Affinage

SLC20A1

Sodium-dependent phosphate transporter 1 · UniProt Q8WUM9

Length
679 aa
Mass
73.7 kDa
Annotated
2026-06-10
40 papers in source corpus 19 papers cited in narrative 19 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 8/8 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

SLC20A1 (PiT1/GLVR1) is a multifunctional 12-transmembrane sodium-dependent inorganic phosphate cotransporter whose biological roles extend well beyond ion transport into cell survival, inflammation, development, and viral entry (PMID:19717569, PMID:20817733, PMID:39287391). As a membrane transport protein it carries out Na-dependent Pi symport, and it serves as the cell-surface receptor for gibbon ape leukemia virus, with residues 550–551 forming the critical determinants of viral entry (PMID:1531369, PMID:8411375). Beyond uptake, PiT1 acts as an extracellular phosphate sensor: Pi-regulated, low-abundance heterodimerization of PiT1 with PiT2/SLC20A2 — dependent on a putative Pi-binding residue Ser-128 — drives Pi-dependent ERK1/2 phosphorylation independently of phosphate transport (PMID:29233890). Several of PiT1's functions are explicitly transport-independent, demonstrated by rescue with Pi-uptake-deficient mutants: it protects cells from TNF-induced apoptosis by restraining caspase-8 and sustained JNK activation (PMID:20817733), it localizes to the endoplasmic reticulum in chondrocytes where it binds protein disulfide isomerase, supports PDI reductase activity, and prevents ER stress and intracellular cargo retention to maintain chondrocyte survival (PMID:30347511), and it sustains LPS-induced NF-κB signaling in macrophages within a positive feedback loop in which p65 directly binds the Pit1 promoter (PMID:30755642). In vivo, PiT1 is essential for fetal liver hematopoiesis and embryonic viability, and is cell-intrinsically required for terminal erythroid differentiation and B-cell development through control of cell-cycle progression, independent of systemic phosphate (PMID:20161774, PMID:23376999). It is required for chorioallantoic placental morphogenesis and serves as the receptor for the endogenous retroviral fusogen syncytin-B that drives syncytiotrophoblast layer II formation (PMID:39287391, PMID:36795703). PiT1 protein abundance is negatively controlled post-transcriptionally by the ESCRT machinery, consistent with ESCRT-mediated lysosomal degradation (PMID:35447110). Additional roles include promotion of hippocampal synaptic plasticity via an Otoferlin-dependent GABAergic mechanism (PMID:38195526) and participation in Pi-induced mineralization and apoptosis of valve interstitial cells upstream of Akt-1 (PMID:23308213).

Mechanistic history

Synthesis pass · year-by-year structured walk · 12 steps
  1. 1992 Medium

    Established the dual identity of GLVR1/SLC20A1 as both a predicted phosphate transport protein and the cell-surface receptor for gibbon ape leukemia virus, framing the protein's two original functional axes.

    Evidence Sequence homology to Neurospora pho-4+ phosphate permease and functional expression conferring GALV susceptibility in mouse cells

    PMID:1531369

    Open questions at the time
    • Transport activity was predicted by homology, not directly measured
    • Did not define which protein regions mediate receptor versus transport functions
  2. 1993 High

    Mapped the structural determinant of viral entry, showing that residues 550–551 are necessary and sufficient for GALV infection and thereby localizing the receptor function to a defined extracellular determinant.

    Evidence Human/mouse hybrid proteins and site-directed mutants assayed for infection susceptibility, confirmed by rat sequence polymorphism

    PMID:8411375

    Open questions at the time
    • Did not address whether the receptor function relates to phosphate transport
    • No structural model of the receptor-virus interface
  3. 1999 Medium

    Defined the transcriptional control of the gene, identifying SP1-dependent promoter activity in osteoblast-like cells and connecting SLC20A1 expression to bone/mineralizing tissue contexts.

