Affinage

CDH5

Cadherin-5 · UniProt P33151

Length
784 aa
Mass
87.5 kDa
Annotated
2026-06-09
45 papers in source corpus 16 papers cited in narrative 16 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 7/7 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

CDH5 (VE-cadherin/CD144) is an endothelial cell-cell adhesion molecule that mediates homophilic, calcium-dependent adhesion at intercellular junctions, where it controls paracellular permeability, contact-inhibited monolayer growth, and angiogenic morphogenesis (PMID:7627717, PMID:10592470). At junctions it recruits beta-catenin and co-distributes with alpha-catenin to reorganize cortical F-actin into parallel bundles, and this junctional/cortical actin organization drives endothelial cell elongation during sprouting angiogenesis (PMID:7627717, PMID:10592470, PMID:25373898). The cytoplasmic domain is required for these functions: a truncated Cdh5 lacking the intracellular domain fails to rescue actin disorganization and elongation defects in vivo, and the phenotype is recapitulated by blocking actin polymerization rather than actomyosin contractility (PMID:25373898). CDH5 also supports lumen and tube formation, acting through cell-cell association and vacuole fusion in a manner distinct from CD31 (PMID:10487846, PMID:10592470). Membrane retention of CDH5 is dynamically regulated: VEGF-C/VEGFR3 signaling drives SRC-mediated phosphorylation and endocytosis of VE-cadherin, while VE-cadherin reciprocally restrains VEGFR3 endocytosis, establishing a reciprocal axis that tunes sinusoidal and lymphatic vessel growth (PMID:36910472). CDH5 expression is transcriptionally activated under hypoxia by HIF1α and HIF2α and by the KAT14–SRF epigenetic axis through H3K9/H3K18 acetylation at the CDH5 locus, the latter being required for placental spiral artery remodeling in vivo (PMID:23645533, PMID:41867034). In cancer, CDH5 is induced by Notch1 and by IGFBP2–SP1 signaling and contributes to vasculogenic mimicry, while it is post-transcriptionally repressed by miR-101 and TNFα-induced miR-6086 to promote endothelial apoptosis (PMID:30368528, PMID:31934175, PMID:29605606, PMID:39172098).

Mechanistic history

Synthesis pass · year-by-year structured walk · 10 steps
  1. 1995 High

    Established that CDH5 is itself sufficient to confer endothelial-type cell-cell adhesion and junctional barrier function, defining its core molecular activity.

    Evidence Full-length CDH5 transfection into CHO cells with aggregation, permeability, migration, and alpha-catenin co-localization assays

    PMID:7627717

    Open questions at the time
    • Did not resolve the cytoplasmic signaling partners beyond alpha-catenin
    • Heterologous cell context rather than native endothelium
  2. 1999 Medium

    Showed that CDH5 is required for endothelial morphogenesis (tube/lumen formation) and links junctional adhesion to beta-catenin recruitment, F-actin reorganization, and contact inhibition of growth.

    Evidence Antibody blockade in 3D collagen gels and CDH5 vs CD31 reconstitution in ECV304 cells with immunofluorescence and proliferation readouts

    PMID:10487846 PMID:10592470

    Open questions at the time
    • Single-lab reconstitution systems
    • Did not define which cytoplasmic domain residues drive actin reorganization
  3. 2014 High

    Demonstrated in vivo that the CDH5 intracellular domain organizes junctional/cortical actin to drive cell elongation during sprouting, distinguishing actin polymerization from contractility as the relevant effector arm.

    Evidence Zebrafish cdh5 null mutants, domain-truncation rescue, live imaging, and pharmacological epistasis on actin polymerization vs contractility

    PMID:25373898

    Open questions at the time
    • Specific actin regulators downstream of the cytoplasmic tail not identified
    • Connection to beta-catenin pool not directly tested
  4. 2013 Medium

    Identified hypoxia-driven transcriptional control of CDH5 by HIF1α/HIF2α and linked CDH5 to vasculogenic mimicry in tumor cells.

    Evidence ChIP for HIF1α/HIF2α at the CDH5 promoter plus shRNA knockdown and tube formation under hypoxia in glioblastoma stem-like cells

    PMID:23645533

    Open questions at the time
    • Promoter binding shown but cooperating co-factors not mapped
    • Single tumor cell context
  5. 2016 Medium

    Placed CDH5 downstream of CD93/Clec14a in an in vivo angiogenic pathway, showing CDH5 junctional localization is a required effector.

