Recombinant Human Parvalbumin Protein Standard (His tag)

Supplementary information

This supplementary information is collated from multiple sources and compiled automatically.

Parvalbumin sometimes referred to as PV is a calcium-binding protein approximately 12 kDa in size. It is recognized for its roles in muscle and neuronal tissues. Within the nervous system parvalbumin is prominently expressed in fast-spiking GABAergic interneurons while in muscle tissues it is present in fast-twitch muscle fibers. Other popular descriptors include anti PV and parvalbumins. These proteins play important roles in the regulation of cellular calcium levels.

Biological function summary

Parvalbumin helps modulate calcium ion concentration which is key in muscle relaxation and neurotransmission. It acts by buffering calcium ions and is not part of a larger protein complex. By impacting calcium transients parvalbumin affects processes like synaptic plasticity and the rapid contractions of muscle fibers. This is especially significant in the brain where rapid neuronal firing is needed and in muscles where quick recovery is essential.

Pathways

Parvalbumin is intimately linked with calcium signaling pathways as well as the regulation of muscle contraction. It ensures proper calcium ion homeostasis thereby aiding muscle relaxation after contraction. In the nervous system calbindin proteins parallel some of parvalbumin's functions participating in calcium ion buffering and modulation of neuron excitability. The balanced action of these proteins helps maintain cellular functions in both neurons and muscles.

Insufficient parvalbumin expression may link to epilepsy and schizophrenia. Deficits in this protein could interfere with normal neurotransmission and muscle relaxation cycles. Parvalbumin deficiency influences neurotransmitter release affecting synaptic transmission which may exacerbate symptoms in these conditions. In disease mechanisms proteins such as calbindin may indirectly relate with parvalbumin showing similar patterns of dysregulation and compensating for its absence in calcium handling.