Ask about this productRelated genes to: PPCDC Blocking Peptide
- Gene:
- PPCDC NIH gene
- Name:
- phosphopantothenoylcysteine decarboxylase
- Previous symbol:
- -
- Synonyms:
- MDS018, FLJ14585
- Chromosome:
- 15q24.2
- Locus Type:
- gene with protein product
- Date approved:
- 2005-07-25
- Date modifiied:
- 2014-11-19
Related products to: PPCDC Blocking Peptide
Related articles to: PPCDC Blocking Peptide
- Osteoarthritis (OA) is a prevalent musculoskeletal disorder causing chronic pain and disability, particularly in older adults. It is a multifactorial disease characterized by joint degeneration, with varying pathophysiological mechanisms across different OA subtypes (knee, hip, spine, hand, etc.). This study aimed to explore the genetic mechanisms underlying various OA subtypes using a novel approach combining protein level ratios (rQTLs) with Mendelian Randomization (MR) analysis. - Source: PubMed
Publication date: 2025/12/05
Wang YuehuaYang XiaozhengZhang QianChe HuiLiao Longteng - The damage of ferroptosis is related to the pathogenesis of intervertebral disc degeneration (IDD). N6-methyladenosine (m6A) modification accounts for more than 80% of RNA modifications in eukaryotic cells. However, the key role of m6A related ferroptosis-related genes (FRGs) in IDD remain explorable. Firstly, batch correction between datasets was performed. Weighted gene co-expression network analysis (WGCNA) was then conducted to acquire the most relevant module genes. Differentially expressed genes (DEGs) between the IDD and Normal Group were obtained by differential analysis subsequently. Next, according to the Pearson correlation and the intersection of m6A and FRGs related genes, m6A-FRGs related genes were selected. Additionally, we intersected module genes, DEGs and m6A-FRGs related genes to obtain DEGs of m6A-FRGs related module genes (m6A-FRGs-DEGs). Least absolute shrinkage and selection operator (LASSO) was applied to get HUBgenes. After, we conducted gene set enrichment analysis (GSEA) to gain function items and related pathways of HUBgenes. Single sample gene set enrichment analysis (ssGSEA) and wilcox.test were proceeded to analyse differences in relative abundance of immune cells between the IDD and Normal Groups, and a nomogram was constructed based on significantly different HUBgenes. The Comparative Toxicogenomics Database (CTDbase) was then applied to predict potential drugs or molecular compounds that could modulate HUBgenes. Last but not least, we performed the quantitative real-time fluorescence PCR (qRT-PCR) to verify HUBgenes. 181 m6A-FRGs-DEGs were acquired by the intersection of key module genes (from MEtan, MEsalmon, MEbrown and MEgreen), 362 DEGs and 15,678 m6A-FRGs related genes. Subsequent analysis showed that HUBgenes (ZNF595, PLXDC1, FNBP1L, KLRB1, NRCAM, PPCDC, C9orf139, SIGLEC17P, RRAS2 and DPRXP4) significantly participated in positive regulation of cytokine production, mitochondrial inner membrane and organellar ribosome. Besides, the relative abundance of neutrophils was found significantly different between IDD and normal groups. A nomogram was constructed based on ZNF595 and RRAS2, and there were 11 drugs targeted on ZNF595, while 118 drugs predicted based on RRAS2 such as Tetrachlorodibenzodioxin, Bisphenol A and Benzo(a)pyrene. Lastly, ZNF595 and RRAS2 were both obviously up-regulated in IDD according to the qRT-PCR. Our research suggested 10 HUBgenes were significantly associated with IDD, providing more evidence about the vital role of HUBgenes in IDD. - Source: PubMed
Publication date: 2025/09/29
Che ZhenChen RuibingLi MingLiao ZhuangyaoWang KunYao DengboLiang YuweiLi YuxiWen GuomingXing TongSu KaihuiLiang ChangchunHuang LinZhao Qun - Gastric cancer (GC) is one of the most prevalent malignancies in the world. Most patients are diagnosed at advanced stages of the disease, primarily attributable to the insidious nature of early symptoms and the infrequent occurrence of routine screening. Further biomarkers are still needed for more comprehensive analysis, targeted prognostication, and effective treatment strategies. Plasma proteins are promising biomarkers and potential drug targets in GC. This study aims to identify potential therapeutic targets for GC by conducting a comprehensive proteome-wide Mendelian randomization (MR) and colocalization analyses. - Source: PubMed
Publication date: 2025/03/18
Wang YongLiu ZongkaiLiu WenjiaSun YingLiu Zhaidong - The role of genetic variants in response to chemotherapy has been investigated in several studies. This study aimed to investigate genetic variants associated with response to chemotherapy in breast cancer (BC) patients. Significant variants (p < 5 × 10) associated with response to chemotherapy were obtained from GWA studies. Candidate variants were identified by haplotype analysis (r2 ≥ 0.9, D'≥0.9) using 1000Genome LD data. To determine the effects of the variants on gene expression, expression quantitative trait loci (eQTL) were evaluated. To compare the expression of the identified genes in tumor samples, expression levels were compared between TCGA tumor types and adjacent normal tissues. Six rs3820706, rs147451859, rs4784750, rs17587029, rs16830728, and rs16972207 variants were significantly associated with response to chemotherapy in BC patients (p < 5 × 10). Seven novel haplotypic structures were identified to be associated with adverse response to chemotherapy in BC patients. These haplotypes formed two genetic structures associated with neutropenia, leukopenia, chemotherapy-induced cytotoxicity (GAG-TTAT), and chemotherapy-induced alopecia (CC-CAACTCCCGTTGCGG). These variants are located on PPCDC, NLRC5, STAM2, and TNFSF13B genes, and the expression of these genes significantly changed in BC tissues than normal tissues (P ≤ 0.05), also showing gene-gene correlation (P ≤ 0.05). These genetic variants and their associated novel haplotypic structures can predict adverse response to chemotherapy in BC patients and could potentially form BC-associated genetic panel for adverse response to chemotherapy. - Source: PubMed
Publication date: 2024/08/28
Gholami MortezaAsouri MohsenAhmadi Ali AsgharNasirikenari Mehrab - Coenzyme A (CoA) is an essential cofactor required for over a hundred metabolic reactions in the human body. This cofactor is synthesized de novo in our cells from vitamin B5, also known as pantothenic acid, a water-soluble vitamin abundantly present in vegetables and animal-based foods. Neurodegenerative disorders, cancer, and infectious diseases have been linked to defects in de novo CoA biosynthesis or reduced levels of this coenzyme. There is now accumulating evidence that CoA limitation is a critical pathomechanism in cardiac dysfunction too. In the current review, we will summarize our current knowledge on CoA and heart failure, with emphasis on two primary cardiomyopathies, phosphopantothenoylcysteine synthetase and phosphopantothenoylcysteine decarboxylase deficiency disorders biochemically characterized by a decreased level of CoA in patients' samples. Hence, we will discuss the potential benefits of CoA restoration in these diseases and, more generally, in heart failure, by vitamin B5 and its derivatives pantethine and 4'-phosphopantetheine. - Source: PubMed
Publication date: 2024/04/09
Wedman J JSibon O C MMastantuono EIuso A