Sentences with phrase «exocytosis of»

Vacuole formation is thought to be a consequence of the uncoupling of exocytosis of zymogens and abnormal intracellular traffi cking of digestive and lysosomal enzymes.

T11 / CD2 activation of cloned human natural killer cells results in increased conjugate formation and exocytosis of cytolytic granules.

Morland C, Nordengen K, Larsson M, Prolo LM, Farzampour Z, Reimer RJ, Gundersen V (2013) Vesicular uptake and exocytosis of L - aspartate is independent of sialin FASEB J, 27 (3), 1264 - 74 PubMed 23221336

In these cells, glucose metabolism inhibits the ATP - dependent potassium channel (KATP channel) and opens voltage - dependent calcium channels (VDCCs), resulting in the exocytosis of insulin - containing granules [41].

Degradation and exocytosis of lipofuscin by RPE cells have not been observed in vivo until now, and no drug is known to eliminate the intracellular amount of lipofuscin.

[MR: The authors of the Remofuscin study apparently show exocytosis of aggregate, but that doesn't prove that the exocytosis is selective!

Regulation of purinergic signaling in biliary epithelial cells by exocytosis of SLC17A9 - dependent ATP - enriched vesicles.

Initiation of purinergic signaling by exocytosis of ATP - containing vesicles in liver epithelium.

Exocytosis of secretory vesicles depends on the consecutive action of tethering factors and SNARE proteins for fusion.

This led to decreased exocytosis of ATP from astrocytes, resulting in decreased purinergic signaling on dopaminergic neurons.

Presynaptic injection of antibodies specific for VAP - 33 inhibited synaptic transmission, which suggests that VAP - 33 is required for the exocytosis of neurotransmitter.

I: Exocytosis of milk protein, lactose, and other components of the aqueous phase in Golgi - derived secretory vesicles.

Not exact matches

The synaptic vesicle protein that mediates membrane fusion during exocytosis also regulates the rate and extent of this process by controlling vesicle tethering.

Dr. Taraska's lab studies the structural cell biology of exocytosis and endocytosis with advanced imaging methods including live cell microscopy, superresolution fluorescence, and electron microscopy.

While working on his Ph.D., Dr. Taraska investigated the processes of triggered exocytosis and endocytosis in neuroendocrine cells with high - resolution microscopy methods.

This unique combination of the genes demonstrates that there is a connection between exocytosis and the remodeling of the cell's internal skeleton, but what that connection is remains unclear.

This regulation is spectacularly apparent in the exquisite speed and precision of synaptic exocytosis, where synaptotagmin (the calcium - ion sensor for fusion) cooperates with complexin (the clamp activator) to control the precisely timed release of neurotransmitters that initiates synaptic transmission and underlies brain function.

The gene discovered in the research couples the exocytosis - regulating protein Sec10 with formin, a protein that regulates the remodeling of the actin cytoskeleton critical to forming cell shapes.

Exocytosis is the process by which cells secrete packets of protein and carbohydrates outside their membranes to support extracellular processes like the construction of cell walls.

The Exocyst complex, which functions in polarized exocytosis, has been involved in regulation of cell motility.

The Calcium Dependence of Kiss - and - Run Exocytosis at the Crayfish Neuromuscular Junction.

Cell motility of neural stem cells is reduced after SPIO - labeling, which is mitigated after exocytosis.

The Palmitoyl Acyltransferase DHHC2 Regulates Recycling Endosome Exocytosis and Synaptic Potentiation through Palmitoylation of AKAP79 / 150.

Myosin II activation and actin reorganization regulate the mode of quantal exocytosis in mouse adrenal chromaffin cells.

Neuraminidase 1 is a negative regulator of lysosomal exocytosis.

The mechanism of loss probably involves exocytosis and possibly blood transport.

This is my postdoctoral work from St Jude Children's Hopsital in Sandra d'Azzo's lab and is an exampe of excessive lysosomal exocytosis being pathological.

Using physiological assays, Scheller demonstrated the importance of these proteins for exocytosis.

... [For example], A deficiency of lysosomal sialidase (Neu1) leads to increased levels of LAMP -1-mediated lysosomal exocytosis by neutrophils in the bone marrow cavity.

In Neu1 - deficient mice the excessive lysosomal exocytosis results in cleavage of VCAM - 1, loss of bone marrow progenitor cells from the bone niche and the onset of spleenic hematopoiesis.

We further demonstrate that lysosomal exocytosis mediates the resealing of primary skin fibroblasts wounded during the contraction of collagen matrices.

[MR: This is because lack of Neu1 means that it's not available to strip sialic acids from LAMP - 1, and oversialylated LAMP - 1 leads to loss of its inhibitory function over lyso exocytosis, apparently leading to a nonspecific puking out of its contents into the ECF].

During an action potential, calcium influx into the presynaptic terminal triggers the fusion of synaptic vesicles with the plasma membrane, leading to the release of transmitter through the process of exocytosis.

The protein is a key regulator of lysosomal exocytosis.

Rothman came from a different background in cell biology to discover first serendipitously, and then with extensive follow - up work, that the same molecules identified by Scheller and Südhof also regulate the transfer of material between compartments in cells, as well as secretion by the process of exocytosis, thus showing the much broader significance of these proteins to biology in general.

Rothman immediately realised the importance of the result, and proposed the «SNARE hypothesis» for vesicle transport and exocytosis as a general process in all cell types: vesicle proteins specifically bind to target proteins in the plasma membrane to form a «v - t» complex which is necessary for vesicle and membrane fusion to proceed.