Affinage

PTPRZ1

Receptor-type tyrosine-protein phosphatase zeta · UniProt P23471

Length
2315 aa
Mass
254.6 kDa
Annotated
2026-04-28
100 papers in source corpus 35 papers cited in narrative 35 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

PTPRZ1 encodes a receptor-type protein tyrosine phosphatase that functions as a major chondroitin sulfate proteoglycan of the central nervous system, regulating neural cell adhesion, neurite outgrowth, oligodendrocyte precursor cell (OPC) differentiation, perineuronal net assembly, and dopaminergic signaling. Its extracellular domain (shed as phosphacan) binds pleiotrophin, midkine, tenascins (C and R), neural cell adhesion molecules (N-CAM, L1/Ng-CAM, TAG-1/contactin-1), and FGF-2 through distinct glycan- and core-protein-mediated interactions, with chondroitin sulfate chains maintaining the receptor in a monomeric active state via electrostatic repulsion until pleiotrophin binding neutralizes this repulsion, induces receptor clustering/inactivation, and activates the AFAP1L2–PI3K–AKT pathway to promote OPC differentiation and remyelination (PMID:27445335, PMID:30667096, PMID:7528221, PMID:8702927). The intracellular phosphatase domain dephosphorylates substrates including GIT1 at Tyr-554 and AFAP1L2 to regulate cell motility and myelination, while PTPRZ1 interactions with tenascin-R are structurally required for perineuronal net lattice formation (PMID:25742295, PMID:31822561, PMID:37356715). Oncogenic PTPRZ1-MET fusion transcripts arising from chromosomal translocation in glioblastoma activate MET kinase in a ligand-independent, coiled-coil-mediated manner, driving glioma stem cell maintenance, migration, and immunosuppressive macrophage polarization (PMID:25135958, PMID:33645009, PMID:38685521).

Mechanistic history

Synthesis pass · year-by-year structured walk · 17 steps
  1. 1994 High

    Establishing PTPRZ1's molecular identity: phosphacan was shown to be the secreted extracellular domain splice variant of receptor-type phosphatase RPTPζ/β, with an N-terminal carbonic anhydrase-like domain, resolving whether the abundant brain proteoglycan was related to a transmembrane signaling receptor.

    Evidence cDNA cloning and peptide sequencing of phosphacan showing 76% identity to RPTPζ/β extracellular domain

    PMID:7511813

    Open questions at the time
    • Full-length transmembrane isoform function not yet tested
    • Relationship between secreted and transmembrane isoforms in vivo unclear
  2. 1994 High

    Defining the extracellular ligand repertoire: phosphacan was found to bind N-CAM, Ng-CAM/L1, and tenascin-C with high affinity via its core glycoprotein (not CS chains), and to inhibit neurite outgrowth on Ng-CAM substrates, establishing PTPRZ1 as a multivalent neural adhesion regulator.

    Evidence Radioligand binding, Scatchard analysis, chondroitinase treatment, neurite outgrowth assays on coated substrates

    PMID:7512960 PMID:7528221

    Open questions at the time
    • Signaling consequences of these interactions on intracellular phosphatase activity unknown
    • In vivo relevance of individual ligand interactions not tested
  3. 1996 High

    Identifying pleiotrophin as a key regulatory ligand: pleiotrophin/HB-GAM bound phosphacan with sub-nanomolar affinity predominantly through chondroitin sulfate chains, and antibody blockade showed this interaction was required for pleiotrophin-induced neurite outgrowth, establishing the ligand–receptor pair central to PTPRZ1 biology.

    Evidence Affinity chromatography, Scatchard analysis, chondroitinase digestion, heparin competition, neurite outgrowth antibody blockade in cortical neurons

    PMID:8702927

    Open questions at the time
    • Whether pleiotrophin binding regulates phosphatase activity was unknown
    • In vivo requirement not yet tested in knockout
  4. 1996 High

    Resolving glycan versus core protein contributions to distinct ligands: TAG-1/contactin binding was ~70% CS-mediated while N-CAM/L1 binding was core-protein-mediated, and asparagine-linked complex oligosaccharides at specific sites (Asn-232, Asn-381) were identified as the core determinants for CAM and tenascin interactions.

    Evidence Chondroitinase treatment, N-glycosidase F/Endo H digestion, tryptic fragment binding assays

    PMID:7559574 PMID:8663515

    Open questions at the time
    • Structural basis of selective glycan recognition not resolved
    • Functional consequence of glycan heterogeneity on signaling not addressed
  5. 1998 High

    Expanding the ligand network to include tenascin-R, amphoterin, and FGF-2: phosphacan core protein bound tenascin-R and FGF-2 with nanomolar affinity, with FGF-2 binding potentiating its mitogenic activity comparably to heparin, broadening PTPRZ1's role beyond adhesion to growth factor co-receptor function.

    Evidence Radioligand binding with chondroitinase treatment, Scatchard analysis, thymidine incorporation mitogenesis assay

    PMID:9507007 PMID:9705269

    Open questions at the time
    • Whether FGF-2 co-receptor activity operates in CNS cells specifically was not tested
    • Signaling downstream of PTPRZ1-FGF-2 not characterized
  6. 2003 High

    Demonstrating that CS sulfation pattern developmentally tunes ligand affinity: adult brain phosphacan carrying D-unit disaccharides bound pleiotrophin ~5-fold more tightly than postnatal phosphacan lacking D-units, providing a glycan-code mechanism for age-dependent signaling regulation.

    Evidence Surface plasmon resonance with chondroitinase digestion and immunochemical CS disaccharide profiling

    PMID:12840014

    Open questions at the time
    • Enzymes responsible for D-unit synthesis on PTPRZ1 not identified
    • Functional consequence of age-dependent affinity shift on OPC biology not tested
  7. 2010 High

    Structural determination of the carbonic anhydrase-like domain revealed the molecular basis of CNTN1-selective binding: crystal structures showed direct interaction with Ig repeats 2–3 of CNTN1 but not other contactins, resolving how PTPRZ1 achieves ligand specificity.

    Evidence X-ray crystallography of PTPRZ1 CA domain, direct binding assays with contactin family members

    PMID:20133774 PMID:21969550

    Open questions at the time
    • Whether CS chains modulate CNTN1 interaction in vivo was unclear
    • Full ectodomain structure not resolved
  8. 2011 High

    Connecting PTPRZ1–CNTN1 binding to oligodendrocyte biology: PTPRZ1 binds CNTN1 on OPC surfaces and this complex inhibits OPC proliferation while promoting differentiation, with Ptprz-deficient mice showing altered glial populations.

