Affinage

TMEM165

Putative divalent cation/proton antiporter TMEM165 · UniProt Q9HC07

Length
324 aa
Mass
34.9 kDa
Annotated
2026-06-10
36 papers in source corpus 18 papers cited in narrative 18 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 7/7 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

TMEM165 is a multi-pass transmembrane cation/H+ antiporter that supplies the secretory pathway with the Mn2+ and Ca2+ required for Golgi glycosylation reactions (PMID:22683087, PMID:27008884, PMID:32047108). Direct transport assays in reconstituted Lactococcus lactis and yeast systems established that TMEM165 (and its yeast ortholog Gdt1p) imports Ca2+ and Mn2+ in exchange for H+, with the direction of H+ flux set by the prevailing ion gradients, and that this activity controls Golgi pH (PMID:27075443, PMID:32047108, PMID:36963491). Its glycosylation function reflects delivery of luminal Mn2+ as a cofactor for glycosyltransferases and glycosidases: TMEM165 loss produces N- and O-glycosylation defects, severe hypogalactosylation and GalNAc-transfer failures, and shortened chondroitin/heparan-sulfate GAG chains, all corrected by Mn2+ (and, for galactosylation, galactose) supplementation (PMID:27008884, PMID:28323990, PMID:34930890). TMEM165 abundance is itself governed by Mn2+: high Golgi Mn2+ pumped by the P-type ATPase SPCA1 triggers lysosomal degradation of TMEM165 via the cytosolic ELGDK motif (E108), coupling the two transporters into a system that detoxifies cytosolic Mn2+ and maintains organellar Mn2+ homeostasis (PMID:28270545, PMID:31652305, PMID:37062452). The conserved UPF0016 E-φ-G-D-[KR]-[TS] motifs form a cytosolic acidic cation-binding site and are required for both transport/glycosylation and Mn2+-induced degradation (PMID:31351090, PMID:37416081). Beyond the Golgi, a lysosomal pool of TMEM165 imports Ca2+ into the lysosomal lumen and mediates Ca2+-induced proton leakage, accelerating recovery from cytosolic Ca2+ overload and promoting cell survival (PMID:40473625). TMEM165 deficiency causes a congenital disorder of glycosylation, and in lactating mammary gland it is required for lactose biosynthesis and normal milk Ca2+/Mn2+ content (PMID:22683087, PMID:30622138).

Mechanistic history

Synthesis pass · year-by-year structured walk · 18 steps
  1. 2012 High

    Established that TMEM165 is functionally required for Golgi glycosylation, defining it as a candidate for congenital disorders of glycosylation rather than an orphan membrane protein.

    Evidence siRNA knockdown in HEK cells with glycosylation readout

    PMID:22683087

    Open questions at the time
    • Did not identify the molecular activity underlying the glycosylation requirement
    • No localization or transport mechanism defined
  2. 2013 Medium

    Mapped TMEM165 to Golgi, plasma membrane, and late endosome/lysosome compartments and showed disease mutations mislocalize the protein, identifying the YNRL motif as a localization determinant.

    Evidence Fluorescence microscopy of WT/mutant constructs plus yeast gdt1Δ complementation

    PMID:23575229

    Open questions at the time
    • Did not establish the biochemical activity
    • Functional significance of the non-Golgi pools left unresolved
  3. 2016 High

    Identified Golgi Mn2+ homeostasis as the mechanistic basis of the glycosylation defect, since Mn2+ supplementation rescues both yeast and mammalian loss-of-function.

    Evidence Yeast/mammalian depletion with Mn2+ rescue and GPP130 Golgi Mn2+ sensor

    PMID:27008884

    Open questions at the time
    • Did not demonstrate direct Mn2+ transport by TMEM165
    • Stoichiometry and coupling ion unknown at this stage
  4. 2016 High

    Demonstrated that the ortholog Gdt1p directly transports Ca2+ as a Ca2+/H+ antiporter, providing the first direct biochemical evidence for transport activity and linking it to cellular calcium stores.

