High impact information on Ppid

• CypA bound Itk via the PPIase active site [1].
• The PTP response to ubiquinone 0, depolarization, pH, adenine nucleotides, and thiol oxidants was similar in mitochondria from wild-type and Ppif-/- mice [2].
• We have identified the binding domain in hsp90 for cyclophilin 40 (CyP40) using a two-hybrid system screen of a mouse cDNA library [3].
• Ssp1 is a site-specific PPIase with respect to the amino acid N-terminal to the proline residue [4].
• Here we describe the purification and characterization of Ssp1, an abundant parvulin homolog from Neurospora crassa, which is unique among the known eucaryotic parvulins in containing a polyglutamine stretch between the N-terminal WW domain and the C-terminal PPIase domain [4].

Biological context of Ppid

• However, Bcl-2 family member-induced cell death does not depend on cyclophilin D, and Ppif null fibroblasts are not protected from staurosporine or tumour-necrosis factor-alpha-induced death [5].
• Ppif null mice are protected from ischaemia/reperfusion-induced cell death in vivo, whereas cyclophilin D-overexpressing mice show mitochondrial swelling and spontaneous cell death [5].
• These hsp90-binding immunophilins possess the signature peptidylprolyl isomerase (PPIase) domain, but no role for their PPIase activity in protein folding has been demonstrated [6].

Anatomical context of Ppid

• We have studied the properties of the permeability transition pore (PTP) in mitochondria from the liver of mice where the Ppif gene encoding for mitochondrial Cyclophilin D (CyP-D) had been inactivated [2].

Associations of Ppid with chemical compounds

• Intracellular distribution of a cytoplasmic progesterone receptor mutant and of immunophilins cyclophilin 40 and FKBP59: effects of cyclosporin A, of various metabolic inhibitors and of several culture conditions [7].
• CsA treatment increased nucleolar staining, while NEM and W7 caused it to decrease; after actinomycin D (1 microM) nucleolar staining of Cyp40 disappeared [7].
• The effect of cyclosporin A (CsA) on the intracellular distribution of a mutated NLS minus rabbit progesterone receptor (PRm) and the receptor-associated immunophilins, cyclophilin 40 (Cyp40) and FKBP59, was tested in Lc13 cells by indirect immunofluorescent staining [7].

Analytical, diagnostic and therapeutic context of Ppid

• Western-blotting experiments following immunoprecipitation of glucocorticosteroid receptor (GR) complexes resulted in coprecipitation of GR, heat shock protein hsp90 and two immunophilins: the FK506-binding protein FKBP59 and the CsA-binding protein cyclophilin 40 (CYP40) [8].

References