    Evidence Co-crystal structure, surface binding assays, Ptprz−/− mouse glial cell analysis

    PMID:21969550

    Open questions at the time
    • Intracellular phosphatase substrates mediating OPC differentiation unknown at this point
    • Whether CNTN1 interaction affects phosphatase activity not tested
  9. 2015 High

    Identifying the first specific intracellular substrate: PTPRZ dephosphorylates GIT1 at Tyr-554, regulating its association with paxillin/Hic-5 and cell motility, validated by elevated GIT1 phosphorylation in Ptprz-knockout mouse brain.

    Evidence In vitro phosphatase assay, Tyr-554 mutagenesis, co-immunoprecipitation, Ptprz−/− mouse biochemistry, wound healing and Boyden chamber assays

    PMID:25742295

    Open questions at the time
    • Whether GIT1 dephosphorylation mediates PTPRZ1's neural functions not tested
    • Full substrate repertoire unknown
  10. 2016 High

    Elucidating the CS-mediated autoinhibition mechanism: chondroitin sulfate chains maintain PTPRZ in a monomeric active state through electrostatic repulsion; pleiotrophin neutralizes this repulsion to induce clustering and phosphatase inactivation, thereby promoting OPC differentiation — a unified model linking ligand binding to phosphatase regulation.

    Evidence Receptor distribution imaging, chondroitinase treatment of OPCs, pleiotrophin stimulation, OPC differentiation assay, Ptn−/− mouse

    PMID:27445335

    Open questions at the time
    • Direct biophysical measurement of clustering (e.g., FRET, single-molecule) not provided
    • Whether other ligands similarly cluster the receptor unknown
  11. 2019 High

    Identifying the downstream signaling axis for OPC differentiation: PTPRZ dephosphorylates AFAP1L2, and pleiotrophin-induced receptor inactivation activates the AFAP1L2–PI3K–AKT–mTOR pathway; catalytically inactive PTPRZ knock-in mice show accelerated OPC differentiation and remyelination after cuprizone demyelination.

    Evidence In vitro phosphatase assay, PTN stimulation in OL1 cells, PTPRZ catalytic-dead knock-in mouse, cuprizone demyelination model

    PMID:30667096

    Open questions at the time
    • Whether AFAP1L2 is the sole mediator or acts with other substrates not resolved
    • Therapeutic potential of PTPRZ inhibition for remyelination not tested in disease models beyond cuprizone
  12. 2019 High

    Establishing PTPRZ1's structural role in perineuronal nets: Ptprz1-knockout mice lose the reticular PNN lattice phenocopying tenascin-R loss, demonstrating that PTPRZ1 anchors PNN components to neuronal surfaces via one of two distinct mechanisms.

    Evidence Ptprz1−/− mouse immunostaining of PNN components, biochemical fractionation, neuronal cultures

    PMID:31822561

    Open questions at the time
    • Molecular details of how PTPRZ1 organizes PNN lattice versus punctate structures unclear
    • Functional consequences for synaptic plasticity not directly measured
  13. 2019 High

    Dissecting phosphatase-dependent versus ectodomain-dependent behavioral functions: using domain-specific knock-in mice, phosphatase activity was shown to be required for dopaminergic regulation (methamphetamine-evoked DA release), while the extracellular domain mediates behavioral responses to novelty and aversive memory.

    Evidence Ptprz-KO, catalytic-dead, and ΔD2 knock-in mice; behavioral testing; nucleus accumbens microdialysis

    PMID:31194769

    Open questions at the time
    • Specific phosphatase substrates mediating dopaminergic regulation not identified
    • Neural circuit basis of behavioral phenotypes not mapped
  14. 2014 High

    Discovery of oncogenic PTPRZ1-MET fusion: recurrent PTPRZ1-MET translocation-derived fusions were identified in secondary glioblastomas and shown to enhance glioma cell migration and invasion upon expression.

    Evidence RNA-seq and genomic analysis of glioblastoma cohorts, RT-PCR validation, Sanger sequencing, migration/invasion assay in U87MG cells

    PMID:25135958

    Open questions at the time
    • Mechanism of constitutive MET activation by fusion not resolved
    • In vivo tumorigenicity of fusion not demonstrated
  15. 2021 Medium

    Mechanism of fusion-driven MET activation clarified: a coiled-coil motif from the PTPRZ1 portion of ZM fusion was proposed to mediate ligand-independent dimerization and constitutive MET kinase activation.

    Evidence 3D structural prediction, coiled-coil analysis, phospho-MET in ZM-expressing cells and clinical specimens

    PMID:33645009

    Open questions at the time
    • Coiled-coil model based on prediction, not experimentally validated structure
    • Mutagenesis of coiled-coil not performed
  16. 2023 High

    Structural basis for PNN assembly resolved: the PTPRZ1 ectodomain–tenascin-R complex structure was determined, and interface mutations disrupted PNN formation in neuronal cultures, directly linking structural interactions to extracellular matrix organization.

    Evidence Structural determination of PTPRZ1-TNR complex, site-directed mutagenesis, Ptprz1−/− neuronal culture PNN analysis

    PMID:37356715

    Open questions at the time
    • In vivo validation of interface mutations not performed
    • Whether tenascin-C binding uses the same or different interface not resolved
  17. 2024 Medium

    ZM fusion drives immunosuppressive tumor microenvironment: PTPRZ1-MET fusion in GSCs activates MET–STAT3–ISG20 signaling, with secreted ISG20 recruiting macrophages and polarizing them to immunosuppressive M2 phenotype.