    Evidence Heterologous expression in L. lactis with Ca2+ uptake assay plus yeast genetics

    PMID:27075443

    Open questions at the time
    • Direct Mn2+ transport by the human protein not yet shown
    • Physiological relevance of Ca2+ vs Mn2+ selectivity unclear
  5. 2017 Medium

    Showed TMEM165 abundance is controlled by Mn2+-induced lysosomal degradation through the cytosolic ELGDK motif (E108), revealing a regulatory feedback layer distinct from its transport function.

    Evidence MnCl2 exposure with WT/mutant western blots and lysosomal inhibitors

    PMID:28270545

    Open questions at the time
    • Degradation machinery and Mn2+-sensing step not identified
    • E108G separates degradation from glycosylation function but its transport effect was not tested here
  6. 2017 High

    Defined the specific glycan lesions (hypogalactosylation, GalNAc-transfer defects) and showed both Mn2+ and galactose correct them in cells and patients, translating the Mn2+ model toward therapy.

    Evidence MS glycomics in KO HEK293, patient galactose treatment, transferrin IEF

    PMID:28323990

    Open questions at the time
    • Mechanism by which galactose bypasses the Mn2+ deficiency not fully resolved
    • Long-term clinical efficacy not assessed
  7. 2017 Medium

    Characterized ER-localized splice isoforms with distinct tissue expression and altered glycosylation effects, indicating isoform-specific regulation of the protein.

    Evidence RT-PCR/RT-qPCR from brain tissue, isoform imaging, glycosylation western blots

    PMID:28088503

    Open questions at the time
    • Physiological role of ER-retained isoforms unknown
    • Whether isoforms transport ions untested
  8. 2018 Medium

    Dissected the route of extracellular Mn2+ rescue, showing SERCA pumps rather than endocytosis or SPCA1 deliver rescuing Mn2+ in TMEM165 KO cells.

    Evidence Thapsigargin/CPA inhibition and SERCA2b overexpression in KO HEK293 cells

    PMID:30307768

    Open questions at the time
    • Quantitative contribution of SERCA vs other pumps unresolved
    • Relationship between SERCA-delivered ER Mn2+ and Golgi Mn2+ not detailed
  9. 2019 High

    Provided direct biochemical proof that human TMEM165 transports both Ca2+ and Mn2+ and that the disease variant E108G reduces transport, unifying the transport and disease mechanisms.

    Evidence Reconstitution in S. cerevisiae and L. lactis, Fura-2 Ca2+ assay, growth/glycosylation assays, mutagenesis

    PMID:32047108

    Open questions at the time
    • Transport stoichiometry not quantified
    • High-resolution structure of the transport site absent
  10. 2019 High

    Established a reciprocal regulatory circuit in which SPCA1-mediated Golgi Mn2+ pumping sustains TMEM165 by preventing constitutive lysosomal degradation.

    Evidence SPCA1-deficient Hap1 cells, SPCA1 transport-selective mutants, western blot, microscopy

    PMID:31652305

    Open questions at the time
    • Molecular sensor coupling Golgi Mn2+ to TMEM165 degradation unidentified
    • Whether SPCA1 and TMEM165 physically interact untested
  11. 2019 High

    Demonstrated a physiological requirement in vivo: mammary TMEM165 supports lactose biosynthesis and normal milk Ca2+/Mn2+, consistent with Ca2+/Mn2+-for-H+ exchange into the Golgi.

    Evidence Tissue-specific conditional knockout mice with milk composition and immunostaining

    PMID:30622138

    Open questions at the time
    • Cell-type contributions within mammary tissue not separated
    • Systemic vs local Mn2+ effects not dissected
  12. 2019 Medium

    Showed the conserved UPF0016 motifs underlie both glycosylation and Mn2+-sensitivity, with individual residues differentially partitioning between the two activities.

