Affinage

DPP4

Dipeptidyl peptidase 4 · UniProt P27487

Round 2 corrected
Length
766 aa
Mass
88.3 kDa
Annotated
2026-04-28
130 papers in source corpus 36 papers cited in narrative 36 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

DPP4 (CD26) is a type II transmembrane serine exopeptidase that cleaves N-terminal dipeptides from substrates bearing a penultimate proline or alanine, thereby inactivating incretin hormones (GLP-1, GIP), chemokines (CXCL12/SDF-1, CCL11/eotaxin), and other bioactive peptides to regulate glucose homeostasis, hematopoietic stem cell homing, and immune cell trafficking (PMID:8100523, PMID:12576320, PMID:30778250). Structurally, the extracellular region forms a homodimer comprising an eight-bladed β-propeller and an α/β-hydrolase domain that together create the catalytic cavity, and the β-propeller additionally serves as the binding site for the MERS-CoV spike receptor-binding domain, establishing DPP4 as the functional entry receptor for MERS-CoV (PMID:12483204, PMID:23486063, PMID:23831647). Beyond its peptidase activity, DPP4 functions as a multivalent signaling scaffold on T cells and antigen-presenting cells by directly associating with adenosine deaminase, CXCR4, caveolin-1, and the adenosine A2A receptor to co-stimulate T cell activation, regulate lymphocyte adhesion, and modulate NF-κB-dependent antigen presentation (PMID:8101391, PMID:11278278, PMID:16622717, PMID:29497379). DPP4 also acts as a hepatocyte- and adipocyte-secreted adipokine that promotes visceral adipose tissue inflammation via a Factor Xa/PAR2 pathway and impairs insulin signaling, and its plasma-membrane localization is regulated by TP53 to control lipid peroxidation and ferroptosis sensitivity (PMID:29562231, PMID:21593202, PMID:28813679).

Mechanistic history

Synthesis pass · year-by-year structured walk · 18 steps
  1. 1993 High

    Identifying DPP4 as the principal serine exopeptidase responsible for incretin inactivation established its central role in glucose homeostasis and provided the mechanistic basis for DPP4 inhibitor (gliptin) drug development.

    Evidence Purified placental DPP4 kinetic assays with GLP-1/GIP substrates and specific inhibitors in human serum

    PMID:8100523

    Open questions at the time
    • Kinetics measured with purified enzyme; in vivo substrate hierarchy not fully resolved
    • Contribution of soluble vs membrane-bound DPP4 to systemic incretin degradation not distinguished
  2. 1993 High

    Demonstrating that CD26 is the lymphocyte surface receptor for adenosine deaminase (ADA) revealed a non-enzymatic scaffolding function and linked DPP4 to purine metabolism and immune regulation.

    Evidence Co-immunoprecipitation and in vitro binding with recombinant extracellular domain, amino acid sequence confirmation

    PMID:8101391

    Open questions at the time
    • Functional consequence of ADA binding on local adenosine concentrations not quantified
    • Whether ADA binding modulates DPP4 catalytic activity was not tested
  3. 1998 Medium

    Domain mapping showed that T cell co-stimulation and ADA binding map to distinct but overlapping regions (aa 248–449) of the extracellular domain, establishing DPP4 as a modular signaling scaffold independent of its peptidase activity.

    Evidence Truncated and human–rat CD26 swap mutants with functional readouts and cross-blocking by 13 anti-CD26 mAbs

    PMID:9683260

    Open questions at the time
    • Downstream signaling pathways triggered by co-stimulation domain not identified
    • Results from chimeric constructs may not capture native folding constraints
  4. 2001 High

    Discovery of a physical CD26/CXCR4 complex that co-internalizes upon SDF-1α stimulation explained how DPP4 coordinates chemokine cleavage with receptor signaling to regulate lymphocyte chemotaxis.

    Evidence Reciprocal co-immunoprecipitation from T/B cell membranes, co-internalization with CXCR4 wild-type and mutants, pertussis toxin treatment

    PMID:11278278

    Open questions at the time
    • Stoichiometry and direct binding interface between CD26 and CXCR4 not determined
    • Whether complex formation alters DPP4 enzymatic kinetics toward SDF-1 is unknown
  5. 2003 High

    High-resolution crystal structures of DPP4 revealed the β-propeller/α/β-hydrolase architecture, the Glu-Glu substrate recognition motif, and dual substrate-access routes, providing the structural framework for understanding catalytic specificity and inhibitor design.

