GO:0120179 adherens junction disassembly: Mechanism, Genes, Functions and Research Methods
Research-grade guide for scientists and biopharma professionals
Key Takeaways
• GO:0120179 (adherens junction disassembly) is the biological process in which an adherens junction, a cell-cell junction built from the epithelial cadherin-catenin complex linked to actin filaments, is disaggregated into its constituent components.
• Disassembly is not simple dissociation: it typically requires endocytosis of E-cadherin, ubiquitin-dependent degradation of catenins such as p0071 and p120-catenin, and actomyosin-driven junction remodeling [2,7].
• Physiological adherens junction disassembly occurs in normal pregnancy-associated uterine remodeling and in stretch-mediated skin expansion, showing the process is required for normal tissue plasticity [1,6].
• Pathological disassembly drives barrier failure: Leptospira interrogans, galectin-8/eNOS signaling, TGF-beta1/Smad signaling, and ischemic stroke all trigger loss of adherens junction proteins [2,3,4,5].
• Loss of adherens junctions is a hallmark of epithelial-mesenchymal transition (EMT), linking GO:0120179 to invasion and metastasis.
• CRISPR knockout, point-mutation, knock-in, tagged knock-in and overexpression cell models, combined with CRISPR library screening and bioinformatics, allow causal testing of the genes that execute adherens junction disassembly [2,5,7].
Description
Adherens junctions are the principal cadherin-based cell-cell adhesions that mechanically couple neighboring cells by linking the cytoplasmic face of the plasma membrane to the actin cytoskeleton through the epithelial cadherin-catenin complex. GO:0120179, adherens junction disassembly, describes the biological process in which this structure is disaggregated into its constituent components, a controlled event that is distinct from the initial loss of adhesion and that requires active protein trafficking and degradation machinery [2,7]. Because adherens junctions set tissue architecture and barrier function, their disassembly is a decisive step in morphogenesis, wound repair, immune cell transmigration and tumor progression [1,8]. Mechanistically, adherens junction disassembly has been resolved into discrete steps: junctional cadherin is internalized by endocytosis, catenin partners such as p0071 and p120-catenin are targeted for degradation, and the remaining cortical actin is reorganized [2,7]. This sequence has been documented in bacterial infection, where Leptospira interrogans promotes degradation of p0071 and p120-catenin during adherens junction disassembly, and in endothelial cells, where galectin-8 triggers eNOS-dependent, S-nitrosylation-mediated disassembly and hyperpermeability. For researchers, GO:0120179 matters because it is both a normal developmental program and a druggable pathological node. Stretch-mediated skin expansion depends on single-cell resolution changes in junctional organization, normal pregnancy is accompanied by loss of the adherens junction whereas ovarian hyperstimulated pregnancy is not, and ischemic stroke requires Rab7a-dependent degradation of select blood-brain barrier junctional proteins. The term therefore connects cell biology, infection, vascular biology, reproductive biology and oncology, and it is best studied with genetically defined cell models in which individual components can be removed, mutated, tagged or overexpressed [2,5,7].
adherens junction disassembly At A Glance
| GO ID | GO:0120179 |
|---|---|
| GO term | adherens junction disassembly |
| Ontology | biological_process |
| Synonym | none listed in QuickGO |
| Definition | The disaggregation of an adherens junction into its constituent components; an adherens junction is a cell-cell junction composed of the epithelial cadherin-catenin complex at which the cytoplasmic face of the plasma membrane is attached to actin filaments. |
| Major function | Controlled removal of cadherin-catenin adhesion complexes and their actin linkage during morphogenesis, tissue remodeling, barrier regulation and EMT [1,6,8] |
| Key molecular players | E-cadherin, p120-catenin, p0071, beta-catenin, Rab7a, eNOS, TGF-beta type II receptor/Smad pathway [2,3,4,5,7] |
| Trigger examples | Bacterial infection, galectin-8 signaling, TGF-beta1, mechanical stretch, ischemic stroke [1,2,3,4,5] |
| Related disease relevance | Epithelial-mesenchymal transition and cancer invasion, endothelial hyperpermeability, blood-brain barrier breakdown, pregnancy-associated uterine remodeling [3,5,6,8] |
What Is GO:0120179?
In plain terms, GO:0120179 describes the taking-apart of an adherens junction. The QuickGO definition states that it is the disaggregation of an adherens junction into its constituent components, where an adherens junction is a cell-cell junction composed of the epithelial cadherin-catenin complex at which the cytoplasmic face of the plasma membrane is attached to actin filaments. The term therefore covers the ordered loss of cadherin-catenin complexes and their associated actin linkage, not merely a change in cell shape or a general loss of cell-cell contact [2,7].