    Evidence Site-directed mutagenesis of conserved motifs with glycosylation and degradation readouts

    PMID:31351090

    Open questions at the time
    • Structural basis of motif function not resolved here
    • Coupling between ion binding and degradation signal unclear
  13. 2020 Medium

    Extended the SPCA1–TMEM165 link to disease cells, showing SPCA1 loss (Hailey-Hailey) sensitizes TMEM165 to Mn2+-induced degradation via cytosolic Mn2+ accumulation.

    Evidence HHD patient fibroblasts/keratinocytes, MnCl2 western blot, ICP-MS, GPP130 sensor

    PMID:32335229

    Open questions at the time
    • Causal contribution of TMEM165 loss to HHD phenotype unproven
    • Patient-derived single-lab data
  14. 2021 Medium

    Showed Mn2+ limitation from TMEM165 loss impairs proteoglycan GAG chain elongation and disrupts TGFβ/BMP signaling and chondrocyte maturation, broadening the functional consequences beyond N/O-glycans.

    Evidence KO cells, GAG chain analysis, Mn2+ rescue, TGFβ/BMP and chondrocyte differentiation assays

    PMID:34930890

    Open questions at the time
    • Direct link between GAG defects and signaling changes not fully traced
    • In vivo skeletal phenotype not established here
  15. 2023 High

    Defined the antiporter mechanism precisely, showing Gdt1p exchanges H+ for Ca2+/Mn2+ with reversible H+ directionality set by gradients and that it shapes Golgi pH.

    Evidence L. lactis pH recording with ion gradients plus genetically encoded cytosolic/Golgi pH probes in yeast

    PMID:36963491

    Open questions at the time
    • Whether human TMEM165 reverses H+ direction in vivo not directly shown
    • Quantitative coupling ratio unresolved
  16. 2023 Medium

    Quantified the cooperative role of TMEM165 and SPCA1 in organellar Mn2+ filling and cytosolic Mn2+ detoxification, tying the degradation mechanism to Mn2+ handling.

    Evidence siRNA depletion of TMEM165/SPCA1, ICP-MS of organellar and cytosolic Mn2+, glycosylation assays

    PMID:37062452

    Open questions at the time
    • Single-lab dataset
    • Dynamic kinetics of Mn2+ partitioning not modeled
  17. 2023 Low

    Proposed a structural model in which the duplicated three-helix repeats place the conserved motifs face-to-face to form a cytosolic acidic cation-binding site, rationalizing distant patient mutations.

    Evidence AlphaFold2 model refined by molecular dynamics with cellular mutation validation

    PMID:37416081

    Open questions at the time
    • Computational model lacks experimental structure
    • Predicted binding-site residues not biochemically confirmed
  18. 2025 High

    Revealed a distinct lysosomal function: a lysosomal pool of TMEM165 imports Ca2+ and drives Ca2+-induced proton leakage, accelerating recovery from cytosolic Ca2+ overload and enhancing survival.

    Evidence Lysosomal patch-clamp electrophysiology, ion-flux imaging, depletion/overexpression, survival assays

    PMID:40473625

    Open questions at the time
    • Relationship between lysosomal and Golgi pools' regulation unresolved
    • Physiological contexts triggering lysosomal Ca2+ handling not defined

Open questions

Synthesis pass · forward-looking unresolved questions
  • How TMEM165 is partitioned and independently regulated between Golgi and lysosomal membranes, and whether its lysosomal Ca2+/H+ activity intersects with Golgi Mn2+ homeostasis, remain open.
  • No experimental structure of the human transporter
  • Mechanism sensing Golgi Mn2+ to trigger lysosomal degradation unidentified
  • Determinants of dual Golgi/lysosomal targeting unknown