    Evidence Zebrafish c1qr/c1qrl single and double mutants with Cdh5 re-expression rescue and ISV imaging

    PMID:28007601

    Open questions at the time
    • Mechanism by which CD93/Clec14a control Cdh5 levels not defined
    • Transcriptional vs post-transcriptional control unresolved
  6. 2018 Medium

    Defined additional inputs to CDH5 regulation: TNFα/miR-6086 post-transcriptional repression promoting endothelial apoptosis, and IGFBP2–integrin–FAK/ERK–SP1 transcriptional activation in glioma vasculogenic mimicry.

    Evidence miRNA mimic/inhibitor with miRNA-insensitive CDH5 rescue in HUVECs; Co-IP, luciferase, and SP1 ChIP at CDH5 promoter with tube formation and orthotopic model

    PMID:29605606 PMID:30368528

    Open questions at the time
    • Direct effect of CDH5 loss on barrier vs apoptosis pathways not separated
    • SP1 and miRNA inputs not tested in native endothelium together
  7. 2019 Medium

    Confirmed miR-101 as a direct 3'-UTR repressor of CDH5 controlling endothelial apoptosis and migration.

    Evidence miR-101 overexpression, 3'-UTR luciferase reporter, and CDH5 siRNA phenocopy in HUVECs

    PMID:31934175

    Open questions at the time
    • In vivo relevance not established
    • Downstream pro-apoptotic effectors not defined
  8. 2022 High

    Established the reciprocal VE-cadherin–VEGFR3 endocytic axis, mechanistically linking SRC-mediated CDH5 phosphorylation and endocytosis to receptor signaling and vessel growth.

    Evidence Mouse genetic models (membrane-retained CDH5 knock-in, conditional knockouts, double mutants) with epistasis and endocytosis/phosphorylation analysis

    PMID:36910472

    Open questions at the time
    • Identity of the SRC-targeted endocytic machinery not fully resolved
    • Whether the axis operates identically in blood vs lymphatic endothelium not separated
  9. 2026 High

    Defined an epigenetic activation mechanism in which KAT14-mediated H3K9/H3K18 acetylation enables SRF binding to drive CDH5 expression, with in vivo requirement for placental spiral artery remodeling.

    Evidence Co-IP, EMSA, luciferase, ChIP for KAT14/SRF at the CDH5 locus, conditional KO mice, and CDH5 overexpression rescue

    PMID:41867034

    Open questions at the time
    • Whether KAT14–SRF control of CDH5 operates in mature vasculature beyond placenta not tested
    • Interplay with HIF-driven activation not addressed
  10. 2024 Medium

    Extended transcriptional control of CDH5 to Notch1, linking it to gastric cancer proliferation, invasion, and vasculogenic mimicry.

    Evidence Notch1 ChIP at the CDH5 promoter with CDH5 shRNA knockdown/rescue and functional assays

    PMID:39172098

    Open questions at the time
    • Cooperating transcription factors not defined
    • Restricted to one cancer cell context

Open questions

Synthesis pass · forward-looking unresolved questions
  • How the multiple transcriptional (HIF, Notch1, SP1, KAT14–SRF), post-transcriptional (miR-101, miR-6086), and post-translational (SRC phosphorylation, proteolysis) inputs are integrated to set CDH5 levels and junctional localization in different vascular beds remains unresolved.
  • No unified model linking the regulatory inputs
  • Proteolytic regulation by MMP-2 and CDH1-dependent membrane retention rest on low-confidence inhibitor/correlation studies
  • Mechanism of CDH1-promoted CDH5 membrane expression undefined

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0008092 cytoskeletal protein binding 3 GO:0098631 cell adhesion mediator activity 2
Localization
GO:0005886 plasma membrane 4 GO:0005856 cytoskeleton 2
Pathway
R-HSA-1266738 Developmental Biology 3 R-HSA-1500931 Cell-Cell communication 2 R-HSA-162582 Signal Transduction 1
Partners
CTNNA1CTNNB1SRCVEGFR3
Complex memberships
VE-cadherin–catenin junctional complex