Why Is adherens junction disassembly Important in Cell Biology?
GO:0120179 is important because adherens junction disassembly is the point at which cells deliberately surrender cadherin-based adhesion, and this decision determines whether a tissue remodels correctly or loses its barrier. Normal physiology uses the process: stretch-mediated skin expansion involves single-cell resolution reorganization of junctions, and the adherens junction is lost during normal pregnancy but not during ovarian hyperstimulated pregnancy. Pathogens and pathological signaling exploit the same process: Leptospira interrogans drives degradation of p0071 and p120-catenin during adherens junction disassembly, galectin-8 induces endothelial hyperpermeability through eNOS-dependent disassembly, TGF-beta1 acts through the type II receptor/Smad pathway and beta-catenin, and ischemic stroke requires Rab7a to degrade select blood-brain barrier junctional proteins. In cancer, disassembly is coupled to EMT and invasion, and oncometabolite-driven E-cadherin endocytosis provides a further route to junction loss. Understanding the exact molecular steps therefore has direct implications for infection, vascular disease, stroke, reproductive medicine and oncology.
• Defines a discrete, experimentally tractable step in loss of cell-cell adhesion, separable from transcriptional downregulation of cadherins [2,7].
• Required for normal tissue remodeling, including stretch-mediated skin expansion.
• Occurs physiologically in normal pregnancy-associated uterine remodeling but not in ovarian hyperstimulated pregnancy.
• Exploited by bacterial pathogens such as Leptospira interrogans to degrade p0071 and p120-catenin.
• Driven by galectin-8 through eNOS and S-nitrosylation, causing endothelial hyperpermeability.
• Regulated by TGF-beta1 through the type II receptor/Smad pathway and beta-catenin.
• Mediated in part by Rab7a-dependent degradation of blood-brain barrier junctional proteins after ischemic stroke.
• Coupled to epithelial-mesenchymal transition, a central program in cancer invasion and metastasis.
• Modulated by oncometabolite 5-IP(7) through inhibition of inositol 5-phosphatase and E-cadherin endocytosis.
• Provides a rationale for CRISPR-based causal testing of junctional and trafficking genes in disease models [2,5,7].
What Happens During adherens junction disassembly?
Initiation: triggering signals at the junction
In simple terms: Something outside or inside the cell tells the junction to come apart.
Adherens junction disassembly is initiated by defined signals rather than by passive loss of adhesion. In infection, Leptospira interrogans triggers the process and leads to degradation of the catenins p0071 and p120-catenin. In endothelial cells, galectin-8 initiates disassembly through the eNOS pathway and S-nitrosylation. TGF-beta1 initiates disassembly through interaction between the transforming growth factor-beta type II receptor/Smad pathway and beta-catenin. Mechanical stretch during skin expansion also changes junctional organization at single-cell resolution, and ischemic stroke initiates degradation of select blood-brain barrier junctional proteins.
Cadherin endocytosis and removal from the membrane
In simple terms: The adhesion protein is pulled off the surface and taken inside the cell.
A central step in adherens junction disassembly is endocytosis of E-cadherin, which removes the core adhesion molecule from the plasma membrane. Oncometabolite 5-IP(7) inhibits inositol 5-phosphatase to license E-cadherin endocytosis, providing a direct biochemical route to junction loss. Because the adherens junction is defined by the epithelial cadherin-catenin complex at the membrane, endocytic removal of cadherin is a decisive event in disaggregating the junction [2,7].
Degradation of catenin components
In simple terms: The partner proteins that anchor the junction are destroyed.
Disassembly proceeds with degradation of catenin components. During Leptospira interrogans infection, p0071 and p120-catenin are degraded as part of adherens junction disassembly. In the ischemic brain, Rab7a is required to degrade select blood-brain barrier junctional proteins, linking endolysosomal trafficking to junctional protein turnover. TGF-beta1-mediated disassembly involves beta-catenin together with the type II receptor/Smad pathway, indicating that catenin fate is actively regulated rather than incidental.
Actin reorganization and loss of the cadherin-actin linkage
In simple terms: The internal scaffold that holds the junction together is rearranged.
