Affinage

PDZK1IP1

PDZK1-interacting protein 1 · UniProt Q13113

Length
114 aa
Mass
12.2 kDa
Annotated
2026-06-10
64 papers in source corpus 24 papers cited in narrative 25 extracted findings
Cross-family judge vs UniProt: tie faithfulness: 6/6 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

PDZK1IP1 (MAP17/DD96/SPAP) is a small dual-pass membrane protein of the proximal tubule brush border that functions both as an obligate accessory subunit for renal sodium-coupled transporters and as a membrane scaffold whose dysregulation drives oncogenic signaling (PMID:8701988, PMID:12812916, PMID:27288013). In the kidney it spans the membrane twice with both termini intracellular, homodimerizes through intracellular Cys55, and is a necessary activator of the Na⁺-glucose cotransporter SGLT2, increasing its activity by roughly two orders of magnitude without altering surface SGLT2 abundance; a homozygous PDZK1IP1 splicing mutation causes familial renal glucosuria, establishing this transporter-activating role in human physiology (PMID:12812916, PMID:27288013, PMID:30156268). Through its C-terminal PDZ-binding domain it interacts with the fourth PDZ domain of PDZK1, anchoring PDZK1 to the apical membrane and assembling a PDZK1/NaPi-IIa/MAP17 complex, and engages NHERF3/NHERF4 to drive PKC-dependent internalization of NaPi-IIa toward the trans-Golgi network, thereby regulating phosphate transport (PMID:12837682, PMID:12754212, PMID:16926447). The same PDZ-binding domain underlies its tumorigenic activity: MAP17 overexpression elevates reactive oxygen species in a manner dependent on Na⁺-coupled cotransport, and this ROS signal activates PI3K/AKT and HIF1α to enhance proliferation, apoptosis resistance, and Warburg-type glycolysis, while ROS instead triggers p38α-dependent senescence in non-transformed cells (PMID:17548903, PMID:17675338, PMID:22266858, PMID:33832535). MAP17 additionally activates Notch signaling by sequestering NUMB to expand cancer stem-like cells, suppresses TGF-β and BMP signaling by binding Smad4 through its central Phe40–Ala49 region and retaining it in the cytoplasm to block R-Smad/Smad4 complex formation, and confers therapy resistance via NF-κB-dependent BCL2 upregulation in glioblastoma-initiating cells and suppression of bortezomib-induced cytoprotective autophagy in breast cancer (PMID:28153862, PMID:30718277, PMID:42043964, PMID:25837675). Its expression is post-transcriptionally constrained by FXR1 and miR-455-5p (PMID:39511680, PMID:36737832).

Mechanistic history

Synthesis pass · year-by-year structured walk · 12 steps
  1. 1996 Medium

    Established the existence and tissue distribution of MAP17 and the first functional clue that it could restrain epithelial tumor growth, framing the protein as both a kidney brush-border component and a growth modulator.

    Evidence Antibody immunolocalization and cDNA transfection with in vitro proliferation and in vivo tumor growth assays in colon carcinoma cells

    PMID:8701988

    Open questions at the time
    • No molecular mechanism for growth suppression
    • No binding partners identified
    • Contrasts with later pro-tumorigenic findings, suggesting context dependence not resolved here
  2. 2003 High

    Defined MAP17 as a PDZ-domain scaffold partner and a transport-activating membrane protein, answering how it physically couples to the brush-border transport machinery.

    Evidence Yeast two-hybrid, in vitro binding, immunofluorescence in OK cells, plus expression cloning in Xenopus oocytes with Cys55 mutagenesis and topology analysis

    PMID:12754212 PMID:12812916 PMID:12837682

    Open questions at the time
    • Identity of the endogenous oocyte transporter being stimulated not defined
    • Mechanism of PDZK1 degradation upon hepatic overexpression unresolved
    • Direct vs indirect basis of transport stimulation unclear
  3. 2006 High

    Showed MAP17 organizes regulated trafficking of phosphate transport, linking the scaffold to NHERF3/4-dependent, PKC-controlled internalization rather than static anchoring.

    Evidence Bacterial and mammalian two-hybrid systems with PKC/dopamine receptor pharmacology and transport assays in OK cells

    PMID:16926447

    Open questions at the time
    • In vivo physiological relevance of TGN-directed internalization not tested
    • Selectivity for NHERF3/4 over NHERF1/2 mechanistically unexplained
  4. 2007 High

    Reframed MAP17 from growth suppressor to oncogenic driver by identifying ROS production through its PDZ-binding domain as the upstream event activating PI3K/AKT and bypassing apoptotic checkpoints.

