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anti-Human PPIF Antikörper:
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Human Monoclonal PPIF Primary Antibody für ELISA, WB - ABIN534876
Bergsma, Eder, Gross, Kersten, Sylvester, Appelbaum, Cusimano, Livi, McLaughlin, Kasyan: The cyclophilin multigene family of peptidyl-prolyl isomerases. Characterization of three separate human isoforms. in The Journal of biological chemistry 1992
Show all 2 Pubmed References
Human Polyclonal PPIF Primary Antibody für IF, IHC - ABIN5664246
Wang, Lin, Chen, Zhu, Jiang, Li, Wang et al.: Overexpression of mitochondrial Hsp75 protects neural stem cells against microglia-derived soluble factor-induced neurotoxicity by regulating mitochondrial permeability transition pore opening in ... in International journal of molecular medicine 2016
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.
Mice containing CypD-deficient T cells exhibited substantially compromised disease tolerance and succumbed to Mycobacterium tuberculosis (Mtb) infection. This study establishes a mechanistic link between T cell-mediated immunity and disease tolerance during Mtb infection.
melatonin treatment inhibited the Ripk3-PGAM5-CypD-mPTP cascade and thus reduced cellular necroptosis, conferring a protective advantage to the endothelial system in IR stress.
Cyclophilin D is an important but non-obligatory regulator of mitoflash activity in cardiac muscle, whereas it is dispensable in the skeletal muscle, due in part to differential cyclophilin D expression.
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, Akt, and ERK 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 and mitochondrial dysfunction in the impairment of bone cells and in aging-related bone loss.
Ppif+/+ and Ppif-/- 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 in regulating cyclophilin-D levels via an Hsp90-dependent mechanism, resulting in protection against activation of mPTP 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 or CypD absence improves the complex I-related mitochondrial function and increases mitochondria stability against Ca(2+) 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.
It regulates Parkinson's disease development.
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 and signaling on mitochondrial trafficking in axons and synaptic degeneration in an environment enriched for Abeta
Cys-203 residue of CypD is necessary for redox stress-induced activation of mPTP.
Data suggest that, in mitochondria exhibiting intact inner membranes, the absence of cyclophilin D or the inhibition of its binding to F(0)F(1)-ATP synthase by cyclosporin A will affect only matrix adenine nucleotides levels.
Regulation of the mPTP by SIRT3-mediated deacetylation of CypD at lysine 166 suppresses age-related cardiac hypertrophy.
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