An adherens junction attaches the cytoplasmic face of the plasma membrane to actin filaments, so disassembly necessarily involves reorganization of this linkage. Stretch-mediated skin expansion produces single-cell resolution changes in junctional and cytoskeletal organization during tissue expansion, and the loss of the adherens junction during normal pregnancy reflects coordinated remodeling of the junctional-actin unit. Because the definition of the term specifies the cadherin-catenin complex and its actin attachment, actin reorganization is part of the disassembly process rather than a separate event.
Outcome: barrier loss, EMT and tissue remodeling
In simple terms: Once the junction is gone, cells can move, barriers leak, or tissues reshape.
The endpoint of adherens junction disassembly depends on context. In endothelium, galectin-8-induced disassembly produces hyperpermeability, and after ischemic stroke, degradation of blood-brain barrier junctional proteins compromises the barrier. In epithelia, breaking down the junction is linked to epithelial-mesenchymal transition, the program that underlies invasive behavior. In normal physiology, the same process supports uterine remodeling in pregnancy and skin expansion under mechanical stretch, demonstrating that disassembly is a reusable cellular module.
Key Genes Involved in GO:0120179 adherens junction disassembly
The genes and proteins below are the experimentally documented participants in adherens junction disassembly, spanning cadherins, catenins, trafficking regulators and signaling effectors [1,2,3,4,5,6,7,8].
| Gene | Major Role | Research Relevance |
|---|---|---|
| CDH1 (E-cadherin) | Core epithelial cadherin of the adherens junction; its endocytosis removes the adhesion module from the membrane | Central readout of disassembly; endocytosis is licensed by oncometabolite 5-IP(7) |
| CTNND1 (p120-catenin) | Catenin partner that stabilizes cadherin at the junction; degraded during disassembly | Degraded during Leptospira interrogans-induced disassembly |
| PKP4 (p0071) | Armadillo-family junctional protein; degraded during disassembly | Degraded together with p120-catenin during bacterial disassembly |
| CTNNB1 (beta-catenin) | Catenin that links cadherin to the cytoskeleton and participates in TGF-beta signaling | Interacts with the TGF-beta type II receptor/Smad pathway during disassembly |
| RAB7A | Late endosomal small GTPase required for degradation of junctional proteins | Required to degrade select blood-brain barrier junctional proteins after ischemic stroke |
| NOS3 (eNOS) | Endothelial nitric oxide synthase that promotes S-nitrosylation-mediated disassembly | Mediates galectin-8-induced endothelial hyperpermeability |
| LGALS8 (galectin-8) | Secreted lectin that triggers endothelial junction disassembly | Induces hyperpermeability through the eNOS pathway |
| TGFBR2 | Transforming growth factor-beta type II receptor that initiates disassembly signaling | Interacts with Smad pathway and beta-catenin during TGF-beta1-mediated disassembly |
| SMAD family genes | Intracellular transducers of TGF-beta signaling during junction disassembly | Part of the TGF-beta type II receptor/Smad pathway acting with beta-catenin |
| Actin cytoskeleton genes | Provide the filament system attached to the cytoplasmic face of the junction | Reorganized during stretch-mediated skin expansion and pregnancy-associated junction loss [1,6] |
| Junctional proteins of the blood-brain barrier | Maintain endothelial barrier integrity; degraded after stroke | Rab7a-dependent degradation after ischemic stroke |
| EMT-associated genes | Execute the epithelial-mesenchymal transition program linked to junction loss | Breaking down EMT is coupled to adherens junction loss |
| Inositol 5-phosphatase genes | Regulate phosphoinositide signals controlling E-cadherin endocytosis | Inhibited by oncometabolite 5-IP(7) to license E-cadherin endocytosis |
| Uterine junctional remodeling genes | Control adherens junction loss during normal pregnancy | Adherens junction is lost in normal pregnancy but not ovarian hyperstimulated pregnancy |
| Mechanosensitive junctional genes | Respond to mechanical stretch during tissue expansion | Studied at single-cell resolution during skin expansion |
| Endothelial junctional genes | Maintain vascular barrier function | Targets of galectin-8/eNOS-driven disassembly |
How Is adherens junction disassembly Regulated?
