The Intracellular Trafficking Of Proteins And Plasma Membrane

-Sarcoplasmic Reticulum (SR) then releases Calcium which binds to troponin in the thin filament, exposing myosin-binding sites;

Exocytosis is the process of how hormones, digestive enzymes and lipids are released from the cell. Vesicles containing the product pinch off from the sacs of the golgi apparatus and move towards the plasma membrane. The vesicles then fuse with the plasma membrane and release the product outside the cell. (CGP, 2009) The cell membrane surrounds all living cells, and is the cell’s most important organelle. It controls how substances can move in and out of the cell and allows cell

Glutamate-receptor-interacting protein (GRIP) is the interacting protein which is associated with AMPAR protein receptor in the postsynaptic cell. Amount of GRIP is associated with AMPAR receptors can lead to the prediction of activity in the presynaptic cell. AMPAR receptor change shape to be ready to receive neurotransmitter when GRIP bind. The presynaptic cell contains vesicle which neurotransmitters are accommodated. When calcium enters the presynaptic cell by calcium channel, vesicles dock to the presynaptic cell to become ready to release neurotransmitters to the synaptic gap. Neurotransmitters are released in a packet called quanta. AMPAR receptor has to change its shape by GRIP to receive the release of quanta in the synaptic

The purpose of these experiments were to gain a better understanding of the movement of vesicles along microtubules and the importance of this in proper nerve transmission. This was accomplished by analyzing the phenotypes of three different strains of Caenorhabditis elegans using microscopy and a fluorescence microscope. The organisms contained fluorescence tags on the membranes of their synaptic vesicles to make it easier to see how the mutations affected the vesicles locations.

After lytic granules approach the membrane with the MTOC, additional obstacles are present which prevents them from immediate priming, docking, and fusion with the plasma membrane (Krzewski and Coligan, 2012). In activated NK cells, there is a dense F-actin meshwork occupying the central region of the synapse which could present as a physical barrier to lytic granule exocytosis. Within this are areas of hypodensity ranging from 200 nm to 500 nm, which could allow for the lytic granules (average diameter 300 nm) to pass through (Brown et al., 2011, Rak et al., 2011, Mace and Orange, 2012). Therefore, lytic granules may require actin clearance machinery and myosin IIA motors to finally reach the plasma membrane. In CTLs, it is suggested that lytic granules reach the plasma membrane via the MTOC, and do not require any microtubule-based or actin-based motors (Stinchcombe et al., 2006). However, it is unclear whether all lytic granule transport to the synapse is based on the close approximation of the MTOC to the synapse and independent of microtubule motors.

Some of these adapter proteins also interact with a docking protein (SNARE) on the plasma membrane and assist FL-myoVa to act as a tether for releasing cargo4-6. For example, Gran A/B directly binds to syntaxin 1a, a SNARE protein responsible for docking the granule at the plasma

The identified candidate protein is Synaptotagmin-1. Synaptotagmin-1 is a protein which positively affects the release of neurotransmitters by acting as a calcium sensor (Lau et al, 2013), so it is expected for the protein to be located in the pre-synaptic terminal of an axon. It has four distinct domains, two of which are very similar. The first domain is the N-terminal transmembrane domain (CDD). This domain was found to be located on the plasma membrane (Feany et al, 1993). Because the role of the protein as a whole is to enable vesicular fusion, it seems logical to assume that the protein must be anchored on the plasma membrane, and it would be a logical assumption to make that the role of this domain is to anchor the protein down.