    Evidence X-ray crystallography of human DPP4 at 2.5 Å (with valine-pyrrolidide) and porcine DPP4 at 1.8 Å; cryo-TEM at ~14 Å confirming dimeric assembly and lateral opening

    PMID:12483204 PMID:12690074 PMID:12705886

    Open questions at the time
    • No structure of full-length membrane-anchored DPP4 in lipid bilayer
    • Dynamics of substrate entry through β-propeller tunnel vs. side opening not resolved
  6. 2003 High

    Showing that DPP4 cleaves CXCL12/SDF-1 to regulate hematopoietic stem cell mobilization and that CD26-truncated CXCL12 acts as a CXCR4 antagonist established a direct mechanism for DPP4 in HSC trafficking.

    Evidence In vitro chemotaxis with truncated CXCL12, DPP4 inhibitor treatment during G-CSF mobilization in mice

    PMID:12576320

    Open questions at the time
    • Relative contributions of membrane-bound vs. soluble DPP4 in HSC niche not distinguished
    • Other DPP4 substrates in the marrow microenvironment not surveyed
  7. 2004 High

    Genetic deletion and pharmacological inhibition of CD26 in donor HSCs dramatically enhanced bone marrow engraftment, validating DPP4 as a therapeutic target for transplantation.

    Evidence CD26 knockout mouse and diprotin A/sitagliptin treatment in bone marrow transplant models with competitive repopulation

    PMID:15310902

    Open questions at the time
    • Long-term engraftment and multilineage reconstitution data limited
    • Whether DPP4 inhibition affects graft-versus-host disease not addressed
  8. 2006 Medium

    Identification of CD26–caveolin-1 binding on APCs that triggers NF-κB activation and CD86 upregulation revealed how DPP4 functions as a co-stimulatory molecule bridging T cells and antigen-presenting cells.

    Evidence Recombinant CD26 binding assays, caveolin-1 siRNA, NF-κB and CD86 readouts, T cell proliferation

    PMID:16622717

    Open questions at the time
    • Direct binding interface between CD26 and caveolin-1 not structurally resolved
    • Single-lab finding; independent replication needed
  9. 2008 Medium

    Demonstrating that DPP4 silencing in melanoma occurs through promoter hypermethylation, and that demethylation restores expression and suppresses growth, linked epigenetic regulation to DPP4's tumor-suppressive function.

    Evidence Bisulfite sequencing of melanoma cell lines, 5-aza-2'-deoxycytidine restoration of DPP4 mRNA/protein/activity, growth inhibition assay

    PMID:17981724

    Open questions at the time
    • Whether restored DPP4 suppresses invasion through the same enzymatic-independent mechanism shown earlier (PMID:11467771) not tested
    • Methylation status in primary melanoma specimens not comprehensively surveyed
  10. 2011 High

    Identification of DPP4 as an adipokine secreted preferentially from visceral adipose tissue that directly impairs insulin signaling revealed an autocrine/paracrine metabolic function beyond incretin degradation.

    Evidence Proteomic profiling of human adipocyte secretome, recombinant DPP4 addition to fat/muscle cells with insulin signaling readout

    PMID:21593202

    Open questions at the time
    • Whether insulin-impairing effect requires DPP4 catalytic activity not determined
    • Receptor or binding partner on target cells mediating this effect not identified
  11. 2013 High

    Identification and structural characterization of DPP4 as the functional receptor for MERS-CoV, with the viral RBD contacting β-propeller blades IV–V, established a non-enzymatic viral entry role and explained species tropism.

    Evidence Affinity pull-down, antibody blocking, ectopic expression conferring susceptibility, crystal structures of MERS-RBD/DPP4 complex at 2.9–3.0 Å, SPR (Kd = 16.7 nM)

    PMID:23486063 PMID:23831647 PMID:23835475

    Open questions at the time
    • Whether DPP4 enzymatic activity is altered upon viral binding not determined
    • Post-binding entry mechanism (endocytic route, membrane fusion) not fully characterized
  12. 2017 High

    Demonstrating that TP53 retains DPP4 in the nucleus to prevent plasma-membrane-associated lipid peroxidation and ferroptosis established a transcription-independent TP53–DPP4 axis controlling cell death through lipid metabolism.

    Evidence DPP4 activity assays, subcellular fractionation, TP53 loss-of-function, lipid peroxidation quantification, erastin-induced ferroptosis model

    PMID:28813679

    Open questions at the time
    • Nuclear function of DPP4 (if any) not characterized
    • Direct physical interaction between TP53 and DPP4 not demonstrated
  13. 2017 High

    Unbiased surfaceome analysis showing selective DPP4 upregulation on senescent cells opened DPP4 as a senescence biomarker and revealed it sensitizes senescent cells to NK-mediated ADCC clearance.

