GO:0045785 positive regulation of cell adhesion: Signaling Mechanisms, Genes, Functions and Research Methods
Research-grade guide for scientists and biopharma professionals
Key Takeaways
• GO:0045785 (positive regulation of cell adhesion) describes any biological process that activates or increases the frequency, rate, or extent of cell adhesion, a fundamental mechanism in development, immunity, and tissue homeostasis.
• Integrin-mediated signaling and inside-out activation are central to positive regulation of cell adhesion, often involving calcium flux and RhoA mechanotransduction.
• Adapter proteins such as Fyb/Slap positively regulate T cell integrin adhesion and activation, linking immune receptor signaling to cytoskeletal remodeling.
• Cell adhesion molecules like CD4 and ITGAV modulate adhesion strength in immune and cancer contexts, with ITGAV influencing LGALS3BP-JUNB signaling in hepatic cancer.
• Matrix metalloproteinases (MMPs) and their inhibitors (TIMPs) act as positive and negative regulators of tumor cell adhesion, highlighting the balance in adhesion regulation.
• Dysregulation of positive regulation of cell adhesion contributes to cancer invasion, cardiovascular disorders, and immune pathologies, making it a key research and therapeutic target.
Description
Cell adhesion is a fundamental biological process that governs how cells interact with their extracellular environment and with each other. The Gene Ontology term GO:0045785, positive regulation of cell adhesion, encompasses any process that activates or increases the frequency, rate, or extent of cell adhesion. This regulation is critical for tissue architecture, immune surveillance, and developmental morphogenesis, and its dysregulation is implicated in numerous diseases including cancer and inflammatory disorders. Understanding the molecular players that positively regulate adhesion is essential for researchers aiming to manipulate these processes experimentally or therapeutically. Integrin-mediated signaling, for example, provides feedback regulation of cell-substratum adhesion through intracellular calcium signaling, establishing a dynamic equilibrium. Moreover, mechanotransduction pathways involving RhoA are regulated by adhesion molecules, linking physical forces to biochemical signals that reinforce adhesion. This article synthesizes authoritative QuickGO data and verified PubMed literature to provide a comprehensive overview of GO:0045785, covering its definition, mechanisms, key genes, disease relevance, and modern research methodologies including CRISPR-based models.
positive regulation of cell adhesion At A Glance
| GO ID | GO:0045785 |
|---|---|
| GO term | positive regulation of cell adhesion |
| Ontology | biological_process |
| Synonym | activation of cell adhesion; stimulation of cell adhesion; up regulation of cell adhesion; up-regulation of cell adhesion; upregulation of cell adhesion |
| Major function | Activates or increases the frequency, rate or extent of cell adhesion |
| Related processes | Integrin signaling, calcium signaling, RhoA mechanotransduction, immune cell activation |
| Key regulators | Integrins, CD4, Fyb/Slap, ITGAV, MMPs/TIMPs, RhoA |
| Disease relevance | Cancer invasion and metastasis, cardiovascular cohesion disorders, immune dysfunction |
What Is GO:0045785?
According to the Gene Ontology, GO:0045785 (positive regulation of cell adhesion) is defined as any process that activates or increases the frequency, rate or extent of cell adhesion. This term is a biological process and includes synonyms such as activation of cell adhesion, stimulation of cell adhesion, up regulation of cell adhesion, up-regulation of cell adhesion, and upregulation of cell adhesion. It encompasses signaling events, molecular interactions, and cellular changes that enhance the ability of cells to adhere to substrates or to one another.
Why Is positive regulation of cell adhesion Important in Cell Biology?
Positive regulation of cell adhesion is vital for numerous physiological processes, including embryonic development, wound healing, immune responses, and tissue integrity. It ensures that cells can form stable contacts with the extracellular matrix or with other cells, which is necessary for building and maintaining multicellular organisms. In the immune system, positive regulation of adhesion is required for leukocyte extravasation and T cell activation, as exemplified by CD4 and Fyb/Slap-mediated integrin adhesion. In the cardiovascular system, desmosomal adhesion regulates cardiac myocyte cohesion and gap junctions, and its disruption leads to arrhythmogenic disorders. In cancer, positive regulation of adhesion can promote invasion and metastasis, as seen with ITGAV regulation of the LGALS3BP-JUNB axis in hepatic cancer cells. Conversely, matrix metalloproteinases and their inhibitors fine-tune tumor cell adhesion, and an imbalance can drive malignant progression. Thus, understanding the mechanisms that positively regulate cell adhesion is crucial for both basic biology and translational medicine.
