Tmem165 deletion in mice
    exposure
    Tissue-specific deletion with milk composition and pup-growth measurements.
    limitations
    The primary abstract supports normalized milk minerals and reduced lactose; altered concentration can reflect less milk dilution. Proposed cation/H+ exchange is an interpretation, not a transport stoichiometry measured here.
    nutrient_topic
    Manganese research collection; topical membership is not evidence of a direct dietary effect. · Manganese
    organism
    Mus musculus
    plain_language
    The defect changed milk manganese and calcium relative to its protein content.
    primary_references
    [mn-gly-milk2019] Milk biosynthesis requires the Golgi cation exchanger TMEM165. (2019). https://pubmed.ncbi.nlm.nih.gov/30622138/ DOI: 10.1074/jbc.ra118.006270
    tissue_or_cell_type
    Lactating mammary gland and milk
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Manganese: enzyme cofactors, glycosylation, transport and nutrient interactions (2026-09-17) · lines 894–906

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Conditional mammary epithelial Tmem165 deletion in mice · source_derived_draft · unverified_draft

    ### mn-gly-mammary-minerals After normalization to milk protein, calcium and manganese were lower in milk from Tmem165-deficient dams. Condition category: machinery_impairment nutrient_topic: Manganese research collection; topical membership is not evidence of a direct dietary effect. plain_language: The defect changed milk manganese and calcium relative to its protein content. organism: Mus musculus tissue_or_cell_type: Lactating mammary gland and milk experimental_model: Conditional mammary epithelial Tmem165 deletion in mice limitations: The primary abstract supports normalized milk minerals and reduced lactose; altered concentration can reflect less milk dilution. Proposed cation/H+ exchange is an interpretation, not a transport stoichiometry measured here. exposure: Tissue-specific deletion with milk composition and pup-growth measurements. cross_nutrient: Mouse TMEM165 (affected_protein); Milk calcium normalized to protein (measured_endpoint); Calcium (affected_nutrient); Manganese (affected_nutrient) evidence_span: {"source_cache": "artifacts/manganese-glycosylation-sources/milk2019.abstract.txt", "locator": "Indexed primary abstract", "file_sha256": "88bcb50ecdb918803c5950bcff8f48665dbd17148b365a4f9f3b463fe7edd2a4", "start_char": 0, "end_char": 1462, "text_sha256": "88bcb50ecdb918803c5950bcff8f48665dbd17148b365a4f9f3b463fe7edd2a4", "text_characters": 1462} [mn-gly-milk2019] Milk biosynthesis requires the Golgi cation exchanger TMEM165. (2019). https://pubmed.ncbi.nlm.nih.gov/30622138/ DOI: 10.1074/jbc.ra118.006270
    Complete structured claim and evidence

  4. Pups nursed by mammary Tmem165-deficient dams had impaired growth.

    Mouse mammary epithelial TMEM165 loss → Growth of nursing mouse pups source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    Mouse TMEM165 (affected_protein); Lactose (affected_product)
    evidence_span
    {"source_cache": "artifacts/manganese-glycosylation-sources/milk2019.abstract.txt", "locator": "Indexed primary abstract", "file_sha256": "88bcb50ecdb918803c5950bcff8f48665dbd17148b365a4f9f3b463fe7edd2a4", "start_char": 0, "end_char": 1462, "text_sha256": "88bcb50ecdb918803c5950bcff8f48665dbd17148b365a4f9f3b463fe7edd2a4", "text_characters": 1462}
    experimental_model
    Conditional mammary epithelial Tmem165 deletion in mice
    exposure
    Tissue-specific deletion with milk composition and pup-growth measurements.
    limitations
    The primary abstract supports normalized milk minerals and reduced lactose; altered concentration can reflect less milk dilution. Proposed cation/H+ exchange is an interpretation, not a transport stoichiometry measured here.
    nutrient_topic
    Manganese research collection; topical membership is not evidence of a direct dietary effect. · Manganese
    organism
    Mus musculus
    plain_language
    The milk-producing-cell defect was accompanied by slower growth in nursing pups.
    primary_references
    [mn-gly-milk2019] Milk biosynthesis requires the Golgi cation exchanger TMEM165. (2019). https://pubmed.ncbi.nlm.nih.gov/30622138/ DOI: 10.1074/jbc.ra118.006270
    tissue_or_cell_type
    Lactating mammary gland and milk
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Manganese: enzyme cofactors, glycosylation, transport and nutrient interactions (2026-09-17) · lines 936–948

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Conditional mammary epithelial Tmem165 deletion in mice · source_derived_draft · unverified_draft

