GO:2000048 negative regulation of cell-cell adhesion mediated by cadherin: Regulation, Genes, Functions and Research Methods
Research-grade guide for scientists and biopharma professionals
Key Takeaways
• GO:2000048 describes any process that stops, prevents, or reduces cadherin-mediated cell-cell adhesion, a key event in tissue remodeling, cell migration, and disease progression [2,3].
• Cadherin adhesion is dynamically regulated by signaling pathways including estrogen receptor signaling, Rho-family GTPases, and kinase/phosphatase networks [2,6].
• Loss of cadherin-mediated adhesion is a hallmark of epithelial-to-mesenchymal transition and is linked to cancer invasion and metastasis [3,8].
• Key proteins involved include E-cadherin, N-cadherin, catenins, filamin A, Cdc42, Rac1, and the estrogen receptor [2,6,7,8].
• Experimental models for studying this process include knockout, point-mutation, knock-in, and overexpression cell lines, as well as CRISPR library screening [2,3,6].
• Understanding negative regulation of cadherin adhesion informs research on cancer, vascular permeability, neuroinflammation, and developmental disorders [1,4,8].
Description
Cell-cell adhesion mediated by cadherins is fundamental for tissue architecture, barrier function, and coordinated cell behavior. Cadherins are transmembrane proteins that form homophilic interactions between adjacent cells, linking to the actin cytoskeleton via catenins. The dynamic modulation of these junctions is essential for processes such as morphogenesis, wound healing, and immune cell transmigration. GO:2000048, negative regulation of cell-cell adhesion mediated by cadherin, captures the biological processes that actively dismantle or weaken these adhesive contacts [2,3]. This term is critical for researchers studying how cells detach during development, how tumor cells acquire invasive capacity, and how endothelial barriers are compromised in inflammation [1,3,4]. Dysregulation of cadherin-mediated adhesion is implicated in a wide range of pathologies, including cancer progression, where loss of E-cadherin promotes metastasis, and vascular diseases, where increased endothelial permeability leads to edema [3,4,8]. The negative regulation of cadherin adhesion is not a passive loss but an actively regulated process involving signaling cascades, endocytosis, and cytoskeletal remodeling [2,6]. For example, estrogen receptor signaling can downregulate N-cadherin-mediated adhesion in pituitary cells, while Cdc42 and Rac1 GTPases modulate junctional stability in epithelial cells. This article synthesizes authoritative QuickGO data and verified PubMed literature to provide a research-grade overview of GO:2000048. We cover the molecular players, regulatory mechanisms, disease relevance, and cutting-edge methods including CRISPR-based models for dissecting this process. By understanding how cadherin adhesion is negatively regulated, researchers can identify therapeutic targets and develop strategies to modulate cell adhesion in disease contexts [3,7,8].
negative regulation of cell-cell adhesion mediated by cadherin At A Glance
| GO ID | GO:2000048 |
|---|---|
| GO term | negative regulation of cell-cell adhesion mediated by cadherin |
| Ontology | biological_process |
| Synonym | none |
| Major function | Actively reduces or prevents cadherin-dependent cell-cell adhesion, facilitating cell detachment, migration, and tissue remodeling [2,3]. |
| Related processes | Epithelial-to-mesenchymal transition, endothelial permeability, smooth muscle proliferation, neuroinflammation [1,3,4]. |
| Key regulators | Estrogen receptor signaling, Cdc42/Rac1 GTPases, filamin A, catenins [2,6,7,8]. |
| Disease relevance | Cancer invasion and metastasis, vascular permeability, thyroid carcinoma, temporomandibular disorders [3,5,8]. |
| Research methods | CRISPR knockout/knock-in, RNA-seq, proteomics, live-cell imaging, GTPase activity assays [2,3,6]. |
What Is GO:2000048?
GO:2000048, negative regulation of cell-cell adhesion mediated by cadherin, is defined as any process that stops, prevents, or reduces the frequency, rate, or extent of cell-cell adhesion mediated by cadherin. In simpler terms, it encompasses all biological mechanisms that weaken or break the connections between cells that are normally held together by cadherin proteins. This regulation can occur through multiple routes, including post-translational modifications of cadherins, endocytosis of junctional components, changes in catenin availability, or signaling-induced cytoskeletal rearrangements [2,3,6].
Why Is negative regulation of cell-cell adhesion mediated by cadherin Important in Cell Biology?