• Essential for tissue morphogenesis and maintenance of organ structure during development.
• Required for immune cell trafficking, antigen presentation, and T cell activation.
• Mediates mechanotransduction, allowing cells to sense and respond to mechanical forces.
• Regulates cardiac myocyte cohesion and gap junction function, with implications for heart disease.
• Promotes cancer cell invasion and metastasis when dysregulated, as in hepatic cancer.
• Involves a balance between MMPs and TIMPs that can be targeted in cancer therapy.
• Feedback regulation via calcium signaling ensures dynamic control of adhesion strength.
• Provides a basis for understanding inflammatory diseases where adhesion is enhanced, such as in EBV-positive NK cell adhesion to endothelium.
• Offers potential therapeutic targets for modulating immune responses and preventing metastasis.
• Serves as a model for studying signal transduction from adhesion receptors to the cytoskeleton.
What Happens During positive regulation of cell adhesion?
Initiation by Adhesion Receptor Engagement
In simple terms: The process starts when adhesion receptors on the cell surface bind to their ligands outside the cell.
Positive regulation of cell adhesion is often initiated by the engagement of adhesion receptors such as integrins with extracellular matrix components or counter-receptors on other cells. This binding triggers conformational changes and clustering of receptors, leading to the recruitment of intracellular adaptor and signaling proteins. For instance, integrin-mediated adhesion is subject to feedback regulation by intracellular calcium signaling, which can strengthen or modulate the adhesive contact. In T cells, CD4 engagement regulates LFA-1-mediated adhesion, enhancing the avidity of integrin binding to ICAM-1 on antigen-presenting cells. Similarly, the adapter protein Fyb/Slap positively regulates T cell activation and integrin adhesion, acting downstream of T cell receptor signaling.
Inside-Out Signaling and Integrin Activation
In simple terms: Signals from inside the cell change the shape of adhesion receptors so they can bind more tightly outside.
Inside-out signaling is a key mechanism in positive regulation of cell adhesion. Intracellular signals, often triggered by chemokines or antigen receptors, induce conformational changes in integrins that increase their affinity for ligands. This process involves the activation of small GTPases like RhoA, which is regulated by adhesion molecules and mechanotransduction pathways. RhoA activation promotes actin cytoskeletal remodeling, which clusters integrins and reinforces adhesion. In T cells, CD4 acts as a positive regulator of LFA-1-mediated adhesion by modulating inside-out signaling, thereby enhancing cell-cell adhesion. The adapter Fyb/Slap also contributes to integrin adhesion by linking receptor signaling to cytoskeletal reorganization.
Cytoskeletal Remodeling and Adhesion Strengthening
In simple terms: The cell's internal skeleton reorganizes to pull receptors together and make the adhesion stronger.
Following integrin activation, the actin cytoskeleton undergoes dynamic remodeling to cluster adhesion receptors and strengthen the adhesive contact. RhoA and other small GTPases play central roles in this process, as they regulate actin polymerization and actomyosin contractility. This cytoskeletal reorganization leads to the formation of focal adhesions and other adhesion structures that anchor the cell. In cardiac myocytes, desmosomal adhesion regulates cohesion and gap junctions, and its positive regulation ensures mechanical integrity of the heart tissue. The interplay between adhesion receptors and the cytoskeleton is also modulated by calcium signaling, which can feed back to regulate adhesion strength.
Modulation by Extracellular Proteases and Matrix Remodeling
In simple terms: Enzymes outside the cell can cut or remodel the matrix, which can either enhance or reduce adhesion.
The extracellular environment is dynamically remodeled by proteases such as matrix metalloproteinases (MMPs) and their inhibitors (TIMPs), which act as positive and negative regulators of tumor cell adhesion. MMPs can cleave matrix components to expose new adhesion sites or release bound growth factors, thereby positively regulating adhesion in certain contexts. Conversely, TIMPs inhibit MMP activity and can negatively regulate adhesion. This balance is critical in cancer, where increased MMP activity often correlates with enhanced adhesion and invasion. In hepatic cancer cells, ITGAV regulates the LGALS3BP-JUNB axis to facilitate cell-to-cell adhesion and invasiveness, highlighting how adhesion molecules can drive malignant phenotypes.
Feedback Regulation and Calcium Signaling
In simple terms: The cell monitors adhesion and adjusts it using calcium signals to maintain the right strength.