    Evidence Mass spectrometry surface proteomics of senescent vs. proliferating fibroblasts, flow cytometry, ADCC functional assay

    PMID:28877934

    Open questions at the time
    • Mechanism driving senescence-specific DPP4 upregulation not defined
    • Whether DPP4 enzymatic activity is required for ADCC sensitization not tested
  14. 2018 High

    Defining a hepatocyte DPP4–Factor Xa–PAR2 pathway that drives adipose tissue macrophage inflammation in obesity revealed a non-enzymatic or paracrine mechanism distinct from the incretin-degradation function targeted by oral gliptins.

    Evidence Hepatocyte-specific DPP4 silencing, caveolin-1 and PAR2 knockdown in macrophages, sitagliptin comparison in obese mice

    PMID:29562231

    Open questions at the time
    • Whether DPP4 directly activates Factor Xa or serves as a co-factor not resolved
    • Relevance of this pathway in human obesity requires clinical validation
  15. 2018 High

    Detection of a trimeric CD26–ADA–A2AR complex spanning two cell surfaces demonstrated how ADA bridges DPP4 on T cells to adenosine receptors on dendritic cells, integrating purine catabolism with immune synapse signaling.

    Evidence Inter-cellular NanoBRET, site-directed ADA mutagenesis, dynamic mass redistribution assay

    PMID:29497379

    Open questions at the time
    • In vivo relevance of the trimeric complex not demonstrated
    • Stoichiometry and structural basis of the ternary complex not resolved
  16. 2019 High

    Showing that DPP4 cleavage of CCL11/eotaxin limits eosinophil tumor infiltration provided a mechanism by which DPP4 inhibition can enhance anti-tumor innate immunity independently of lymphocytes.

    Evidence Sitagliptin treatment in syngeneic HCC and breast cancer models, eosinophil depletion, lymphocyte-deficient mice, CCL11 quantification

    PMID:30778250

    Open questions at the time
    • Whether other DPP4 chemokine substrates contribute to eosinophil exclusion not addressed
    • Human clinical relevance of eosinophil-mediated anti-tumor effect with DPP4 inhibition not established
  17. 2021 High

    Placing DPP4 downstream of Wnt/β-catenin signaling as a required effector of skin fibrosis expanded DPP4's role to extracellular matrix remodeling and identified it as a druggable node in fibrotic disease.

    Evidence Genetically inducible Wnt activation with Dpp4 knockout epistasis, DPP4 inhibitor reversal of established fibrosis in mouse skin

    PMID:34808238

    Open questions at the time
    • DPP4 substrate(s) mediating fibrotic remodeling downstream of Wnt not identified
    • Applicability to organ fibrosis beyond skin not tested
  18. 2023 Medium

    Discovery that DPP4 on senescence-associated extracellular vesicles renders them refractory to uptake by proliferating cells suggested a mechanism for selective senescent cell communication.

    Evidence Surface proteomics of EVs from three senescence models; DPP4 overexpression in HeLa producing EVs with reduced uptake

    PMID:37862381

    Open questions at the time
    • Mechanism by which surface DPP4 blocks EV uptake (receptor masking, repulsion) not defined
    • In vivo consequences of altered EV uptake not examined
    • Overexpression system may not recapitulate physiological DPP4 density on S-EVs

Open questions

Synthesis pass · forward-looking unresolved questions
  • Key unresolved questions include the structural basis of full-length membrane-anchored DPP4 in lipid bilayers, the precise mechanism by which TP53 directs DPP4 nuclear retention, the identity of DPP4 substrates mediating Wnt-driven fibrosis, and whether the hepatocyte DPP4–Factor Xa–PAR2 inflammatory pathway operates through DPP4's catalytic or scaffolding function.
  • No structure of full-length membrane-embedded DPP4
  • TP53–DPP4 physical interaction and nuclear DPP4 function uncharacterized
  • Substrate identity in fibrosis context unknown