    Evidence Stable transfection in tumor and Rat1a cells with ROS measurement, PDZ-domain mutagenesis, antioxidant rescue, dominant-negative AKT, and nude mouse tumor assays; plus a genetic screen for TNF-induced arrest bypass

    PMID:17230460 PMID:17548903 PMID:17675338

    Open questions at the time
    • Source of MAP17-driven ROS not molecularly defined
    • How AKT Thr308 phosphorylation occurs independently of PI3K unexplained
    • Reconciliation with earlier growth-suppressive role incomplete
  5. 2012 Medium

    Resolved the suppressor/promoter paradox by showing the same ROS signal produces p38α-dependent senescence in normal cells but tumorigenic enhancement where p38α signaling is lost, making cellular context the determinant of outcome.

    Evidence Gain- and loss-of-function in breast cell lines with ROS, senescence, p38α phosphorylation, and tumor growth assays

    PMID:22266858

    Open questions at the time
    • Single lab
    • Threshold of p38α activity that switches outcomes not quantified
  6. 2016 High

    Established MAP17 as a necessary activator of SGLT2 and linked PDZK1IP1 loss to human disease, anchoring its physiological transport role in genetics.

    Evidence Expression cloning in oocytes and OK cells, surface SGLT2 quantification, and identification of a homozygous PDZK1IP1 splicing mutation in familial renal glucosuria

    PMID:27288013

    Open questions at the time
    • Structural basis of SGLT2 activation without changing surface levels unknown
    • Whether activation requires homodimerization not tested for SGLT2 specifically
  7. 2017 High

    Identified NUMB sequestration as a discrete oncogenic mechanism, explaining how MAP17 activates Notch signaling and expands cancer stem-like cells beyond its ROS activity.

    Evidence Co-immunoprecipitation, PDZ-binding domain interaction studies, Notch reporter assays, knockdown, and tumorsphere/PDX models

    PMID:28153862

    Open questions at the time
    • Stoichiometry of NUMB sequestration not defined
    • Crosstalk between NUMB/Notch and ROS/AKT arms unresolved
  8. 2019 High

    Defined a Smad4-trapping mechanism mapped to the central Phe40–Ala49 region, showing MAP17 suppresses TGF-β/BMP signaling without altering R-Smad phosphorylation.

    Evidence Co-IP, deletion mutagenesis, R-Smad phosphorylation assays, nuclear/cytoplasmic fractionation, reporter assays, and xenograft model

    PMID:30718277

    Open questions at the time
    • How a membrane protein retains Smad4 cytoplasmically not structurally explained
    • Interplay with PDZ-domain-dependent functions not addressed
  9. 2021 High

    Integrated the ROS arm into tumor metabolism, showing MAP17 drives the Warburg effect via ROS-mediated AKT and HIF1α activation in a PDZ-binding-domain-dependent manner.

    Evidence Gain/loss-of-function with PDZ-domain mutant, Seahorse metabolic assays, ROS measurement, RNA-seq, and xenograft model in HCC

    PMID:33832535

    Open questions at the time
    • Direct connection between transporter activity and HIF1α stabilization not biochemically dissected
  10. 2023 Medium

    Placed PDZK1IP1 under post-transcriptional control and extended its scaffolding role to renal stress responses, defining regulatory inputs and an in vivo transporter-complex context.

    Evidence RNA-IP and 3'UTR/mRNA stability assays (FXR1), proteomic and Western analyses in diabetic and heart-failure renal models, and molecular docking for fenofibrate

    PMID:36524468 PMID:38042280 PMID:39511680

    Open questions at the time
    • Fenofibrate binding inferred from docking only
    • MAP17 scaffolding of SGLT2/NHE3 in stressed kidney is interpretive in these studies
    • Direct vs indirect FXR1 effects on downstream phenotype incomplete
  11. 2024 Medium

    Added miR-455-5p as a direct repressor and reinforced the TGF-β-suppressive role by showing PDZK1IP1 loss promotes EMT and metastasis.

