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**Transient pore formation in plasma membrane** refers to a biophysical phenomenon where short-lived, nanoscale openings (pores) are formed in the lipid bilayer of the cell membrane. Such pores can be induced by physical stresses (like electroporation[3], mechanical stretch[2][5]), chemical agents (detergents, peptides such as melittin or alamethicin[4]), or protein toxins (pore-forming proteins, PFPs[1]). These pores typically exist for milliseconds to seconds before resealing, leading to transient loss of membrane barrier function. This process plays roles in physiological events (membrane repair, endocytosis), in cell death (necrosis, apoptosis via Bax/Bak pores), in infections (bacterial toxins), and is exploited for drug delivery (e.g., polymer transfection reagents[6]). It is not a “target” in the sense of a receptor or single protein but a physical state exploited or modulated by drugs or peptides. Control over transient pore formation is a major challenge due to unpredictable size, lifetime, and non-specificity, making safety and efficacy hard to manage in therapeutic contexts[5][6]. Note: - This is not a canonical molecular target (not a protein, enzyme, receptor, etc.), but a cellular event or membrane state. - The entry is "incorrect" as a target in drug discovery informatics; it refers to a process, not a discrete targetable biomolecule. - For actual “targets,” consider specific pore-forming proteins (e.g., Perforin, Bax, MAC) or agents (e.g., Melittin) that induce transient pore formation[1][4].
Direct physical disruption of lipid bilayer Formation of transient, non-equilibrium pores allowing leakage of cellular contents and influx of ions Facilitation of molecular or ion passage via short-lived defects
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