In the contraction of the muscle, action potentials are needed. Action potentials travel down the T-tubules of the sarcolemma, in which they are able to activate the release of Ca++ from the sarcoplasmic reticulum. Then the Ca++ binds to the troponin. This then allows tropomyosin to move since it is currently in the way of the interaction of

When an action potential races along the axon of a neuron, activating sodium and potassium channels in a wave, it eventually comes down to the presynaptic terminal, and activates the VGCC channels to release calcium into the neurons cytoplasm. This flow of positively-charged calcium ions causes the synaptic vesicles to fuse with the cell membrane and release their chemical messengers. It’s these neurotransmitters that act like couriers diffusing across the synaptic cleft and binding to receptor sites on the post synaptic

Endocytosis is a form of active transport that transports materials into a cell through bulk movement (Daempfle, 2016). Furthermore, the bulk movement of the materials include particles, large molecules, and parts of a cell. Moreover, the mentioned bulk materials are moved into a cell (Cohen-Fix, & Askjaer, 2017). Cell Biology of the Caenorhabditis elegans Nucleus. Genetics, 205(1), 25-59. The type of endocytosis that involves the movement of large amounts of water is called pinocytosis. Pinocytosis is when the cell is taking in extracellular fluid. This process is when the cell takes in molecules, including water, which the cell needs. During this process, large food particles that cannot pass through the plasma membrane are broken down by

Cells release diverse types of membrane-bound extracellular vesicles into the extracellular milieu. These can be further classified into three main subgroups based on their cellular biogenesis: exosomes, microvesicles, and apoptotic bodies.21 Exosomes (~50-100 nm diameter) originate from the multivesicular body (MVB); MVBs are well-characterized endosomal precursors of the lysosomal degradation pathway. MVBs can also fuse with the plasma membrane. In this case, their intraluminal vesicle contents are released into the extracellular space; thus becoming “exosomes”.22 Microvesicles (~50-1000 nm diameter) bud directly from the plasma membrane. Apoptotic bodies (more than 500 nm in diameter) represent

Active transport is a process that requires ATP in order for molecules to move. There are several reasons why active transport is required as oppose to passive transport: substances may be too large to pass through the membrane, substances may move against the concentration gradient as oppose to with it, or some substances may not be lipid soluble. v Amino acids and some sugars are transported into cells by solute pumps. An example of a solute pump is a sodium-potassium pump. Within a sodium-potassium pump, both K+ and Na+ are pushed into opposite regions across the cell membrane. Other processes that require ATP are pinocytosis and phagocytosis. Both pinocytosis and phagocytosis occurs when the cell membrane descends beneath the material in order to create a small vesicle, then pinches off into the cell. vi Phagocytosis is the process of cell eating, and phagocytic cells work

Ceramides are an example of a family of cellular lipids (Yasuda et al., 2001). Ceramides are synthesised at the endoplasmic reticulum from precursor compounds and are transported to the Golgi apparatus for conversion into one of the several sphingolipids (Yasuda et al., 2001). The transport of such compounds is highly selective if not specific (Kumagai et al., 2005; Yasuda et al., 2001). Inhibiting transport is a useful tool in investigating the role of substrates (Yasuda et al., 2001) and makes an attractive target for biochemical manipulation of the cell (Ueno et al., 2001).

Overexpression of the HEPN domain in HeLa cells following three hours of starvation indicates that sacsin plays a key role in lysosomal transport due to the reduced efficiency of perinuclear lysosomal clustering. HEPN’s property of dimerizing may be disrupting the function of with full-length sacsin by preventing endogenous sacsin from dimerizing within the cell. Thus, dimerization may be essential to sacsin’s function, particularly for binding JIP3, which is necessary for lysosomal transport7. HATPase 3 overexpression may be occupying JIP3 binding, but was not found to disrupt lysosomal localization following starvation, perhaps due to the truncated size of this deletion construct.

Exocyst is an octameric protein complex that mediates the initial contact between secretory vesicles and the plasma membrane. The final fusion event is mediated by SNAREs (Soluble N-ethylmaleimide Sensitive Factor Attachment Protein Receptor), proteins residing on both vesicles and the PM. The assembly of the SNARE complex drives membrane fusion. SNARE mediated fusion at the plasma membrane in yeast begins with the formation of a binary t SNARE complex composed of Sso1/2 and Sec9 followed by its binding to the v SNARE protein Snc1/2. It was previously shown that SNARE assembly is