Evidence

Reading pass · 16 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1995 VE-cadherin (CDH5/7B4) mediates homophilic, calcium-dependent cell aggregation and cell-to-cell adhesion when expressed in transfected CHO cells; it localizes to intercellular junctions where it co-distributes with alpha-catenin, decreases intercellular permeability to high-molecular-weight molecules, and reduces cell migration rate across a wounded area. Transfection of full-length CDH5 cDNA into CHO cells, cell aggregation assays, permeability assays, wound-healing migration assay, co-localization with alpha-catenin Arteriosclerosis, thrombosis, and vascular biology High 7627717
1999 Antibody blockade of VE-cadherin (CD144) in 3D collagen gel cultures impairs endothelial tube formation by inhibiting cell-cell association and reducing vacuole formation or vacuole fusion required for intercellular lumen formation, a role distinct from that of CD31. Monoclonal antibody inhibition in 3D type I collagen gel angiogenesis assay with morphological analysis The American journal of pathology Medium 10487846
1999 VE-cadherin (CD144) expression in transfected ECV304 cells (which lack endogenous VE-cadherin) recruits beta-catenin to junctional regions, reorganizes F-actin into parallel bundles, enables 3D tube formation, and enforces contact-inhibited monolayer growth with dramatic reduction of cell cycling after confluence — properties absent in CD31 transfectants and empty-vector controls. Stable transfection of VE-cadherin or CD31 cDNA into ECV304 cells, immunofluorescence for beta-catenin and F-actin, 3D collagen gel tube assay, cell proliferation analysis International archives of allergy and immunology Medium 10592470
2014 Cdh5 (zebrafish ortholog of CDH5) organizes junctional and cortical actin cytoskeleton to support cell elongation during angiogenic sprouting; loss of cdh5 by null mutation impairs junctional remodeling and cell elongation associated with disorganized actin, and a truncated Cdh5 (lacking intracellular domain) fails to rescue these defects. Pharmacological inhibition of actin polymerization (but not actin-myosin contractility) phenocopies cdh5 mutation. Zebrafish cdh5 null mutant generation, in vivo live imaging of sprouting angiogenesis, rescue with truncated Cdh5 construct, pharmacological inhibition of actin polymerization vs. contractility Cell reports High 25373898
2013 In glioblastoma stem-like cells (GSCs), both HIF1α and HIF2α transcriptionally activate CDH5 under hypoxia by directly binding its promoter (shown by ChIP), and CDH5 expression contributes to vasculogenic mimicry formation by GSCs, especially under hypoxic conditions (shown by CDH5 shRNA knockdown and tube formation assay). shRNA knockdown of CDH5, chromatin immunoprecipitation (ChIP) for HIF1α/HIF2α at CDH5 promoter, vasculogenic tube formation assay under normoxia and 1% O2 Neuro-oncology Medium 23645533
2022 VEGF-C/VEGFR3 signaling induces VE-cadherin (CDH5) endocytosis and loss of function via SRC-mediated phosphorylation, while VE-cadherin reciprocally prevents VEGFR3 endocytosis required for optimal receptor signaling. Mice with membrane-retained (non-endocytosable) VE-cadherin exhibit defects in sinusoidal and lymphatic vessel growth identical to loss of VEGFR3. Genetic loss of VE-cadherin rescues sinusoidal/lymphatic growth defects caused by VEGFR3 loss (but not VEGF-C loss) by potentiating VEGFR2 signaling. Mouse genetic models (membrane-retained CDH5 knock-in, conditional CDH5 knockout, VEGFR3 knockout, VEGF-C knockout, double mutants), genetic epistasis, mechanistic analysis of receptor endocytosis and SRC-mediated phosphorylation Nature cardiovascular research High 36910472
2018 IGFBP2 interacts with integrin α5β1 and activates the FAK/ERK pathway to upregulate CDH5 (CD144) expression in glioma cells, promoting vasculogenic mimicry formation. SP1, activated downstream of IGFBP2, binds directly to the CDH5 promoter (shown by luciferase reporter and ChIP assay). Co-immunoprecipitation of IGFBP2 with integrin α5/β1, IGFBP2 stable knockdown, luciferase reporter assay, ChIP assay for SP1 at CDH5 promoter, vasculogenic tube formation assay, orthotopic mouse model Oncogene Medium 30368528