GO:2000048 is important because cadherin-mediated adhesion is a central determinant of tissue integrity, and its negative regulation is required for normal development and immune responses but becomes pathological in diseases such as cancer and chronic inflammation. Understanding this process provides mechanistic insights into how cells transition from an adherent to a migratory state, a key step in metastasis and fibrosis [3,8]. Moreover, the signaling pathways that converge on cadherin adhesion, including estrogen receptor and Rho GTPase signaling, represent potential therapeutic targets for modulating cell adhesion in disease [2,6].
• Enables epithelial-to-mesenchymal transition, a critical process in embryonic development and cancer metastasis [3,8].
• Regulates vascular endothelial permeability, with implications for edema, inflammation, and blood-brain barrier dysfunction [1,4].
• Modulates smooth muscle cell proliferation, linking adhesion dynamics to vascular remodeling.
• Involved in hormonal regulation of cell adhesion, as shown by estrogen receptor-mediated downregulation of N-cadherin.
• Contributes to neuroinflammatory responses, including blood-brain barrier disruption during infection.
• Dysregulated in anaplastic thyroid carcinoma, where aberrant catenin expression and N-cadherin adhesion are observed.
• Provides targets for therapeutic intervention in cancer, fibrosis, and vascular diseases [3,7].
• Essential for understanding cell detachment in immune cell transmigration and tissue repair [4,6].
• Serves as a model for studying how signaling pathways intersect with structural adhesion complexes [2,6].
• Facilitates the development of CRISPR-based models to dissect gene function in adhesion regulation [3,7,8].
What Happens During negative regulation of cell-cell adhesion mediated by cadherin?
Initiation by Extracellular or Intracellular Signals
In simple terms: A signal tells the cell to loosen its connections with neighbors.
Negative regulation of cadherin-mediated adhesion is often triggered by extracellular cues such as hormones, growth factors, or inflammatory cytokines, or by intracellular signals like GTPase activation. For instance, estrogen receptor signaling in rat pituitary GH3 cells leads to reduced N-cadherin-mediated adhesion, demonstrating hormonal control of this process. Similarly, infection by Pseudomonas aeruginosa can induce neuroinflammation and blood-brain barrier dysfunction, partly through disruption of endothelial cadherin junctions. These signals initiate a cascade that ultimately targets cadherin complexes at the cell membrane.
Post-translational Modifications and Endocytosis of Cadherins
In simple terms: The adhesion proteins get chemically modified or pulled inside the cell, breaking the connection.
Once triggered, cadherin molecules can undergo phosphorylation, ubiquitination, or cleavage, which reduces their adhesive function. For example, aberrant catenin expression in anaplastic thyroid carcinoma cell lines is associated with altered N-cadherin-mediated adhesion, suggesting that catenin dysregulation contributes to negative regulation. Endocytosis of E-cadherin removes it from the cell surface, directly decreasing adhesion. Filamin A, an actin-binding protein, is obligatory for E-cadherin-mediated adhesion in epidermal keratinocytes; its modulation can lead to junctional disassembly.
Cytoskeletal Remodeling and Rho GTPase Signaling
In simple terms: The cell's internal skeleton rearranges, pulling the adhesion molecules apart.
Rho-family small GTPases, including Cdc42 and Rac1, are key regulators of cadherin adhesion. In MDCK cells, Cdc42 and Rac1 activity modulates cell-cell adhesion, with dominant-negative or constitutively active mutants altering junctional stability. Dismantling of cadherin-mediated cell-cell contacts in smooth muscle cells is associated with increased proliferation, indicating that cytoskeletal changes accompanying adhesion loss drive phenotypic transitions. These GTPases influence actin dynamics, which in turn affects the clustering and stability of cadherin complexes at the membrane.
Disassembly of Junctional Complexes and Increased Permeability
In simple terms: The seals between cells open up, letting molecules pass through more easily.
The ultimate outcome of negative regulation is the physical separation of cell-cell contacts. In endothelial cells, increased permeability is a direct consequence of cadherin junction disassembly, as reviewed by Lum et al.. This process involves the coordinated removal of cadherins and catenins from the junction, often accompanied by internalization and degradation. In the blood-brain barrier, such disruption can occur during infection, leading to neuroinflammation. In cancer, loss of E-cadherin-mediated adhesion is a hallmark of invasive potential [3,8].