    Evidence Gene cloning, 5'-RACE, and reporter promoter-deletion assays in SaOS-2 cells

    PMID:9889306

    Open questions at the time
    • Single cell type; physiological relevance of SP1 sites not tested in vivo
    • Did not connect promoter regulation to functional output
  4. 2009 High

    Resolved the membrane architecture and defined the regulatory logic of phosphate-responsive expression, revising the topology to 12 transmembrane helices and showing Pi up-regulates SLC20A1 via ERK1/2 signaling.

    Evidence SCAM live-cell topology mapping; RT-PCR and ERK1/2 phosphorylation with UO126 inhibition and calcium-free conditions in odontoblast-like cells

    PMID:19232318 PMID:19717569

    Open questions at the time
    • Topology mapping did not assign substrate-binding or dimerization residues
    • Did not establish whether ERK activation depends on transport
  5. 2010 High

    Separated PiT1's survival function from its transport activity and established its in vivo essentiality, showing transport-independent protection from TNF apoptosis and embryonic lethality from defective fetal liver hematopoiesis.

    Evidence RNAi/KO MEFs with transport-deficient mutant rescue and caspase-8/JNK assays; mouse knockout allelic series with embryo histology and colony assays

    PMID:20161774 PMID:20817733

    Open questions at the time
    • Molecular mechanism by which PiT1 restrains caspase-8/JNK undefined
    • Direct partner mediating apoptosis protection not identified
  6. 2013 High

    Demonstrated a cell-intrinsic, phosphate-independent requirement for PiT1 in hematopoietic differentiation and positioned it upstream of Akt-1 in Pi-driven mineralization, broadening its roles in cell-cycle and survival control.

    Evidence Conditional KO mice with transplantation and cell-cycle analysis; siRNA, phosphonoformic acid inhibition and Akt-1 overexpression in valve interstitial cells

    PMID:23308213 PMID:23376999

    Open questions at the time
    • Cell-cycle target of PiT1 in hematopoiesis not defined
    • Mechanism linking PiT1 to Akt-1 regulation unresolved
  7. 2017 High

    Defined PiT1 as a bona fide extracellular phosphate sensor, showing Pi-regulated PiT1–PiT2 heterodimerization drives ERK1/2 signaling independently of Pi uptake and identified candidate Pi-binding residues.

    Evidence Genetic deletion, Pi-dependent ERK1/2 assays, chemical cross-linking, BRET, and transport-deficient/Pi-binding-residue mutagenesis

    PMID:29233890

    Open questions at the time
    • Downstream effectors linking heterodimer to ERK not identified
    • Structural basis of Pi sensing not resolved
  8. 2018 High

    Revealed an intracellular ER-resident function, showing PiT1 binds PDI and maintains ER homeostasis and chondrocyte survival in a transport-independent manner, a localization distinct from its plasma-membrane transporter role.

    Evidence Conditional chondrocyte deletion, ER-marker co-localization, PiT1-PDI co-IP, PDI reductase assay, ER stress markers, and transport-deficient mutant rescue

    PMID:30347511

    Open questions at the time
    • How PiT1 traffics to/is retained in the ER unknown
    • Whether ER localization occurs outside chondrocytes untested
  9. 2019 High

    Connected PiT1 to innate immune signaling, establishing a transport-independent role in LPS-induced NF-κB activation and a positive feedback loop in which p65 directly drives Pit1 transcription.

    Evidence Conditional KO macrophages, cytokine ELISA, IκB/p65 immunoblots, in vivo LPS challenge, promoter-reporter and ChIP assays

    PMID:30755642

    Open questions at the time
    • Molecular step at which PiT1 acts in the NF-κB cascade undefined
    • Direct PiT1 effector partner in macrophages not identified
  10. 2022 Medium

    Identified post-transcriptional control of PiT1 abundance, implicating ESCRT-mediated lysosomal degradation in setting phosphate uptake capacity in phosphate-replete cells.

    Evidence Genome-wide CRISPR loss-of-function screen with co-localization and phosphate uptake validation

    PMID:35447110

    Open questions at the time
    • Direct ubiquitination/ESCRT recognition of SLC20A1 not biochemically demonstrated
    • Trigger coupling phosphate status to degradation unknown
  11. 2023 Medium

    Extended PiT1 function to placental development and metabolic signaling, showing a transport-dependent requirement for chorioallantoic morphogenesis and an NPP1-associated role in podocyte insulin signaling.