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140096 catalytic activity, acting on a protein 5 GO:0001618 virus receptor activity 4 GO:0060090 molecular adaptor activity 4 GO:0016787 hydrolase activity 3 GO:0098772 molecular function regulator activity 2
Localization
GO:0005886 plasma membrane 5 GO:0005576 extracellular region 3 GO:0005634 nucleus 1 GO:0031410 cytoplasmic vesicle 1
Pathway
R-HSA-168256 Immune System 8 R-HSA-162582 Signal Transduction 6 R-HSA-1643685 Disease 6 R-HSA-392499 Metabolism of proteins 4 R-HSA-1430728 Metabolism 3 R-HSA-5357801 Programmed Cell Death 1
Partners
ADACAV1CXCR4F10F2RL1TP53
Complex memberships
CD26-ADA-A2AR trimeric complexCD26/CXCR4 signaling complex

Evidence

Reading pass · 36 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1993 DPP4 (CD26) enzymatically hydrolyzes GIP, GLP-1(7-36)amide, and peptide histidine methionine by removing N-terminal dipeptides (His-Ala or Tyr-Ala), inactivating these incretin hormones; DPP4-specific inhibitors (diprotin A, Lys-pyrrolidide) completely abolished serum degradation of GIP and GLP-1, establishing DPP4 as the principal serine exopeptidase responsible for incretin inactivation in human serum. In vitro enzymatic assay with purified DPP4 from human placenta; kinetic analysis (Km, Vmax); serum incubation with DPP4-specific inhibitors; fragment identification European journal of biochemistry High 8100523
1993 CD26 (DPP4) directly associates with adenosine deaminase (ADA) on the T cell surface through its extracellular domain; co-immunoprecipitation and in vitro binding assays demonstrated that the 43-kDa protein co-purifying with CD26 is ADA, establishing CD26 as the lymphocyte surface receptor for ADA. Immunoprecipitation, amino acid sequence analysis, in vitro binding assay with recombinant extracellular domain Science High 8101391
1997 The extracellular portion of human DPP4 (starting at Gly-31) forms a homodimer and contains at least two independently folding domains: one stabilized by disulfide bonds (not required for catalytic activity or ADA binding) and one containing the active site; FTIR spectrometry showed ~45% beta-sheet content, and low-angle X-ray scattering supported a three-domain structure per subunit with flexible linker regions. Biochemical purification from seminal plasma, FTIR spectrometry, low-angle X-ray scattering, unfolding experiments under reducing conditions Biochimica et biophysica acta Medium 9252108
1998 CD26 delivers a co-stimulatory T cell activation signal through the CD3 pathway; epitope mapping using truncated and swap mutants localized T-cell costimulation activity to the 248–358 and 359–449 amino acid regions, and the ADA-binding domain to the 359–449 region, demonstrating functionally distinct domains within the extracellular portion of CD26. Truncated and human-rat CD26 swap mutants, cross-blocking with 13 anti-CD26 mAbs, DPP4 enzymatic activity as functional readout Molecular immunology Medium 9683260
2001 CD26 physically co-distributes and co-immunoprecipitates with CXCR4 on T and B cell membranes; upon SDF-1α stimulation, CD26 is co-internalized with CXCR4 in a CXCR4 internalization-dependent manner (blocked by CXCR4 internalization mutants but not pertussis toxin), indicating a functional CD26/CXCR4 complex in which CD26 can modulate SDF-1α-induced chemotaxis. Additionally, HIV-1 gp120 interacts with CD26 and disrupts the ADA/CD26 interaction through a site distinct from the ADA-binding domain. Co-immunoprecipitation from membrane fractions, co-internalization experiments with CXCR4 mutants, pertussis toxin treatment, flow cytometry The Journal of biological chemistry High 11278278
2002 Cell-surface ADA-CD26 interaction mediates adhesion of T lymphocytes to epithelial cells; CD26 overexpression increased T-cell adhesion to Caco-2 epithelial monolayers by ~50%, whereas anti-CD26 antibody targeting the ADA-binding site or exogenous ADA reduced adhesion by 50–70%. This adhesion was mediated by LFA-1 (lymphocyte function-associated antigen) integrin activation. Cell adhesion assays with CD26-overexpressing T cell lines, antibody blocking, FACS integrin activation assay The Biochemical journal Medium 11772392
2003 Crystal structure of the extracellular region of human DPP4 at 2.5 Å (in complex with the inhibitor valine-pyrrolidide) revealed two domains: an eight-bladed β-propeller and an α/β-hydrolase domain; the catalytic site is located in a large cavity between these two domains, and both domains participate in inhibitor/substrate binding, explaining how substrate specificity (N-terminal dipeptides with penultimate Pro or Ala) is achieved. X-ray crystallography at 2.5 Å resolution, inhibitor complex Nature structural biology High 12483204
2003 Crystal structure of native porcine DPP4 at 1.8 Å revealed a 2-2-2 symmetric tetrameric assembly dependent on glycosylation of β-propeller blade IV, and identified a Glu-Glu motif as a key substrate-recognition element (distinguishing DPP4 as an aminopeptidase) and an oxyanion trap that activates the P2-carbonyl oxygen for efficient post-proline cleavage. Structure also suggested dual routes for substrate access (β-propeller tunnel) and product exit (side opening). X-ray crystallography at 1.8 Å of native glycosylated porcine DPP4; dipeptide inhibitor complex Proceedings of the National Academy of Sciences of the United States of America High 12690074