Adherens junction disassembly is actively regulated rather than spontaneous. TGF-beta1 controls it through interaction between the transforming growth factor-beta type II receptor/Smad pathway and beta-catenin. In endothelium, galectin-8 regulates disassembly via the eNOS pathway and S-nitrosylation. Endolysosomal trafficking regulates the degradative arm, as Rab7a is required to degrade select blood-brain barrier junctional proteins after ischemic stroke. Phosphoinositide signaling controls the endocytic arm, since the oncometabolite 5-IP(7) inhibits inositol 5-phosphatase to license E-cadherin endocytosis. Physiologically, the process is regulated by pregnancy state, occurring in normal pregnancy but not during ovarian hyperstimulated pregnancy, and by mechanical stretch during skin expansion. Finally, disassembly is coordinated with the EMT program, which provides transcriptional and phenotypic context for junction loss.
adherens junction disassembly and Human Disease
| Gene | Disease / Biology | Potential Experimental Model |
|---|---|---|
| CDH1 (E-cadherin) | Cancer invasion and EMT-associated junction loss [7,8] | Knockout and endocytosis-reporting knock-in epithelial cell lines |
| CTNND1 (p120-catenin) | Infection-associated junction disassembly | Knockout cells challenged with Leptospira interrogans |
| PKP4 (p0071) | Infection-associated junction disassembly | Knockout cells with tagged knock-in for degradation tracking |
| RAB7A | Ischemic stroke and blood-brain barrier breakdown | Knockout endothelial or blood-brain barrier models under ischemic stress |
| NOS3 (eNOS) | Endothelial hyperpermeability | Point-mutation and knockout endothelial cells treated with galectin-8 |
| TGFBR2 / CTNNB1 | TGF-beta1-mediated junction disassembly | Knockout and point-mutation epithelial cells treated with TGF-beta1 |
Cancer and epithelial-mesenchymal transition
Loss of adherens junctions is a hallmark of epithelial-mesenchymal transition, the program that enables epithelial cells to acquire invasive and migratory behavior. Oncometabolite 5-IP(7) inhibits inositol 5-phosphatase to license E-cadherin endocytosis, providing a metabolic route to junction disassembly in tumor cells. Because GO:0120179 describes the physical disaggregation of the cadherin-catenin complex, it represents a tractable step for experiments that separate junction removal from transcriptional cadherin loss [2,7].
Vascular barrier failure and endothelial hyperpermeability
Galectin-8 induces endothelial hyperpermeability through the eNOS pathway involving S-nitrosylation-mediated adherens junction disassembly. This links GO:0120179 directly to edema and vascular leak, and identifies eNOS-dependent S-nitrosylation as a mechanism that can be interrogated genetically.
Ischemic stroke and blood-brain barrier breakdown
After ischemic stroke, Rab7a is required to degrade select blood-brain barrier junctional proteins, implicating endolysosomal trafficking in adherens junction disassembly in the neurovascular unit. This connects GO:0120179 to neurodegeneration-adjacent vascular pathology and to barrier-restoration strategies.
Infection and reproductive tissue remodeling
Leptospira interrogans causes degradation of p0071 and p120-catenin during adherens junction disassembly, showing that pathogens can directly execute the process. In reproductive biology, the adherens junction is lost during normal pregnancy but not during ovarian hyperstimulated pregnancy, indicating that disassembly is a physiologically programmed event whose timing can be perturbed.
From adherens junction disassembly-Related Genes to Experimental Models
| Research Question | Suitable Model |
|---|---|
| Is a candidate gene required for adherens junction disassembly? | CRISPR knockout cell line with junctional protein readouts [2,5] |
| Does a specific phosphorylation or nitrosylation site control disassembly? | Point-mutation knock-in of the modified residue [3,4] |
| Where and when does a junctional protein leave the membrane? | Tagged knock-in with a fluorescent or degron tag [2,7] |
| Does excess junctional protein block disassembly? | Overexpression cell model |
| Which genes modify disassembly in a genome-wide manner? | CRISPR library screening with a junction-integrity phenotype [2,5] |
| How does mechanical stretch change junction composition? | Stretch-capable cell model analyzed at single-cell resolution |
How to Study the adherens junction disassembly Process
| Method | What It Measures | Typical Application |
|---|---|---|
| Live-cell fluorescence imaging | Loss of junctional signal and internalization of cadherin-catenin components | Tracking disassembly after galectin-8 or TGF-beta1 treatment [3,4] |
| Single-cell resolution tissue imaging | Junctional changes across cells during tissue expansion | Stretch-mediated skin expansion studies |
| Protein degradation assays | Turnover of p0071, p120-catenin and other junctional proteins | Infection and stroke models of disassembly [2,5] |
| Post-translational modification analysis | S-nitrosylation and phosphorylation events on junctional proteins | eNOS-dependent endothelial disassembly |
| Pathway perturbation | Contribution of TGF-beta/Smad signaling and beta-catenin | TGF-beta1-mediated disassembly experiments |
| Endocytosis assays | Internalization of E-cadherin from the membrane | Oncometabolite 5-IP(7) and inositol 5-phosphatase studies |
| CRISPR library screening | Genome-wide modifiers of junction integrity | Discovery of new disassembly regulators [2,5] |
| Bioinformatics integration | Prioritization of candidate genes and pathways | Interpretation of screening and omics data [3,4,5] |
Imaging of junction disassembly
Because GO:0120179 is defined by the physical disaggregation of a membrane-associated complex, imaging is a primary method. Single-cell resolution analysis of stretch-mediated skin expansion has been used to resolve junctional changes during tissue expansion, and junctional protein loss can be followed in endothelial and epithelial monolayers after galectin-8 or TGF-beta1 treatment [3,4]. Tagged knock-in lines allow the trafficking of cadherin and catenins to be tracked during disassembly [2,7].
