CD230 _ Human Prion Protein (PrP)
- Known as:
- CD230 _ Human Prion Protein (PrP)
- Catalog number:
- 11-593-C100
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- Exbio
- Gene target:
- CD230 _ Human Prion Protein (PrP)
Ask about this productRelated genes to: CD230 _ Human Prion Protein (PrP)
- Gene:
- DHX15 NIH gene
- Name:
- DEAH-box helicase 15
- Previous symbol:
- DDX15
- Synonyms:
- HRH2, DBP1, PRP43, PrPp43p, PRPF43
- Chromosome:
- 4p15.2
- Locus Type:
- gene with protein product
- Date approved:
- 1997-12-05
- Date modifiied:
- 2016-10-05
- Gene:
- PRND NIH gene
- Name:
- prion like protein doppel
- Previous symbol:
- -
- Synonyms:
- DPL, dJ1068H6.4, DOPPEL, PrPLP
- Chromosome:
- 20p13
- Locus Type:
- gene with protein product
- Date approved:
- 2001-05-30
- Date modifiied:
- 2017-02-15
- Gene:
- PRNP NIH gene
- Name:
- prion protein
- Previous symbol:
- PRIP, GSS, CJD
- Synonyms:
- CD230, PRP, AltPrP
- Chromosome:
- 20p13
- Locus Type:
- gene with protein product
- Date approved:
- 1986-01-01
- Date modifiied:
- 2015-08-25
Related products to: CD230 _ Human Prion Protein (PrP)
Related articles to: CD230 _ Human Prion Protein (PrP)
- Sporadic Creutzfeldt-Jakob disease (sCJD) is a rapidly progressive prion disorder whose heterogeneous manifestations may overlap with potentially treatable neurological conditions. We report an atypical sCJD phenotype dominated by progressive dysarthria and an opsoclonus-myoclonus-ataxia-plus (OMAS-plus) phenotype, highlighting the diagnostic pitfalls relative to treatable mimics. - Source: PubMed
Publication date: 2026/09/21
Hulej RichardSkáčik PavolŽáková DanaKoprušáková-Turčanová MonikaGrofik MilanKurča Egon - - Source: PubMed
Publication date: 2026/09/10
Ganguly JackyMarconi MartinaMead SimonGiunti Paola - Prion diseases are rare, transmissible, and invariably fatal neurodegenerative disorders caused by the conformational conversion of cellular prion protein (PrP) into its pathogenic isoform (PrP). Despite decades of research, no licensed disease-modifying therapies are currently available. This reflects the rapid clinical course of these disorders, the difficulty of early diagnosis, and the biological challenge of targeting a self-propagating protein misfolding process within the central nervous system. - Source: PubMed
Publication date: 2026/09/03
Zhu YixinBradford Barry MMabbott Neil A - Scrapie is a fatal transmissible spongiform encephalopathy affecting small ruminants, with susceptibility strongly influenced by polymorphisms in the prion protein gene (PRNP). The aim of this study was to evaluate trends in PRNP haplotype and genotype frequencies in the Valle del Belìce sheep breed before and after the implementation of the Sicilian scrapie Resistance Plan. Furthermore, a simulation analysis was performed to assess the expected genetic response under a revised selection strategy. A total of 4341 animals were genotyped for the PRNP gene. In the overall population, ARR (0.543) and ARQ (0.406) were the most frequent haplotypes. In animals born before the implementation of the selection plan (pre-2016), the frequency of the ARR haplotype was 0.462 (females = 0.459; males = 0.537). In animals born after the introduction of the plan, ARR frequency increased to 0.589 (females = 0.566; males = 0.774), reflecting the greater selection intensity applied to breeding rams. These results support the effectiveness of targeted genetic selection in increasing the frequency of the resistant ARR haplotype, while emphasizing the often-overlooked role of ewes as a reservoir of susceptible genotypes. Simulation results suggest that extending selection to ewes and implementing controlled mating schemes could accelerate genetic progress, leading to near-fixation of the ARR haplotype within approximately seven to eight years. This study demonstrates that the inclusion of the entire breeding population is essential to optimize scrapie resistance programs. The findings provide a quantitative basis for revising current regional guidelines and offer broader insights for the design of sustainable genetic control strategies. - Source: PubMed
Publication date: 2026/09/11
Riggio SilviaMastrangelo SalvatoreCarta FedericaPortolano BaldassareSardina Maria Teresa - BackgroundAlzheimer's disease (AD) is characterized by progressive cognitive decline and neuropsychiatric symptoms, including chronic neuropathic pain. However, the molecular mechanisms linking pain sensitivity to early AD pathology remain poorly understood. - Source: PubMed
Publication date: 2026/08/26
Sheng ZhutaoXu FuYan YuqingChen LingDou BaominLiu NaZhou SichengZhu XiongweiTao Yuan-XiangXu Ying