    Evidence Dual-luciferase reporter, qRT-PCR, migration/invasion and in vivo metastasis assays, and fractionation in OSCC cells

    PMID:36737832

    Open questions at the time
    • Tissue specificity of tumor-suppressive versus oncogenic behavior not reconciled
    • Single lab
  12. 2026 Medium

    Defined an NF-κB/BCL2 axis underlying therapy resistance and tied renal complex regulation to sympathetic ERK/NF-κB signaling, broadening MAP17's roles in chemoresistance and cardiorenal physiology.

    Evidence Overexpression/knockdown with NF-κB and BCL2 epistasis and TMZ resistance assays in glioblastoma-initiating cells; CHF rat model with renal denervation and norepinephrine treatment of human proximal tubular cells

    PMID:41549941 PMID:42043964

    Open questions at the time
    • Whether NF-κB activation depends on the ROS or scaffolding arm not resolved
    • Direct molecular link between MAP17 and RELA activation unknown
    • Single-lab findings

Open questions

Synthesis pass · forward-looking unresolved questions
  • How a single small membrane protein integrates its transporter-activating scaffolding function with its multiple cytoplasmic signaling effects (NUMB, Smad4, ROS, NF-κB) at the structural and stoichiometric level remains unresolved.
  • No structure of MAP17 or its complexes
  • Mechanism linking Na⁺-coupled transport to ROS generation undefined
  • No unified model reconciling growth-suppressive and oncogenic contexts

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0060090 molecular adaptor activity 4 GO:0098772 molecular function regulator activity 3 GO:0005215 transporter activity 2
Localization
GO:0005886 plasma membrane 5 GO:0005794 Golgi apparatus 1 GO:0005829 cytosol 1
Pathway
R-HSA-162582 Signal Transduction 4 R-HSA-1643685 Disease 3 R-HSA-382551 Transport of small molecules 3
Partners
NAPI-IIANHE3NHERF3NHERF4NUMBPDZK1SLC5A2SMAD4
Complex memberships
PDZK1/NaPi-IIa/MAP17 complexSGLT2-MAP17-PDZK1 complex