    Evidence RNA-seq of sGBM tissues, ISG20 knockdown/overexpression, macrophage polarization assays, conditioned medium experiments

    PMID:38685521

    Open questions at the time
    • In vivo immune phenotype of ZM-positive tumors not validated in immunocompetent models
    • Whether ISG20 secretion is the dominant immunosuppressive mechanism unclear

Open questions

Synthesis pass · forward-looking unresolved questions
  • Key unresolved questions include the full substrate repertoire of PTPRZ1 phosphatase in neural and non-neural contexts, the structural basis of CS-mediated receptor clustering upon pleiotrophin binding, whether pharmacological PTPRZ1 inhibition can promote remyelination in human demyelinating disease, and the therapeutic vulnerability of PTPRZ1-MET fusion-driven gliomas to targeted MET inhibition in clinical settings.
  • Complete phosphatase substrate repertoire not systematically identified
  • No high-resolution structure of full-length transmembrane PTPRZ1
  • Clinical translation of PTPRZ1 inhibitors for remyelination or glioma therapy untested

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140096 catalytic activity, acting on a protein 4 GO:0098631 cell adhesion mediator activity 3 GO:0098772 molecular function regulator activity 2
Localization
GO:0005576 extracellular region 5 GO:0005886 plasma membrane 3 GO:0031012 extracellular matrix 2
Pathway
R-HSA-1643685 Disease 4 R-HSA-162582 Signal Transduction 3 R-HSA-1266738 Developmental Biology 2 R-HSA-1474244 Extracellular matrix organization 2 R-HSA-112316 Neuronal System 1
Partners
AFAP1L2CNTN1GIT1L1CAMNCAM1PTNTNCTNR

