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The protein encoded by CYPD is a member of the peptidyl-prolyl cis-trans isomerase (PPIase) family.
Data show that cyclophilin 40 (CyP40) interacts with and dissolves amyloids forming proteins tau and alpha-synuclein aggregates.
This review discusses previous studies to provide comprehensive information on the physiological role of cyclophilin D as well as PTP opening in the cell that can be taken into consideration for the development of new PTP inhibitors. [review]
The influx of unfolded p53 (zeige TP53 ELISA Kits) into the mitochondrial matrix in response to oxidative stress indirectly activates the normally inhibited CypD by displacing it from Trap1 (zeige TRAP1 ELISA Kits) complexes. This activates CypD's isomerase activity. Liberated CypD then isomerizes multiple proteins including p53 (zeige TP53 ELISA Kits) (causing p53 (zeige TP53 ELISA Kits) aggregation) and the structural components of the mPTP (zeige PTPN2 ELISA Kits) pore, inducing pore opening.
The present study is to investigate the role of CypD in regulating the mitochondrial dynamics relevant to oxidative stress induced (zeige SQSTM1 ELISA Kits) neuron dysfunctions.
CyPD regulates mitochondrial metabolism, and likely cell survival, by promoting more efficient electrons flow through the respiratory chain via increased supercomplex formation
cyclophilin D (zeige PPIF ELISA Kits) may modify mitochondrial features by inducing the translocation of molecules to the mitochondria through the mechanism associated with cellular energy metabolism
The thermodynamics of binding of Cyp-40 (zeige PPID ELISA Kits) to Hsp90 (zeige HSP90 ELISA Kits) shows remarkable temperature sensitivity in the physiological temperature range.
cyclophilin-D (zeige PPIF ELISA Kits) protein could increase oxidative stress and cause endothelial cell injury and apoptosis. cyclophilin-D (zeige PPIF ELISA Kits) protein is the key factor in reactive oxygen species-induced mitochondrial damage, leading to apoptosis of endothelial cells.
Results show that CypD interacts with SPG7 and VDAC to form the mitochondrial permeability transition pore complex (PTP)and its CsA-binding region is necessary for PTP formation.
molecular determinants necessary for Cyclophilin D (zeige PPIF ELISA Kits) activity regulation and binding to proposed pore constituents thereby regulating the mitochondrial permeability transition pore.
Mannheimia haemolytica leukotoxin binds cyclophilin D (zeige PPIF ELISA Kits) on bovine neutrophil mitochondria.
these data demonstrate that mitochondria are impaired in aging bone and that CypD deletion protects against this impairment to prevent bone loss. This implicates CypD-regulated MPTP (zeige PTPN2 ELISA Kits) and mitochondrial dysfunction in the impairment of bone cells and in aging-related bone loss.
Ppif (zeige PPID ELISA Kits)+/+ and Ppif (zeige PPID ELISA Kits)-/- eosinophils exhibited no significant difference in apoptosis or secondary necrosis.
Ischemic postconditioning might prevent lethal reperfusion injury through an increased SIRT3 (zeige SIRT3 ELISA Kits) activity and subsequent attenuation of CyPD acetylation at reperfusion.
These findings reveal the role of HAX-1 (zeige HAX1 ELISA Kits) in regulating cyclophilin-D (zeige PPIF ELISA Kits) levels via an Hsp90 (zeige HSP90 ELISA Kits)-dependent mechanism, resulting in protection against activation of mPTP (zeige PTPN2 ELISA Kits) and subsequent cell death responses
study identifies a novel signaling pathway composed of E2F1 (zeige E2F1 ELISA Kits), miR (zeige MLXIP ELISA Kits)-30b and CypD that regulates myocardial necrosis.
It is concluded that CypD sensitizes the brain mitochondria to PT, and its inhibition by CsA (zeige HSPA9 ELISA Kits) or CypD absence improves the complex I-related mitochondrial function and increases mitochondria stability against Ca(2 (zeige CA2 ELISA Kits)+) stress.
Data indicate that Ppif (zeige PPID ELISA Kits) protein cyclophilin D (CypD)-dependent protein kinase A (PKA)/cAMP regulatory-element-binding (CREB (zeige CREB1 ELISA Kits)) signaling is responsible for amyloid beta (Abeta (zeige APP ELISA Kits))-induced synaptic injury.
Ablation of CypD leads to changes in the mitochondrial acetylome which may contribute to altered mitochondrial metabolism in CypD-deficient mice.
These results suggest a physiologic function for CypD and the mitochondrial permeability transition in the regulation of starvation-induced autophagy.
new insights into CypD-dependent mitochondrial mPTP (zeige PTPN2 ELISA Kits) and signaling on mitochondrial trafficking in axons and synaptic degeneration in an environment enriched for Abeta (zeige APP ELISA Kits)
The protein encoded by this gene is a member of the peptidyl-prolyl cis-trans isomerase (PPIase) family. PPIases catalyze the cis-trans isomerization of proline imidic peptide bonds in oligopeptides and accelerate the folding of proteins. This protein has been shown to possess PPIase activity and, similar to other family members, can bind to the immunosuppressant cyclosporin A.
40 kDa peptidyl-prolyl cis-trans isomerase
, Cyclophilin D
, PPIase D
, peptidyl-prolyl cis-trans isomerase D
, rotamase D
, 40 kDa peptidyl-prolyl cis-trans isomerase D
, cyclophilin 40
, cyclophilin D
, cyclophilin-related protein
, PPIase F
, cyclophilin F
, peptidyl-prolyl cis-trans isomerase F, mitochondrial
, peptidyl-prolyl cis-trans isomerase, mitochondrial
, peptidylprolyl isomerase F (cyclophilin F)
, rotamase F
, mitochondrial Cyclophilin D