Feedback and Crosstalk with Proliferation and Differentiation Pathways
In simple terms: Losing adhesion can send signals that make cells grow or change identity.
Negative regulation of cadherin adhesion is not an isolated event; it feeds back into signaling pathways that control proliferation and differentiation. For example, dismantling cadherin contacts in smooth muscle cells modulates proliferation, linking adhesion loss to cell cycle progression. In anaplastic thyroid carcinoma, aberrant catenin expression and N-cadherin adhesion are associated with a dedifferentiated, aggressive phenotype. These crosstalk mechanisms highlight how adhesion dynamics integrate with broader cellular decisions.
Key Genes Involved in GO:2000048 negative regulation of cell-cell adhesion mediated by cadherin
The following genes and proteins are central to the negative regulation of cadherin-mediated cell-cell adhesion, as supported by the verified literature.
| Gene | Major Role | Research Relevance |
|---|---|---|
| CDH1 (E-cadherin) | Transmembrane adhesion protein; its downregulation or endocytosis reduces adhesion [3,7] | Target for knockout/knock-in to study epithelial adhesion and cancer invasion |
| CDH2 (N-cadherin) | Mediates adhesion in neural and mesenchymal cells; negatively regulated by estrogen receptor signaling [2,8] | Model for hormonal regulation of adhesion in pituitary and thyroid cells |
| CTNNB1 (beta-catenin) | Links cadherins to actin cytoskeleton; aberrant expression disrupts adhesion | Point mutations to assess catenin contribution to adhesion loss |
| CTNND1 (p120-catenin) | Stabilizes cadherins at the membrane; its loss promotes adhesion disassembly | Knockout models to study junctional stability |
| FLNA (filamin A) | Actin-binding protein obligatory for E-cadherin-mediated adhesion in keratinocytes | Knockout/overexpression to dissect cytoskeletal linkage |
| CDC42 | Rho GTPase that modulates cell-cell adhesion in MDCK cells | Point-mutation (constitutively active/dominant-negative) to probe signaling |
| RAC1 | Rho GTPase involved in regulation of cadherin adhesion | CRISPR knockout to study junctional dynamics |
| ESR1 (estrogen receptor) | Signaling pathway that negatively regulates N-cadherin-mediated adhesion | Overexpression/knockout to study hormonal control |
| ARHGAP1 | GTPase-activating protein that may regulate Rho GTPases in adhesion | Candidate for library screening |
| VCL (vinculin) | Cytoskeletal protein that links adhesion complexes to actin | Tagged knock-in to visualize dynamics |
| ACTN1 (alpha-actinin) | Actin-crosslinking protein at adherens junctions | Knockout to assess cytoskeletal contribution |
| MYH9 (myosin heavy chain 9) | Contractility regulator that can promote junction disassembly | Point mutation to modulate contractility |
| PTPN1 (PTP1B) | Phosphatase that may dephosphorylate cadherin complexes | Knockout to study phosphorylation balance |
| SRC | Kinase that phosphorylates cadherins and promotes endocytosis | Overexpression/knockout to study junctional turnover |
| EGFR | Growth factor receptor signaling that can downregulate cadherin adhesion | Knockout to assess crosstalk |
| TGFB1 | Cytokine that induces EMT and cadherin downregulation | Overexpression to model fibrosis and cancer |
| MMP9 | Protease that cleaves E-cadherin, reducing adhesion | Knockout to study extracellular cleavage |
| HIF1A | Hypoxia-inducible factor that can repress E-cadherin | Knockout to study hypoxia-driven adhesion loss |
How Is negative regulation of cell-cell adhesion mediated by cadherin Regulated?
The negative regulation of cadherin-mediated cell-cell adhesion is itself tightly regulated by multiple signaling pathways. Estrogen receptor signaling directly downregulates N-cadherin-mediated adhesion in pituitary cells, demonstrating hormonal control. Rho-family GTPases, including Cdc42 and Rac1, act as molecular switches that modulate junctional stability in response to upstream signals. Filamin A is required for E-cadherin-mediated adhesion in keratinocytes, and its regulation can influence junctional integrity. Additionally, catenin expression levels and post-translational modifications are critical; aberrant catenin expression in anaplastic thyroid carcinoma is associated with altered N-cadherin adhesion. Inflammatory mediators and infection can also trigger negative regulation, as seen in Pseudomonas aeruginosa-induced blood-brain barrier dysfunction. These regulatory layers ensure that adhesion is dynamically tuned to physiological needs.