Evidence

Reading pass · 35 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1994 Phosphacan (the extracellular domain of PTPRZ1/RPTPζ/β) binds with high affinity (Kd ~0.1 nM) to neural cell adhesion molecules N-CAM and Ng-CAM/L1 via its core glycoprotein (not chondroitin sulfate chains), and inhibits neuronal adhesion and neurite outgrowth when neurons are incubated on dishes co-coated with phosphacan and Ng-CAM. Radioligand binding assay (125I-phosphacan), Scatchard analysis, chondroitinase treatment, antibody inhibition, neurite outgrowth assay The Journal of cell biology High 7528221
1994 Phosphacan represents an mRNA splicing variant encoding the entire extracellular portion of the transmembrane receptor-type protein tyrosine phosphatase RPTP zeta/beta (PTPRZ1), established by cDNA cloning and peptide sequencing showing 76% identity to human RPTP zeta/beta extracellular domain; the N-terminal domain is homologous to carbonic anhydrases. cDNA cloning, peptide sequencing (CNBr, tryptic, endoproteinase Lys-C fragments), RNA analysis with domain-specific probes Proceedings of the National Academy of Sciences of the United States of America High 7511813
1994 Phosphacan (PTPRZ1 extracellular domain) binds specifically and with high affinity to tenascin-C via the core glycoprotein (not chondroitin sulfate chains), as demonstrated by bead co-aggregation and solid-phase radioligand binding, and inhibits C6 glioma cell adhesion to tenascin. Fluorescent microbead co-aggregation, solid-phase radioligand binding, Scatchard analysis, chondroitinase treatment, Fab' antibody inhibition, cell adhesion assay The Journal of biological chemistry High 7512960
1995 The interactions of phosphacan/PTPRZ1 with neural cell adhesion molecules (Ng-CAM/L1, N-CAM) and tenascin are mediated by asparagine-linked complex-type oligosaccharides located in the carbonic anhydrase-like and fibronectin type III-like domains (at Asn-232 and Asn-381), rather than by the proteoglycan chains. Tryptic digest radioligand binding, peptide N-glycosidase F treatment under non-denaturing conditions, endo-β-N-acetylglucosaminidase H treatment, size analysis of glycopeptides The Journal of biological chemistry High 7559574
1996 6B4 proteoglycan/phosphacan (PTPRZ1 extracellular domain) binds pleiotrophin/HB-GAM with high affinity (Kd = 0.25 nM high-affinity site, 3 nM low-affinity site); chondroitin sulfate chains mediate differential binding affinities, and heparin potently inhibits binding (IC50 = 3.5 ng/ml). Anti-6B4 antibody added to cortical neuron cultures suppressed pleiotrophin-induced neurite outgrowth, indicating the interaction is required for pleiotrophin action. Affinity chromatography purification, N-terminal amino acid sequencing, Scatchard analysis, chondroitinase ABC digestion, heparin competition assay, neurite outgrowth assay with antibody blockade The Journal of biological chemistry High 8702927
1996 Phosphacan/PTPRZ1 adsorbed as substrate exerts repulsive effects on cortical and thalamic neurons, preventing adhesion, but when sparsely seeded on poly-L-lysine co-coated with phosphacan it promotes neurite outgrowth and dendrite development of cortical neurons (not thalamic neurons) through a protein moiety (chondroitinase- and keratanase-resistant activity); this effect correlates with transient tyrosine phosphorylation of an 85 kDa protein in cortical neurons. Stripe/pattern substrate assay, chondroitinase/keratanase treatment, antibody neutralization, Western blot for tyrosine phosphorylation Development (Cambridge, England) High 8625816
1996 Phosphacan/PTPRZ1 binds TAG-1/axonin-1 with very high affinity (Kd ~0.04 nM); approximately 70% of binding is mediated by chondroitin sulfate chains (opposite to binding of Ng-CAM/L1 and N-CAM where core protein dominates); N-deglycosylation does not affect binding to TAG-1. Radioligand binding assay, chondroitinase treatment, N-deglycosylation, Scatchard analysis The Journal of biological chemistry High 8663515
1997 Phosphacan/PTPRZ1 binds to the fibrinogen-like globe of tenascin-C (Kd ~12 nM for this single domain, nearly same as native tenascin-C); binding is calcium-dependent and mediated by the proteoglycan core protein rather than glycosaminoglycan chains; rotary shadowing EM shows phosphacan apposed to the fibrinogen globe. Recombinant tenascin-C deletion variants, radioligand binding, inhibition studies, calcium chelation, chondroitinase treatment, rotary shadowing electron microscopy The Journal of biological chemistry High 9182584
1998 Phosphacan/PTPRZ1 binds tenascin-R with high affinity (Kd 2–7 nM) via its core glycoprotein, and also binds amphoterin and HB-GAM (Kd 0.3–8 nM) predominantly through its chondroitin sulfate chains (>80% of binding); amphoterin increases phosphacan binding to contactin 5-fold. Radioligand binding assay, chondroitinase treatment, calcium chelation, Scatchard analysis The Journal of biological chemistry High 9507007
1998 Phosphacan/PTPRZ1 core protein (not chondroitin sulfate chains) binds fibroblast growth factor-2 (FGF-2) with high affinity (Kd ~6 nM) and potentiates FGF-2 mitogenic activity on NIH/3T3 cells by 75–90%, comparable to heparin. Radioligand binding assay, chondroitinase treatment, Scatchard analysis, [3H]thymidine incorporation mitogenic assay The Journal of biological chemistry High 9705269
2003 The chondroitin sulfate heterogeneity on phosphacan/PTPRZ1 regulates binding affinity for pleiotrophin: adult brain phosphacan containing the D unit (GlcA(2S)-GalNAc(6S)) binds pleiotrophin ~5-fold more strongly (KD = 0.14 nM) than postnatal phosphacan lacking D units (KD ~1.5 nM); chondroitinase treatment abolishes this difference. Surface plasmon resonance biosensor, chondroitinase ABC digestion, immunochemical characterization of CS disaccharide composition The Journal of biological chemistry High 12840014