    Evidence Knockout mouse placental analysis with BeWo Pi uptake assays; NPP1/PiT1 co-IP and siRNA with insulin signaling and GLUT4 glucose-uptake assays in podocytes

    PMID:36795703 PMID:37269459

    Open questions at the time
    • Podocyte NPP1-PiT1 interaction shown by single Co-IP without reciprocal validation
    • Whether placental requirement is transport-dependent versus a sensing/structural role not fully separated
  12. 2024 High

    Defined a developmental receptor function and a neuronal role, identifying PiT1 as the syncytin-B fusogen receptor for syncytiotrophoblast formation and as a promoter of hippocampal synaptic plasticity via an Otoferlin-dependent GABAergic mechanism.

    Evidence Cell-cell fusion ORFeome screening, immunoprecipitation, chimera/truncation mapping and in vivo KO placental EM; conditional KO mice with electrophysiology, behavior, and Otoferlin/GABAergic marker analysis

    PMID:38195526 PMID:39287391

    Open questions at the time
    • Structural basis of PiT1–syncytin-B recognition beyond N-terminus mapping unknown
    • Otoferlin link in synaptic plasticity mechanistically proposed but pathway not reconstituted

Open questions

Synthesis pass · forward-looking unresolved questions
  • How PiT1 integrates its transport, sensing, ER-resident, and receptor functions through shared structural determinants — and what distinguishes its many transport-independent activities mechanistically — remains unresolved.
  • No high-resolution structure assigning transport, dimerization, and receptor surfaces
  • Direct effectors mediating transport-independent apoptosis, NF-κB, and ER functions not identified
  • Mechanistic basis of tissue-specific localization (plasma membrane vs ER) unknown

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0005215 transporter activity 4 GO:0001618 virus receptor activity 3 GO:0140096 catalytic activity, acting on a protein 1 GO:0140299 molecular sensor activity 1
Localization
GO:0005886 plasma membrane 3 GO:0005783 endoplasmic reticulum 1
Pathway
R-HSA-1266738 Developmental Biology 3 R-HSA-162582 Signal Transduction 2 R-HSA-382551 Transport of small molecules 2 R-HSA-5357801 Programmed Cell Death 2 R-HSA-168256 Immune System 1
Partners
NPP1PDISLC20A2

