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Alpha-Latrotoxin: Wikis

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The best-studied latrotoxin is alpha-latrotoxin, which acts presynaptically to release neurotransmitters[1] from sensory and motor neurons, as well as on endocrine cells (to release insulin, for example).[2] It is a ~130 kDa protein[3] which exists mainly in its dimerized or tetramerized forms.

Contents

Mechanism of action

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Pore formation

α-latrotoxin tetramers can form ion-permeable pores in the membrane of target cells, causing influx of calcium ions and thus leading to massive neurotransmitter release. Eventually, the cellular membrane can be disrupted, leading to cell death. The insertion of α-latrotoxin into artificial membranes is a rare event, and it is only when specific receptors are present on the surface of biological membranes that membrane insertion occurs efficiently.

Membrane penetration

Although tetrameric pore formation of α-latrotoxin has been shown conclusively, some authors still dispute whether this is the main mode of action of α-latrotoxin, and believe that α-latrotoxin (tetrameric or not) may penetrate through the membrane of target cells to interact directly with intracellular neurotransmitter release machinery.

Receptors

Three receptors for α-latrotoxin have been described:

It is the expression patterns of these receptors which confers specificity to α-latrotoxin. So far, only latrophilin has been shown to be able to signal. In addition, because of its ability to bind α-latrotoxin in the absence of calcium, it may be involved in the intriguing and unexplained calcium-independent actions of α-latrotoxin. A secretory cell that is not sensitive to α-latrotoxin has yet to be found[3]

Signaling

As well as the major effects of α-latrotoxin pore formation, other effects of α-latrotoxin are mediated by interaction with latrophilin and intracellular signalling (see signal transduction).

References

External links


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