Rough endoplasmic reticulum binding

The first step is the synthesis of the enzymes that are involved in the formation of the neurotransmitters, which occurs on the rough endoplasmic reticulum in the cell body. They are then transferred to the terminus of the presynaptic neurone by axonal transport. Here the neurotransmitters are synthesized prior to packaging into vesicles. The contents of the vesicles are, upon stimulation of the presynaptic neurone, released into the synaptic cleft. After binding to the postsynaptic receptor they are inactivated either by uptake from the cleft back into the presynaptic neurone or by enzymic degradation (Figure 14.9). After exocytosis, the membrane of the vesicle can be recycled back into the presynaptic neurone for re-filling and further exocytosis (see Figure 14.8). 

In any battle, when the defence is outnumbered by the enemy, more troops are brought into the battle from the reserve. However, in the immune system, there are initially no reserve troops. When an antigen binds to its complementary antibody-receptor on B-cells, these are strongly stimulated to proliferate (clonal expansion). In addition, not only does the number of daughter cells increase but each quickly develops into what is known as an effector (or plasma) cell, in which the protein synthetic machinery increases through the development of the rough endoplasmic reticulum, so that there is a large increase in the number of antibodies synthesised and secreted. A simple description of the sequence of events is as follows ... 

Liver Storage and Release of Retinol Tissues can take up retinyl esters from chylomicrons, but most is left in the chylomicron remnants that are taken up into the liver by endocytosis. The retinyl esters are hydrolyzed at the hepatocyte cell membrane, and free retinol is transferred to the rough endoplasmic reticulum, where it binds to apo-RBP. Holo-RBP then migrates through the smooth endoplasmic reticulum to the Golgi and is secreted as a 1 1 complex with the thyroid hormone binding protein, transthyretin (Section 2.2.3). 

Neurotransmission is based on the secretion of neurotransmitters from secretory vesicles in the presynaptic membrane and the binding of the agonists by receptors on the postsynaptic membrane. The transmitters have to travel only about 20 nm across the synaptic cleft, whereas neurohormones may act on much more distant receptors. The biogenesis of the secretory vesicles and the receptors are intimately connected with the secretory pathway of the eukaryotic cells. In this system a series of membrane-bound structures mediate the transfer of exported proteins from their site of synthesis at the rough endoplasmic reticulum to their site of discharge at the plasma membrane. We will use the chromaffin granules (storage vesicles of the adrenal medulla) as an example for secretory vesicles, and the acetylcholine receptor for receptors of neurotransmitters. 

During translation, messenger RNA (mRNA) binds to ribosomes, where its nucleotide base code is decoded into the amino acid sequence of polypeptides. Ribosomes, which are located free in the cytoplasm or on the rough endoplasmic reticulum (an organelle located within cells), consist of ribosomal RNA (rRNA) and several proteins. 

Fig. 34.2. Summary of the major pathways for the biosynthesis and secretion of the thyroid hormones. When thyrotropin (TSH) binds to the TSH receptor at the basal membrane of the follicular cell, the biosynthesis of thyroglobulin (TG) is stimulated, as is that of thyroperoxidase (TPO) and the production of hydrogen peroxide. Noniodinated TG is synthesized by the rough endoplasmic reticulum of the follicular cell and secreted through the apical membrane of the follicular cell into the follicular lumen. Iodide enters the follicular cell by the iodide pump (NIS, sodium iodide symporter) and is then transported into the follicular lumen. In the lumen, the iodide is oxidized by TPO-O (a Ti-cation radical intermediate formed from TPO and hydrogen peroxide) at the apical...

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