Evidence

Reading pass · 19 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1992 GLVR1/SLC20A1 protein is homologous to pho-4+, a phosphate permease of Neurospora crassa, predicting that GLVR1 functions as a transport protein; it also serves as the cell-surface receptor for gibbon ape leukemia virus (GALV). Sequence homology analysis; functional expression in mouse cells conferring GALV susceptibility Journal of virology Medium 1531369
1993 Human GLVR1 residues 550–551, located in a cluster of seven positions differing between human and mouse proteins, are the critical determinants that allow GALV infection; substitution or hybrid constructs demonstrated these residues are necessary and sufficient for viral entry. Construction of human/mouse hybrid proteins and site-directed mutants; infection susceptibility assay in mouse cells Journal of virology High 8411375
1999 The human GLVR1 gene consists of 11 exons over ~18 kb; its promoter contains a GC-rich region with two SP1 binding sites required for high promoter activity in osteoblast-like SaOS-2 cells, as shown by reporter gene assays. Gene cloning, 5'-RACE, reporter gene (promoter) assays in transiently transfected SaOS-2 cells Gene Medium 9889306
2000 TGF-β1 selectively increases sodium-dependent Pi transport and Glvr-1 (SLC20A1) mRNA expression in chondrogenic ATDC5 cells via a mechanism dependent on new RNA and protein synthesis; the response does not involve protein kinase C or MAPK (ERK/p38) pathways but likely involves Smad-dependent signaling. Northern blotting, radiolabeled Pi uptake assays, pharmacological inhibitors (PKC, ERK, p38 inhibitors), and Smad pathway analysis in ATDC5 cells Endocrinology Medium 10830313
2009 Substituted cysteine accessibility mutagenesis (SCAM) of SLC20A1 in live cells revealed a revised topology of 12 transmembrane helices and 7 extracellular regions, superseding earlier 10-helix models, and identified extracellular regions accessible to the cell surface milieu. Substituted cysteine accessibility mutagenesis (SCAM); HMMTOP hidden Markov model-constrained topology prediction The Journal of biological chemistry High 19717569
2009 Inorganic phosphate (Pi) up-regulates Glvr-1 (SLC20A1) expression in MO6-G3 odontoblast-like cells via ERK1/2 signaling; this effect requires extracellular calcium and is blocked by the ERK inhibitor UO126. Real-time RT-PCR, ERK1/2 phosphorylation assays, calcium-free conditions, UO126 pharmacological inhibition Biochemical and biophysical research communications Medium 19232318
2010 Complete deletion of PiT1/SLC20A1 in mice causes embryonic lethality at E12.5 due to severely hypoplastic fetal livers with decreased proliferation and massive apoptosis, leading to reduced hematopoiesis and anemia; hematopoietic progenitors show no cell-autonomous proliferation/differentiation defect, placing the essential function in fetal liver stroma. Mouse knockout/hypomorphic allelic series; histology, FACS, colony assays, embryo analysis PloS one High 20161774
2010 PiT1/SLC20A1 has a transport-independent role in protecting cells from TNF-induced apoptosis: PiT1-depleted cells show increased caspase-8 activation and sustained JNK activation in response to TNF; re-expression of a Pi-uptake-deficient PiT1 mutant rescues the apoptosis phenotype as effectively as wild-type PiT1. RNA interference in HeLa cells; PiT1 knockout MEFs; re-expression of transport-deficient PiT1 mutant; caspase-8 and JNK activity assays; JNK-specific inhibitor rescue The Journal of biological chemistry High 20817733
2013 Conditional deletion of PiT1/SLC20A1 in bone marrow causes a profound block in terminal erythroid differentiation and severe B-cell lymphopenia (pro-B cell block) and mild neutropenia; the phenotype is hematopoietic-cell-intrinsic, associated with a cell-cycle progression defect, and occurs independently of changes in serum phosphate or cellular phosphate uptake. Conditional knockout mice; transplantation experiments; flow cytometry; cell-cycle analysis Experimental hematology High 23376999
2013 SLC20A1/PiT1 silencing reduces Pi-induced mineralization of valve interstitial cells (VICs) and prevents Pi-mediated Akt-1 downregulation and apoptosis; pharmacological block of Pi transport (phosphonoformic acid) or siRNA against SLC20A1 restores Akt-1 levels; overexpression of Akt-1 prevents Pi-induced apoptosis and mineralization, placing SLC20A1 upstream of Akt-1 in this pathway. siRNA knockdown in VIC cultures; phosphonoformic acid inhibition; Akt-1 overexpression; mitochondrial membrane potential and cytochrome c assays PloS one Medium 23308213
2017 Pi-regulated heterodimerization of PiT1/SLC20A1 and PiT2/SLC20A2 mediates extracellular Pi sensing independently of Pi uptake: deletion of either PiT blunts Pi-dependent ERK1/2 phosphorylation; transport-deficient PiT mutants rescue ERK1/2 signaling; cross-linking and BRET show Pi-regulated low-abundance PiT1-PiT2 heterodimers; mutation of putative Pi-binding residues Ser-128 (PiT1) and Ser-113 (PiT2) abolishes Pi regulation of heterodimerization. Genetic deletion (siRNA/KO); Pi-dependent ERK1/2 phosphorylation assay; chemical cross-linking; bioluminescence resonance energy transfer (BRET); site-directed mutagenesis of Pi-binding residues The Journal of biological chemistry High 29233890