Positive regulation of cell adhesion is subject to feedback regulation to prevent excessive or insufficient adhesion. Integrin-mediated intracellular calcium signaling provides a feedback loop that can either enhance or dampen adhesion depending on the cellular context. For example, calcium influx can activate calpain proteases that cleave adhesion proteins, leading to turnover, while also triggering signaling that reinforces adhesion. This dynamic balance ensures that cells can rapidly adapt to changes in their environment. In inflammatory conditions, cytokines can stimulate endothelial cells to increase adhesion molecule expression, promoting the adhesion of immune cells such as EBV-positive NK cells. Thus, positive regulation of cell adhesion integrates multiple signaling pathways to fine-tune cellular interactions.
Key Genes Involved in GO:0045785 positive regulation of cell adhesion
The following genes and proteins are key players in the positive regulation of cell adhesion, as supported by the verified literature.
| Gene | Major Role | Research Relevance |
|---|---|---|
| ITGB1 (Integrin beta 1) | Forms heterodimers with alpha subunits to mediate cell-matrix adhesion; activates intracellular signaling | Central to mechanotransduction and adhesion strengthening; target for cancer and fibrosis studies |
| ITGAV (Integrin alpha V) | Binds to RGD-containing matrix proteins; regulates cell-to-cell adhesion and invasion | Implicated in hepatic cancer progression via LGALS3BP-JUNB axis |
| CD4 | Co-receptor on T cells; positively regulates LFA-1-mediated adhesion | Model for studying immune synapse formation and T cell activation |
| LFA-1 (ITGAL/ITGB2) | Integrin mediating leukocyte adhesion to ICAMs; regulated by inside-out signaling | Key in immune cell trafficking and inflammatory diseases |
| Fyb/Slap (FYB) | Adapter protein linking T cell receptor signaling to integrin activation | Positive regulator of T cell adhesion and activation; knockout models available |
| RhoA | Small GTPase regulating actin cytoskeleton and adhesion complex assembly | Critical for mechanotransduction and adhesion feedback |
| MMP2 | Matrix metalloproteinase that remodels extracellular matrix; can enhance adhesion | Positive regulator in tumor cell adhesion; balance with TIMPs is crucial |
| MMP9 | Matrix metalloproteinase involved in matrix degradation and adhesion modulation | Associated with cancer invasion and immune cell migration |
| TIMP1 | Tissue inhibitor of metalloproteinases; negatively regulates MMPs | Modulates adhesion balance; potential therapeutic target |
| TIMP2 | Tissue inhibitor of metalloproteinases; inhibits MMP activity | Regulates adhesion in cancer and fibrosis |
| LGALS3BP | Secreted glycoprotein that interacts with integrins; modulates adhesion | Involved in hepatic cancer cell adhesion and invasion |
| JUNB | Transcription factor downstream of ITGAV signaling; promotes adhesion and invasion | Potential target in liver cancer |
| Desmoglein 2 (DSG2) | Desmosomal cadherin mediating cardiac myocyte cohesion | Regulates gap junctions and heart function |
| Desmocollin 2 (DSC2) | Desmosomal cadherin; component of desmosomal adhesion | Cardiac cohesion and arrhythmia research |
| Plakoglobin (JUP) | Armadillo protein linking desmosomes to intermediate filaments | Cardiac and skin adhesion disorders |
| ICAM-1 (ICAM1) | Cell surface glycoprotein binding LFA-1; enhances leukocyte adhesion | Inflammatory and immune response studies |
| VCAM-1 (VCAM1) | Adhesion molecule on endothelial cells; binds VLA-4 | Mediates immune cell adhesion in inflammation |
| Calpain | Calcium-dependent protease that cleaves adhesion proteins | Feedback regulation of adhesion turnover |
How Is positive regulation of cell adhesion Regulated?