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0005215 transporter activity 4 GO:0140104 molecular carrier activity 3
Localization
GO:0005764 lysosome 3 GO:0005794 Golgi apparatus 3 GO:0005783 endoplasmic reticulum 1 GO:0005886 plasma membrane 1
Pathway
R-HSA-382551 Transport of small molecules 4 R-HSA-1643685 Disease 3 R-HSA-392499 Metabolism of proteins 3
Partners
ATP2C1

Evidence

Reading pass · 18 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2012 TMEM165 is required for Golgi glycosylation; siRNA-mediated knockdown of TMEM165 in HEK cells causes Golgi glycosylation defects, identifying it as a protein involved in congenital disorders of glycosylation. siRNA knockdown in HEK cells with glycosylation readout American journal of human genetics High 22683087
2013 Wild-type TMEM165 localizes to the Golgi compartment, plasma membrane, and late endosomes/lysosomes; disease-causing mutations alter subcellular localization differentially depending on the mutation. The YNRL motif is critical for TMEM165 subcellular localization. Fluorescence microscopy of wild-type and mutant TMEM165 constructs; yeast complementation assay with gdt1Δ strain Human molecular genetics Medium 23575229
2016 Glycosylation defects in Gdt1p/TMEM165-deficient cells result from a defect in Golgi manganese (Mn2+) homeostasis; Mn2+ supplementation restores normal glycosylation in both yeast gdt1Δ mutants and TMEM165-depleted mammalian cells. GPP130 Mn2+ sensitivity is altered in TMEM165-depleted cells. Yeast and mammalian cell knockout/depletion with Mn2+ supplementation rescue; GPP130 as Golgi Mn2+ sensor Human molecular genetics High 27008884
2016 Yeast Gdt1p (TMEM165 ortholog) has direct Ca2+ transport activity functioning as a Ca2+/H+ antiporter, demonstrated by heterologous expression in Lactococcus lactis; Gdt1p controls cellular calcium stores and is required for glycosylation at high external calcium concentrations, with glycosylation restored by Mn2+ supplementation. Heterologous expression in Lactococcus lactis with Ca2+ uptake assay; yeast genetic analysis; glycosylation assays Scientific reports High 27075443
2017 High Mn2+ concentrations cause lysosomal degradation of TMEM165. The glutamic acid at position E108 within the cytosolic ELGDK motif is crucial for Mn2+-induced degradation; the E108G variant is insensitive to Mn2+-induced degradation but does not abolish TMEM165 function in Golgi glycosylation. Western blot of TMEM165 levels upon MnCl2 exposure in cell lines expressing wild-type or mutant TMEM165; lysosomal inhibitor experiments The Biochemical journal Medium 28270545
2017 TMEM165 deficiency causes severe hypogalactosylation and GalNAc transfer defects; these N-glycosylation defects are corrected by Mn2+ supplementation and also rescued by galactose supplementation in cells and in patients. Mass spectrometry glycan analysis in TMEM165 KO HEK293 cells; patient treatment with oral galactose; transferrin isoelectrofocusing The Journal of clinical endocrinology and metabolism High 28323990