2016 C1qr (CD93) and C1qrl (Clec14a) redundantly regulate angiogenesis in zebrafish by controlling Cdh5 expression; double mutation of c1qr/c1qrl abolishes Cdh5 from inter-segmental vessel endothelial junctions, and replenishment of Cdh5 rescues the angiogenic defects in double mutants. Zebrafish single and double mutant analysis, in vivo imaging of inter-segmental vessel formation, rescue by Cdh5 re-expression Biochemical and biophysical research communications Medium 28007601
2014 IL-2 induces vascular leak syndrome through redistribution (altered membrane distribution) of CD144 (VE-cadherin) in primary human pulmonary microvascular endothelial cells, demonstrated by ex vivo studies using serum from IL-2-treated patients. Ex vivo primary human pulmonary microvascular endothelial cell model, in vitro IL-2 treatment, immunofluorescence-based analysis of CD144 distribution, patient serum studies Journal of translational medicine Medium 24885155
2019 miR-101 represses CDH5 expression by targeting its 3'-UTR in HUVECs, and this suppression mediates promotion of endothelial cell apoptosis and inhibition of cell migration; silencing CDH5 alone recapitulates the pro-apoptotic and anti-migratory effects of miR-101 overexpression. miR-101 overexpression in HUVECs, 3'-UTR luciferase reporter assay, CDH5 siRNA knockdown, apoptosis and migration assays International journal of clinical and experimental pathology Medium 31934175
2018 TNFα induces hsa-miR-6086 in HUVECs, which in turn downregulates CDH5 expression by targeting it; inhibition of hsa-miR-6086 or exogenous CDH5 re-expression protects HUVECs from TNFα-induced apoptosis and growth inhibition, placing CDH5 as a downstream effector of TNFα/miR-6086 signaling in endothelial cells. miR-6086 mimic/inhibitor transfection in HUVECs, CDH5 cDNA re-expression (insensitive to miRNA), apoptosis and proliferation assays Gene Medium 29605606
2024 Notch1 directly transcriptionally activates CDH5 in gastric cancer cells, as demonstrated by ChIP assay showing Notch1 binding to the CDH5 gene promoter; CDH5 silencing attenuates the Notch1-driven enhancement of proliferation, migration, invasion, and vasculogenic mimicry. ChIP assay for Notch1 at CDH5 promoter, CDH5 shRNA knockdown with rescue, proliferation (EdU), migration, invasion, and tube formation assays Aging Medium 39172098
2022 ANGPTL4 upregulates ETV5 expression in ovarian cancer cells; ETV5 binds the CDH5 promoter region to activate CDH5 transcription; CDH5 in turn activates AKT phosphorylation and upregulates MMP9, promoting angiogenesis and metastasis. CDH5 expression is required for ANGPTL4-driven tumorigenic effects. shRNA knockdown of ANGPTL4 and ETV5, Western blotting for CDH5/p-AKT/MMP9, promoter binding by ETV5 (inferred by expression correlation and transcription factor binding analysis), in vivo xenograft model Journal of ovarian research Low 36517864
2026 KAT14 (lysine acetyltransferase 14) acetylates histones H3K9 and H3K18 at the CDH5 locus, facilitating binding of serum response factor (SRF) to activate CDH5 expression in trophoblast/endothelial cells; CDH5 overexpression rescues placental vascular defects in KAT14-deficient mice, and CDH5-Cre; KAT14 KO mice show defective spiral artery remodeling. Co-immunoprecipitation, EMSA, luciferase reporter assay, ChIP for KAT14/SRF at CDH5 locus, conditional knockout mouse models (CYP19A1-Cre and CDH5-Cre), RNA sequencing, CDH5 overexpression rescue Hypertension (Dallas, Tex. : 1979) High 41867034
2026 MMP-2 promotes degradation of CDH5 (VE-cadherin), thereby increasing vascular permeability and facilitating inflammatory cell infiltration in heterotopic ossification; inhibition of MMP-2 preserves CDH5 and suppresses ectopic bone formation. In vitro and in vivo heterotopic ossification models, MMP-2 inhibition by Forsythoside A, assessment of CDH5 protein levels and vascular permeability Materials today. Bio Low 42099999
2025 CDH1 (E-cadherin) reduces endothelial cell permeability under chronic intermittent hypoxia by promoting CDH5 (VE-cadherin) membrane expression; loss of CDH1 from the cell membrane (caused by ox-LDL) correlates with reduced CDH5 membrane localization and increased permeability. Endothelial cell CIH model, immunofluorescence for CDH5 membrane localization, FITC-dextran permeability assay, CDH1 overexpression/knockdown European journal of medical research Low 41419959

