Fasciculin 2

From WikiMD's Wellness Encyclopedia


Overview[edit | edit source]

Fasciculin 2 is a potent neurotoxin derived from the venom of the green mamba snake, Dendroaspis angusticeps. It is a member of the fasciculin family of toxins, which are known for their ability to inhibit acetylcholinesterase (AChE), an enzyme crucial for the breakdown of the neurotransmitter acetylcholine in the synaptic cleft. By inhibiting AChE, fasciculin 2 causes an accumulation of acetylcholine, leading to prolonged muscle contraction and potentially resulting in paralysis.

Structure[edit | edit source]

Fasciculin 2 is a small protein consisting of 61 amino acids. It belongs to the three-finger toxin superfamily, characterized by a compact structure stabilized by disulfide bonds. The three-finger motif is a common structural feature among snake venom proteins, contributing to their stability and functional diversity.

Mechanism of Action[edit | edit source]

Fasciculin 2 exerts its effects by binding to the active site of acetylcholinesterase, thereby preventing the enzyme from hydrolyzing acetylcholine into acetate and choline. This inhibition leads to an accumulation of acetylcholine at neuromuscular junctions, causing continuous stimulation of muscles. The resulting effect is sustained muscle contraction, which can lead to paralysis if not counteracted.

Biological Significance[edit | edit source]

The ability of fasciculin 2 to inhibit acetylcholinesterase makes it a valuable tool in neurobiological research. It is used to study the role of acetylcholine in synaptic transmission and to investigate the pathophysiology of diseases characterized by cholinergic dysfunction, such as Alzheimer's disease and myasthenia gravis.

Therapeutic Potential[edit | edit source]

While fasciculin 2 itself is not used therapeutically due to its toxicity, understanding its mechanism of action has contributed to the development of drugs that target acetylcholinesterase. These drugs, known as acetylcholinesterase inhibitors, are used in the treatment of Alzheimer's disease to enhance cholinergic transmission in the brain.

Also see[edit | edit source]


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Contributors: Prab R. Tumpati, MD