Evidence

Reading pass · 25 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1996 MAP17 (DD96/PDZK1IP1) is a 17 kDa membrane-associated protein localized to the brush border of proximal tubular epithelial cells in normal kidney, and to cell membranes at areas of cell-cell contact in tissue culture. Transfection of full-length DD96 cDNA into HT-29 colon carcinoma cells markedly decreased cell proliferation in vitro and tumor growth in vivo. Polyclonal antibody characterization, immunolocalization, cDNA transfection with in vitro proliferation assay and in vivo tumor growth assay The American journal of pathology Medium 8701988
2003 MAP17 interacts specifically with the fourth PDZ domain of PDZK1 (but not other PDZ proteins in the proximal tubule brush border), associates with the NH2-terminus of NaPi-IIa within a PDZK1/NaPi-IIa/MAP17 complex, and acts as an apical anchoring site for PDZK1. MAP17 apical localization is independent of PDZK1, but MAP17 is required for apical localization of PDZK1 in opossum kidney cells. Yeast two-hybrid screen, in vitro binding assays, immunofluorescence, transfection studies in opossum kidney (OK) cells American journal of physiology. Renal physiology High 12837682
2003 Rat kidney MAP17 induces high-affinity, Na-dependent cotransport of D-mannose and D-glucose in Xenopus laevis oocytes, likely by stimulating an endogenous oocyte transport system. MAP17 spans the membrane twice with both termini inside the cell, and forms homodimers through intracellular Cys55; mutation of Cys55 abolishes transport activity. Expression cloning in Xenopus oocytes, transport assays, site-directed mutagenesis (Cys55), membrane topology analysis American journal of physiology. Renal physiology High 12812916
2003 SPAP (MAP17/DD96/PDZK1IP1) is an in vivo PDZK1-interacting protein in liver. Hepatic overexpression of SPAP in transgenic mice leads to degradation of PDZK1 via a proteasome-independent pathway, resulting in loss of SR-BI from the liver cell surface and markedly elevated plasma HDL levels. In vivo transgenic mouse model, metabolic labeling, proteasome inhibitor experiments, Western blot The Journal of biological chemistry High 12754212
2006 MAP17 interacts with all four NHERF proteins, NaPi-IIa, and NHE3 via its PDZ-binding domain. Co-expression of MAP17 with NHERF3 or NHERF4 (but not NHERF1/2) induces internalization of NaPi-IIa, MAP17, and the PDZ protein to the trans-Golgi network (TGN). This internalization is prevented by PKC inhibition and is triggered by PKC activation or dopamine D1-like receptor activation. Co-transfection of MAP17 and NHERF3 prevents adaptive upregulation of phosphate transport in response to low phosphate. Bacterial and mammalian two-hybrid systems, transfection in OK cells, immunofluorescence, PKC inhibition/activation assays, lysosomal inhibition, dopamine receptor activation American journal of physiology. Renal physiology High 16926447
2007 MAP17 overexpression in tumor cells increases reactive oxygen species (ROS) production, enhancing proliferation, migration, resistance to apoptosis, and tumor growth in nude mice. The tumorigenic effects are abolished by antioxidant treatment. MAP17-dependent ROS increase requires its PDZ-binding domain, as point mutations disrupting this domain abolish ROS production and tumorigenesis. Na+-coupled co-transporter inhibitors reduce ROS increase and malignant behavior. Stable transfection in tumor cell lines, ROS measurement, antioxidant treatment, PDZ-binding domain point mutagenesis, nude mouse tumor assay, Na+-coupled cotransporter inhibition Carcinogenesis High 17548903
2007 MAP17 overexpression in Rat1a fibroblasts protects against Myc-induced apoptosis through ROS-mediated activation of the PI3K/AKT signaling pathway. This is associated with absence of Bax translocation to mitochondria, reduced caspase-3 activation, and oxidation of a fraction of PTEN. AKT activation (Thr308 phosphorylation) by MAP17 is independent of PI3K activity. Antioxidant treatment prevents AKT activation and restores apoptosis. Stable transfection in Rat1a cells, apoptosis assays, Bax translocation, caspase-3 activation measurement, PTEN oxidation assay, PI3K inhibition, dominant-negative AKT overexpression, antioxidant treatment Carcinogenesis High 17675338
2007 MAP17 expression bypasses TNF-alpha-induced G1 growth arrest by impairing p21waf1 induction in tumor cells, but does not inhibit TNF-induced apoptosis. The effect is specific to TNF and does not alter IFN-gamma response. Large-scale genetic screen, cell cycle analysis, p21waf1 Western blot, cytokine treatment assays Journal of cellular biochemistry Medium 17230460