Source papers

Stage 0 corpus · 45 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
1995 Functional properties of human vascular endothelial cadherin (7B4/cadherin-5), an endothelium-specific cadherin. Arteriosclerosis, thrombosis, and vascular biology 243 7627717
1999 Functional roles for PECAM-1 (CD31) and VE-cadherin (CD144) in tube assembly and lumen formation in three-dimensional collagen gels. The American journal of pathology 197 10487846
2014 Cdh5/VE-cadherin promotes endothelial cell interface elongation via cortical actin polymerization during angiogenic sprouting. Cell reports 137 25373898
2013 CDH5 is specifically activated in glioblastoma stemlike cells and contributes to vasculogenic mimicry induced by hypoxia. Neuro-oncology 131 23645533
2018 IGFBP2 promotes vasculogenic mimicry formation via regulating CD144 and MMP2 expression in glioma. Oncogene 94 30368528
2005 CD144 (VE-cadherin) is transiently expressed by fetal liver hematopoietic stem cells. Blood 85 15831702
2014 Elevated circulating VE-cadherin+CD144+endothelial microparticles in ischemic cerebrovascular disease. Thrombosis research 44 25523345
1996 Genomic structure and chromosomal mapping of the mouse VE-cadherin gene (Cdh5). Genomics 43 8786117
2018 Whole-Transcriptome Analysis of CD133+CD144+ Cancer Stem Cells Derived from Human Laryngeal Squamous Cell Carcinoma Cells. Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology 38 29949786
2023 Cdh5-mediated Fpn1 deletion exerts neuroprotective effects during the acute phase and inhibitory effects during the recovery phase of ischemic stroke. Cell death & disease 30 36841833
2016 Elevated levels of circulating CDH5 and FABP1 in association with human drug-induced liver injury. Liver international : official journal of the International Association for the Study of the Liver 29 27224670
2008 High-reproducible flow cytometric endothelial progenitor cell determination in human peripheral blood as CD34+/CD144+/CD3- lymphocyte sub-population. Journal of immunological methods 24 18402976
2020 Utility of LysM-cre and Cdh5-cre Driver Mice in Retinal and Brain Research: An Imaging Study Using tdTomato Reporter Mouse. Investigative ophthalmology & visual science 20 32232350
2014 Interleukin-2 alters distribution of CD144 (VE-cadherin) in endothelial cells. Journal of translational medicine 20 24885155
1999 Vascular-endothelial cadherin (CD144)- but not PECAM-1 (CD31)-based cell-to-cell contacts convey the maintenance of a quiescent endothelial monolayer. International archives of allergy and immunology 20 10592470
2023 A comprehensive pan-cancer analysis of CDH5 in immunological response. Frontiers in immunology 18 37809080
2016 C1qr and C1qrl redundantly regulate angiogenesis in zebrafish through controlling endothelial Cdh5. Biochemical and biophysical research communications 18 28007601
2015 CD144, CD146 and VEGFR-2 properly identify circulating endothelial cell. Revista brasileira de hematologia e hemoterapia 16 25818819
2021 Calcium Signal Profiles in Vascular Endothelium from Cdh5-GCaMP8 and Cx40-GCaMP2 Mice. Journal of vascular research 15 33706307
2019 The Cdh5-CreERT2 transgene causes conditional Shb gene deletion in hematopoietic cells with consequences for immune cell responses to tumors. Scientific reports 12 31101877
2022 Sinusoidal and lymphatic vessel growth is controlled by reciprocal VEGF-C-CDH5 inhibition. Nature cardiovascular research 10 36910472
2021 Inverse correlation of miR-27a-3p and CDH5 expression serves as a diagnostic biomarker of proliferation and metastasis of clear cell renal carcinoma. Pathology, research and practice 9 33740544
2020 Fenretinide reduces angiogenesis by downregulating CDH5, FOXM1 and eNOS genes and suppressing microRNA-10b. Molecular biology reports 9 31925643