2003 Cryo-TEM and single-particle analysis of rat DPP4/CD26 at ~14 Å resolution confirmed that the protein exists as a dimer and revealed a second lateral opening to the active site distinct from the β-propeller tunnel, suggesting that substrate selectivity and binding rate mechanisms differ from the structurally related serine peptidase POP. Cryo-TEM, single particle analysis, structural comparison by docking calculations Biochemical and biophysical research communications Medium 12705886
2003 CD26 mediates G-CSF-induced mobilization of hematopoietic stem/progenitor cells (HSCs/HPCs) by cleaving CXCL12 at its position-2 proline; CD26-truncated CXCL12(3-68) failed to induce migration of Sca-1+c-kit+lin- cells and acted as an antagonist to intact CXCL12. CD26 inhibition during G-CSF treatment reduced peripheral progenitor cell numbers, demonstrating a mechanistic role in mobilization. Flow cytometry for CD26 expression, in vitro chemotaxis assays with truncated CXCL12, CD26 inhibitor treatment, in vivo G-CSF mobilization model in mice Blood High 12576320
2004 Endogenous CD26 expression on donor hematopoietic stem cells negatively regulates homing and bone marrow engraftment; pharmacological inhibition or genetic deletion of CD26 greatly increased transplantation efficiency in mice, demonstrating that CD26 peptidase activity (by cleaving CXCL12/SDF-1) limits HSC homing. CD26 inhibitor treatment and CD26 knockout mouse bone marrow transplantation experiments; engraftment quantification Science High 15310902
2000 DPPIV expression in melanoma cells inhibits cellular invasion: stable transfection of full-length DPPIV cDNA reduced Matrigel invasion by >75% compared to parental or vector-transfected cells. Neither the extracellular serine protease activity nor the 6-amino-acid cytoplasmic domain was required for anti-invasive activity, as mutants lacking either function retained the phenotype. Stable transfection of DPPIV cDNA and active-site/cytoplasmic-domain mutants into melanoma cell lines; Matrigel invasion assays Clinical & experimental metastasis High 11467771
2006 CD26 binds to caveolin-1 on antigen-presenting cells (APCs) through residues 201–211 of CD26 together with the serine catalytic site at residue 630; this interaction triggers caveolin-1 phosphorylation and NF-κB activation in APCs, leading to CD86 upregulation and subsequent antigen-specific T cell activation. Reduced caveolin-1 expression on APCs abolished CD26-mediated CD86 upregulation and T cell proliferation. Recombinant CD26 binding assays, caveolin-1 siRNA knockdown, NF-κB activation assay, CD86 upregulation measurement, T cell proliferation assay, immunohistochemistry of rheumatoid synovium Modern rheumatology Medium 16622717
2013 DPP4 (CD26) is identified as the functional receptor for MERS-CoV (hCoV-EMC); the receptor-binding S1 domain of the MERS-CoV spike protein specifically co-purified with DPP4 from susceptible Huh-7 cell lysates. Anti-DPP4 antibodies blocked MERS-CoV infection of primary human bronchial epithelial cells. Expression of human or bat DPP4 in non-susceptible COS-7 cells conferred susceptibility to infection. Co-purification/affinity pull-down of viral S1 domain with DPP4; antibody inhibition of infection; ectopic DPP4 expression in COS-7 cells enabling infection Nature High 23486063
2013 Crystal structures of both the free MERS-CoV spike receptor-binding domain (RBD) and its complex with human DPP4 were determined; the viral RBD contacts blades IV and V of the CD26 β-propeller through a strand-dominated external receptor-binding motif. Binding was confirmed by surface plasmon resonance (Kd = 16.7 nM). The interface is mediated mainly by hydrophilic residues, distinct from other coronavirus-receptor interactions. X-ray crystallography of free RBD and RBD-DPP4 complex; surface plasmon resonance binding assay Nature High 23831647
2013 Crystal structure of MERS-CoV RBD bound to the extracellular domain of human DPP4 at 3.0 Å resolution showed that the receptor-binding subdomain of MERS-CoV RBD interacts with the DPP4 β-propeller but not its hydrolase domain. Mutagenesis of key residues in the receptor-binding subdomain abrogated viral binding to DPP4 and cell entry. X-ray crystallography (3.0 Å); site-directed mutagenesis of receptor-binding subdomain residues; viral entry assays Cell research High 23835475
2014 CD26 (DPP4) expressed on CML leukemic stem cells (LSCs) disrupts the SDF-1-CXCR4 axis by cleaving SDF-1, facilitating abnormal extramedullary spread of BCR/ABL1+ LSCs. CD26+ LSCs engrafted NSG mice with BCR/ABL1+ cells, whereas CD26- stem cells from the same patients produced multilineage BCR/ABL1- engraftment. Gliptin-mediated CD26 inhibition suppressed BCR/ABL1+ cell expansion. Functional xenograft engraftment assays (NSG mice), flow cytometry cell sorting, CD26 enzymatic inhibition with gliptins, SDF-1 cleavage assay Blood High 24778155