    ### mn-gly-mammary-pup-growth Pups nursed by mammary Tmem165-deficient dams had impaired growth. Condition category: machinery_impairment nutrient_topic: Manganese research collection; topical membership is not evidence of a direct dietary effect. plain_language: The milk-producing-cell defect was accompanied by slower growth in nursing pups. organism: Mus musculus tissue_or_cell_type: Lactating mammary gland and milk experimental_model: Conditional mammary epithelial Tmem165 deletion in mice limitations: The primary abstract supports normalized milk minerals and reduced lactose; altered concentration can reflect less milk dilution. Proposed cation/H+ exchange is an interpretation, not a transport stoichiometry measured here. exposure: Tissue-specific deletion with milk composition and pup-growth measurements. cross_nutrient: Mouse TMEM165 (affected_protein); Lactose (affected_product) evidence_span: {"source_cache": "artifacts/manganese-glycosylation-sources/milk2019.abstract.txt", "locator": "Indexed primary abstract", "file_sha256": "88bcb50ecdb918803c5950bcff8f48665dbd17148b365a4f9f3b463fe7edd2a4", "start_char": 0, "end_char": 1462, "text_sha256": "88bcb50ecdb918803c5950bcff8f48665dbd17148b365a4f9f3b463fe7edd2a4", "text_characters": 1462} [mn-gly-milk2019] Milk biosynthesis requires the Golgi cation exchanger TMEM165. (2019). https://pubmed.ncbi.nlm.nih.gov/30622138/ DOI: 10.1074/jbc.ra118.006270
    Complete structured claim and evidence

  5. MnCl2 restored the decorin glycosaminoglycan readout in mouse Tmem165-knockout ATDC5 cells.

    Manganese(II) chloride → Decorin glycosaminoglycan modification source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    Manganese(II) ion (supplied_ion); Mouse TMEM165 (affected_protein)
    evidence_span
    {"source_cache": "artifacts/manganese-glycosylation-sources/morelle2022.txt", "locator": "Results and Figure 5; decorin migration", "file_sha256": "91d05677c6d7bb4224f71742888e39533e3f130d59e6b2ffcae3e2b2c058e9aa", "start_char": 25939, "end_char": 27086, "text_sha256": "d94138936b018635104317fedba6c1298f0d54c6cd7b3f578b60000cea925bf5", "text_characters": 1147}
    experimental_model
    Tmem165-knockout mouse ATDC5 chondrogenic cells
    exposure
    Decorin-transfected ATDC5 cells: 1 micromolar MnCl2, 1 millimolar galactose or 1 millimolar xylose for 36 hours.
    limitations
    Decorin chondroitin-sulfate elongation in mouse chondrogenic cells. This is a separate model from the human HEK N/O-glycosylation assays and does not establish clinical cartilage rescue.
    nutrient_topic
    Manganese research collection; topical membership is not evidence of a direct dietary effect. · Manganese
    organism
    Mus musculus
    plain_language
    Manganese restored the measured sugar-chain modification on a matrix proteoglycan.
    primary_references
    [mn-gly-morelle2022] Differential Effects of D-Galactose Supplementation on Golgi Glycosylation Defects in TMEM165 Deficiency. (2022). https://pubmed.ncbi.nlm.nih.gov/35693943/ DOI: 10.3389/fcell.2022.903953
    tissue_or_cell_type
    Mouse chondrogenic ATDC5 cells and secreted decorin
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Manganese: enzyme cofactors, glycosylation, transport and nutrient interactions (2026-09-17) · lines 782–794

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Tmem165-knockout mouse ATDC5 chondrogenic cells · source_derived_draft · unverified_draft

    ### mn-gly-mn-gag-rescue MnCl2 restored the decorin glycosaminoglycan readout in mouse Tmem165-knockout ATDC5 cells. Condition category: machinery_impairment nutrient_topic: Manganese research collection; topical membership is not evidence of a direct dietary effect. plain_language: Manganese restored the measured sugar-chain modification on a matrix proteoglycan. organism: Mus musculus tissue_or_cell_type: Mouse chondrogenic ATDC5 cells and secreted decorin experimental_model: Tmem165-knockout mouse ATDC5 chondrogenic cells limitations: Decorin chondroitin-sulfate elongation in mouse chondrogenic cells. This is a separate model from the human HEK N/O-glycosylation assays and does not establish clinical cartilage rescue. exposure: Decorin-transfected ATDC5 cells: 1 micromolar MnCl2, 1 millimolar galactose or 1 millimolar xylose for 36 hours. cross_nutrient: Manganese(II) ion (supplied_ion); Mouse TMEM165 (affected_protein) evidence_span: {"source_cache": "artifacts/manganese-glycosylation-sources/morelle2022.txt", "locator": "Results and Figure 5; decorin migration", "file_sha256": "91d05677c6d7bb4224f71742888e39533e3f130d59e6b2ffcae3e2b2c058e9aa", "start_char": 25939, "end_char": 27086, "text_sha256": "d94138936b018635104317fedba6c1298f0d54c6cd7b3f578b60000cea925bf5", "text_characters": 1147} [mn-gly-morelle2022] Differential Effects of D-Galactose Supplementation on Golgi Glycosylation Defects in TMEM165 Deficiency. (2022). https://pubmed.ncbi.nlm.nih.gov/35693943/ DOI: 10.3389/fcell.2022.903953
    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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