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抗Human PPIF 抗体:
抗Rat (Rattus) PPIF 抗体:
抗Mouse (Murine) PPIF 抗体:
Cyclophilin D protects cell from cell death.
There was increased [Ca(2+)](c), [Ca(2+)](m), mCICR, MPTP opening, and expression of cyclophilin D and decreased DeltaPsim in POAG TM cells compared with control cells.
Mannheimia haemolytica leukotoxin binds cyclophilin D on bovine neutrophil mitochondria.
Both male and female cypD heterozygous but not gene knockout mice exhibited increased lifespans compared to wild-type littermates, associated with alterations in the protein expression of some markers, albeit without exhibiting changes in behaviour.
Ablation of Cyclophilin D Results in an Activation of FAK (显示 PTK2 抗体), Akt (显示 AKT1 抗体), and ERK (显示 EPHB2 抗体) Pathways in the Mouse Heart.
Binding of signal transducer and activator of transcription 3 (STAT3) to cyclophilin D (CypD) was important for reducing mitochondrial reactive oxygen species (ROS) production after oxidative stress.
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 (显示 PTPN2 抗体) and mitochondrial dysfunction in the impairment of bone cells and in aging-related bone loss.
Ppif (显示 PPID 抗体)+/+ and Ppif (显示 PPID 抗体)-/- eosinophils exhibited no significant difference in apoptosis or secondary necrosis.
Ischemic postconditioning might prevent lethal reperfusion injury through an increased SIRT3 activity and subsequent attenuation of CyPD acetylation at reperfusion.
These findings reveal the role of HAX-1 (显示 HAX1 抗体) in regulating cyclophilin-D levels via an Hsp90 (显示 HSP90 抗体)-dependent mechanism, resulting in protection against activation of mPTP (显示 PTPN2 抗体) and subsequent cell death responses
study identifies a novel signaling pathway composed of E2F1, miR-30b and CypD that regulates myocardial necrosis.
It is concluded that CypD sensitizes the brain mitochondria to PT, and its inhibition by CsA (显示 HSPA9 抗体) or CypD absence improves the complex I-related mitochondrial function and increases mitochondria stability against Ca(2 (显示 CA2 抗体)+) stress.
Data indicate that Ppif protein cyclophilin D (CypD)-dependent protein kinase A (PKA)/cAMP regulatory-element-binding (CREB) signaling is responsible for amyloid beta (Abeta)-induced synaptic injury.
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 is part of the mitochondrial permeability transition pore in the inner mitochondrial membrane. Activation of this pore is thought to be involved in the induction of apoptotic and necrotic cell death.
peptidyl-prolyl cis-trans isomerase A
, peptidylprolyl isomerase F (cyclophilin F)
, peptidyl-prolyl cis-trans isomerase F, mitochondrial
, cyclophilin D
, cyclophilin F
, ppiase F
, rotamase F
, peptidylprolyl isomerase F
, PPIase F
, cyclophilin 3
, mitochondrial cyclophilin
, peptidyl-prolyl cis-trans isomerase, mitochondrial
, mitochondrial Cyclophilin D