2016 DPP4 in hepatocytes is regulated by DNA methylation: demethylation of four intronic CpG sites amplifies glucose-induced DPP4 transcription; this epigenetic reprogramming occurs early in life (6 weeks) in obesity-prone mice, preceding hepatic triglyceride accumulation, and correlates with subsequent hepatosteatosis. Bisulfite sequencing of DPP4 CpG sites, glucose stimulation experiments, longitudinal mouse model comparing obese-prone vs normal mice, human liver biopsy analysis Diabetes Medium 27999105
2017 TP53 (p53) limits ferroptosis by blocking DPP4 activity in a transcription-independent manner: loss of TP53 prevents nuclear accumulation of DPP4, allowing plasma-membrane-associated DPP4-dependent lipid peroxidation that triggers ferroptosis. This establishes a direct molecular link between TP53 and DPP4 in the control of lipid metabolism. DPP4 activity assays, subcellular fractionation, TP53 loss-of-function experiments, lipid peroxidation assays, erastin-induced ferroptosis model in colorectal cancer cells Cell reports High 28813679
2017 DPP4 is selectively expressed on the surface of senescent (but not proliferating) human diploid fibroblasts, as identified by mass spectrometry surfaceome analysis. Surface DPP4 preferentially sensitizes senescent cells to NK cell-mediated antibody-dependent cell-mediated cytotoxicity (ADCC), enabling their selective elimination. Mass spectrometry surface proteome analysis, flow cytometry with anti-DPP4 antibodies for cell sorting, ADCC assays with NK cells Genes & development High 28877934
2018 In obesity, hepatocytes synthesize and secrete DPP4, which acts together with plasma factor Xa to activate ATM (adipose tissue macrophage) inflammation via PAR2 signaling, promoting visceral adipose tissue inflammation and insulin resistance. Silencing hepatocyte DPP4 or macrophage caveolin-1 or PAR2 suppressed inflammation and insulin resistance; the oral DPP4 inhibitor sitagliptin did not recapitulate this effect, indicating a non-enzymatic or paracrine mechanism. Hepatocyte-specific DPP4 siRNA silencing in mice; caveolin-1 and PAR2 knockdown in macrophages; measurement of VAT inflammation and insulin sensitivity; sitagliptin comparison Nature High 29562231
2018 Adenosine deaminase (ADA) bridges CD26 on T cells and adenosine A2A receptor (A2AR) on dendritic cells to form a trimeric CD26-ADA-A2AR complex spanning two cell surfaces. This was demonstrated by NanoBRET (inter-cellular BRET), site-directed mutagenesis of ADA residues involved in A2AR binding, and functional dynamic mass redistribution assays, suggesting ADA acts as a cell-to-cell connector. NanoBRET (inter-cellular bioluminescence resonance energy transfer), site-directed mutagenesis, dynamic mass redistribution assay, ligand binding assay Frontiers in pharmacology High 29497379
2019 DPP4 enzymatic cleavage of CCL11 (eotaxin) regulates eosinophil trafficking into tumors; inhibition of DPP4 by sitagliptin preserved functional CCL11, increased eosinophil tumor infiltration, and enhanced tumor control in hepatocellular carcinoma and breast cancer models. This mechanism was independent of lymphocytes and required IL-33 expression by tumor cells and eosinophil degranulation. DPP4 inhibitor (sitagliptin) treatment in syngeneic mouse tumor models; eosinophil depletion experiments; lymphocyte-deficient mice; IL-33 manipulation; CCL11 quantification Nature immunology High 30778250
2019 Oxidized LDL upregulates DPP4 expression on macrophages through a TLR4/TRIF/CD36 signaling pathway; oxLDL (but not native LDL) increased DPP4 expression preferentially in CD36+ macrophages, and this effect was substantially reduced by TLR4 knockdown, CD36 deficiency, or TRIF (but not MyD88) deficiency. Flow cytometry, TLR4 knockdown, CD36-deficient macrophages, TRIF/MyD88-deficient cells, DPP4 enzymatic activity assay EBioMedicine Medium 30738832
2020 Glucocorticoid receptor (GR) directly induces DPP4 gene transcription in macrophages by binding to two glucocorticoid-responsive elements (GREs) within the DPP4 promoter; glucocorticoid-induced DPP4 expression mediates macrophage migration, as siRNA-mediated knockdown of GR or DPP4 blocked dexamethasone-induced macrophage migration in THP-1 cells and murine peritoneal macrophages. Transcriptome analysis (RNA-seq), ChIP (GR binding to DPP4 promoter GREs), siRNA knockdown of GR and DPP4, GR antagonist (RU-486), macrophage migration assays, DPP4 enzymatic activity measurement The Journal of biological chemistry High 31988243
2011 DPP4 was identified as a novel adipokine secreted from differentiated human adipocytes; DPP4 protein concentration in visceral fat was ~5-fold higher than in subcutaneous fat in obese patients. Direct addition of soluble DPP4 to fat, skeletal muscle, and smooth muscle cells impaired insulin signaling in an autocrine/paracrine manner. DPP4 release from adipose tissue strongly correlated with adipocyte volume. Proteomic profiling of human adipocyte secretome, depot-specific DPP4 expression measurement, direct addition of recombinant DPP4 to target cells with insulin signaling readout, adipose tissue explant release assays Diabetes High 21593202