2009 Overexpression of MAP17 in HaCaT keratinocytes significantly decreases the expression of filaggrin, suggesting that Th cell cytokine-induced up-regulation of MAP17 may link to down-regulation of filaggrin and abnormal epidermal differentiation. Microarray meta-analysis, cytokine stimulation of NHEK cells, MAP17 overexpression in HaCaT cells, gene expression analysis Experimental dermatology Low 19601982
2012 In non-tumoral breast epithelial cells, MAP17-induced ROS triggers a senescence-like response mediated by p38α activation. In tumor cells lacking p38α phosphorylation, MAP17-induced ROS instead enhances tumorigenic properties. Knockdown of MAP17 in protein-expressing tumor cells reduces tumorigenic capabilities. Stable transfection and shRNA knockdown in breast cell lines, ROS measurement, senescence assays, p38α activation/phosphorylation analysis, tumor growth assays Oncogene Medium 22266858
2015 MAP17 is associated with proteins involved in protein degradation and suppresses bortezomib-induced cytoprotective autophagy and NFκB nuclear translocation in breast cancer cells both in vitro and in vivo. This MAP17-induced sensitivity to bortezomib depends on oxidative status and Na+-coupled transporter activity, as antioxidants or furosemide treatment restores cytoprotective responses. In vitro bortezomib treatment, autophagy assay, NFκB nuclear translocation assay, antioxidant treatment, furosemide inhibition, xenograft tumor model Molecular cancer therapeutics Medium 25837675
2016 MAP17 is a necessary activator of SGLT2 (SLC5A2): co-expression of MAP17 with SGLT2 in Xenopus oocytes increases SGLT2 activity by two orders of magnitude, and significant stimulation also occurs in opossum kidney cells co-transfected with SGLT2 and MAP17. MAP17 does not change the quantity of SGLT2 protein at the cell surface. A patient with familial renal glucosuria without SGLT2 mutations was found to carry a homozygous splicing mutation in PDZK1IP1 (c.176+1G>A). Expression cloning in Xenopus oocytes, glucose transport assay, co-transfection in opossum kidney cells, cell surface SGLT2 quantification, genetic analysis of patient cohort Journal of the American Society of Nephrology : JASN High 27288013
2017 MAP17 (PDZK1IP1) interacts with NUMB through its PDZ-binding domain, sequestering NUMB and thereby activating the Notch signaling pathway. This leads to increased stem cell factor expression and expansion of cancer stem-like cells. MAP17 downregulation in tumor cell lines reduces Notch pathway activation and stemness. MAP17 levels directly correlate with tumorsphere formation capability in PDX models. Co-immunoprecipitation, PDZ-binding domain interaction studies, Notch pathway reporter assays, MAP17 overexpression/knockdown in cell lines, tumorsphere formation assay, PDX models Clinical cancer research High 28153862
2017 MAP17 expression directly regulates NFAT2 and IL-6 activation and induces differentiation of monocytes to dendritic cells, suggesting a causal role for MAP17 in inflammation. MAP17 overexpression experiments, NFAT2 and IL-6 reporter/activation assays, monocyte differentiation assay Oncotarget Low 29228712
2018 MAP17 colocalizes and co-immunoprecipitates with SGLT2 in HEK293T cells co-expressing V5-tagged SGLT2 and HA-tagged MAP17. In human kidney sections, both proteins overlap at the apical surface of tubular epithelia. Co-immunoprecipitation, colocalization by immunofluorescence in HEK293T cells, immunohistochemistry in human kidney sections FEBS letters Medium 30156268
2019 PDZK1IP1 (MAP17) interacts with Smad4 protein. PDZK1IP1 inhibits both TGF-β and BMP signaling pathways without affecting R-Smad phosphorylation, instead interfering with R-Smad/Smad4 complex formation and retaining Smad4 in the cytoplasm. The middle region of PDZK1IP1 (Phe40–Ala49) is required for Smad4-regulating activity. PDZK1IP1 knockdown enhances TGF-β target gene expression; overexpression suppresses TGF-β-induced reporter activity, cell migration, and cell growth inhibition, and decreases tumor size in a xenograft model. Co-immunoprecipitation, PDZK1IP1 deletion/variant mutagenesis, R-Smad phosphorylation assays, Smad complex formation assay, cytoplasmic/nuclear fractionation, TGF-β reporter assay, siRNA knockdown, cell migration assay, xenograft tumor model The Journal of biological chemistry High 30718277