2018 PiT1/SLC20A1 localizes to the endoplasmic reticulum (not the plasma membrane) in chondrocytes, co-localizing with ER marker ERp46; it binds the ER chaperone protein disulfide isomerase (PDI) and is required for PDI reductase activity; PiT1 ablation causes uncompensated ER stress (elevated Chop, Atf4, Bip), intracellular retention of aggrecan and VEGF-A, and chondrocyte death; a phosphate transport-deficient PiT1 mutant rescues ER stress and cargo retention, establishing a transport-independent ER homeostasis function. Conditional gene deletion in chondrocytes; immunofluorescence co-localization with ER markers; co-immunoprecipitation (PiT1-PDI interaction); PDI reductase activity assay; ER stress markers (RT-PCR/immunoblot); rescue with transport-deficient PiT1 mutant Journal of bone and mineral research High 30347511
2019 PiT1/SLC20A1 has a novel transport-independent role in LPS-induced NF-κB signaling: PiT1-deficient macrophages show reduced IκB degradation, lower p65 nuclear translocation, and impaired MCP-1/IL-6 production upon LPS stimulation; ChIP assays show p65 directly binds the mPit1 promoter, and an NF-κB inhibitor abolishes LPS-induced PiT1 expression, establishing a positive feedback loop between PiT1 and NF-κB. PiT1 conditional knockout macrophages; ELISA for cytokines; immunoblot for IκB/p65; in vivo LPS challenge; promoter-reporter assay; chromatin immunoprecipitation (ChIP) Scientific reports High 30755642
2022 ESCRT machinery negatively regulates SLC20A1/PiT1 protein abundance post-transcriptionally in phosphate-replete cells: ESCRT deficiency increases SLC20A1 protein levels and phosphate uptake; SLC20A1 co-localizes with ESCRT components, suggesting direct ESCRT-mediated lysosomal degradation of SLC20A1. Genome-wide CRISPR loss-of-function screen; immunofluorescence co-localization; phosphate uptake assays in ESCRT-deficient cells The Journal of biological chemistry Medium 35447110
2023 PiT1/SLC20A1 interacts with NPP1 in podocytes under hyperinsulinemic conditions; knockdown of SLC20A1 in podocytes under normal conditions induces insulin resistance manifested as loss of insulin signaling and inhibition of GLUT4-mediated glucose uptake, placing PiT1 as a required factor in NPP1-mediated insulin signaling. Co-immunoprecipitation (NPP1/PiT1 interaction); siRNA knockdown of SLC20A1; insulin signaling assays; glucose uptake measurement via GLUT4 Journal of cellular physiology Medium 37269459
2024 PiT1/SLC20A1 is the receptor for syncytin-B (SynB), the endogenous retroviral fusogen responsible for mouse syncytiotrophoblast layer II (ST-II) formation: cell-cell fusion assays with ORFeome screening identified PiT1 (but not PiT2/SLC20A2) as the SynB receptor; the interaction was confirmed by immunoprecipitation; PiT1 N-terminus is the major determinant for SynB-mediated fusion; PiT1 null embryos display absence of ST-II syncytialization, phenocopying SynB null placenta. Cell-cell fusion assay with ORFeome library screening; immunoprecipitation; PiT1/PiT2 chimera and truncation experiments; RT-qPCR expression analysis; electron microscopy of PiT1 null placenta Journal of virology High 39287391
2024 Slc20a1 (PiT-1) promotes synaptic plasticity in the hippocampus via a likely Otoferlin-dependent regulation of synaptic vesicle trafficking that impacts the GABAergic system; this role is distinct from and independent of its phosphate transport activity, as demonstrated by behavioral and electrophysiological analyses in conditional knockout mice. Conditional knockout mice; electrophysiology; behavioral analysis; molecular analysis of Otoferlin and GABAergic markers Cell death & disease Medium 38195526
2023 Slc20a1/SLC20A1 is required for chorioallantoic placental morphogenesis: Slc20a1-/- embryos at E9.5 show reduced placenta size and structural abnormalities in the chorioallantois, with reduced MCT1+ syncytiotrophoblast coverage; SLC20A1 mediates sodium-dependent Pi symport into syncytiotrophoblast cells supporting their differentiation. Knockout mouse analysis; P33 phosphate uptake assays in BeWo cells; microarray, RT-PCR, RNA-seq expression profiling; immunohistochemistry of trophoblast markers Vascular biology Medium 36795703
2020 Simultaneous conditional deletion of both Pit1 and Pit2 in skeletal muscle causes fatal muscle atrophy by P13; single or partial deletions produce a gene-dose-dependent reduction in running activity associated with reduced ERK1/2 activation and stimulated AMP kinase in skeletal muscle, indicating Pi transport-dependent and ERK1/2-dependent metabolic Pi sensing pathways for myofiber function. Skeletal muscle conditional double knockout mice; grip strength and running activity assays; ERK1/2 and AMPK immunoblots; C2C12 oxygen consumption rate assays Scientific reports Medium 32080237