2016 DPP4 knockdown in human preadipocytes using lentiviral shRNA altered gene expression (upregulating metabolic genes PDK4 and PGC1α, downregulating proliferation genes including FGF7), retarded preadipocyte proliferation, and markedly diminished basal and insulin-induced ERK (but not Akt) activation by ~60%, indicating DPP4 modulates growth factor signaling during adipocyte differentiation. Lentiviral DPP4 knockdown, whole-genome DNA array, quantitative PCR, western blotting for ERK and Akt phosphorylation Scientific reports Medium 26983599
2014 DPP4 inhibition combined with dmPGE2 treatment synergistically enhances bone marrow HSC engraftment; pretreatment of donor cells with diprotin A (DPP4 inhibitor) or dmPGE2 and pretreatment of irradiated recipients with sitagliptin each improved engraftment, and the combined approach was significantly superior to either treatment alone in a congenic competitive repopulation model. Congenic CD45+ mouse bone marrow transplantation, pharmacological DPP4 inhibition (diprotin A, sitagliptin), dmPGE2 treatment, competitive repopulation assay Blood cells, molecules & diseases Medium 24602918
2021 Skin fibrosis driven by Wnt/β-catenin signaling requires DPP4 as a downstream effector: DPP4 is a Wnt/β-catenin-responsive gene, and genetic evidence showed the Wnt/DPP4 axis is required for fibrotic dermal remodeling including ECM expansion and dermal adipocyte shrinkage. DPP4 inhibitors reversed established Wnt-induced fibrosis in mouse skin. Genetically inducible/reversible Wnt activation mouse model, Dpp4 genetic knockout, DPP4 inhibitor treatment, skin architecture analysis, human skin fibrosis correlation The Journal of investigative dermatology High 34808238
2022 CD26 promotes colorectal cancer angiogenesis and metastasis through a CAV1/MMP1 signaling axis: CD26 overexpression upregulated MMP1 expression, and caveolin-1 (CAV1) overexpression abrogated CD26-regulated MMP1 induction. CD26 functionally regulated CRC cell migration and invasion in vitro and angiogenesis and metastasis in vivo. Genome-wide mRNA expression array, qPCR, wound healing and invasion assays, mouse models of CRC metastasis, CAV1 overexpression rescue experiments International journal of molecular sciences Medium 35163100
2020 Purified recombinant human DPP4 (produced in insect cells) does not bind SARS-CoV-2 full-length spike protein or its receptor-binding domain, as measured by surface plasmon resonance and ELISA, demonstrating that unlike MERS-CoV, SARS-CoV-2 does not use DPP4 as a receptor. Recombinant protein purification, surface plasmon resonance, ELISA binding assay Molecules High 33218025
2023 DPP4 on the surface of senescence-associated extracellular vesicles (S-EVs) renders them refractory to uptake by proliferating cells; surfaceome proteomics of EVs from multiple senescence models consistently showed DPP4 enrichment on S-EVs, and ectopic DPP4 overexpression in HeLa cells produced EVs that were no longer taken up by proliferating cells. Surface proteomics of EVs from replicative, radiation-induced, and etoposide-induced senescent cells; DPP4 overexpression in HeLa cells; EV uptake assays Proceedings of the National Academy of Sciences of the United States of America Medium 37862381
2014 Bat coronavirus HKU4-RBD binds human DPP4 (hCD26) and pseudotyped viruses with HKU4 spike infect cells via hCD26, supporting a bat origin for MERS-CoV. Crystal structure of HKU4-RBD/hCD26 complex revealed a binding mode similar to MERS-RBD but with lower affinity, explained by fewer optimized contact residues. Receptor binding assays, pseudovirus infection assays, X-ray crystallography of HKU4-RBD/hCD26 complex Cell host & microbe High 25211075
2008 Loss of DPPIV expression in melanomas occurs at the RNA level and is attributable to promoter hypermethylation: DPPIV gene promoter is methylated in 8 of 10 melanoma cell lines, and demethylating agent 5-aza-2'-deoxycytidine restored DPPIV mRNA, protein, and enzyme activity, correlating with growth inhibition and apoptosis in melanoma cells. Bisulfite genomic sequencing, 5-aza-2'-deoxycytidine treatment, RT-PCR, western blot, DPPIV enzyme activity assay, growth inhibition assay Frontiers in bioscience Medium 17981724
2011 CD26 deficiency in mice leads to enhanced ovalbumin-induced airway inflammation characterized by increased eosinophilic infiltrates, elevated Th2 cytokines (IL-4, IL-5, IL-13) in bronchoalveolar lavage, and increased eotaxin/RANTES and their receptors CCR3/CCR5, suggesting CD26 normally restricts Th2-mediated airway inflammation, likely through chemokine cleavage. CD26 knockout mice, OVA sensitization/challenge model, cytokine measurement in BAL, immunohistochemistry, qRT-PCR European journal of immunology Medium 22101691
2014 CD26 signaling promotes human osteoclast (OC) differentiation via the MKK3/6–p38 MAPK–mi/Mitf phosphorylation pathway; M-CSF and sRANKL induced CD26 expression on OC precursors concomitantly with p38 MAPK phosphorylation. Anti-CD26 monoclonal antibody (huCD26mAb) blocked early OC differentiation by inactivating MKK3/6 and p38 MAPK, and p38 MAPK inhibitor phenocopied the effect. Human OC differentiation assay with M-CSF/sRANKL, anti-CD26 mAb treatment, p38 MAPK inhibitor, western blotting for MKK3/6 and MAPK phosphorylation, TRAP staining, OC functional assays Journal of bone and mineral research Medium 24821427