2003 A novel truncated isoform of PTPRZ1 (phosphacan short isoform, PSI), corresponding to N-terminal carbonic anhydrase- and fibronectin type III-like domains, is expressed in the CNS and can interact with Ig-CAMs F3/contactin and L1, and promotes neurite outgrowth of cortical neurons as a coated substrate; PSI is not a proteoglycan (lacks GAG chains) but carries HNK-1 oligosaccharides. cDNA library screening, Northern blot, Western blot with N-terminal sequencing, co-immunoprecipitation/binding assays with F3/contactin and L1, neurite outgrowth assay The Journal of biological chemistry High 12700241
2007 PTPRZ1 (RPTPβ/ζ) forms a functional complex with ERBB4 bridged by MAGI scaffolding proteins: MAGI interacts with both ERBB4 and RPTPβ; ERBB4 expression leads to tyrosine phosphorylation of MAGI proteins that is enhanced by neuregulin, and RPTPβ shows spatial and functional association with ERBB4/MAGI in cultured cells. Yeast two-hybrid, co-immunoprecipitation in mammalian cells, tyrosine phosphorylation assay, neuregulin stimulation Molecular psychiatry Medium 17579610
2007 PTPRZ1 amplification and overexpression in renal cell carcinoma activates the beta-catenin pathway: PTPRZ1 knockdown (siRNA) in RCC cell lines decreases nuclear beta-catenin and suppresses expression of target genes (cyclin D1, c-myc, c-jun, fra-1, CD44) and cellular proliferation, without involvement of Wnt signaling. Gene expression microarray, CGH array, siRNA knockdown, Western blot for nuclear beta-catenin, gene expression analysis The American journal of pathology Medium 18055543
2008 The transcription factor Egr-1 directly regulates PTPRZ1 (phosphacan) expression in astrocytes after ischemic injury: Egr-1 binds to a site within the phosphacan promoter and transactivates its expression; Egr-1-deficient mice show reduced phosphacan RNA and protein after experimental stroke. Gain/loss-of-function in primary astrocytes, promoter-reporter assay, chromatin immunoprecipitation (ChIP), knockout mouse model, RT-PCR, Western blot The American journal of pathology High 18556777
2010 Crystal structures of the carbonic anhydrase-like domain of PTPRZ show it interacts directly with the second and third Ig repeats of CNTN1; PTPRZ binds specifically CNTN1 (but not CNTN3/4/5/6), establishing binding specificity determined by the carbonic anhydrase-like domain. X-ray crystallography, direct binding assays Proceedings of the National Academy of Sciences of the United States of America High 20133774
2011 PTPRZ binds specifically to CNTN1 expressed at the surface of oligodendrocyte precursor cells (OPCs); this PTPRZ/CNTN1 complex inhibits OPC proliferation and promotes their differentiation into mature oligodendrocytes, as shown in PTPRZ-deficient mice. Cocrystal structure of PTPRZ carbonic anhydrase-like domain with CNTN1 Ig repeats, surface binding assays, glial cell population analysis in Ptprz-/- vs. wild-type mice Proceedings of the National Academy of Sciences of the United States of America High 21969550
2012 RPTPζ/phosphacan (PTPRZ1) undergoes aberrant O-mannosyl glycosylation in the brain: it is a major substrate for POMGnT1-mediated O-mannosylation; in POMGnT1-knockout mice modeling muscle-eye-brain disease, RPTPζ/phosphacan shifts to lower molecular weight and loses HNK-1 epitopes. Western blot, immunoprecipitation, glycan epitope analysis in POMGnT1 knockout mouse brain Neuroscience High 22728091
2013 Phosphacan/PTPRZ1 is identified as the major carrier of O-mannose-linked HNK-1 glycan in developing mouse brain; GlcAT-P specifically synthesizes O-linked HNK-1 onto phosphacan; the 6B4 monoclonal antibody epitope is O-mannose-linked HNK-1 on phosphacan, as shown in GlcAT-P-deficient mice. Mass spectrometric glycan analysis, GlcAT-P knockout mice, co-expression in cultured cells, immunoblot Glycobiology High 24352591
2014 PTPRZ1-MET (ZM) fusion transcripts arise from chromosomal translocation involving introns 3 or 8 of PTPRZ1 and intron 1 of MET in secondary glioblastomas; exogenous expression of ZM fusion in U87MG cells enhances cell migration and invasion. RNA-seq, RT-PCR, Sanger sequencing, genomic translocation analysis, cell migration/invasion assay after ZM overexpression Genome research High 25135958
2015 ZM fusion proteins preserve wild-type MET processing and dimerization properties, and enhance MET phosphorylation in both HGF-dependent and HGF-independent manners, with increased MET mRNA expression induced by fusion with PTPRZ1 promoter. Western blot for phospho-MET, HGF stimulation assays, dimerization analysis, mRNA expression analysis in patient samples and transfected cells FEBS letters Medium 25935522
2015 PTPRZ specifically dephosphorylates GIT1 at Tyr-554 in vitro and in HEK293T cells; this dephosphorylation promotes GIT1 association with paxillin and Hic-5; in Ptprz-deficient mice, GIT1 Tyr-554 phosphorylation is higher and paxillin binding is lower; cyclic phosphorylation-dephosphorylation at GIT1 Tyr-554 is critical for cell motility. In vitro phosphatase assay, site-directed mutagenesis of GIT1 Tyr-554, co-immunoprecipitation, Ptprz-/- mouse brain biochemistry, random motility/wound healing/Boyden chamber assays with GIT1 mutants PloS one High 25742295
2016 The chondroitin sulfate (CS) moiety of PTPRZ-A maintains it in a monomeric active (dephosphorylated-substrate) state by electrostatic repulsion between CS chains, preventing spontaneous clustering; pleiotrophin (PTN) binding induces receptor clustering/inactivation by neutralizing CS repulsion, thereby promoting OPC differentiation. CS removal by chondroitinase ABC similarly inactivates PTPRZ and promotes OPC differentiation. Surface receptor localization imaging (punctate vs. diffuse distribution), chondroitinase ABC treatment of OPCs, PTN ligand application, oligodendrocyte differentiation assay, Ptn-deficient mouse analysis The Journal of biological chemistry High 27445335
2016 Crystal structure of the PTPRZ catalytic domain was determined; SCB4380 binds stoichiometrically to the catalytic pocket and inhibits PTPRZ phosphatase activity; site-directed mutagenesis validated the docking-predicted binding mode; intracellular delivery of SCB4380 in C6 glioblastoma cells inhibits PTPRZ activity, suppresses migration and proliferation in vitro, and reduces tumor growth in vivo. X-ray crystallography, biochemical phosphatase assay, mass spectrometry, molecular docking, site-directed mutagenesis, liposome drug delivery, in vitro migration/proliferation assay, rat allograft tumor model Scientific reports High 26857455
