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Genes affecting secretory pathway traffic are also reported to be affected in those with ASD [12], [24].
When the ER encounters high protein flux or intractable heterologous proteins, its folding capacity could be transiently saturated, thus leading to a secretory pathway traffic jam and causing ER stress [ 6, 7].
As the picture of how proteins found within the exocytotic pathway traffic in astrocytes is being elucidated, there are no comparative data as to the trafficking of receptors, such as GPCRs (G-protein-coupled receptors), in astrocytes.
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If the Arf6/TC10-dependent recycling pathway traffics AMPARs out of the spines then blocking it would act to reduce LTD, as we observed with TC10DN expression.
Activity-dependent events during cLTP increase AMPAR recycling through the dynamin-dependent pathway, trafficking AMPARs from clathrin-coated pits distant from the stimulated synapse to sites accessible to the stimulated PSD.
To date, the downstream effects of highly fluctuating calcium concentrations on the ER membrane surface have been speculative as little research has been done into the effects of calcium fluctuation on early secretory pathway trafficking.
Our finding that TC10WT expression had opposite effects on synaptic AMPAR currents, a measure of functional synaptic AMPARs, and the cell-surface levels of dendritic AMPARs suggests that the Arf6/TC10-dependent recycling pathway traffics AMPARs out of synaptic spines.
In contrast, liposomes targeted to the E-selectin, a transmembrane glycoprotein that is taken up by clathrin-mediated endocytosis, enter cells via this pathway and traffic to lysosomes.
These proteins are described to be involved in MAPK, JNK and ERK pathways, vesicular traffic and DNA repair.
Cellular endocytosis of bound HPV16 virions is thought to occur via a classical clathrin-mediated pathway with trafficking through the endosomal/lysosomal compartments [10], [11].
Gene Shaving and Robust Bayesian Network Analysis detect interactions between the AR pathway, EGFR trafficking signals, and ErbB2.
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