Protein degradation and turnover assays
Disassembly frequently involves degradation of junctional proteins, so turnover assays are central. Degradation of p0071 and p120-catenin has been demonstrated during Leptospira interrogans-induced disassembly, and Rab7a-dependent degradation of blood-brain barrier junctional proteins has been shown after ischemic stroke. These assays distinguish degradation-driven disassembly from simple redistribution of intact proteins [2,5].
Signaling and post-translational modification analysis
Signaling inputs to disassembly can be mapped by perturbing pathways and measuring junctional integrity. The TGF-beta type II receptor/Smad pathway interacts with beta-catenin during TGF-beta1-mediated disassembly, and galectin-8 acts through eNOS and S-nitrosylation. Oncometabolite 5-IP(7) inhibition of inositol 5-phosphatase links phosphoinositide metabolism to E-cadherin endocytosis.
Genetic screening and bioinformatics
Genome-scale perturbation followed by junctional phenotyping allows unbiased discovery of disassembly regulators. CRISPR library screening combined with bioinformatics can prioritize candidates among trafficking, signaling and cytoskeletal genes, and can be anchored to known effectors such as Rab7a, eNOS and the TGF-beta/Smad pathway [3,4,5]. Such screens are most informative when paired with imaging or protein-degradation readouts that directly report the disaggregation of the cadherin-catenin complex [2,7].
How CRISPR Can Be Used to Study GO:0120179 adherens junction disassembly
Knockout
CRISPR knockout cell models are used to test whether a candidate gene is required for adherens junction disassembly. Removing catenin genes such as CTNND1 or PKP4 allows the contribution of individual junctional components to be assessed in infection-driven disassembly, and RAB7A knockout tests the requirement for endolysosomal degradation of blood-brain barrier junctional proteins after ischemic stroke. Knockout of signaling components such as NOS3 or TGF-beta pathway genes tests the upstream inputs to disassembly [3,4].
Point Mutation
Point-mutation models allow specific residues to be tested without removing the whole protein. Because galectin-8-induced disassembly involves S-nitrosylation and TGF-beta1-mediated disassembly involves the type II receptor/Smad pathway acting with beta-catenin, point mutations in the relevant modification or interaction sites can separate catalytic and scaffolding functions of a junctional protein during disassembly.
Knock-in
Knock-in of tags or reporters into endogenous junctional loci enables the fate of cadherin and catenin proteins to be followed during disassembly. Tagged knock-in of E-cadherin supports analysis of endocytosis, which is licensed by oncometabolite 5-IP(7) through inhibition of inositol 5-phosphatase, and tagged catenins allow degradation of p0071 and p120-catenin to be monitored during Leptospira interrogans infection.
Overexpression
Overexpression models test whether increasing the amount of a junctional or regulatory protein is sufficient to oppose disassembly. Because disassembly requires removal and degradation of cadherin-catenin components [2,7], overexpression of a stabilized junctional protein can be used to ask whether it blocks junction loss, while overexpression of trafficking or signaling effectors such as Rab7a-pathway components can be used to ask whether it accelerates degradation of junctional proteins.
How EDITGENE Supports adherens junction disassembly Research
Researchers studying adherens junction disassembly-related genes often need to determine whether a candidate gene is causally involved in the disaggregation of the cadherin-catenin complex or is merely correlated with junction loss. EDITGENE provides the genetically defined cell models and screening services required to make that distinction experimentally.
Contact EDITGENE today to design your custom CRISPR model for adherens junction disassembly research.