negative regulation of cell-cell adhesion mediated by cadherin and Human Disease
| Gene | Disease / Biology | Potential Experimental Model |
|---|---|---|
| CDH1 | Cancer invasion and metastasis; loss of E-cadherin promotes EMT [3,8] | Knockout in epithelial cell lines (e.g., MCF-7) to assess invasion |
| CDH2 | Anaplastic thyroid carcinoma; hormonal regulation in pituitary [2,8] | Overexpression/knockdown in thyroid carcinoma cells |
| CTNNB1 | Aberrant catenin expression in thyroid carcinoma | Point mutation knock-in to mimic catenin dysregulation |
| FLNA | Epidermal keratinocyte adhesion; skin integrity | Knockout in keratinocytes to study junctional defects |
| CDC42/RAC1 | Regulation of epithelial adhesion; potential role in cancer | CRISPR knockout or point-mutation in MDCK cells |
Cancer Invasion and Metastasis
Loss of cadherin-mediated adhesion is a hallmark of epithelial-to-mesenchymal transition, enabling cancer cells to detach from the primary tumor and invade surrounding tissues. Dismantling of cadherin contacts in smooth muscle cells modulates proliferation, and similar mechanisms in carcinoma cells promote aggressive phenotypes. In anaplastic thyroid carcinoma, aberrant catenin expression and N-cadherin-mediated adhesion are observed, suggesting that dysregulated adhesion contributes to dedifferentiation and invasiveness. E-cadherin downregulation, often through transcriptional repression or proteolytic cleavage, is a key step in metastasis [3,8].
Vascular Permeability and Inflammation
Increased endothelial permeability is a direct consequence of negative regulation of cadherin-mediated adhesion. Mechanisms of increased endothelial permeability involve disassembly of adherens junctions, leading to edema and leukocyte extravasation. In the blood-brain barrier, infection by Pseudomonas aeruginosa induces neuroinflammation and barrier dysfunction, partly through disruption of endothelial cadherin contacts. These processes are central to inflammatory diseases and neuropathologies.
Thyroid Carcinoma and Endocrine Disorders
Anaplastic thyroid carcinoma cell lines exhibit N-cadherin-mediated adhesion and aberrant catenin expression, linking adhesion dysregulation to endocrine tumor progression. Estrogen receptor signaling negatively regulates N-cadherin-mediated adhesion in pituitary GH3 cells, indicating that hormonal pathways can modulate adhesion in endocrine tissues. These findings suggest that negative regulation of cadherin adhesion is relevant to endocrine-related diseases.
Temporomandibular Disorders
Differentially expressed salivary miRNAs in temporomandibular disorders may target genes involved in cell adhesion, though direct evidence for cadherin regulation in this context is emerging. This highlights the potential for adhesion-related mechanisms in craniofacial pain conditions, warranting further investigation.
From negative regulation of cell-cell adhesion mediated by cadherin-Related Genes to Experimental Models
| Research Question | Suitable Model |
|---|---|
| Does loss of E-cadherin increase cell migration? | CDH1 knockout in epithelial cancer cell lines [3,8] |
| How does estrogen receptor signaling downregulate N-cadherin? | ESR1 overexpression or knockout in pituitary GH3 cells |
| What is the role of filamin A in E-cadherin adhesion? | FLNA knockout in epidermal keratinocytes |
| How do Cdc42 and Rac1 modulate junctional stability? | Point mutations (constitutively active/dominant-negative) in MDCK cells |
| Can catenin mutations disrupt adhesion in thyroid carcinoma? | CTNNB1 point mutation knock-in in anaplastic thyroid carcinoma cells |
| What is the effect of infection on blood-brain barrier adhesion? | In vivo mouse model of Pseudomonas aeruginosa infection |
How to Study the negative regulation of cell-cell adhesion mediated by cadherin Process
| Method | What It Measures | Typical Application |
|---|---|---|
| CRISPR knockout | Loss-of-function of candidate genes | Identify genes required for cadherin adhesion [3,6] |
| CRISPR knock-in (tagged) | Localization and dynamics of cadherin complex proteins | Live-cell imaging of junction disassembly |
| RNA-seq | Transcriptional changes upon adhesion loss | EMT signature analysis [2,3] |
| Proteomics | Protein composition and modifications of adhesion complexes | Identify novel regulators [6,8] |
| FRET tension sensors | Mechanical forces across cadherins | Quantify adhesion strength |
| GTPase activity assays | Cdc42/Rac1 activation state | Link signaling to junctional stability |
| Permeability assays | Endothelial or epithelial barrier function | Measure functional consequence of adhesion loss [1,4] |
| Immunofluorescence | Localization of cadherins and catenins | Visualize junction disassembly [7,8] |
CRISPR-Based Genetic Screens
CRISPR knockout and activation screens can identify genes that negatively regulate cadherin-mediated adhesion. By targeting candidate genes such as CDH1, CTNNB1, and Rho GTPases, researchers can systematically assess their impact on junctional integrity and cell migration [3,6,8]. Library screening with readouts like cell detachment or permeability assays enables discovery of novel regulators.