2019 The upregulation of miR-101 promotes vascular endothelial cell apoptosis and suppresses cell migration in acute coronary syndrome by targeting CDH5. International journal of clinical and experimental pathology 9 31934175
2024 Notch1 signaling pathway promotes growth and metastasis of gastric cancer via modulating CDH5. Aging 5 39172098
2021 CDH5, a Possible New Candidate Gene for Genetic Testing of Lymphedema. Lymphatic research and biology 5 34882481
2018 Inhibition of hsa-miR-6086 protects human umbilical vein endothelial cells against TNFα-induced proliferation inhibition and apoptosis via CDH5. Gene 5 29605606
2022 ANGPTL4 functions as an oncogene through regulation of the ETV5/CDH5/AKT/MMP9 axis to promote angiogenesis in ovarian cancer. Journal of ovarian research 4 36517864
2010 mRNA levels of CD31, CD144, CD146 and von Willebrand factor do not serve as surrogate markers for circulating endothelial cells. Thrombosis and haemostasis 4 20589320
2022 The rs7404339 AA Genotype in CDH5 Contributes to Increased Risks of Kawasaki Disease and Coronary Artery Lesions in a Southern Chinese Child Population. Frontiers in cardiovascular medicine 3 35571208
2012 Decreased pre-surgical CD34+/CD144+ cell number in patients undergoing coronary artery bypass grafting compared to coronary artery disease-free valvular patients. Journal of cardiothoracic surgery 3 22214418
2024 Changes in the Release of Endothelial Extracellular Vesicles CD144+, CCR6+, and CXCR3+ in Individuals with Acute Myocardial Infarction. Biomedicines 2 39335632
2018 Generation of reporter hESCs by targeting EGFP at the CD144 locus to facilitate the endothelial differentiation. Development, growth & differentiation 2 29696633
2025 CDH1 reduces endothelial cell permeability by enhancing CDH5 membrane expression under chronic intermittent hypoxia. European journal of medical research 1 41419959
2024 Determination of blood biochemical indices and research of egg quality-related candidate gene CDH5 in Putian black duck. Gene 1 39643146
2023 Genetic Variants in Genes Correlated to the PI3K/AKT Pathway: The Role of ARAP3, CDH5, KIF11 and RELN in Primary Lymphedema. Lymphology 1 39207407
2000 Molecular analysis of human immunoglobulin heavy chain variable region associated determinants recognized by anti-VH3 antibodies 7B4, B6 and D12. Scandinavian journal of immunology 1 11013004
2026 Histone Acetyltransferase KAT14 Mediates CDH5 to Regulate Spiral Artery Remodeling in Preeclampsia via Cooperation With SRF. Hypertension (Dallas, Tex. : 1979) 0 41867034
2026 A Novel Anti-CDH5/VE-Cadherin Monoclonal Antibody (Ca5Mab-8) for Flow Cytometry, Western Blotting, and Immunohistochemistry. Monoclonal antibodies in immunodiagnosis and immunotherapy 0 41954588
2026 miR-142-3p regulates RDH13 to impair trophoblast function via regulating CDH5/LFA-1/L-SELECTIN axis: a novel mechanism and diagnostic/therapeutic for pre-eclampsia. Frontiers in medicine 0 41958596
2026 Treatment of heterotopic ossification via inhibiting the MMP-2/CDH5 axis through oral delivery of network pharmacology-predicted Chinese medicine. Materials today. Bio 0 42099999
2026 Protocol to generate endothelial cell-specific knockout mouse models using Cas9/Cdh5-Cre mice coupled with sgRNA. STAR protocols 0 42105238
2025 DMP1-mediated transformation of DPSCs to CD31+/CD144+ cells demonstrate endothelial phenotype both in vitro and in vivo. Frontiers in cell and developmental biology 0 40861275
2023 Comparison the therapeutic effects of bone marrow CD144+ endothelial cells and CD146+ mesenchymal stem cells in POF rats. BioImpacts : BI 0 38022384
2022 Mutations in the Spliceosome Component prp-6 and Overexpression of cdh-5 Suppress Axon Guidance Defects of cdh-4 Mutants in Caenorhabditis elegans. Neuroscience insights 0 36090596

Missed literature

Know a paper Affinage missed for CDH5? Flag it for the maintainers and the community.

No submissions yet.