Cleft cells

Granular cells Melanotrophs Corticotrophs PAS-positive cells Agranular cells Cleft cells... 

Each precursor protein molecule is cleaved only once to generate one molecule of the coat protein, and catalytic activity is restricted to the precursor protein. Why is the coat protein itself catalytically inactive The structure of the coat protein shows that its C-terminus is bound in the active site cleft and thereby prevents other proteins entering the cleft and being cleaved. Tbis arrangement allows the precursor protein to fulfill its function to generate the coat protein and prevents the coat protein from destroying other proteins in the infected cell, including other coat proteins. 

The disruption of C1C-2 in mice leads to male infertility, blindness, and leukodystrophy, and was attributed to defective extracellular ion homeostasis in narrow clefts. C1C-2 yields currents that slowly activate upon hyperpolarization. It is also activated by cell swelling and by extracellular acidification. Structural determinants that are essential for these types of activation were identified by mutagenesis. There is a report that C1C-2 might be mutated in human epilepsy, but this has not been confirmed in fiuther studies. 

Non-selective Cation Channels. Figure 1 The nicotinic acetylcholine receptor (nAChR) is localized within the cell membrane above the cell membrane is the synaptic cleft, below the cytoplasm. Drawing of the closed (left) and open (right) nAChR showing acetylcholine (ACh) binding and cation movement. Dimensions of the receptor were taken from references [2, 3]. 

Class IIHLA molecules are expressed on the surface of antigen-presenting cells. They play a key role in presentation of processed linear peptide antigens of at least nine amino acids to T cells. Antigen is bound to the HLA antigen binding cleft formed by the a and 3 chains of the HLA class II molecule. This tri-molecular HLA-antigen complex binds in turn to the variable portion of the T-cell receptor. 

Communication between neurons involves neurotransmitters. Up until the beginning of the last century, synaptic transmission was regarded as probably electrical. It was suggested that the close apposition of two neurons allowed the current to jump the synaptic cleft, rather like an electrical spark between two closely positioned wires. There is indeed evidence for electrical synapses in animal species where the synaptic cleft is particularly narrow (2 nm, or nanometres), as well as in the myocardium where the close coupling of cells allows electrical current to flow from one cell to the next,... 

Schmidt-Lantermann clefts are structures where the cytoplasmic surfaces of the myelin sheath have not compacted to form the major dense line and therefore contain Schwann or glial cell cytoplasm (Fig. 4-9). They are common in peripheral myelin but rare in the CNS. These inclusions of cytoplasm are present in each layer of myelin. The clefts can be visualized in the unrolled myelin sheet as tubes of cytoplasm similar to the tubes making up the lateral loops but in the middle regions of the sheet, rather than at the edges (Fig. 4-9). 

The postsynaptic receptors on any given neuron receive information from transmitters released from another neuron. Typically, postsynaptic receptors are located on dendrites or cell bodies of neurons, but may also occur on axons or nerve terminals in the latter case, an axoaxonic synaptic relationship may cause increases or decreases in transmitter release. In contrast, autoreceptors are found on certain neurons and respond to transmitter molecules released from the same neuron. Autoreceptors may be widely distributed on the surface of the neuron. At the nerve terminal, they respond to transmitter molecules released into the synaptic cleft on the cell body, they may respond to transmitter molecules released by dendrites. Functionally, most autoreceptors appear to decrease further transmitter release in a kind of negative feedback loop. Autoreceptors have been identified for all the catecholamines, as well as for several other neurotransmitters. a2-adrenergic receptors are often found on noradrenergic nerve terminals of postganglionic sympathetic nerves, as well as on noradrenergic neurons in the CNS [36], and activation of these receptors decreases further norepinephrine release. Dopamine autoreceptors,... 

Air concentrations of 28.5 mg/m3 for 4 h daily on days 9-12 of gestation caused fetotoxic effects and chromosomal damage to liver cells by day 18 effects included reduced survival, impaired growth, retarded limb ossification, and bone abnormalities. At 2.9 mg/m3, a 9.9% decrease in fetal weight was recorded at 0.26 mg/m3, a 3.1% decrease was measured Oral dosages of 400-600 mg/kg BW on days 7-16 of gestation produces fetal malformations (cleft palate), delayed skeletal ossification, and fetal weight reduction 200-600 mg/kg BW daily for 10 days (DMA) produced fetal and maternal toxicity... 

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