2017 TMEM165 exists as splice-transcript isoforms (Short Form 129 aa and Long Form 259 aa in addition to full-length 324 aa); both isoforms localize to the endoplasmic reticulum (not Golgi), the Short Form forms homodimers and is expressed at low levels broadly but enriched in brain, and the Long Form is expressed only in the temporal lobe. These isoforms have different effects on glycosylation compared to wild-type protein. RT-PCR from human brain tissue, RT-Q-PCR, fluorescence microscopy of expressed isoforms, western blot for glycosylation readout Biochimica et biophysica acta. General subjects Medium 28088503
2018 The rescue of Golgi N-glycosylation defects in TMEM165 KO cells by extracellular Mn2+ is mediated by thapsigargin- and cyclopiazonic acid-sensitive pumps (SERCA pumps), not by endocytosis or SPCA1. Overexpression of SERCA2b partially rescues LAMP2 glycosylation defect in TMEM165 KO cells. Pharmacological inhibition with thapsigargin/CPA in TMEM165 KO HEK293 cells; SERCA2b overexpression; glycosylation readout by western blot FASEB journal Medium 30307768
2019 TMEM165 directly mediates Ca2+ and Mn2+ transport when expressed heterologously in yeast and Lactococcus lactis; expression in a yeast strain lacking Golgi Ca2+/Mn2+ transporters abrogates Mn2+-induced growth defects, excessive Mn2+ accumulation, and glycosylation defects. The E108G disease-causing mutation significantly reduces TMEM165 transport activity. Heterologous expression in S. cerevisiae and L. lactis; Fura-2 fluorescent probe Ca2+ influx assay in bacteria; yeast growth assays; glycosylation assays; site-directed mutagenesis The Journal of biological chemistry High 32047108
2019 TMEM165 abundance is directly dependent on SPCA1 function—specifically SPCA1's capacity to pump Mn2+ into the Golgi lumen. In SPCA1-deficient cells, TMEM165 is constitutively degraded in lysosomes; the SPCA1 Q747A mutant that favors Mn2+ pumping rescues TMEM165 abundance and Golgi localization. SERCA2b overexpression also rescues TMEM165 expression. SPCA1-deficient Hap1 cells; complementation with SPCA1 mutants differentially impairing Mn2+/Ca2+ transport; western blot; fluorescence microscopy; lysosomal inhibitors The Biochemical journal High 31652305
2019 TMEM165 is crucial in the lactating mammary gland for normal biosynthesis of lactose and affects milk calcium and manganese levels; conditional knockout mice show decreased lactose biosynthesis and only calcium and manganese levels are significantly lower in milk (normalized to protein), consistent with TMEM165 supplying Ca2+ and Mn2+ to the Golgi in exchange for H+. Conditional tissue-specific knockout mice; biochemical assays of milk composition; immunostaining The Journal of biological chemistry High 30622138
2019 The conserved UPF0016 consensus motifs E-φ-G-D-[KR]-[TS] in TMEM165 are crucial for both Golgi glycosylation function and Mn2+-induced sensitivity; specific amino acids within these motifs differentially contribute to these two activities. Site-directed mutagenesis of conserved motifs; glycosylation assays; western blot for Mn2+-induced degradation Biochimie Medium 31351090
2020 TMEM165 depletion in SPCA1-deficient context (Hailey-Hailey disease fibroblasts and keratinocytes) leads to increased sensitivity to Mn2+-induced degradation, linked to cytosolic Mn2+ accumulation as measured by ICP-MS and GPP130 as Golgi Mn2+ sensor. HHD patient fibroblasts and keratinocytes; western blot for TMEM165 upon MnCl2; ICP-MS for Mn2+ levels; GPP130 immunofluorescence as Golgi Mn2+ sensor Biochimie Medium 32335229
