Ask about this productRelated genes to: PPP5C antibody
- Gene:
- PPP5C NIH gene
- Name:
- protein phosphatase 5 catalytic subunit
- Previous symbol:
- PPP5
- Synonyms:
- PP5
- Chromosome:
- 19q13.32
- Locus Type:
- gene with protein product
- Date approved:
- 1993-02-05
- Date modifiied:
- 2016-10-05
Related products to: PPP5C antibody
Related articles to: PPP5C antibody
- Chemoselective cysteine modification is pivotal for chemical biology and drug discovery. While photochemical strategies offer spatiotemporal control, most current methods rely on exogenous catalysts, complicating purification processes. Furthermore, the structural diversity of accessible conjugates remains limited. Here, we report an additive/catalyst-free, visible-light-driven platform for divergent cysteine modification via indole isocyanide photochemistry. This strategy eliminates the need for external additives or photocatalysts, ensuring excellent biocompatibility and operational simplicity. A key practical advantage of this method is its compatibility with both solution-phase and solid-phase reaction systems, offering unmatched flexibility for diverse experimental setups. By leveraging the tunable structure of indole isocyanides, this photoreaction readily generates a diverse array of indole-fused or indole-spiro aza-cycles at cysteine residues. We demonstrate broad utility of this method, ranging from site-specific modification of peptides and proteins to the synthesis of cyclic peptides and the assembly of proteolysis-targeting chimeras (PROTACs). Moreover, a chemical proteomics profiling employing indole isocyanide-based photoprobe achieved selective modification of C77 within the therapeutic phosphatase target PPP5C. This interaction revealed a novel druggable pocket at the TPR-catalytic domain interface, uncovering a previously unknown allosteric inhibition strategy. Collectively, this work establishes a robust, versatile platform for advancing therapeutic discovery and chemical biology. - Source: PubMed
Publication date: 2026/04/24
Wei HanZhu GuangheZhu RuiyingMiao RuoyangLu XinyuCheng WeiyanTian Xin - Hepatic fibrosis (HF) represents a critical stage in the progression of chronic liver disease, for which effective treatments remain limited. Cichorium pumilum Jacq (CG), a traditional Chinese medicinal herb abundant in Xinjiang, is commonly used by the local Uyghur population for therapeutic purposes. Modern pharmacology indicates that CG possesses anti-fibrotic, anti-steatotic, anti-inflammatory, and antibacterial properties. However, the primary chemical constituents of Cichorium pumilum Jacq water extract (CGEF) and its anti-fibrotic mechanisms remain unclear. This study induced HF in SD rats using 40% carbon tetrachloride-olive oil and found that CGEF improved serum markers and mitigated hepatic pathological damage. CGEF components were identified via HPLC-MS/MS, with network pharmacology predicting key targets and enrichment analysis conducted. A total of 72 major compounds were identified, network pharmacology predicted 45 key targets, and enrichment results indicated CGEF may alleviate HF through a regulatory network centered on the TGF-β/Smad pathway. To validate this hypothesis, immunohistochemical analysis was performed on liver tissues from experimental animals. In vitro, TGF-β-induced HSC-T6 cell models were treated with CGEF to evaluate changes in TGF-β/Smad pathway-related gene expression. Immunohistochemical results indicated that CGEF significantly downregulated TGF-β1, TLR4, and α-SMA expression. In cell experiments, CGEF significantly reduced the gene expression of Smad2, Smad3, Smad7, TGF-β1, and PPP5C at 24 h. At 48 h, CGEF decreased the gene expression of Smad2, Smad3, TGF-β1, and PPP5C while increasing the gene expression of Smad7. Thus, CGEF may alleviate HF primarily by regulating the TGF-β/Smad pathway. - Source: PubMed
Publication date: 2026/03/21
Chen WeijunDong NuanLu XueQin Dongmei - Tourette syndrome (TS) is a highly heritable childhood-onset neuropsychiatric disorder characterized by persistent motor and vocal tics. While both common and rare variants contribute to TS susceptibility, the role of rare mutations (DNMs) remains incompletely characterized. Here, we report findings from the largest TS whole-exome sequencing study to date, analyzing 1,466 TS trios alongside 6,714 autism spectrum disorder (ASD) trios and 5,880 unaffected sibling controls from the Simons Simplex Collection (SSC) and SPARK cohorts. Leveraging a trio-based design across these cohorts enabled calibrated assessment of DNM burden while controlling for background mutation rates. We observed a significant exome-wide enrichment of protein-truncating DNMs in TS probands, particularly within genes intolerant to loss-of-function variation (pLI ≥ 0.9), with little contribution from damaging missense variants. Notably, TS probands did not exhibit enrichment in previously implicated ASD or developmental delay (DD) genes, but elsewhere in the genome, suggesting a distinct rare variant architecture. Using a Bayesian statistical framework that integrates both and rare inherited coding variants, we identified three candidate TS risk genes with FDR ≤ 0.05: , , and . Literature shows that they have prior links to neurodevelopmental and psychiatric disorders. These findings reveal a rare variant burden in TS that is genetically distinguishable from ASD, underscore the importance of loss-of-function mutations in TS risk, and nominate novel candidate genes for future functional investigation. - Source: PubMed
Publication date: 2025/11/05
Zhan LingyuYu DongmeiIvankovic FranjoNiarchou MariaDomenech-Salgado LauraBarr Cathy LBenarroch FortuBudman Cathy LCath Danielle CFreimer Nelson BGarrido HelenaGrados Marco AGross-Tsur VardaHerrera-Amighetti LuisKing Robert AKurlan RogerLeckman James FLyon Gholson JMcMahon William MPauls David LPollak YehudaRobertson Mary MRomero RoxanaRouleau Guy ASandor PaulSinger Harvey SGiusti-Rodriguez PaolaDavis Lea KMathews Carol AScharf Jeremiah MOphoff Roel A - Emerging evidence suggesting a possible link between the PPP5C gene (protein phosphatase 5 catalytic subunit; OMIM#600658) and developmental and epileptic encephalopathy (DEE, OMIM#308350), although the clinical significance of pathogenic variants in this gene remains unclear. PPP5C is a member of the protein phosphatase catalytic subunit family, which is involved in various signaling pathways governing cell growth, differentiation, and responses to hormonal signals or cellular stress. To date, only one case with a PPP5C variant has been reported, associated with a severe neurological phenotype, including microcephaly, failure to thrive, and early-onset seizures. - Source: PubMed
Publication date: 2025/04/02
Falsaperla RaffaeleSapuppo AnnamariaPappalardo Xena GiadaRizzo RobertaRocca RobertaFusto GaiaMarino SilviaSortino VincenzoSaccuzzo LuciaRuggieri MartinoFichera Marco - Circadian rhythm is crucial to the function of the immune system. Disorders of the circadian rhythm can contribute to inflammatory diseases such as Ulcerative colitis (UC). This Mendelian Randomization (MR) analysis applies genetic tools to represent the aggregated statistical results of exposure to circadian rhythm disorders and UC and its comorbidities, allowing for causal inferences. - Source: PubMed
Publication date: 2024/02/01
Huang MengfenWu YuanLi YitingChen XueruFeng JieniLi ZumingLi JiqiangChen JiankunLu YueFeng Yan