2017 TAMs secrete pleiotrophin (PTN) to activate PTPRZ1 signaling in glioma stem cells (GSCs); disrupting PTPRZ1 (shRNA or anti-PTPRZ1 antibody) abrogates GSC maintenance and tumorigenicity; silencing PTN in M2-like macrophages reduces their pro-tumorigenic activity; PTPRZ1 is preferentially expressed on GSCs. GSC co-implantation with M2 macrophages, shRNA knockdown, antibody blockade, neurosphere formation assay, in vivo tumor growth assay Nature communications High 28569747
2017 PTPRZ knockdown in C6 and U251 glioblastoma sphere-forming cells alters expression of stem cell transcription factors SOX2, OLIG2, and POU3F2 and decreases sphere-forming ability; the small-molecule allosteric inhibitor NAZ2329 reduces SOX2 expression and sphere-forming ability, and slows tumor growth in xenograft model when combined with temozolomide. Stable PTPRZ shRNA knockdown, small-molecule inhibitor (NAZ2329) treatment, sphere-forming assay, Western blot for transcription factors, C6 xenograft mouse model Scientific reports High 28717188
2019 PTPRZ dephosphorylates AFAP1L2 at tyrosine residues in vitro and in HEK293T cells; PTN-PTPRZ signaling enhances phosphorylation of AFAP1L2, AKT, and mTOR in OPC-like cells to activate the PI3K-AKT pathway for OPC differentiation; catalytically inactive PTPRZ knock-in mice (CS mutation) show higher AFAP1L2/AKT/mTOR phosphorylation and accelerated OPC differentiation and remyelination. In vitro phosphatase assay with AFAP1L2 substrate, HEK293T cell transfection, PTN stimulation of OL1 cells, PTPRZ catalytic dead knock-in mouse (Cys-to-Ser), cuprizone demyelination model, Western blot for phosphoproteins Glia High 30667096
2019 RPTPζ/PTPRZ1 is required for perineuronal net (PNN) reticulated structure: in Ptprz1-/- mice, PNNs lose their reticular lattice and form puncta, phenocopying tenascin-R knockout; RPTPζ mediates one of two distinct modes of PNN component anchoring to the neuronal surface (the other requiring hyaluronan). Ptprz1-/- mouse analysis, immunostaining of PNN components, biochemical fractionation, neuronal culture experiments The Journal of biological chemistry High 31822561
2019 Ptprz-knockout mice lacking all three isoforms show increased exploratory activity, deficits in spatial and contextual learning, and reduced responses to methamphetamine including reduced methamphetamine-evoked dopamine release in nucleus accumbens; phosphatase activity of PTPRZ receptor isoforms (CS mutant mice) is specifically required for dopaminergic regulation, while the extracellular region (including secretory isoform) mediates behavioral responses to novelty and aversive memory. Behavioral testing (open field, inhibitory avoidance), Ptprz-KO and knock-in mouse lines (CS catalytic dead, ΔD2 domain deletion), microdialysis for dopamine measurement PloS one High 31194769
2019 GlcNAc6ST3 (encoded by Chst5, expressed in oligodendrocytes in adult brain) is a major keratan sulfate sulfotransferase for PTPRZ1; a KS-modified isoform of PTPRZ1 is a major R-10G-reactive KS proteoglycan associated with perineuronal nets in adult brain. Immunostaining with R-10G anti-KS antibody, Chst5-specific in situ hybridization, mass spectrometry-based proteoglycan identification, adult visual cortex analysis Scientific reports Medium 30867513
2021 ZM fusion protein activates MET kinase in a ligand-independent manner, attributed to a coiled-coil motif from the PTPRZ1 fusion partner that promotes dimerization/activation of the MET extracellular domain; ZM-positive clinical specimens show hyperactivation of MET signaling. 3D structural prediction, coiled-coil motif analysis, cell line experiments with ZM expression, phospho-MET analysis in patient specimens CNS neuroscience & therapeutics Medium 33645009
2023 RPTPζ/PTPRZ1 ectodomain forms direct protein-protein complexes with tenascin-R and tenascin-C; structural basis for these interactions was determined; mutations at the RPTPζ-TNR interface impair PNN formation in dissociated neuronal cultures; TNR is absent from net structures in Ptprz1-/- neuronal cultures. Structural determination of PTPRZ1 ectodomain-TNR complex, binding assays, Ptprz1-/- neuronal cultures, site-directed mutagenesis at interface residues, immunostaining of PNN components The Journal of biological chemistry High 37356715
2023 PTPRZ1 deletion or pharmacological inhibition of its phosphatase activity in endothelial cells activates c-Met and Akt kinase, increasing angiogenesis; PTPRZ1 mediates c-Met activation by VEGFA165 and pleiotrophin in endothelial cells, and this effect is abolished by the c-Met inhibitor crizotinib; Ptprz1-/- mice show enhanced LUAD growth and lung angiogenesis. Ptprz1-/- mouse model, lung microvascular endothelial cell isolation, PTPRZ1 pharmacological inhibitor, Western blot for c-Met/Akt phosphorylation, in vitro angiogenesis assay, LUAD urethane model, crizotinib rescue experiment International journal of cancer High 37260355
2024 PTPRZ1-MET (ZM) fusion in GSCs activates MET-STAT3-ISG20 axis; ZM-positive GSCs secrete ISG20 extracellularly to recruit macrophages and drive their polarization toward an immunosuppressive M2-like phenotype, thereby promoting tumor progression. RNA-seq of sGBM patient tissues, GSC sphere cultures with ZM, ISG20 knockdown/overexpression, macrophage polarization assays, conditioned medium experiments Cellular signalling Medium 38685521
2025 Curcumin directly interacts with PTPRZ1 to maintain its enzymatic phosphatase activity, which in turn regulates phosphorylation of the m6A-reader YTHDF2; this PTPRZ1-YTHDF2 axis modulates expression of inflammatory genes to reduce microglial inflammatory responses. Binding assay of curcumin with PTPRZ1, phosphatase activity assay, phosphorylation analysis of YTHDF2, gene expression analysis, microglial inflammatory assay Advanced science (Weinheim, Baden-Wurttemberg, Germany) Medium 39921492

