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A cell is enclosed by a plasma membrane, which forms a selective barrier that allows nutrients to enter and waste products to leave.
Extraction with the use of a porous membrane which forms an interphase between two bulk phases and provides the physical surface for mass transfer is, in a number of applications, more efficient than that carried out in conventional devices.
The first step of antibiotic interaction with Gram-negative bacteria is to cross the outer membrane, which forms a protective barrier against hostile environments [3], [4].
Following initiation, nucleation generates a phagophore, or a cup-shaped double-bilipid membrane, which forms at the initiation site.
The myo-epithelium of the alveoli is discontinuous so that the luminal cells directly contact the underlying basement membrane, which forms part of the extracellular matrix.
DOI: http://dx.doi.org/10.7554/eLife.07118.001 All bacterial cells are surrounded by a membrane, which forms a protective barrier around the cell.
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Synaptic vesicle fusion with the presynaptic plasma membrane is mediated by the three neuronal SNARE proteins synaptobrevin-2 (on the synaptic vesicle membrane), SNAP-25 and syntaxin-1 (on the presynaptic plasma membrane), which form the synaptic SNARE-complex.
In forming multiple anastomosing strands surrounding the cells they allow close contacts between opposing cytoplasma membranes which form a barrier regulating the passage of small molecules, ions, water and pathogens, thereby protecting subepithelial and -endothelial tissues from the external environment [ 1- 3].
Model studies have proposed that trimerization involves not only the coiled-coil stem but also the C-terminal membrane anchor, which forms a 12-strand β-barrel from the four transmembrane β-strands of the three monomers.
Further, insect chitinases modulate the thickness of the peritrophic membrane (PM) which forms a film-like structure separating undigested nutrients from epithelial cells protecting the epithelium from food abrasion and enteric pathogens (reviewed by [32].
The 'membrane repair hypothesis' postulates that dysferlin is a key component of the muscle membrane repair system, which forms vesicle plugs over membrane lesions, maintaining cell homeostasis before the formation of new membrane (16, 17).
More suggestions(15)
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