2020 MAP17 increases exosome production in breast cancer tumor cells, and MAP17 protein is released as cargo in exosomes. Exosomal MAP17 transfer to recipient cells increases EMT. An antibody against MAP17 in conditioned media reduces EMT and stemness alterations in recipient cells. MAP17 expression is regulated by demethylation-induced miRNA changes dependent on Notch pathway activation. Exosome isolation, Western blot for MAP17 in exosomes, conditioned media transfer experiments, EMT and stemness assays, antibody blocking experiment, methylation analysis Oncogenesis Medium 33106480
2021 MAP17 expression is hypoxia-dependent in HCC. MAP17 knockdown reduces glucose uptake, lactate release, extracellular acidification rate, and glycolytic gene expression. Ectopic expression of wild-type MAP17, but not a PDZ-binding domain mutant (MAP17-PDZm), increases tumor glycolysis. Mechanistically, MAP17 increases ROS, which activates AKT and HIF1α downstream effectors to enhance the Warburg effect. RNA sequencing after MAP17 knockdown reveals transcriptional changes in ROS metabolic processes. Gain/loss-of-function studies, PDZ-binding domain mutagenesis, Seahorse metabolic assay, ROS measurement, co-immunoprecipitation, immunofluorescence, Western blotting, RNA sequencing, xenograft tumor model Journal of experimental & clinical cancer research High 33832535
2023 FXR1 negatively regulates PDZK1IP1 mRNA by promoting its degradation via direct interaction with the 3'UTR of PDZK1IP1. PDZK1IP1 overexpression inhibits the tumor-promotive phenotype in FXR1-overexpressed esophageal cancer cells. RNA-binding protein immunoprecipitation, mRNA stability assay, 3'UTR interaction analysis, PDZK1IP1 overexpression rescue experiments, xenograft tumor model Biology direct Medium 39511680
2023 Fenofibrate binds tightly to PDZK1IP1 protein (assessed by molecular docking), inhibits its hepatic expression in NIAAA model mice independently of PPARα signaling, and reduces lipid deposition, oxidative stress and inflammation. Molecular docking, Western blot in mouse liver, PPARα gene silencing, NIAAA alcoholic liver disease mouse model Life sciences Low 38042280
2023 MAP17 up-regulation in kidneys of diabetic mice is observed with combined empagliflozin (SGLT2i) and ramipril (RAS blocker) treatment, suggesting MAP17 acts as a scaffolding protein placing SGLT2 and NHE3 together in proximal tubular cells. High-throughput proteomic analysis by TMT-labeled mass spectrometry, Western blot validation in db/db diabetic mouse kidneys Clinical science Low 36524468
2024 miR-455-5p directly suppresses PDZK1IP1 (MAP17) expression by targeting it post-transcriptionally. PDZK1IP1 knockdown promotes migration, metastasis, EMT, and increases TGF-β signaling in OSCC cells. Dual-luciferase reporter assay, qRT-PCR, wound-healing assay, transwell invasion assay, in vivo metastasis assay, nuclear/cytoplasmic fractionation, Western blot Journal of experimental & clinical cancer research Medium 36737832
2026 MAP17 activates the RELA-dependent NF-κB pathway in glioblastoma-initiating cells (GICs), increasing BCL2 expression, which promotes TMZ resistance and tumorigenicity. MAP17 overexpression in GICs increases proliferation, TMZ resistance, and tumorigenicity; knockdown impairs these properties. BCL2 overexpression phenocopies MAP17 overexpression, and BCL2 knockdown impairs TMZ resistance in MAP17-high resistant GICs. Stable overexpression and shRNA knockdown in GICs, gene expression profiling, NF-κB pathway assays, BCL2 overexpression/knockdown, TMZ resistance assays, tumorigenicity assays Cancer science Medium 42043964
2026 In rats with congestive heart failure (CHF), renal sympathetic nerve activity activates the ERK/NF-κB pathway, which increases SGLT2, MAP17, and PDZK1 expression and their translocation to the luminal membrane. Renal denervation mitigates enhanced expression of the SGLT2-MAP17-PDZK1 complex. Norepinephrine directly triggers SGLT2-MAP17-PDZK1 upregulation via ERK/NF-κB in human proximal tubular cells. Coronary artery ligation CHF rat model, bilateral renal denervation, Western blot, immunohistochemistry, norepinephrine treatment of human proximal tubular cells Hypertension Medium 41549941
2025 SGLT2 is enriched within proximal tubular microvilli and partially colocalizes with its co-factor PDZK1IP1 (MAP17) at this subcellular location, as shown using knockout-validated antibodies in rodent and human kidney tissue. Immunohistochemistry with SGLT2-knockout rodent negative controls, subcellular colocalization analysis bioRxiv (preprint)preprint Medium