Positive regulation of cell adhesion is tightly controlled by multiple signaling pathways. RhoA activity is regulated by adhesion molecules and mechanotransduction, creating a feedback loop that adjusts adhesion strength in response to mechanical forces. Intracellular calcium signaling downstream of integrin engagement provides another layer of feedback regulation, modulating adhesion dynamics. In immune cells, adapter proteins such as Fyb/Slap transmit signals from the T cell receptor to integrins, positively regulating adhesion. Cytokines can stimulate endothelial cells to upregulate adhesion molecules like ICAM-1 and VCAM-1, enhancing the adhesion of leukocytes such as EBV-positive NK cells. Additionally, the balance between matrix metalloproteinases (MMPs) and their tissue inhibitors (TIMPs) regulates tumor cell adhesion, with MMPs often promoting adhesion and TIMPs inhibiting it. These regulatory mechanisms ensure that cell adhesion is appropriately modulated in response to physiological and pathological cues.
positive regulation of cell adhesion and Human Disease
| Gene | Disease / Biology | Potential Experimental Model |
|---|---|---|
| ITGAV | Hepatic cancer invasion and metastasis | Knockout or knockdown in liver cancer cell lines; overexpression in normal hepatocytes |
| MMP2/MMP9 | Tumor cell adhesion and metastasis | CRISPR knockout in cancer cell lines; TIMP overexpression |
| DSG2/DSC2 | Arrhythmogenic cardiomyopathy | Point mutations in induced pluripotent stem cell-derived cardiomyocytes |
| CD4 | Autoimmune diseases and HIV | Knockout in T cell lines; point mutations affecting LFA-1 regulation |
| FYB (Fyb/Slap) | Immunodeficiency and autoimmunity | Knockout mice or CRISPR knockout in Jurkat T cells |
Cancer Invasion and Metastasis
Positive regulation of cell adhesion is frequently dysregulated in cancer, contributing to invasion and metastasis. In hepatic cancer cells, ITGAV regulates the LGALS3BP-JUNB axis to facilitate cell-to-cell adhesion and invasiveness, suggesting that targeting this pathway could reduce metastatic spread. Matrix metalloproteinases (MMPs) and their inhibitors (TIMPs) act as positive and negative regulators of tumor cell adhesion, and an imbalance favoring MMP activity is associated with enhanced adhesion and invasion. Thus, positive regulation of adhesion can be a double-edged sword: while necessary for tissue integrity, its aberrant activation promotes cancer progression.
Cardiovascular Disorders
Desmosomal adhesion is critical for cardiac myocyte cohesion and gap junction function. Positive regulation of desmosomal adhesion helps maintain the mechanical integrity of the heart, and its disruption leads to arrhythmogenic cardiomyopathy and other cardiac disorders. Research into the regulation of desmosomal adhesion may reveal therapeutic targets for preventing arrhythmias and heart failure.
Immune and Inflammatory Diseases
Positive regulation of cell adhesion is essential for immune responses, but excessive adhesion can contribute to inflammatory diseases. For example, inflammatory cytokines stimulate endothelial cells to increase adhesion molecule expression, promoting the adhesion of EBV-positive NK cells to cultured endothelial cells. CD4 and Fyb/Slap positively regulate T cell adhesion, and dysregulation of these pathways can lead to autoimmune conditions. Modulating positive regulation of adhesion is therefore a potential strategy for treating inflammatory and autoimmune diseases.
From positive regulation of cell adhesion-Related Genes to Experimental Models
| Research Question | Suitable Model |
|---|---|
| Does ITGAV promote hepatic cancer cell adhesion via LGALS3BP-JUNB? | ITGAV knockout in HepG2 or Huh7 cells; rescue with wild-type ITGAV |
| How does RhoA mechanotransduction regulate adhesion strength? | RhoA knockout or point mutation (constitutively active/inactive) in fibroblasts; traction force microscopy |
| What is the role of Fyb/Slap in T cell integrin adhesion? | FYB knockout in Jurkat T cells; re-expression of wild-type or mutant Fyb/Slap |
| How do desmosomal mutations affect cardiac myocyte cohesion? | Knock-in of patient mutations in DSG2 or DSC2 in iPSC-derived cardiomyocytes |
| Does TIMP1 overexpression inhibit tumor cell adhesion? | TIMP1 overexpression in cancer cell lines; adhesion assays |
| Can CD4 point mutations alter LFA-1-mediated adhesion? | CD4 knockout T cells reconstituted with CD4 mutants |
How to Study the positive regulation of cell adhesion Process
| Method | What It Measures | Typical Application |
|---|---|---|
| Static adhesion assay | Number of adherent cells after washing | Screening for positive regulators of adhesion |
| Flow chamber assay | Adhesion strength under shear stress | Leukocyte adhesion to endothelial cells |
| TIRF microscopy | Real-time dynamics of adhesion complexes | Integrin clustering and cytoskeletal remodeling |
| Co-immunoprecipitation | Protein-protein interactions | Identifying components of adhesion signaling complexes |
| Phosphoproteomics | Global phosphorylation changes | Mapping signaling downstream of adhesion receptors |
| CRISPR knockout screen | Gene requirement for adhesion | Discovery of novel adhesion regulators |
| Traction force microscopy | Mechanical forces exerted by cells | Mechanotransduction studies |
| Calcium imaging | Intracellular calcium flux | Feedback regulation of adhesion |
Adhesion Assays
Cell adhesion assays are fundamental for studying positive regulation of cell adhesion. These include static adhesion assays where cells are allowed to attach to coated surfaces (e.g., fibronectin, ICAM-1) and non-adherent cells are washed away, followed by quantification of adherent cells. Dynamic assays under flow conditions can measure adhesion strength and rolling behavior. Such assays have been used to demonstrate the positive regulation of T cell adhesion by CD4 and Fyb/Slap.