Source papers

Stage 0 corpus · 40 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
1992 GLVR1, a receptor for gibbon ape leukemia virus, is homologous to a phosphate permease of Neurospora crassa and is expressed at high levels in the brain and thymus. Journal of virology 129 1531369
2017 Phosphate (Pi)-regulated heterodimerization of the high-affinity sodium-dependent Pi transporters PiT1/Slc20a1 and PiT2/Slc20a2 underlies extracellular Pi sensing independently of Pi uptake. The Journal of biological chemistry 90 29233890
2010 The phosphate transporter PiT1 (Slc20a1) revealed as a new essential gene for mouse liver development. PloS one 87 20161774
1999 In vivo expression of transcripts encoding the Glvr-1 phosphate transporter/retrovirus receptor during bone development. Bone 76 9916777
1993 Definition of a domain of GLVR1 which is necessary for infection by gibbon ape leukemia virus and which is highly polymorphic between species. Journal of virology 67 8411375
2000 Transforming growth factor-beta stimulates inorganic phosphate transport and expression of the type III phosphate transporter Glvr-1 in chondrogenic ATDC5 cells. Endocrinology 59 10830313
2010 Identification of a novel transport-independent function of PiT1/SLC20A1 in the regulation of TNF-induced apoptosis. The Journal of biological chemistry 56 20817733
2013 High expression of the Pi-transporter SLC20A1/Pit1 in calcific aortic valve disease promotes mineralization through regulation of Akt-1. PloS one 48 23308213
2018 PiT1/Slc20a1 Is Required for Endoplasmic Reticulum Homeostasis, Chondrocyte Survival, and Skeletal Development. Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research 30 30347511
2013 Mice with hypomorphic expression of the sodium-phosphate cotransporter PiT1/Slc20a1 have an unexpected normal bone mineralization. PloS one 29 23785462
2019 Novel function of PiT1/SLC20A1 in LPS-related inflammation and wound healing. Scientific reports 28 30755642
2006 The Na+/PO4 cotransporter SLC20A1 gene labels distinct restricted subdomains of the developing pronephros in Xenopus and zebrafish embryos. Gene expression patterns : GEP 28 16531124
2016 Vitamin-D receptor agonist calcitriol reduces calcification in vitro through selective upregulation of SLC20A2 but not SLC20A1 or XPR1. Scientific reports 27 27184385
2009 Inorganic phosphate regulates Glvr-1 and -2 expression: role of calcium and ERK1/2. Biochemical and biophysical research communications 27 19232318
2009 New structural arrangement of the extracellular regions of the phosphate transporter SLC20A1, the receptor for gibbon ape leukemia virus. The Journal of biological chemistry 24 19717569
2020 SLC20A1 Is Involved in Urinary Tract and Urorectal Development. Frontiers in cell and developmental biology 23 32850778
2020 Slc20a1/Pit1 and Slc20a2/Pit2 are essential for normal skeletal myofiber function and survival. Scientific reports 21 32080237
2013 Mice lacking the sodium-dependent phosphate import protein, PiT1 (SLC20A1), have a severe defect in terminal erythroid differentiation and early B cell development. Experimental hematology 21 23376999
2017 Identification of SLC20A1 and SLC15A4 among other genes as potential risk factors for combined pituitary hormone deficiency. Genetics in medicine : official journal of the American College of Medical Genetics 20 29261175
2019 LincRNA-SLC20A1 (SLC20A1) promotes extracellular matrix degradation in nucleus pulposus cells in human intervertebral disc degeneration by targeting the miR-31-5p/MMP3 axis. International journal of clinical and experimental pathology 19 31934214
