A team of researchers led by Associate Professor Ken Natsuga found that cell-cell adhesion governs pattern formation in keratinocytes. Starvation also plays a crucial role in the formation of these patterns, which are influenced by cell proliferation and differentiation.
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Researchers found phosphatidylinositol bisphosphate (PIP2) essential for epithelial cell-cell adhesion and maintaining cellular identity. PIP2 regulates epithelial properties by recruiting Par3 to the plasma membrane, facilitating the formation of adherens junctions and preventing epithelial-mesenchymal transformation.
Researchers found that RNAi machinery primarily localizes at apical adherens junctions in healthy colon cells but becomes mis-localized in colon cancer. This localization plays a crucial role in maintaining epithelial homeostasis, with restoration of the RNAi machinery potentially serving as a brake on tumor progression.
E-cadherin molecules form small clusters of about five molecules, which then recruit more molecules and organize into the adherens junction. The actin cytoskeleton fences these clusters, preventing them from merging to form a belt.
Researchers have uncovered evidence that adherens junctions actively respond to mechanical cues by remodeling their own position and intensity. This discovery sheds light on the organization of multi-cellularity, from cell-cell contacts to the remodeling of tissues and organs during life.
Researchers at Penn find that mechanical forces reinforce and grow endothelial cell connections, creating stronger adhesions. This discovery has implications for therapies targeting vascular dysfunction in diseases like septic shock and diabetes.
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The study reveals that the NF2 gene's protein, merlin, organizes cellular structures facilitating cell-to-cell communication and plays a crucial role in tumor development. Loss of merlin function may contribute to cancer progression and metastasis, providing potential therapeutic targets for NF2-associated cancers.
Researchers have identified a key function of merlin in maintaining adherens junctions, which are essential for suppressing cancer development and progression. The study reveals that loss of merlin results in destabilization of these junctions, leading to unchecked cell proliferation and tumor formation.