Imaging and Microscopy
Advanced imaging techniques such as total internal reflection fluorescence (TIRF) microscopy, confocal microscopy, and live-cell imaging allow visualization of adhesion complex formation, integrin clustering, and cytoskeletal remodeling in real time. These methods are essential for understanding the spatiotemporal dynamics of positive regulation of cell adhesion. For example, imaging of GFP-tagged integrins and actin has revealed how RhoA activation promotes adhesion strengthening.
Biochemical and Proteomic Approaches
Co-immunoprecipitation, pull-down assays, and mass spectrometry-based proteomics can identify protein-protein interactions and post-translational modifications that regulate adhesion. Phosphoproteomics can reveal signaling events downstream of adhesion receptor engagement. These techniques have been used to map the interactions of Fyb/Slap with cytoskeletal and signaling proteins.
Genetic and CRISPR Screens
CRISPR-based knockout, knock-in, and overexpression models enable systematic interrogation of genes involved in positive regulation of cell adhesion. Pooled CRISPR screens can identify novel regulators of adhesion under specific conditions. For instance, knockout of ITGAV in hepatic cancer cells has been used to demonstrate its role in adhesion and invasion.
How CRISPR Can Be Used to Study GO:0045785 positive regulation of cell adhesion
Knockout
CRISPR knockout is a powerful approach to study positive regulation of cell adhesion by eliminating candidate genes. For example, knocking out ITGAV in hepatic cancer cells can reduce cell-to-cell adhesion and invasiveness, confirming its positive regulatory role. Knockout of FYB in T cells impairs integrin adhesion, demonstrating its necessity. Knockout models are also used to study RhoA and calcium signaling components in adhesion.
Point Mutation
Point mutations can be introduced to dissect specific domains or phosphorylation sites in adhesion regulators. For instance, mutating key residues in CD4 can reveal how it regulates LFA-1-mediated adhesion. Point mutations in desmosomal genes like DSG2 can model arrhythmogenic cardiomyopathy and study effects on cardiac myocyte cohesion. CRISPR-mediated point mutation allows precise interrogation of signaling mechanisms.
Knock-in
Knock-in of tagged or reporter genes enables visualization and tracking of adhesion proteins. For example, knocking in a fluorescent tag on integrins allows live-cell imaging of adhesion dynamics. Knock-in of patient-specific mutations in DSG2 or DSC2 can model cardiac adhesion disorders. Knock-in of wild-type or mutant FYB can rescue knockout phenotypes and test structure-function relationships.
Overexpression
CRISPR activation (CRISPRa) or traditional overexpression can increase levels of positive regulators to study gain-of-function effects. Overexpressing TIMP1 can inhibit tumor cell adhesion, while overexpressing MMPs can enhance it. Overexpression of ITGAV or LGALS3BP can promote adhesion and invasion in cancer models. Overexpression studies complement knockout approaches to establish causality.
How EDITGENE Supports positive regulation of cell adhesion Research
Researchers studying positive regulation of cell adhesion-related genes often need to determine whether a candidate gene is causally involved in enhancing adhesion, and to dissect the underlying molecular mechanisms. This requires precise genetic manipulation, which can be achieved through CRISPR-based knockout, point mutation, knock-in, or overexpression models. EDITGENE provides comprehensive services to support such studies, from cell line generation to library screening and bioinformatics analysis.
Contact EDITGENE today to design your custom CRISPR model for positive regulation of cell adhesion research.
Frequently Asked Questions About positive regulation of cell adhesion
What is GO:0045785 positive regulation of cell adhesion?
GO:0045785 is a Gene Ontology biological process term defined as any process that activates or increases the frequency, rate or extent of cell adhesion. It includes signaling events and molecular changes that enhance cell attachment.