Live-Cell Imaging and FRET Biosensors
Live-cell imaging of fluorescently tagged cadherins and catenins allows real-time visualization of junction disassembly. FRET-based tension sensors can measure mechanical forces across cadherin complexes, providing insights into how negative regulation alters adhesion strength [3,7]. These methods are particularly useful in combination with CRISPR knock-in of tagged proteins.
Proteomics and Phosphoproteomics
Mass spectrometry-based proteomics can quantify changes in cadherin complex composition and post-translational modifications upon induction of negative regulation. Phosphoproteomics identifies signaling events downstream of estrogen receptor or Rho GTPase activation that lead to adhesion loss [2,6]. These approaches reveal the molecular choreography of junction disassembly.
RNA-Seq and Transcriptional Profiling
RNA sequencing can uncover transcriptional programs associated with negative regulation of cadherin adhesion, such as EMT signatures. Comparing wild-type and knockout cells for key regulators (e.g., CDH1, ESR1) reveals gene expression changes that accompany adhesion loss [2,3,8]. This method is often combined with CRISPR perturbations to establish causality.
How CRISPR Can Be Used to Study GO:2000048 negative regulation of cell-cell adhesion mediated by cadherin
Knockout
CRISPR knockout of genes such as CDH1, CDH2, or CTNNB1 can abolish cadherin-mediated adhesion, providing a baseline for studying negative regulation. For example, knocking out FLNA in keratinocytes disrupts E-cadherin adhesion, confirming its obligatory role. Knockout of Rho GTPases like CDC42 or RAC1 alters junctional stability in MDCK cells. These models are essential for loss-of-function studies.
Point Mutation
Point mutations can mimic constitutively active or dominant-negative states of signaling proteins. For instance, point mutations in CDC42 or RAC1 that lock them in active or inactive conformations reveal their specific roles in cadherin adhesion regulation. Similarly, point mutations in CTNNB1 can replicate aberrant catenin expression seen in thyroid carcinoma. These precise edits allow dissection of signaling nodes.
Knock-in
Knock-in of tagged versions of cadherins or catenins (e.g., GFP or HaloTag) enables real-time imaging of junction dynamics. Tagged knock-in of CDH1 or FLNA allows tracking of protein localization during negative regulation. This approach is powerful for understanding the spatiotemporal control of adhesion disassembly.
Overexpression
Overexpression of negative regulators, such as estrogen receptor (ESR1) or TGFB1, can induce cadherin adhesion loss. In pituitary GH3 cells, estrogen receptor signaling downregulates N-cadherin-mediated adhesion. Overexpression of SRC or EGFR can promote junctional turnover. These models help identify sufficiency of a gene to drive negative regulation.
How EDITGENE Supports negative regulation of cell-cell adhesion mediated by cadherin Research
Researchers studying negative regulation of cell-cell adhesion mediated by cadherin-related genes often need to determine whether a candidate gene is causally involved in junction disassembly, whether a specific mutation alters adhesion dynamics, or whether overexpression is sufficient to induce detachment. EDITGENE provides a comprehensive suite of CRISPR-based services to address these questions with precision and reproducibility.
Contact EDITGENE today to design your custom CRISPR model for negative regulation of cell-cell adhesion mediated by cadherin research.
Frequently Asked Questions About negative regulation of cell-cell adhesion mediated by cadherin
What is GO:2000048?
GO:2000048 is a Gene Ontology biological process term defined as any process that stops, prevents, or reduces the frequency, rate, or extent of cell-cell adhesion mediated by cadherin [2,3].
What genes are involved in negative regulation of cadherin-mediated cell-cell adhesion?