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2003 The chondroitin sulfate proteoglycans neurocan, brevican, phosphacan, and versican are differentially regulated following spinal cord injury. Experimental neurology 422 12895450
1999 The chondroitin sulfate proteoglycans neurocan and phosphacan are expressed by reactive astrocytes in the chronic CNS glial scar. The Journal of neuroscience : the official journal of the Society for Neuroscience 375 10594061
2014 RNA-seq of 272 gliomas revealed a novel, recurrent PTPRZ1-MET fusion transcript in secondary glioblastomas. Genome research 329 25135958
1994 Interactions of the chondroitin sulfate proteoglycan phosphacan, the extracellular domain of a receptor-type protein tyrosine phosphatase, with neurons, glia, and neural cell adhesion molecules. The Journal of cell biology 299 7528221
1994 Phosphacan, a chondroitin sulfate proteoglycan of brain that interacts with neurons and neural cell-adhesion molecules, is an extracellular variant of a receptor-type protein tyrosine phosphatase. Proceedings of the National Academy of Sciences of the United States of America 285 7511813
2017 Tumour-associated macrophages secrete pleiotrophin to promote PTPRZ1 signalling in glioblastoma stem cells for tumour growth. Nature communications 281 28569747
1996 6B4 proteoglycan/phosphacan, an extracellular variant of receptor-like protein-tyrosine phosphatase zeta/RPTPbeta, binds pleiotrophin/heparin-binding growth-associated molecule (HB-GAM). The Journal of biological chemistry 262 8702927
1994 Interactions with tenascin and differential effects on cell adhesion of neurocan and phosphacan, two major chondroitin sulfate proteoglycans of nervous tissue. The Journal of biological chemistry 231 7512960
1996 TAG-1/axonin-1 is a high-affinity ligand of neurocan, phosphacan/protein-tyrosine phosphatase-zeta/beta, and N-CAM. The Journal of biological chemistry 182 8663515
1998 High affinity binding and overlapping localization of neurocan and phosphacan/protein-tyrosine phosphatase-zeta/beta with tenascin-R, amphoterin, and the heparin-binding growth-associated molecule. The Journal of biological chemistry 168 9507007
1999 DSD-1-proteoglycan is the mouse homolog of phosphacan and displays opposing effects on neurite outgrowth dependent on neuronal lineage. The Journal of neuroscience : the official journal of the Society for Neuroscience 159 10234020
2004 Decorin suppresses neurocan, brevican, phosphacan and NG2 expression and promotes axon growth across adult rat spinal cord injuries. The European journal of neuroscience 154 15016081
1996 Neurocan and phosphacan: two major nervous tissue-specific chondroitin sulfate proteoglycans. Perspectives on developmental neurobiology 143 9117260
1996 Chondroitin sulfate proteoglycans in the developing central nervous system. II. Immunocytochemical localization of neurocan and phosphacan. The Journal of comparative neurology 134 8866845
1995 Purification, characterization and developmental expression of a brain-specific chondroitin sulfate proteoglycan, 6B4 proteoglycan/phosphacan. Neuroscience 124 7477903
1995 Chondroitin sulfate and chondroitin/keratan sulfate proteoglycans of nervous tissue: developmental changes of neurocan and phosphacan. Journal of neurochemistry 116 7595522
1996 Chondroitin sulfate proteoglycans in the developing central nervous system. I. cellular sites of synthesis of neurocan and phosphacan. The Journal of comparative neurology 108 8866844
2017 Tumour exosomes from cells harbouring PTPRZ1-MET fusion contribute to a malignant phenotype and temozolomide chemoresistance in glioblastoma. Oncogene 106 28504721
2010 The protein tyrosine phosphatases PTPRZ and PTPRG bind to distinct members of the contactin family of neural recognition molecules. Proceedings of the National Academy of Sciences of the United States of America 106 20133774
1996 6B4 proteoglycan/phosphacan is a repulsive substratum but promotes morphological differentiation of cortical neurons. Development (Cambridge, England) 105 8625816
2001 Inhibitory effects of neurocan and phosphacan on neurite outgrowth from retinal ganglion cells in culture. Investigative ophthalmology & visual science 95 11431463
1997 The fibrinogen-like globe of tenascin-C mediates its interactions with neurocan and phosphacan/protein-tyrosine phosphatase-zeta/beta. The Journal of biological chemistry 91 9182584
2003 Heterogeneity of the chondroitin sulfate portion of phosphacan/6B4 proteoglycan regulates its binding affinity for pleiotrophin/heparin binding growth-associated molecule. The Journal of biological chemistry 89 12840014
1996 Comparison of RPTP zeta/beta, phosphacan, and trkB mRNA expression in the developing and adult rat nervous system and induction of RPTP zeta/beta and phosphacan mRNA following brain injury. Brain research. Molecular brain research 87 8840016
2011 A complex between contactin-1 and the protein tyrosine phosphatase PTPRZ controls the development of oligodendrocyte precursor cells. Proceedings of the National Academy of Sciences of the United States of America 84 21969550
2003 Phosphacan short isoform, a novel non-proteoglycan variant of phosphacan/receptor protein tyrosine phosphatase-beta, interacts with neuronal receptors and promotes neurite outgrowth. The Journal of biological chemistry 82 12700241
1998 The core protein of the chondroitin sulfate proteoglycan phosphacan is a high-affinity ligand of fibroblast growth factor-2 and potentiates its mitogenic activity. The Journal of biological chemistry 82 9705269
1996 Expression of polypeptide variants of receptor-type protein tyrosine phosphatase beta: the secreted form, phosphacan, increases dramatically during embryonic development and modulates glial cell behavior in vitro. Journal of neuroscience research 78 8984199
2003 Regulation of RPTPbeta/phosphacan expression and glycosaminoglycan epitopes in injured brain and cytokine-treated glia. Molecular and cellular neurosciences 75 14697661
2009 NG2 and phosphacan are present in the astroglial scar after human traumatic spinal cord injury. BMC neurology 72 19604403
2007 Molecular dissection of NRG1-ERBB4 signaling implicates PTPRZ1 as a potential schizophrenia susceptibility gene. Molecular psychiatry 70 17579610
1997 Isolation of a tenascin-R binding protein from mouse brain membranes. A phosphacan-related chondroitin sulfate proteoglycan. The Journal of biological chemistry 69 9405406
2006 DSD-1-Proteoglycan/Phosphacan and receptor protein tyrosine phosphatase-beta isoforms during development and regeneration of neural tissues. Advances in experimental medicine and biology 64 16955703
2006 Monoclonal antibody Cat-315 detects a glycoform of receptor protein tyrosine phosphatase beta/phosphacan early in CNS development that localizes to extrasynaptic sites prior to synapse formation. Neuroscience 64 16989954
1995 Complex-type asparagine-linked oligosaccharides on phosphacan and protein-tyrosine phosphatase-zeta/beta mediate their binding to neural cell adhesion molecules and tenascin. The Journal of biological chemistry 64 7559574
2008 Egr-1 regulates expression of the glial scar component phosphacan in astrocytes after experimental stroke. The American journal of pathology 53 18556777
2001 Tenascin glycoproteins and the complementary ligand DSD-1-PG/ phosphacan--structuring the neural extracellular matrix during development and repair. Restorative neurology and neuroscience 51 12082229
2017 Targeting PTPRZ inhibits stem cell-like properties and tumorigenicity in glioblastoma cells. Scientific reports 50 28717188
2003 Phosphacan and neurocan are repulsive substrata for adhesion and neurite extension of adult rat dorsal root ganglion neurons in vitro. Experimental neurology 50 12821372
2003 Kainic acid-induced convulsions cause prolonged changes in the chondroitin sulfate proteoglycans neurocan and phosphacan in the limbic structures. Experimental neurology 49 14637091
1998 Coordinate expression of L1 and 6B4 proteoglycan/phosphacan is correlated with the migration of mesencephalic dopaminergic neurons in mice. Brain research. Developmental brain research 47 9593903
2007 Chronic oxidative stress causes amplification and overexpression of ptprz1 protein tyrosine phosphatase to activate beta-catenin pathway. The American journal of pathology 45 18055543
2016 Small-molecule inhibition of PTPRZ reduces tumor growth in a rat model of glioblastoma. Scientific reports 43 26857455
2016 Role of Chondroitin Sulfate (CS) Modification in the Regulation of Protein-tyrosine Phosphatase Receptor Type Z (PTPRZ) Activity: PLEIOTROPHIN-PTPRZ-A SIGNALING IS INVOLVED IN OLIGODENDROCYTE DIFFERENTIATION. The Journal of biological chemistry 43 27445335
2019 The protein tyrosine phosphatase RPTPζ/phosphacan is critical for perineuronal net structure. The Journal of biological chemistry 39 31822561
2005 Neuronal expression of the chondroitin sulfate proteoglycans receptor-type protein-tyrosine phosphatase beta and phosphacan. Neuroscience 39 15708477