What genes are involved in positive regulation of cell adhesion?
Key genes include ITGB1, ITGAV, CD4, LFA-1, FYB (Fyb/Slap), RhoA, MMPs, TIMPs, and desmosomal genes like DSG2 and DSC2, as supported by the literature.
How is cell adhesion positively regulated?
Positive regulation occurs through inside-out signaling, integrin activation, cytoskeletal remodeling, and feedback loops involving calcium and RhoA. Adapter proteins like Fyb/Slap link receptor signaling to integrin activation.
What diseases are associated with dysregulated positive regulation of cell adhesion?
Dysregulation is linked to cancer invasion and metastasis, cardiovascular disorders like arrhythmogenic cardiomyopathy, and inflammatory/autoimmune diseases.
How can CRISPR be used to study positive regulation of cell adhesion?
CRISPR knockout, point mutation, knock-in, and overexpression models allow precise manipulation of candidate genes to test their role in adhesion. For example, ITGAV knockout reduces hepatic cancer cell adhesion.
What are common methods to measure positive regulation of cell adhesion?
Common methods include static and flow adhesion assays, TIRF microscopy, co-immunoprecipitation, phosphoproteomics, and traction force microscopy.
What is the role of RhoA in positive regulation of cell adhesion?
RhoA is a small GTPase that regulates actin cytoskeleton dynamics and adhesion complex assembly, and its activity is modulated by adhesion molecules and mechanotransduction.
How do MMPs and TIMPs regulate cell adhesion?
MMPs can enhance tumor cell adhesion by remodeling the extracellular matrix, while TIMPs inhibit MMPs and can negatively regulate adhesion. The balance between them is critical.
What is the role of CD4 in T cell adhesion?
CD4 positively regulates LFA-1-mediated T cell adhesion by modulating inside-out signaling, thereby enhancing T cell conjugation with antigen-presenting cells.
Can EDITGENE help create custom cell models for adhesion research?
Yes, EDITGENE provides CRISPR knockout, point mutation, knock-in, overexpression, library screening, and bioinformatics services tailored to study positive regulation of cell adhesion.
Conclusion
Positive regulation of cell adhesion (GO:0045785) is a fundamental biological process that controls how cells interact with their environment and with each other. It is driven by complex signaling networks involving integrins, adapter proteins, small GTPases, and extracellular proteases, and its dysregulation underlies cancer, cardiovascular, and immune disorders. Researchers can leverage CRISPR-based models and advanced assays to dissect these mechanisms. EDITGENE offers comprehensive services to support such studies, from custom cell line generation to high-throughput screening and bioinformatics, empowering discoveries in adhesion biology.
References
- 1. Marjoram RJ et al.. 2014. Regulation of RhoA activity by adhesion molecules and mechanotransduction.. Curr Mol Med 14(2):199-208 PMID: 24467208
- 2. Sjaastad MD et al.. 1994. Feedback regulation of cell-substratum adhesion by integrin-mediated intracellular Ca2+ signaling.. Proc Natl Acad Sci U S A 91(17):8214-8 PMID: 8058782
- 3. Shim HJ et al.. 2025. ITGAV Regulation of LGALS3BP-JUNB Axis Facilitates the Cell-to-Cell Adhesion and Invasiveness of Hepatic Cancer Cells.. Anticancer Res 45(7):2997-3008 PMID: 40578967
- 4. Mazerolles F et al.. 1991. Regulation of LFA-1-mediated T cell adhesion by CD4.. Eur J Immunol 21(4):887-94 PMID: 1826886
- 5. Griffiths EK et al.. 2001. Positive regulation of T cell activation and integrin adhesion by the adapter Fyb/Slap.. Science 293(5538):2260-3 PMID: 11567140
- 6. Kanno H et al.. 2008. Adhesion of Epstein-Barr virus-positive natural killer cell lines to cultured endothelial cells stimulated with inflammatory cytokines.. Clin Exp Immunol 151(3):519-27 PMID: 18190605
- 7. Schinner C et al.. 2019. Regulation of cardiac myocyte cohesion and gap junctions via desmosomal adhesion.. Acta Physiol (Oxf) 226(2):e13242 PMID: 30582290
- 8. Bourboulia D et al.. 2010. Matrix metalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMPs): Positive and negative regulators in tumor cell adhesion.. Semin Cancer Biol 20(3):161-8 PMID: 20470890