Source papers

Stage 0 corpus · 130 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2014 Biological insights from 108 schizophrenia-associated genetic loci. Nature 5878 25056061
2020 Functional assessment of cell entry and receptor usage for SARS-CoV-2 and other lineage B betacoronaviruses. Nature microbiology 2243 32094589
2020 Structural and Functional Basis of SARS-CoV-2 Entry by Using Human ACE2. Cell 2225 32275855
2013 Dipeptidyl peptidase 4 is a functional receptor for the emerging human coronavirus-EMC. Nature 1527 23486063
2002 Generation and initial analysis of more than 15,000 full-length human and mouse cDNA sequences. Proceedings of the National Academy of Sciences of the United States of America 1479 12477932
2020 Characterization of the receptor-binding domain (RBD) of 2019 novel coronavirus: implication for development of RBD protein as a viral attachment inhibitor and vaccine. Cellular & molecular immunology 1164 32203189
2003 Genome-wide survey of human alternative pre-mRNA splicing with exon junction microarrays. Science (New York, N.Y.) 1117 14684825
1993 Dipeptidyl-peptidase IV hydrolyses gastric inhibitory polypeptide, glucagon-like peptide-1(7-36)amide, peptide histidine methionine and is responsible for their degradation in human serum. European journal of biochemistry 980 8100523
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