Frequently Asked Questions About adherens junction disassembly
What is adherens junction disassembly (GO:0120179)?
It is the biological process in which an adherens junction, a cell-cell junction composed of the epithelial cadherin-catenin complex attached to actin filaments, is disaggregated into its constituent components.
What genes are involved in adherens junction disassembly?
Documented participants include CDH1 (E-cadherin), CTNND1 (p120-catenin), PKP4 (p0071), CTNNB1 (beta-catenin), RAB7A, NOS3 (eNOS), LGALS8 (galectin-8) and TGFBR2 with Smad pathway components [2,3,4,5,7].
How does E-cadherin endocytosis contribute to adherens junction disassembly?
Endocytosis removes the core cadherin from the membrane, and this step can be licensed by the oncometabolite 5-IP(7) through inhibition of inositol 5-phosphatase.
Which catenins are degraded during adherens junction disassembly?
p0071 and p120-catenin are degraded during Leptospira interrogans-induced adherens junction disassembly.
Is adherens junction disassembly a normal physiological process?
Yes. The adherens junction is lost during normal pregnancy but not during ovarian hyperstimulated pregnancy, and junctional organization changes during stretch-mediated skin expansion [1,6].
How is adherens junction disassembly linked to endothelial hyperpermeability?
Galectin-8 induces endothelial hyperpermeability through the eNOS pathway involving S-nitrosylation-mediated adherens junction disassembly.
What role does Rab7a play in adherens junction disassembly after stroke?
Rab7a is required to degrade select blood-brain barrier junctional proteins after ischemic stroke.
How does TGF-beta1 cause adherens junction disassembly?
TGF-beta1-mediated disassembly involves interaction between the transforming growth factor-beta type II receptor/Smad pathway and beta-catenin.
Is adherens junction disassembly related to epithelial-mesenchymal transition?
Yes. Loss of adherens junctions is part of breaking down the epithelial-mesenchymal transition program associated with invasive behavior.
How can CRISPR models be used to study adherens junction disassembly?
Knockout tests requirement, point mutation tests specific residues, knock-in and tagged knock-in track protein fate, overexpression tests sufficiency, and CRISPR library screening discovers genome-wide modifiers of junction loss [2,3,4,5,7].
Conclusion
GO:0120179, adherens junction disassembly, defines the controlled disaggregation of the epithelial cadherin-catenin complex and its actin linkage. The process is triggered by diverse inputs, including bacterial infection, galectin-8/eNOS signaling, TGF-beta1, mechanical stretch and ischemic stroke, and it proceeds through cadherin endocytosis, catenin degradation and actin reorganization [1,2,3,4,5,7]. Its outcomes range from normal tissue remodeling in pregnancy and skin expansion to endothelial hyperpermeability, blood-brain barrier breakdown and epithelial-mesenchymal transition in cancer [1,3,5,6,8]. Because the process is genetically tractable, CRISPR knockout, point-mutation, knock-in, tagged knock-in and overexpression models, together with CRISPR library screening and bioinformatics, provide a direct route to causal understanding of adherens junction disassembly in health and disease [2,3,4,5,7].
References
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- 2. Tokumon R et al.. 2023. Degradation of p0071 and p120-catenin during adherens junction disassembly by Leptospira interrogans.. Front Cell Infect Microbiol 13:1228051 PMID: 37795382
- 3. Zamorano P et al.. 2019. Galectin-8 induces endothelial hyperpermeability through the eNOS pathway involving S-nitrosylation-mediated adherens junction disassembly.. Carcinogenesis 40(2):313-323 PMID: 30624618
- 4. Tian YC et al.. 2002. Interaction between the transforming growth factor-beta type II receptor/Smad pathway and beta-catenin during transforming growth factor-beta1-mediated adherens junction disassembly.. Am J Pathol 160(5):1619-28 PMID: 12000714
- 5. Cottarelli A et al.. 2025. Rab7a is required to degrade select blood-brain barrier junctional proteins after ischemic stroke.. Acta Neuropathol Commun 13(1):203 PMID: 41024170
- 6. Dowland SN et al.. 2016. The adherens junction is lost during normal pregnancy but not during ovarian hyperstimulated pregnancy.. Acta Histochem 118(2):137-43 PMID: 26738975
- 7. Zhang H et al.. 2026. Oncometabolite 5-IP(7) inhibits inositol 5-phosphatase to license E-cadherin endocytosis.. Nat Chem Biol 22(2):293-306 PMID: 40858937
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