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The underlying mechanism forAT1-autoantibody induced podocyte damage might involve activation of the TRPC6 -calcium/calcineurin pathway.
A short-linear interaction motif between residues 337-343 of AKAP79 is the sole PP2B-anchoring determinant sustaining these diverse topologies.
Mutation in PPP3CA gene is associated with Severe Neurodevelopmental Disease with Seizures.
identify a distinct C-terminal autoinhibitory four-residue sequence in CNAbeta1, (462)LAVP(465), which competitively inhibits substrate dephosphorylation. In vitro and cell-based assays revealed that the CNAbeta1-containing holoenzyme, CNbeta1, is autoinhibited at a single site by either of two inhibitory regions, CBD and LAVP, which block substrate access to the substrate-binding groove.
Studies indicate the importance of the AKAP79/PP2B/protein kinase A complex's role in synaptic long-term depression in the CA1 region of the hippocampus.
Ca(2+)/calcineurin (CaN)/nuclear factor of activated T-cells (NFAT) c4 axis is required for neuritin-induced Kv4.2 transcriptional expression and potentiation of IA densities in cerebellum granule neurons.
CN-A and nephrin were clearly reduced in the kidneys of a 10-year-old boy who had relapsing steroid-resistant nephrotic syndrome.
that KIF1Bbeta affects mitochondrial dynamics through calcineurin-dependent dephosphorylation of Dynamin-related protein 1 (DRP1), causing mitochondrial fission and apoptosis
for Aspergillus fumigatus, activation of macrophage calcineurin-NFAT occurs via a phagosomal TLR9-dependent and Bruton's tyrosine kinase-dependent signalling pathway that is independent of MyD88
Data indicate that both nuclear factors of activated T cells (NFATs) motifs partially compete for binding but do not fully displace each other on the calcineurin (Cn) epitope.
Lysosomal calcium signaling regulates autophagy through calcineurin and TFEB.
Human herpesvirus 6B U54 binds the calcineurin (CaN) phosphatase enzyme, causing improper dephosphorylation and nuclear translocation of NFAT (nuclear factor of activated T cells) proteins, resulting in suboptimal IL-2 gene transcription.
KSR2 deficiency affects stromal interaction molecule 1 (STIM1)/ORAI1 puncta formation, which is correlated with cytoskeleton disorganization.
These findings therefore provide initial support for the novel mechanistic hypothesis that oxidation-induced global and/or local conformational changes within calcineurin
PKCepsilon may negatively regulate adverse myocardial remodeling by cooperating with calcineurin to downregulate fibrosis and induce transcription of cardioprotective wound healing genes, including COX-2
Mutations on the hydrophobic face of Calcineurin distal helix disrupt the structure gained upon CaM binding.
Bile-induced NF-kappaB activation and acinar cell injury are mediated by calcineurin.
Dephosphorylation of Aly1 by calcineurin serves as a regulatory switch to promote Aly1-mediated trafficking to the vacuole.
lower expression of PPP3CA and PPP3CB genes in atrium myocardium can be related to expressed postinfarction LV remodeling.
PPP3CA down-regulation is associated with hepatocellular carcinoma infected with hepatitis C virus.
calcineurin in astrocytes may be activated in response to neuronal activity.
calcineurin is a key regulator of Wnt5a-induced AQP2 activation without affecting intracellular cAMP level and PKA activity.
Redirected splicing of calcineurin A to the fetal isoforms in adult muscle and in differentiated C2C12 slows the timing of muscle relaxation, promotes nuclear localization of calcineurin target Nfatc3, and/or affects expression of Nfatc transcription targets.
these results demonstrate that increased susceptibility to Aspergillus fumigatus is dependent on calcineurin signaling in myeloid cells
the CaN-Nfat pathway regulates development and function of IFN-gamma-producing gammadelta T cells.
the expression of the full-length 60-kDa calcineurin protein is down-regulated due to over-activated calpain that cleaves calcineurin to form a 45-kDa fragment.
AKAP150-calcineurin signaling dyad is essential for the activation of the phosphatase and the subsequent down-regulation of Kv channel currents following myocardial infarction.
Calcineurin inhibitor tacrolimus ameliorated proteinuria in nephrotic model by inhibiting the redistribution of CN-A and nephrin at the slit diaphragm.
global deficiency of catalytic subunit Ppp3cb, and tissue-specific ablation of regulatory subunit Ppp3r1 from skeletal muscle, but not adipose tissue or liver, led to protection from high-fat-diet-induced obesity
Overexpression of the phosphatase calcineurin A prevents the development of a capillary/myocyte mismatch despite progressive myocardial hypertrophy.
Catalytic subunits of the phosphatase calcineurin interact with NF-kappaB-inducing kinase (NIK) and attenuate NIK-dependent gene expression
Data indicate that calcineurin (CnAalpha-/- or CnAbeta-/-) is required for pathological but not compensatory renal hypertrophy.
We also confirmed that overexpression of RCAN1-1L could inhibit the transcriptional activation of an NFAT-dependent promoter in response to PMA and ionomycin by inhibiting Calcineurin activity in HEK293T cells
A calcineurin- and NFAT-dependent pathway is involved in alpha-synuclein-induced degeneration of midbrain dopaminergic neurons in a Parkinson's disease mouse model.
Calcineurin and its regulator, RCAN1, confer time-of-day changes in susceptibility of the heart to ischemia/reperfusion.
Data indicate that reduction in connexin43 (Cx43) and sodium channel NaV1.5 expression coincided with overexpression of transgene calcineurin A (CnA) and hypertrophy development and preceded significant presence of fibrosis.
Calcineurin regulates Nirr1 expression in a cell-autonomous, neural activity-dependent manner.
Muscle-specific RING finger 1 negatively regulates pathological cardiac hypertrophy through downregulation of calcineurin A.
The calmodulin binding region from residues 389 to 420 was modeled based on the structure of two other proteins having calmodulin binding domains with the same 1-8-14 structural motif as calcineurin.
molecular cloning and characterization of expression in skeletal muscle
The findings reveal a novel mechanism by which Ca2+ overload disrupts myofibril integrity by activating a Calcineurin-FoxO-MuRF1-proteosome signaling pathway.
catalytic subunit of Calcineurin (CaN), ubiquitously expressed Ca2+/CaM-dependent protein phosphatase\; mediates activities of transcription factors and ion channels\; involved in regulation of T-cell activation
CAM-PRP catalytic subunit
, calcineurin A alpha
, calmodulin-dependent calcineurin A subunit alpha isoform
, protein phosphatase 2B, catalytic subunit, alpha isoform
, protein phosphatase 3 (formerly 2B), catalytic subunit, alpha isoform
, serine/threonine-protein phosphatase 2B catalytic subunit alpha isoform
, PP2B alpha 1
, PP2BA alpha
, protein phosphatase 3 (formerly 2B), catalytic subunit, alpha isoform (calcineurin A alpha)
, protein phosphatase 3, catalytic subunit, alpha isoform
, Calcineurin subunit A alpha
, protein phosphatase-2Ba
, calcineurin catalytic subunit delta isoform
, calcineurin catalytic subunit
, protein phosphatase 3, catalytic subunit, alpha isozyme
, serine/threonine-protein phosphatase 2B catalytic subunit alpha isoform-like