Source papers

Stage 0 corpus · 64 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
1999 Virulence of a spaP mutant of Streptococcus mutans in a gnotobiotic rat model. Infection and immunity 89 10024561
2016 MAP17 Is a Necessary Activator of Renal Na+/Glucose Cotransporter SGLT2. Journal of the American Society of Nephrology : JASN 81 27288013
1996 Identification and partial characterization of a novel membrane-associated protein (MAP17) up-regulated in human carcinomas and modulating cell replication and tumor growth. The American journal of pathology 63 8701988
2017 Streptococcus mutans SpaP binds to RadD of Fusobacterium nucleatum ssp. polymorphum. Molecular oral microbiology 61 27976528
2017 The Cargo Protein MAP17 (PDZK1IP1) Regulates the Cancer Stem Cell Pool Activating the Notch Pathway by Abducting NUMB. Clinical cancer research : an official journal of the American Association for Cancer Research 58 28153862
2007 MAP17 enhances the malignant behavior of tumor cells through ROS increase. Carcinogenesis 55 17548903
2003 Identification of small PDZK1-associated protein, DD96/MAP17, as a regulator of PDZK1 and plasma high density lipoprotein levels. The Journal of biological chemistry 51 12754212
2003 Interactions of MAP17 with the NaPi-IIa/PDZK1 protein complex in renal proximal tubular cells. American journal of physiology. Renal physiology 51 12837682
2006 Interaction of MAP17 with NHERF3/4 induces translocation of the renal Na/Pi IIa transporter to the trans-Golgi. American journal of physiology. Renal physiology 49 16926447
2007 MAP17 overexpression is a common characteristic of carcinomas. Carcinogenesis 48 17426052
1991 Restriction fragment length polymorphisms and sequence variation within the spaP gene of Streptococcus mutans serotype c isolates. Infection and immunity 39 1673448
2003 Rat kidney MAP17 induces cotransport of Na-mannose and Na-glucose in Xenopus laevis oocytes. American journal of physiology. Renal physiology 38 12812916
2009 MAP17 is associated with the T-helper cell cytokine-induced down-regulation of filaggrin transcription in human keratinocytes. Experimental dermatology 35 19601982
2012 MAP17 and the double-edged sword of ROS. Biochimica et biophysica acta 30 22465409
2007 MAP17 inhibits Myc-induced apoptosis through PI3K/AKT pathway activation. Carcinogenesis 30 17675338
2007 Large scale genetic screen identifies MAP17 as protein bypassing TNF-induced growth arrest. Journal of cellular biochemistry 28 17230460
2019 PDZK1-interacting protein 1 (PDZK1IP1) traps Smad4 protein and suppresses transforming growth factor-β (TGF-β) signaling. The Journal of biological chemistry 26 30718277
2018 MAP17 predicts sensitivity to platinum-based therapy, EGFR inhibitors and the proteasome inhibitor bortezomib in lung adenocarcinoma. Journal of experimental & clinical cancer research : CR 26 30119639
2017 The cargo protein MAP17 (PDZK1IP1) regulates the immune microenvironment. Oncotarget 26 29228712
2000 The membrane-associated protein pKe#192/MAP17 in human keratinocytes. The Journal of investigative dermatology 26 10951271
1994 Detection of Streptococcus mutans by PCR amplification of spaP gene. Journal of medical microbiology 26 7932616
1989 Clinical significance of SP/AP ratio in inner ear diseases. ORL; journal for oto-rhino-laryngology and its related specialties 25 2748143
2019 Diversity of SpaP in genetic and salivary agglutinin mediated adherence among Streptococcus mutans strains. Scientific reports 24 31882747
2016 Efficacy of bortezomib in sarcomas with high levels of MAP17 (PDZK1IP1). Oncotarget 24 27563810
2015 MAP17 (PDZKIP1) Expression Determines Sensitivity to the Proteasomal Inhibitor Bortezomib by Preventing Cytoprotective Autophagy and NFκB Activation in Breast Cancer. Molecular cancer therapeutics 24 25837675
2012 p38α limits the contribution of MAP17 to cancer progression in breast tumors. Oncogene 23 22266858
2023 MiR-455-5p suppresses PDZK1IP1 to promote the motility of oral squamous cell carcinoma and accelerate clinical cancer invasion by regulating partial epithelial-to-mesenchymal transition. Journal of experimental & clinical cancer research : CR 22 36737832
2012 MAP17, a ROS-dependent oncogene. Frontiers in oncology 20 22973555
2021 Hypoxia-dependent expression of MAP17 coordinates the Warburg effect to tumor growth in hepatocellular carcinoma. Journal of experimental & clinical cancer research : CR 19 33832535
2020 Breast tumor cells promotes the horizontal propagation of EMT, stemness, and metastasis by transferring the MAP17 protein between subsets of neoplastic cells. Oncogenesis 19 33106480
2018 MAP17 (PDZK1IP1) and pH2AX are potential predictive biomarkers for rectal cancer treatment efficacy. Oncotarget 16 30250642
2019 Combined Fascin-1 and MAP17 Expression in Breast Cancer Identifies Patients with High Risk for Disease Recurrence. Molecular diagnosis & therapy 15 31273628
2020 Sarcoma stratification by combined pH2AX and MAP17 (PDZK1IP1) levels for a better outcome on doxorubicin plus olaparib treatment. Signal transduction and targeted therapy 14 32963243