2021 High SLC20A1 Expression Is Associated With Poor Prognoses in Claudin-low and Basal-like Breast Cancers. Anticancer research 18 33419798
2014 High levels of the type III inorganic phosphate transporter PiT1 (SLC20A1) can confer faster cell adhesion. Experimental cell research 16 24880124
2019 Impact of SLC20A1 on the Wnt/β‑catenin signaling pathway in somatotroph adenomas. Molecular medicine reports 13 31432167
2002 Overexpression of gibbon ape leukemia virus (GALV) receptor (GLVR1) on human CD34(+) cells increases gene transfer mediated by GALV pseudotyped vectors. Molecular therapy : the journal of the American Society of Gene Therapy 13 12231177
2024 Slc20a1 and Slc20a2 regulate neuronal plasticity and cognition independently of their phosphate transport ability. Cell death & disease 12 38195526
1999 Characterization of the human Glvr-1 phosphate transporter/retrovirus receptor gene and promoter region. Gene 11 9889306
2022 Cellular abundance of sodium phosphate cotransporter SLC20A1/PiT1 and phosphate uptake are controlled post-transcriptionally by ESCRT. The Journal of biological chemistry 10 35447110
2024 Spitz Melanoma With SLC20A1::ALK Fusion: A Novel Fusion Previously Undescribed in Spitz Melanocytic Neoplasm. The American Journal of dermatopathology 7 38941542
2022 High expression of SLC20A1 is less effective for endocrine therapy and predicts late recurrence in ER-positive breast cancer. PloS one 6 35605014
2024 Sodium-dependent phosphate transporter PiT1/SLC20A1 as the receptor for the endogenous retroviral envelope syncytin-B involved in mouse placenta formation. Journal of virology 5 39287391
2023 Computational analysis of sodium-dependent phosphate transporter SLC20A1/PiT1 gene identifies missense variations C573F, and T58A as high-risk deleterious SNPs. Journal of biomolecular structure & dynamics 5 37286379
2019 Transgenic mouse model for conditional expression of influenza hemagglutinin-tagged human SLC20A1/PIT1. PloS one 4 31613887
2023 SLC20a1/PiT-1 is required for chorioallantoic placental morphogenesis. Vascular biology (Bristol, England) 3 36795703
2023 Pit 1 transporter (SLC20A1) as a key factor in the NPP1-mediated inhibition of insulin signaling in human podocytes. Journal of cellular physiology 2 37269459
2022 Long Noncoding RNA SLC20A1-1 Induces Nucleus Pulposus Apoptosis by Sponging miR-146a-5p. Genetic testing and molecular biomarkers 2 35349375
2011 Association between SLC20A1 and sodium-lithium countertransport. American journal of hypertension 2 21796222
2026 Homozygous Loss-of-Function Variant in SLC20A1 Coding for Ubiquitous Phosphate Transporter PiT1 Is Associated With Multiple Developmental Abnormalities. Clinical genetics 0 41906789
2026 Investigating the role of the TGF-β-SLC20A1 axis in the spatial heterogeneity of hepatocellular carcinoma through single-cell and spatial transcriptomics. Frontiers in immunology 0 41953013
2025 A matrix stiffness gene signature identifies SLC20A1 as a novel mechano-immunological checkpoint enabling synergistic immunotherapy in pancreatic ductal adenocarcinoma. Cancer immunology, immunotherapy : CII 0 41222719
2025 SLC20A1 knockout to stably express a fusogenic gibbon ape leukemia virus envelope glycoprotein for lentiviral vector production. Molecular therapy. Methods & clinical development 0 41281711

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