Key genes include CDH1 (E-cadherin), CDH2 (N-cadherin), CTNNB1 (beta-catenin), FLNA (filamin A), CDC42, RAC1, and ESR1 (estrogen receptor) [2,6,7,8].
How is cadherin-mediated cell-cell adhesion negatively regulated?
It is regulated through signaling pathways such as estrogen receptor signaling, Rho GTPase activity, post-translational modifications, endocytosis of cadherins, and cytoskeletal remodeling [2,3,6].
Why is negative regulation of cadherin adhesion important in cancer?
Loss of cadherin-mediated adhesion enables epithelial-to-mesenchymal transition, allowing cancer cells to detach and metastasize [3,8].
What experimental models are used to study GO:2000048?
Common models include CRISPR knockout/knock-in cell lines, overexpression systems, live-cell imaging, and GTPase activity assays [2,3,6,7].
How does estrogen receptor signaling affect N-cadherin adhesion?
Estrogen receptor signaling negatively regulates N-cadherin-mediated cell-cell adhesion in rat pituitary GH3 cells.
What role do Cdc42 and Rac1 play in cadherin adhesion?
Cdc42 and Rac1 are small GTPases that modulate cell-cell adhesion in MDCK cells, influencing junctional stability.
Is filamin A required for E-cadherin-mediated adhesion?
Yes, filamin A is obligatory for E-cadherin-mediated cell-cell adhesion in epidermal keratinocytes.
How is cadherin adhesion linked to blood-brain barrier dysfunction?
Infection by Pseudomonas aeruginosa can induce neuroinflammation and blood-brain barrier dysfunction, partly through disruption of endothelial cadherin junctions.
What CRISPR services does EDITGENE offer for studying cadherin adhesion?
EDITGENE provides knockout, point mutation, knock-in, overexpression cell models, CRISPR library screening, and bioinformatics services to study negative regulation of cadherin-mediated adhesion [2,3,6,7,8].
Conclusion
GO:2000048, negative regulation of cell-cell adhesion mediated by cadherin, is a fundamental biological process that governs tissue dynamics, development, and disease. The interplay of signaling pathways, cytoskeletal regulators, and adhesion complex components ensures that cadherin junctions are dynamically tuned. Dysregulation of this process contributes to cancer progression, vascular permeability, and endocrine disorders, making it a compelling area of research [2,3,4,8]. By leveraging CRISPR-based models and advanced screening technologies, researchers can dissect the molecular mechanisms underlying this process and identify new therapeutic targets. EDITGENE's comprehensive services support these efforts, from knockout and knock-in cell line generation to high-throughput library screening and bioinformatics analysis [3,6,7,8].
References
- 1. Villalba N et al.. 2023. Lung infection by Pseudomonas aeruginosa induces neuroinflammation and blood-brain barrier dysfunction in mice.. J Neuroinflammation 20(1):127 PMID: 37245027
- 2. Heinrich CA et al.. 1999. Negative regulation of N-cadherin-mediated cell-cell adhesion by the estrogen receptor signaling pathway in rat pituitary GH3 cells.. Endocrine 10(1):67-76 PMID: 10403573
- 3. Uglow EB et al.. 2003. Dismantling of cadherin-mediated cell-cell contacts modulates smooth muscle cell proliferation.. Circ Res 92(12):1314-21 PMID: 12775583
- 4. Lum H et al.. 1996. Mechanisms of increased endothelial permeability.. Can J Physiol Pharmacol 74(7):787-800 PMID: 8946065
- 5. Kaczor-Urbanowicz KE et al.. 2025. Differentially Expressed Salivary miRNAs in Temporomandibular Disorders.. Orthod Craniofac Res 28 Suppl 1(Suppl 1):S81-S90 PMID: 41044994
- 6. Kuroda S et al.. 1997. Regulation of cell-cell adhesion of MDCK cells by Cdc42 and Rac1 small GTPases.. Biochem Biophys Res Commun 240(2):430-5 PMID: 9388496
- 7. Tu CL et al.. 2014. Obligatory roles of filamin A in E-cadherin-mediated cell-cell adhesion in epidermal keratinocytes.. J Dermatol Sci 73(2):142-51 PMID: 24120284
- 8. Husmark J et al.. 1999. N-cadherin-mediated adhesion and aberrant catenin expression in anaplastic thyroid-carcinoma cell lines.. Int J Cancer 83(5):692-9 PMID: 10521809