2018 Chemotherapy-driven increases in the CDKN1A/PTN/PTPRZ1 axis promote chemoresistance by activating the NF-κB pathway in breast cancer cells. Cell communication and signaling : CCS 38 30497491
2016 Early remodelling of the extracellular matrix proteins tenascin-C and phosphacan in retina and optic nerve of an experimental autoimmune glaucoma model. Journal of cellular and molecular medicine 37 27374750
2012 RPTPζ/phosphacan is abnormally glycosylated in a model of muscle-eye-brain disease lacking functional POMGnT1. Neuroscience 37 22728091
2019 The PTN-PTPRZ signal activates the AFAP1L2-dependent PI3K-AKT pathway for oligodendrocyte differentiation: Targeted inactivation of PTPRZ activity in mice. Glia 36 30667096
2013 Structural and biochemical characterization of O-mannose-linked human natural killer-1 glycan expressed on phosphacan in developing mouse brains. Glycobiology 36 24352591
2001 Expression of brain specific chondroitin sulfate proteoglycans, neurocan and phosphacan, in the developing and adult hippocampus of Ihara's epileptic rats. Brain research 32 11292447
2017 Development of inhibitors of receptor protein tyrosine phosphatase β/ζ (PTPRZ1) as candidates for CNS disorders. European journal of medicinal chemistry 30 29275231
2015 Neurons and glia modify receptor protein-tyrosine phosphatase ζ (RPTPζ)/phosphacan with cell-specific O-mannosyl glycans in the developing brain. The Journal of biological chemistry 30 25737452
2004 Keratan sulfate proteoglycan phosphacan regulates mossy fiber outgrowth and regeneration. The Journal of neuroscience : the official journal of the Society for Neuroscience 30 14724244
2004 Activity-dependent regulation of a chondroitin sulfate proteoglycan 6B4 phosphacan/RPTPbeta in the hypothalamic supraoptic nucleus. Brain research 30 15261112
2012 PTPRZ1 regulates calmodulin phosphorylation and tumor progression in small-cell lung carcinoma. BMC cancer 29 23170925
2014 Intracellular and extracellular domains of protein tyrosine phosphatase PTPRZ-B differentially regulate glioma cell growth and motility. Oncotarget 27 25238264
2007 Differential expression of phosphacan/RPTPbeta isoforms in the developing mouse visual system. The Journal of comparative neurology 27 17722031
2015 Requirement of keratan sulfate proteoglycan phosphacan with a specific sulfation pattern for critical period plasticity in the visual cortex. Experimental neurology 26 26277687
2019 GlcNAc6ST3 is a keratan sulfate sulfotransferase for the protein-tyrosine phosphatase PTPRZ in the adult brain. Scientific reports 25 30867513
2010 Characterization of the activation of protein tyrosine phosphatase, receptor-type, Z polypeptide 1 (PTPRZ1) by hypoxia inducible factor-2 alpha. PloS one 25 20224786
2000 Dynamic spatiotemporal expression patterns of neurocan and phosphacan indicate diverse roles in the developing and adult mouse olfactory system. The Journal of comparative neurology 23 10861539
1996 Cell surface-associated extracellular distribution of a neural proteoglycan, 6B4 proteoglycan/phosphacan, in the olfactory epithelium, olfactory nerve, and cells migrating along the olfactory nerve in chick embryos. Neuroscience research 22 8861104
2023 Protein-protein interactions between tenascin-R and RPTPζ/phosphacan are critical to maintain the architecture of perineuronal nets. The Journal of biological chemistry 21 37356715
2014 Major glycan structure underlying expression of the Lewis X epitope in the developing brain is O-mannose-linked glycans on phosphacan/RPTPβ. Glycobiology 21 25361541
2015 Enhanced expression and phosphorylation of the MET oncoprotein by glioma-specific PTPRZ1-MET fusions. FEBS letters 20 25935522
2010 Glypican-1, phosphacan/receptor protein-tyrosine phosphatase-ζ/β and its ligand, tenascin-C, are expressed by neural stem cells and neural cells derived from embryonic stem cells. ASN neuro 20 20689858
2005 No association of FOXP2 and PTPRZ1 on 7q31 with autism from the Japanese population. Neuroscience research 20 15998549
2018 Pharmacological inhibition of Receptor Protein Tyrosine Phosphatase β/ζ (PTPRZ1) modulates behavioral responses to ethanol. Neuropharmacology 19 29753117
2005 Chondroitin sulfate proteoglycan phosphacan associates with parallel fibers and modulates axonal extension and fasciculation of cerebellar granule cells. Molecular and cellular neurosciences 18 16150606
2000 Spatiotemporal expression patterns of 6B4 proteoglycan/phosphacan in the developing rat retina. Investigative ophthalmology & visual science 18 10845626
2022 Targeted OUM1/PTPRZ1 silencing and synergetic CDT/enhanced chemical therapy toward uveal melanoma based on a dual-modal imaging-guided manganese metal-organic framework nanoparticles. Journal of nanobiotechnology 17 36335349
2022 HOXA5 is amplified in glioblastoma stem cells and promotes tumor progression by transcriptionally activating PTPRZ1. Cancer letters 16 35219772
2010 Significance of PTPRZ1 and CIN85 expression in cervical carcinoma. Archives of gynecology and obstetrics 16 20882291
2004 Expression of phosphacan and neurocan during early development of mouse retinofugal pathway. Brain research. Developmental brain research 16 15283989
2025 Curcumin Modulates PTPRZ1 Activity and RNA m6A Modifications in Neuroinflammation-Associated Microglial Response. Advanced science (Weinheim, Baden-Wurttemberg, Germany) 15 39921492
2011 Phosphacan and receptor protein tyrosine phosphatase β expression mediates deafferentation-induced synaptogenesis. Hippocampus 15 20014386
2007 Brevican and phosphacan expression and localization following transient middle cerebral artery occlusion in the rat. Biochemical Society transactions 15 17635124
2005 Cortical neurons express PSI, a novel isoform of phosphacan/RPTPbeta. Cell and tissue research 14 16028071
2001 Developmentally regulated expression of brain-specific chondroitin sulfate proteoglycans, neurocan and phosphacan, in the postnatal rat hippocampus. Cell and tissue research 14 11702233
2023 PTPRZ1-METFUsion GENe (ZM-FUGEN) trial: study protocol for a multicentric, randomized, open-label phase II/III trial. Chinese neurosurgical journal 13 37443050
2021 High-sensitive clinical diagnostic method for PTPRZ1-MET and the characteristic protein structure contributing to ligand-independent MET activation. CNS neuroscience & therapeutics 13 33645009
2019 A novel PTPRZ1-ETV1 fusion in gliomas. Brain pathology (Zurich, Switzerland) 13 31381204
2021 Recurrent PTPRZ1-MET fusion and a high occurrence rate of MET exon 14 skipping in brain metastases. Cancer science 12 34812554
2022 A comprehensive atlas of Aggrecan, Versican, Neurocan and Phosphacan expression across time in wildtype retina and in retinal degeneration. Scientific reports 11 35508614
2020 Soluble protein tyrosine phosphatase receptor type Z (PTPRZ) in cerebrospinal fluid is a potential diagnostic marker for glioma. Neuro-oncology advances 11 32642707
2020 PTN-PTPRZ signalling is involved in deer antler stem cell regulation during tissue regeneration. Journal of cellular physiology 9 33111346
2002 Chondroitin sulfate proteoglycan phosphacan/RPTPbeta in the hypothalamic magnocellular nuclei. Brain research 9 12213306
2020 Up-regulation of miR-137 can inhibit PTN in target manner to regulate PTN/PTPRZ pathway to prevent cognitive dysfunction caused by propofol. American journal of translational research 8 33312384
2019 Behavioral and neurological analyses of adult mice carrying null and distinct loss-of-receptor function mutations in protein tyrosine phosphatase receptor type Z (PTPRZ). PloS one 8 31194769
2019 MiR-1261/circ-PTPRZ1/PAK1 pathway regulates glioma cell growth and invasion. Human cell 8 31364003
2019 L1 Cell Adhesion Molecule Overexpression Down Regulates Phosphacan and Up Regulates Structural Plasticity-Related Genes Rostral and Caudal to the Complete Spinal Cord Transection. Journal of neurotrauma 8 31426714
2024 The PTPRZ1-MET/STAT3/ISG20 axis in glioma stem-like cells modulates tumor-associated macrophage polarization. Cellular signalling 7 38685521
2024 PTPRZ1-Targeting RNA CAR T Cells Exert Antigen-Specific and Bystander Antitumor Activity in Glioblastoma. Cancer immunology research 7 39269445
2023 Genetic deletion or tyrosine phosphatase inhibition of PTPRZ1 activates c-Met to up-regulate angiogenesis and lung adenocarcinoma growth. International journal of cancer 7 37260355
2016 Tailor-Made Protein Tyrosine Phosphatases: In Vitro Site-Directed Mutagenesis of PTEN and PTPRZ-B. Methods in molecular biology (Clifton, N.J.) 7 27514801
2015 Specific dephosphorylation at tyr-554 of git1 by ptprz promotes its association with paxillin and hic-5. PloS one 7 25742295
2014 Expression of the heparin-binding growth factor midkine and its receptor, Ptprz1, in adult rat pituitary. Cell and tissue research 7 25519047
2001 Recombinant core protein fragment of phosphacan, a brain specific chondroitin sulfate proteoglycan, promote excitotoxic cell death of cultured rat hippocampal neurons. Neuroscience letters 7 11343829