2021 TMEM165 deficiency impairs elongation of chondroitin- and heparan-sulfate glycosaminoglycan chains of proteoglycans (producing shorter GAG chains) not by defects in Golgi elongating enzymes but by reduced Mn2+ cofactor availability; Mn2+ supplementation rescues the elongation defect. TMEM165 deficiency also impairs TGFβ and BMP signaling in chondrocytes and accelerates chondrocyte maturation/hypertrophy. TMEM165 KO cells; GAG chain analysis; Mn2+ rescue; TGFβ/BMP signaling assays; chondrocyte differentiation assays Cell death & disease Medium 34930890
2023 Yeast Gdt1p transports H+ ions in exchange for Ca2+ and Mn2+ cations (antiporter mechanism); the direction of H+ transport can be reversed depending on physiological concentration gradients. Direct transport measurements were made by expressing Gdt1p in L. lactis and recording extracellular/intracellular pH during application of Ca2+, Mn2+ or H+ gradients; in vivo cytosolic and Golgi pH measurements confirmed Gdt1p influences Golgi pH. Heterologous expression in L. lactis with pH recording; genetically encoded pH probes in S. cerevisiae targeting cytosol and Golgi The Journal of biological chemistry High 36963491
2023 Mn2+ supplementation fully rescues the Mn2+ content in secretory pathway organelles of TMEM165-depleted cells and restores glycosylation. Both TMEM165 and SPCA1 are crucial for cellular Mn2+ homeostasis; cytosolic Mn2+ accumulation in TMEM165- and SPCA1-depleted cells is demonstrated by ICP-MS upon increasing Mn2+ concentrations. The Mn2+-detoxifying capacity through SPCA1 relies on the Mn2+-induced degradation mechanism of TMEM165. TMEM165 siRNA depletion; SPCA1 siRNA depletion; ICP-MS for organellar and cytosolic Mn2+; glycosylation assays Biochimica et biophysica acta. Molecular basis of disease Medium 37062452
2023 AlphaFold2 structural modeling of TMEM165, refined by molecular dynamics simulation with membrane lipids, reveals a two-fold repeat of three transmembrane helices where the conserved consensus motifs face each other to form a putative acidic cation-binding site at the cytosolic side. This model explains the functional impact of patient mutations including G304R, which is distant from the consensus motifs in sequence. AlphaFold2 structural prediction refined by molecular dynamics simulation; functional validation of mutations by expression in cells Computational and structural biotechnology journal Low 37416081
2025 A fraction of TMEM165 localizes to the lysosomal limiting membrane (in addition to its Golgi localization) where it imports calcium into the lysosomal lumen and mediates calcium-induced lysosomal proton leakage. This lysosomal TMEM165 activity accelerates cellular recovery from cytosolic calcium overload, enhancing cell survival, and causes significant cytosolic acidification. Genetic depletion and overexpression; electrophysiology (patch-clamp of lysosomes); visualization of subcellular ion concentrations and fluxes across lysosomal membrane; cell survival assays Nature communications High 40473625

