Ask about this productRelated genes to: PPIL3 Blocking Peptide
- Gene:
- PPIL3 NIH gene
- Name:
- peptidylprolyl isomerase like 3
- Previous symbol:
- -
- Synonyms:
- CyPJ
- Chromosome:
- 2q33.1
- Locus Type:
- gene with protein product
- Date approved:
- 2000-05-31
- Date modifiied:
- 2015-11-23
Related products to: PPIL3 Blocking Peptide
Related articles to: PPIL3 Blocking Peptide
- Dysfunction in mitochondrial oxidative phosphorylation (OXPHOS) has been implicated in the pathophysiology of schizophrenia, yet its molecular underpinnings remain poorly defined. In this study, we performed an integrative multi-omics analysis to delineate these molecular signatures. - Source: PubMed
Publication date: 2025/10/23
Zhou YuZhang ShuangLiu Yao-XiaDai XinZhang TingXu Xiao-TaoDeng Sheng-NanYang Min-YanFan Zhen - Bladder cancer (Bca) remains a major genitourinary malignancy with unmet needs in immunotherapy optimization. Despite advancements in immune checkpoint inhibitors (ICIs), challenges persist, including low response rates and drug resistance. Emerging evidence links tumor cell senescence to immunotherapy efficacy, yet predictive biomarkers are lacking. - Source: PubMed
Publication date: 2025/06/26
Du KaixuanKang NingLin YudaJia KaipengShen ChongWu ZhouliangHu Hailong - The mechanisms underlying the complex relationship between autoimmune hypothyroidism and neurological disorders remain unclear. We conducted a comprehensive analysis of associations between alternative splicing, transcriptomics, and proteomics data and autoimmune hypothyroidism. - Source: PubMed
Publication date: 2024/12/28
Yu HongLi ZuoxiGao XiaoLiu XuehuanCui WeiweiLi NingjunLian XinyingLi CanLiu Jun - The RNA-dependent RNA polymerase (RdRp) is a crucial element in the replication and transcription of RNA viruses. Although the RdRps of lethal human coronaviruses severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), SARS-CoV, and Middle East respiratory syndrome coronavirus (MERS-CoV) have been extensively studied, the molecular mechanism of the catalytic subunit NSP12, which is involved in pathogenesis, remains unclear. In this study, the biochemical and cell biological results demonstrate the interactions between SARS-CoV-2 NSP12 and seven host proteins, including three splicing factors (SLU7, PPIL3, and AKAP8). The entry efficacy of SARS-CoV-2 considerably decreased when SLU7 or PPIL3 was knocked out, indicating that abnormal splicing of the host genome was responsible for this occurrence. Furthermore, the polymerase activity and stability of SARS-CoV-2 RdRp were affected by the three splicing factors to varying degrees. In addition, NSP12 and its homologues from SARS-CoV and MERS-CoV suppressed the alternative splicing of cellular genes, which were influenced by the three splicing factors. Overall, our research illustrates that SARS-CoV-2 NSP12 can engage with various splicing factors, thereby impacting virus entry, replication, and gene splicing. This not only improves our understanding of how viruses cause diseases but also lays the foundation for the development of antiviral therapies. - Source: PubMed
Yang LiZeng Xiao-TaoLuo Rong-HuaRen Si-XueLiang Lin-LinHuang Qiu-XiaTang YingFan HongRen Hai-YanZhang Wan-JiangZheng Yong-TangCheng Wei - Lack of FMR1 protein results in fragile X syndrome (FXS), which is the most common inherited intellectual disability syndrome and serves as an excellent model disease to study molecular mechanisms resulting in neuropsychiatric comorbidities. We compared the transcriptomes of human neural progenitors (NPCs) generated from patient-derived induced pluripotent stem cells (iPSCs) of three FXS and three control male donors. Altered expression of and in FXS NPCs suggested changes related to triplet repeat instability, RNA splicing, testes development, and pathways previously shown to be affected in FXS. LYNX1 is a cholinergic brake of tissue plasminogen activator (tPA)-dependent plasticity, and its reduced expression was consistent with augmented tPA-dependent radial glial process growth in NPCs derived from FXS iPSC lines. There was evidence of human iPSC line donor-dependent variation reflecting potentially phenotypic variation. NPCs derived from an FXS male with concomitant epilepsy expressed differently several epilepsy-related genes, including genes shown to cause the auditory epilepsy phenotype in the murine model of FXS. Functional enrichment analysis highlighted regulation of insulin-like growth factor pathway in NPCs modeling FXS with epilepsy. Our results demonstrated potential of human iPSCs in disease modeling for discovery and development of therapeutic interventions by showing early gene expression changes in FXS iPSC-derived NPCs consistent with the known pathophysiological changes in FXS and by revealing disturbed FXS progenitor growth linked to reduced expression of LYNX1, suggesting dysregulated cholinergic system. - Source: PubMed
Publication date: 2022/11/21
Talvio KaroMinkeviciene RimanteTownsley Kayla GAchuta Venkat SwaroopHuckins Laura MCorcoran PadraicBrennand Kristen JCastrén Maija L