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Manipulating the Intracellular Trafficking of Nucleic Acids
Published in Kenneth L. Brigham, Gene Therapy for Diseases of the Lung, 2020
Kathleen E. B Meyer, Lisa S. Uyechi, Francis C. Szoka
Nuclear envelope assembly occurs in anaphase and telophase, and begins with dephosphorylation of the putative nuclear envelope receptor, which permits the sequential targeting of membrane components to the chromatin surface. Vesicles (80 to 200 nm in diameter) containing the lamin B receptor, an inner membrane protein, are the first components to initiate the assembly process (167-169). Experiments employing tryptic digestion have shown that vesicle chromatin association requires proteins on both the vesicle and the chromatin to interact for the priming of the spontaneous reassociation of nuclear envelope components (156,166). The fusion of membrane vesicles follows vesicle coating of chromatin, producing a double lipid bilayer structure. Nuclear membrane reassembly then proceeds by the incorporation of NPCs and reassembly of the lamina matrix. Vesicle binding to chromatin is independent of ATP (166); however, vesicle fusion requires the presence of both ATP and GTP (166,170). Vesicle fusion is inhibited by treatment of both cytoplasmic and membrane fractions with NEM, confirming the involvement of protein interaction in vesicle binding, and is inhibited by treatment with the calcium chelator BAPTA suggesting a role of calcium in the fusion process (169).
Homeostasis of Dopamine
Published in Nira Ben-Jonathan, Dopamine, 2020
Despite the abovementioned differences in the origin and trafficking between synaptic and secretory vesicles, three over-encompassing models of exocytosis and its coupling to endocytosis have emerged [75]. The first model has been coined “full-collapse fusion.” According to this model, in response to a stimulus, vesicles are collapsed into the plasma membrane, followed by a clathrin-dependent endocytosis that involves membrane invagination and vesicular reformation. The full-collapse fusion is associated with a rapidly expanding vesicular pore and a complete release of the vesicular content. The second model is named “kiss-and-run.” According to this model, the fusion pore opens and closes rapidly, and it is associated with a fast disengagement of the vesicle from the active zone. The third model is known as the “compound exocytosis.” According to this model, exocytosis includes very large vesicles that are formed by vesicle–vesicle fusion, followed by bulk endocytosis that retrieves giant vesicles. A schematic illustration of the various models of exocytosis is shown in Figure 1.11.
Cytotoxicology Studies of 2-D Nanomaterials
Published in Suresh C. Pillai, Yvonne Lang, Toxicity of Nanomaterials, 2019
Priyanka Ganguly, Ailish Breen, Suresh C. Pillai
Clathrin-coated vesicles are utilised to internalise NMs of size usually <100 nm. It is a receptor-mediated endocytosis pathway, where the plasma membrane undergoes inward budding and forms vesicles. The vesicles are layered with various protein receptors permitted to internalise the specific molecule (Sorkin and Puthenveedu, 2013). In this energy-dependent process the clathrin does not interact with the membrane or the ingested particles. It completely depends on the protein receptors and the accessory proteins present on the walls of the vesicles. The accessory proteins are the cytoplasmic proteins which are later subjected to reuse for another endocytosis cycle. The internalised NMs experience organization in the endosomes and are later sent to the surface or delivered to other mature endosomes like lysosomes (McMahon and Boucrot, 2011). The uptake of nutrients, activation of signalling pathways, regulation of surface expression of proteins, and retrieval of proteins deposited after vesicle fusion are some of the functions associated with clathrin-mediated endocytosis (Chen et al., 1998; Liu et al., 2001; McMahon and Boucrot, 2011; Motley et al., 2003; Sikora et al., 2017).
Homocysteine can aggravate depressive like behaviors in a middle cerebral artery occlusion/reperfusion rat model: a possible role for NMDARs-mediated synaptic alterations
Published in Nutritional Neuroscience, 2023
Mengying Wang, Xiaoshan Liang, Qiang Zhang, Suhui Luo, Huan Liu, Xuan Wang, Na Sai, Xumei Zhang
VGLUT1 is a specific presynaptic protein that uploads glutamate in the synaptic vesicle before its release, and thus is one of the synaptic plasticity markers linked to glutamate neurotransmission. Complexins and SNAP-25, as the key players of the synaptic-vesicle fusion machinery, participate in glutamate transmission [44, 45]. These synaptic vesicle-associated proteins, which are required for vesicle fusion and neurotransmitter release, have been identified as possible factors involved in the pathophysiology of psychiatric disorders including depression. At present, many studies have found the changes in synaptic protein expression in neurological diseases including cerebral ischemia, Alzheimer's disease and memory dysfunction. For instance, in an animal model of electroconvulsive therapy, the mRNA levels of 6 synaptic-vesicle proteins were significantly regulated in the hippocampus [46]. Similarly, Kamat et al. [43] found that several synaptic vesicle-associated proteins including synaptophysin and SNAP-25 decreased in HCY-injected mice brain and further impaired the function of memory. Here, VGLUT1, Complexins and SNAP-25 were significantly reduced in HCY-treated MCAO rats and depression-like behavior occurred. This suggests that abnormalities in synaptic function may lead to the progression of depression in HCY-treated MCAO rats.
The neurosciences at the Max Planck Institute for Biophysical Chemistry in Göttingen
Published in Journal of the History of the Neurosciences, 2023
Whittaker and his colleagues were able to show that the neurotransmitters were not released from the cytoplasmic pool, but through fusion of the vesicle with the presynaptic membrane. They were also able to demonstrate that vesicles are “created” in the cell body and are then transported to the synapse in Fast Axonal Transport. Following vesicle fusion with the presynaptic membrane when the neurotransmitters are released, there is a reuptake of the vesicle, which is once again loaded with neurotransmitters. Whittaker and his colleagues studied this vesicle cycle with radioactive marker substances (e.g., Dextran) and with antibodies against specific proteoglycanes they had identified in the vesicle membranes. They also identified and localized other elements of the vesicle membrane. Figure 4 shows how far their knowledge had reached in the year 1984 (Whittaker 1984).
New insights into human prefrontal cortex aging with a lipidomics approach
Published in Expert Review of Proteomics, 2021
Mariona Jové, Natalia Mota-Martorell, Pascual Torres, Manuel Portero-Otin, Isidre Ferrer, Reinald Pamplona
Lipids have been key players in human brain’s evolution toward complexity [19]. As an example of this relevance, lipids not only represent up to 50% of the dry matter of the human brain [20], but also present the greatest structural and functional diversity of molecular species in the human body [19]. Lipids are mainly involved in cell membrane generation, protection against oxidative damage through the modulation of the degree of membrane unsaturation and the induction of antioxidant response systems (such as Nrf2, REST, and uncoupling proteins) via lipid peroxidation-derived compounds, cell signaling, energy supply and cell physiology [19,21], and most categories of lipids are present in human brain conferring it a wide range of functionalities. Thus, for instance, by determining the membrane composition and regulating the chemical-physical properties of lipid bilayer, lipids direct a multitude of mechanisms such as vesicle fusion and fission processes, ion flux, lateral diffusion of membrane proteins, vulnerability to lipid oxidation, and formation of microdomains necessary for optimal cellular communication [19,22–24].