5 results match your criteria cn-mediated dephosphorylation

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Q134R: Small chemical compound with NFAT inhibitory properties improves behavioral performance and synapse function in mouse models of amyloid pathology.

Aging Cell 2021 07 12;20(7):e13416. Epub 2021 Jun 12.

Sanders-Brown Center on Aging, University of Kentucky College of Medicine, Lexington, KY, USA.

Inhibition of the protein phosphatase calcineurin (CN) ameliorates pathophysiologic and cognitive changes in aging rodents and mice with aging-related Alzheimer's disease (AD)-like pathology. However, concerns over adverse effects have slowed the transition of common CN-inhibiting drugs to the clinic for the treatment of AD and AD-related disorders. Targeting substrates of CN, like the nuclear factor of activated T cells (NFATs), has been suggested as an alternative, safer approach to CN inhibitors. Read More

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Alzheimer's Disease, Dendritic Spines, and Calcineurin Inhibitors: A New Approach?

ACS Chem Neurosci 2018 06 14;9(6):1233-1234. Epub 2018 May 14.

Department of Pathology, O'Donnell Brain Institute , UT Southwestern Medical Center , Dallas , Texas 75390-9072 , United States.

Therapeutics to effectively treat Alzheimer's disease (AD) are lacking. In vitro, animal and human studies have implicated the excessive activation of the protein phosphatase calcineurin (CN) as an early step in the pathogenesis of AD. We discuss recent data showing that the prolyl isomerase Pin1 is suppressed by CN-mediated dephosphorylation induced by Aβ42 signaling. Read More

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Calcineurin-mediated YB-1 dephosphorylation regulates CCL5 expression during monocyte differentiation.

J Biol Chem 2014 Aug 19;289(31):21401-12. Epub 2014 Jun 19.

From the Department of Nephrology and Clinical Immunology, University Hospital RWTH-Aachen, Pauwelsstrasse 30, 52057 Aachen, Germany,

Y-box (YB) protein-1 serves as a master regulator in gene transcription and mRNA translation. YB-1 itself is regulated at various levels, e.g. Read More

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A new calcineurin inhibition domain in Cabin1.

Biochem Biophys Res Commun 2007 Jul 21;359(1):129-35. Epub 2007 May 21.

Department of Biochemistry and Molecular Biology, Cancer Research Institute, Interdisciplinary Program in Genetic Engineering, Seoul National University College of Medicine, 28 Yongon-dong, Chongro-gu, Seoul 110-799, Republic of Korea.

Calcineurin (CN), a calcium-activated phosphatase, plays a critical role in various biological processes including T cell activation. Cabin1, a calcineurin binding protein 1, has been shown to bind directly to CN using its C-terminal region and inhibit CN activity. However, no increase in CN activity has been found in Cabin1DeltaC T cells, which produce a truncated Cabin1 lacking the C-terminal CN binding region. Read More

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Mitochondria to nucleus stress signaling: a distinctive mechanism of NFkappaB/Rel activation through calcineurin-mediated inactivation of IkappaBbeta.

J Cell Biol 2003 May 5;161(3):507-19. Epub 2003 May 5.

Dept. of Animal Biology, Mari Lowe Center for Comparative Oncology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA.

Mitochondrial genetic and metabolic stress causes activation of calcineurin (Cn), NFAT, ATF2, and NFkappaB/Rel factors, which collectively alter the expression of an array of nuclear genes. We demonstrate here that mitochondrial stress-induced activation of NFkappaB/Rel factors involves inactivation of IkappaBbeta through Cn-mediated dephosphorylation. Phosphorylated IkappaBbeta is a substrate for Cn phosphatase, which was inhibited by FK506 and RII peptide. Read More

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