Source papers

Stage 0 corpus · 36 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2012 TMEM165 deficiency causes a congenital disorder of glycosylation. American journal of human genetics 172 22683087
2016 Glycosylation abnormalities in Gdt1p/TMEM165 deficient cells result from a defect in Golgi manganese homeostasis. Human molecular genetics 97 27008884
2017 Galactose Supplementation in Patients With TMEM165-CDG Rescues the Glycosylation Defects. The Journal of clinical endocrinology and metabolism 72 28323990
2016 Yeast Gdt1 is a Golgi-localized calcium transporter required for stress-induced calcium signaling and protein glycosylation. Scientific reports 53 27075443
2017 Manganese-induced turnover of TMEM165. The Biochemical journal 48 28270545
2012 Bone Dysplasia as a Key Feature in Three Patients with a Novel Congenital Disorder of Glycosylation (CDG) Type II Due to a Deep Intronic Splice Mutation in TMEM165. JIMD reports 44 23430531
2016 TMEM165 deficiencies in Congenital Disorders of Glycosylation type II (CDG-II): Clues and evidences for roles of the protein in Golgi functions and ion homeostasis. Tissue & cell 40 27401145
2013 Impact of disease-causing mutations on TMEM165 subcellular localization, a recently identified protein involved in CDG-II. Human molecular genetics 40 23575229
2020 The human Golgi protein TMEM165 transports calcium and manganese in yeast and bacterial cells. The Journal of biological chemistry 36 32047108
2015 Abnormal cartilage development and altered N-glycosylation in Tmem165-deficient zebrafish mirrors the phenotypes associated with TMEM165-CDG. Glycobiology 32 25609749
2018 Involvement of thapsigargin- and cyclopiazonic acid-sensitive pumps in the rescue of TMEM165-associated glycosylation defects by Mn2. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 28 30307768
2019 Dissection of TMEM165 function in Golgi glycosylation and its Mn2+ sensitivity. Biochimie 26 31351090
2015 TMEM165 Deficiency: Postnatal Changes in Glycosylation. JIMD reports 24 26238249
2014 The Ca(2+)/H(+) antiporter TMEM165 expression, localization in the developing, lactating and involuting mammary gland parallels the secretory pathway Ca(2+) ATPase (SPCA1). Biochemical and biophysical research communications 20 24530912
2000 gdt1, a new signal transduction component for negative regulation of the growth-differentiation transition in Dictyostelium discoideum. Molecular biology of the cell 20 10793140
2018 TMEM165, a Golgi transmembrane protein, is a novel marker for hepatocellular carcinoma and its depletion impairs invasion activity. Oncology reports 19 30015898
2021 TMEM165 a new player in proteoglycan synthesis: loss of TMEM165 impairs elongation of chondroitin- and heparan-sulfate glycosaminoglycan chains of proteoglycans and triggers early chondrocyte differentiation and hypertrophy. Cell death & disease 17 34930890
2020 Novel role for the Golgi membrane protein TMEM165 in control of migration and invasion for breast carcinoma. Oncotarget 17 32733646
2019 Milk biosynthesis requires the Golgi cation exchanger TMEM165. The Journal of biological chemistry 17 30622138
2019 Fetal bovine serum impacts the observed N-glycosylation defects in TMEM165 KO HEK cells. Journal of inherited metabolic disease 17 31415112
2020 From the Uncharacterized Protein Family 0016 to the GDT1 family: Molecular insights into a newly-characterized family of cation secondary transporters. Microbial cell (Graz, Austria) 16 32743000
2019 Investigating the functional link between TMEM165 and SPCA1. The Biochemical journal 15 31652305
2014 Antisense-mediated therapeutic pseudoexon skipping in TMEM165-CDG. Clinical genetics 13 24720419
2024 Insights into molecular and cellular functions of the Golgi calcium/manganese-proton antiporter TMEM165. The Journal of biological chemistry 10 39002685
2023 Insights into the regulation of cellular Mn2+ homeostasis via TMEM165. Biochimica et biophysica acta. Molecular basis of disease 9 37062452
2017 Evidence for splice transcript variants of TMEM165, a gene involved in CDG. Biochimica et biophysica acta. General subjects 9 28088503
2020 SPCA1 governs the stability of TMEM165 in Hailey-Hailey disease. Biochimie 8 32335229
2023 The yeast Gdt1 protein mediates the exchange of H+ for Ca2+ and Mn2+ influencing the Golgi pH. The Journal of biological chemistry 7 36963491
2023 New insights into the pathogenicity of TMEM165 variants using structural modeling based on AlphaFold 2 predictions. Computational and structural biotechnology journal 6 37416081
2023 Efficacy of oral manganese and D-galactose therapy in a patient bearing a novel TMEM165 variant. Translational research : the journal of laboratory and clinical medicine 6 38013006
2001 Interaction of gdt1 and protein kinase A (PKA) in the growth-differentiation-transition in Dictyostelium. Differentiation; research in biological diversity 6 11270120
2025 Lysosomal TMEM165 controls cellular ion homeostasis and survival by mediating lysosomal Ca2+ import and H+ efflux. Nature communications 4 40473625
2021 The Relationship between rs534654 Polymorphism in TMEM165 Gene and Increased Risk of Bipolar Disorder Type 1. International journal of molecular and cellular medicine 1 34703799
2026 Putative role of TMEM165 in congenital cardiomyopathies. Frontiers in molecular neuroscience 0 41583011
2025 TMEM165 promotes glioblastoma progression through epithelial-mesenchymal transition-mediated invasion and temozolomide chemoresistance. International journal of biological macromolecules 0 41308767
2024 Sharing is caring: TMEM165 a Golgi calcium importer used by the lysosome. Trends in biochemical sciences 0 38816278

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