calcineurin


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cal·ci·neu·rin

(kal'sē-nyūr'in),
A calcium-dependent serine-threonine phosphatase involved in T-cell signaling transcription; the target of cyclosporine immunosuppression; the reaction cascade in which it resides is referred to as the calcineurin pathway.
[calcium + G. neuron, nerve, + -in]

calcineurin

An enzyme which binds Ca2+ and calmodulin, inhibiting calmodulin activity. Calcineurin alters proteins by removing phosphate groups, shortening duration of NMDA channel opening, resulting in synaptic desensitisation of NMDA receptors. Calcineurin activates T cells via transcription factor NFATc (Nuclear Factor of Activated T cell, cytoplasmic) by dephosphorylation. Activated NFATc is translocated into the nucleus, where it upregulates IL-2 expression, and, by extension, the T cell response. Calcineurin is most concentrated in the CNS, and is inhibited by immunophilin ligand, tacrolimus and cyclosporin, both immunosuppressants. Because rejection can be mediated by calcineurin, calcineurin inhibitors (cyclosporine, pimecrolimus and tacrolimus) are used to prevent or manage rejection.

cal·ci·neu·rin

(kal'sē-nūr'in)
A calcium-dependent serine-threonine phosphatase involved in T-cell signaling transcription; the reaction cascade in which it resides is referred to as the calcineurin pathway.
[calcium + G. neuron, nerve, + -in]
References in periodicals archive ?
This stimulates a molecular gas pedal, of sorts, known as calcineurin, which revs up CRTC2, activating genes that allow the liver to drive the metabolic engine by producing more glucose.
CONCLUSION: The calcineurin inhibitor tacrolimus (TCR) and the pineal gland hormone and antioxidant melatonin (MLT) have been shown to possess otoprotective properties against noise-induced hearing loss (NIHL).
It is activated by calcineurin and biomechanical stress.
Currently, the most common topical prescription treatments, corticosteroids and calcineurin inhibitors, carry concerns about their long-term safety, so their continuous application for long periods of time is not recommended.
Drugs have been analyzed by segments such as Calcineurin Inhibitors, Anti-proliferative Agents, mTOR Inhibitors, Antibodies, and Steroids.
The clinical management of calcineurin inhibitors (CNIs) [7] in organ transplantation is complex owing to their narrow therapeutic range and poor correlation between trough blood concentrations and clinical response.
Endothelial dysfunction and hypertension are common complications of calcineurin inhibitors, such a cyclosporine and Tacrolimus.
6 mm Hg in patients on either of the topical calcineurin inhibitors.
Current research shows that calcium-sensitive proteins found in the body, for example calcineurin, promote inflammation, but it is not known exactly how.
Ophthalmologists and eye specialists from the US and Europe focus on recent innovative treatment options, but begin with an outline of treatment principles and the most conventional treatments, including corticosteroids and other immunosuppresant agents, then discuss the newer available agents for intraocular inflammation, such as drugs adopted from rheumatology, mycophenolate mofetil, anti-tumor necrosis factor-alpha agents, anti-interleuken therapy, interferon-alpha therapy, rituximab, intravitreal injection therapy, corticosteroid intravitreal implants, and calcineurin inhibitor voclosporin, mammalian target of rapamycin inhibitor sirolumus, and the IL-1 trap rilonacept.
Its lead drug, voclosporin, is a calcineurin inhibitor, and is targeted at the estimated US$3.
The mechanism of the development of PTDM is not entirely understood but is thought to involve the effects of corticosteroids and calcineurin inhibitors.