2024 FXR1 associates with and degrades PDZK1IP1 and ATOH8 mRNAs and promotes esophageal cancer progression. Biology direct 13 39511680
2018 EGFR-TKI resistance and MAP17 are associated with cancer stem cell like properties. Oncology letters 12 29616128
2020 MAP17 contributes to non-small cell lung cancer progression via suppressing miR-27a-3p expression and p38 signaling pathway. Cancer biology & therapy 11 33280497
2017 Elevation of MAP17 enhances the malignant behavior of cells via the Akt/mTOR pathway in hepatocellular carcinoma. Oncotarget 11 29190940
2010 Role of the cell wall microenvironment in expression of a heterologous SpaP-S1 fusion protein by Streptococcus gordonii. Applied and environmental microbiology 11 21193663
1998 Detection of Streptococcus mutans by PCR amplification of the spaP gene in teeth rendered caries free. Journal of dentistry 10 9699435
2023 Fenofibrate inhibits MOXD1 and PDZK1IP1 expression and improves lipid deposition and inflammation in mice with alcoholic fatty liver. Life sciences 9 38042280
2018 The Na+ -coupled glucose transporter SGLT2 interacts with its accessory unit MAP17 in vitro and their expressions overlap in the renal proximal tubule. FEBS letters 8 30156268
2023 The membrane-associated protein 17 (MAP17) is up-regulated in response to empagliflozin on top of RAS blockade in experimental diabetic nephropathy. Clinical science (London, England : 1979) 7 36524468
2014 Molecular characterization of the dextran-binding lectin B gene dblB of Streptococcus criceti in Streptococcus mutans strain GS-5 with mutations in both gbpC and spaP genes. Genes & genetic systems 7 25224970
2011 A mechanism for extremely weak SpaP-expression in Streptococcus mutans strain Z1. Journal of oral microbiology 7 21541094
2011 spaP gene of Streptococcus mutans in dental plaque and its relationship with early childhood caries. European journal of paediatric dentistry 7 22185244
2008 The SP-AP compound wave in patients with auditory neuropathy. Acta oto-laryngologica 7 18612852
2024 TAPSE/SPAP ratio stratifies mortality risk in mild-to-moderate idiopathic pulmonary fibrosis. The international journal of tuberculosis and lung disease : the official journal of the International Union against Tuberculosis and Lung Disease 6 38563341
2024 Exosomal LINC00853 promotes progression of gastric cancer via the MAP17/PDZK1/AKT signaling pathway. Non-coding RNA research 6 38586313
2022 PDZK1IP1 gene promotes proliferation, migration, and invasion in papillary thyroid carcinoma. Pathology, research and practice 6 36057192
2023 LINC00853 contributes to tumor stemness of gastric cancer through FOXP3-mediated transcription of PDZK1IP1. Biological procedures online 5 37403034
2016 Overexpression of PDZK1IP1, EEF1A2 and RPL41 genes in intrahepatic cholangiocarcinoma. Molecular medicine reports 4 27082702
2025 Glioblastoma Stem Cells: MAP17 as a Novel Predictive Biomarker and Therapeutic Target Associated with Quiescence and Immune Evasion. Discovery medicine 2 39851232
2025 Efficacy of NAMPT Inhibitors in Pancreatic Cancer After Stratification by MAP17 (PDZK1IP1) Levels. Cancers 2 40805270
2022 PDZK1-interacting protein 1(PDZK1IP1) promotes subcutaneous preadipocyte proliferation in goats. Animal biotechnology 2 36244042
2025 MAP17 contributes to the tumorigenesis of papillary thyroid carcinoma by activating the AKT signaling pathway. Archives of endocrinology and metabolism 1 40062974
2009 [Construction and expression of spap/A eukaryotic expression plasmid of Streptococcus mutans in mammalian cells]. Shanghai kou qiang yi xue = Shanghai journal of stomatology 1 19290430
2026 Neural Upregulation of SGLT2-MAP17-PDZK1 Complex in Kidneys of Rats With Heart Failure. Hypertension (Dallas, Tex. : 1979) 0 41549941
2026 Pan-cancer analysis of PDZK1IP1 reveals its role in tumorigenesis and tumor immunity: focused validation in thyroid carcinoma. Hereditas 0 41761346
2026 MAP17 Enhances Chemoresistance and Tumorigenicity of Glioblastoma-Initiating Cells via the Canonical NF-кB Pathway. Cancer science 0 42043964
2026 The miR-4512/PDZK1IP1 axis in hepatocellular carcinoma: clinical significance, diagnostic value, and functional validation. BMC medical genomics 0 42260473
2025 MAP17 is a Novel NASH Progression Biomarker Associated with Macrophage Infiltration, Immunotherapy Response, and Oxidative Stress. Journal of inflammation research 0 39839187
2025 MAP17 as a Mediator of HGF-induced Proliferation and Invasion in Gastric Cancer. Anticancer research 0 40295039
2025 SPAP: Soluble Human Plasma Proteoform Analysis via Acetonitrile Precipitation and Top-Down Mass Spectrometry. Journal of the American Society for Mass Spectrometry 0 41412792
2024 Cell penetrable peptide nucleic acids targeting PDZK1IP1 with anti-inflammatory potential in human keratinocytes. Bioorganic & medicinal chemistry letters 0 39557312

Missed literature

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