PPID _ CyP_40
- Known as:
- PPID _ CyP_40
- Catalog number:
- Y213700
- Product Quantity:
- 200ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- PPID _ CyP_40
Related genes to: PPID _ CyP_40
- Gene:
- PPID NIH gene
- Name:
- peptidylprolyl isomerase D
- Previous symbol:
- -
- Synonyms:
- CYP-40
- Chromosome:
- 4q32.1
- Locus Type:
- gene with protein product
- Date approved:
- 1995-08-23
- Date modifiied:
- 2016-10-05
Related products to: PPID _ CyP_40
1,25-dihydroxyvitamin D(3) 24-hydroxylase, mitochondrial,24-OHase,Cyp24,Cyp-24,Cyp24a1,Cytochrome P450 24A1,Cytochrome P450-CC24,Mouse,Mus musculus,Vitamin D(3) 24-hydroxylase40 kDa peptidyl-prolyl cis-trans isomerase,Bos taurus,Bovine,Cyclophilin-40,Cyclophilin-related protein,CYP-40,CYPD,Estrogen receptor-binding cyclophilin,Peptidyl-prolyl cis-trans isomerase D,PPIase D40 kDa peptidyl-prolyl cis-trans isomerase,Cyclophilin-40,Cyclophilin-related protein,CYP40,CYP-40,CYPD,Homo sapiens,Human,Peptidyl-prolyl cis-trans isomerase D,PPIase D,PPID,Rotamase D40 kDa peptidyl-prolyl cis-trans isomerase,Cyclophilin-40,CYP-40,Mouse,Mus musculus,Peptidyl-prolyl cis-trans isomerase D,PPIase D,Ppid,Rotamase D40 kDa peptidyl-prolyl cis-trans isomerase,Cyclophilin-40,CYP-40,Peptidyl-prolyl cis-trans isomerase D,PPIase D,Ppid,Rat,Rattus norvegicus,Rotamase DAnti- PPID CyP-40 Antibodyanti-Cyclophilin D，PPIDanti-PPID (4C7)Anti-PPID Antibodyanti-PPID(4C7)Anti-recombinant CYP-33E1 Monoclonal AntibodyAntibodies: PPID _ CyP-40 HOST: Goat Clonality: pAbAntigens Cyclophilin D(PPID), 1- 370aa, Human, His-tagged, Recombinant, E.coliBovine Peptidyl-prolyl cis-trans isomerase D(PPID) ELISA kitBovine Peptidyl-prolyl cis-trans isomerase D(PPID) ELISA kit SpeciesBovine Related articles to: PPID _ CyP_40
- Insulin dysregulation (ID) is common and diminishes welfare of horses. Current management relies on diet and exercise, with variable responses and limited medical options. Alpha-glucosidase inhibitors (AGIs) might provide adjunctive therapy. - Source: PubMed
Whitfield-Cargile CanaanColeman MichelleHart KelseyGomes DanielBerghaus LondaDuberstein Kylee JoEllis KenzieTinkle AmandaShirzad Roya - Pituitary pars intermedia dysfunction (PPID) is an age-related endocrinopathy associated with elevated systemic inflammation, and specifically an upregulation of interleukin-8 (IL-8). It is unknown if PPID in concomitant with reproductive tract inflammation. This is a pertinent question, as chronic inflammation of the endometrium and ovary would impede fertility. Therefore, the objective of this study was to evaluate the impact of PPID on the reproductive tract of the mare. - Source: PubMed
Publication date: 2026/03/26
Howard JocelynHamner IsabellaCrook Rebecca AElliott CheyenneCarnevale ElaineColeman Stephen JKlinglesmith Brody AMcCue Patrick MSones Jenny LFedorka Carleigh E - Currently, no therapies are approved for alcohol-associated liver disease (ALD). Here, we identify cyclophilin D (CypD) as a critical mediator in the progression of ALD. We observe elevated expression of CypD in ALD patients and a corresponding mouse model. Hepatocyte-specific knockout of CypD mitigates hepatic mitochondrial dysfunction, steatosis, inflammation, and oxidative stress. Conversely, overexpression of CypD exacerbates hepatic mitochondrial stress. In vivo and in vitro experiments demonstrate that a CypD inhibitor, RN-0001, effectively and safely alleviates hepatic damage induced by ethanol exposure; these protective effects are absent in CypD-deficient mice. Biophysical assays indicate that RN-0001 directly binds to CypD. Additionally, absorption, distribution, metabolism, excretion, and toxicity (ADMET) tests and first-in-human phase I clinical trial identify RN-0001 as a promising translational candidate for ALD therapy. Collectively, our study highlights the pathological role of CypD in ALD and introduces a preclinical candidate for its management. This study was registered at chictr.org.cn (ChiCTR2500106709). - Source: PubMed
Che ZhaoyiLuo ZhihuiXiao DongMa FashuZhou HaoxiongSong YaliGuo ShanshanYuan YuanWang HaoMak Ching-PongSo Kwok-FaiXiao Jia - Environmental stressors, host condition, and parasitic infections are closely linked, as adverse conditions may compromise individual health and increase susceptibility to parasitism. This study evaluated the influence of intrinsic (body condition) and extrinsic host factors (farm, mining activity, cattle load, and dog abundance) on prevalence and parasite load in the Endangered subpopulation of from eastern Buenos Aires Province, Argentina. Fecal samples from 45 individuals were analyzed using coproparasitological techniques, including modified Ritchie sedimentation combined with Ziehl–Neelsen staining and Willis flotation to estimate prevalence, and a McMaster chamber to quantify parasite load. Body condition was estimated using a weight-to-total length index. All samples were parasitized. Oocysts of spp. and sp., as well as helminth eggs (Cestoda and Nematoda), were identified. spp., sp. 1, and sp. 4 showed the highest prevalences, while spp. exhibited the highest parasite loads. None of the models were statistically significant; however, infections with sp. 3 were the closest to significance, being more frequent in farms with low mining and cattle activity and high dog abundance. This pattern may reflect higher vegetation cover and soil moisture favoring oocyst survival. Further research is needed to disentangle the effects of specific anthropogenic pressures on host–parasite–environment interactions. - Source: PubMed
Publication date: 2026/03/16
Pagnutti NoralíLacunza JosefinaVercellini ClaraPlez Ragusa María CarolinaFux LuisinaMinardi GracielaAbba Agustín ManuelEzquiaga María Cecilia - Heart failure remains a major global health burden, with mitochondrial dysfunction recognized as a key contributor to its onset and progression. This review highlights three critical regulators of mitochondrial integrity phosphocreatine (PCr), cyclophilin D (CypD), and signal transducer and activator of transcription 3 (STAT3) and their coordinated roles in cardiac function. PCr is vital for sustaining myocardial energy balance, particularly under metabolic stress. CypD controls the mitochondrial permeability transition pore, regulating cell death pathways that contribute to cardiac injury. Beyond its classical nuclear actions, STAT3 supports mitochondrial respiration, biogenesis, and resistance to oxidative damage. Evidence reveals a functional interplay among these regulators, forming a protective network that preserves mitochondrial performance. Disruption of this network promotes energetic failure, mitochondrial injury, and heart failure progression. Targeting PCr metabolism, CypD activity, and STAT3 signaling may represent a promising therapeutic approach to enhance mitochondrial resilience and improve clinical outcomes in heart failure patients. - Source: PubMed
Publication date: 2026/03/06
Qaed EskandarLiu WuAldahmash WaleedMahyoub Mueataz AElshafei Haya ATang Zeyao