Ask about this productRelated genes to: PDE8A antibody
- Gene:
- PDE8A NIH gene
- Name:
- phosphodiesterase 8A
- Previous symbol:
- -
- Synonyms:
- HsT19550
- Chromosome:
- 15q25.3
- Locus Type:
- gene with protein product
- Date approved:
- 1998-06-12
- Date modifiied:
- 2014-11-19
Related products to: PDE8A antibody
Related articles to: PDE8A antibody
- Thoracic aortic aneurysm (TAA) is driven by complex molecular mechanisms beyond size thresholds, yet the role of cyclic nucleotide metabolism remains unclear. Phosphodiesterases (PDEs), which hydrolyze cAMP and cGMP in compartmentalized microdomains, act as key regulators of vascular integrity and remodeling. - Source: PubMed
Publication date: 2026/01/01
Magouliotis Dimitrios ESicouri SergeAndroutsopoulou VasilikiBaudo MassimoCabrucci FrancescoZotos Prokopis-AndreasXanthopoulos AndrewRamlawi Basel - Dysregulation in the production of cyclic nucleotides and the upregulation of cyclic nucleotide phosphodiesterases (PDEs) are implicated in many tumor pathologies. Therefore, a comprehensive investigation of PDEs and their dysfunction across different cancers is necessary. In this study, we conducted an in-depth analysis of the genomic expression and variation profiles of PDEs across multiple cancer types. We found that PDE6C, PDE6D, PDE6H, and PDE7A were significantly upregulated in nearly all types of cancer, whereas PDE2A was downregulated in 15 cancer types. Our results demonstrated that somatic copy number alterations (SCNAs) and promoter DNA methylation in pan-cancer samples were heterogeneous and may regulate the expression of PDEs in tumors. We further observed that the expression of PDEs predominantly influences the prognosis of solid tumors. Five differentially expressed PDEs (PDE5A, PDE6D, PDE8A, PDE8B, and PDE9A) were identified as independent prognostic factors for patients with pan-cancer in both the training and testing cohorts. To our knowledge, this is the first study to construct a PDE signature in pan-cancer and to highlight the pivotal role of PDE4D in LIHC (liver hepatocellular carcinoma). - Source: PubMed
Publication date: 2025/12/12
Wu ZenghongRen HuiliGuo Feng - Medication-related osteonecrosis of the jaw (MRONJ) is a severe adverse effect of antiresorptive agents, including bisphosphonates (BPs) and denosumab (DMB). We conducted a case-control epigenome-wide association study (EWAS) of 24 cancer patients treated with BPs or BPs + DMB using the Infinium MethylationEPIC v2.0 to explore epigenetic differences associated with MRONJ. Differentially methylated positions (DMPs) and regions (DMRs) were assessed across three analyses: MRONJ vs. controls (main), BPs-MRONJ vs. BPs-controls, and BPs/DMB-MRONJ vs. BPs/DMB-controls. Eight plasma bone biomarkers were quantified by Luminex and correlated with top methylation sites. We identified 10 DMPs and 4 DMRs at suggestive significance ( < 1 × 10). cg1913766 in the promoter was hypomethylated in the main analysis ( = 2.19 × 10) and in BPs-MRONJ ( = 4.80 × 10), correlating with osteocalcin ( = 0.02 and 0.03, respectively). cg21289669 was hypermethylated in the main analyses ( = 6.31 × 10), and TNXB locus formed a DMR ( = 3.30 × 10) in the main and BPs-MRONJ analyses ( = 2.76 × 10). cg11392877 in was hypomethylated in BPs/DMB-MRONJ ( = 5.35 × 10). was a significant DMR in BPs-MRONJ and the main analysis ( = 3.30 × 10). , , and regulate collagen I, while supports ribosome biogenesis, potentially contributing to MRONJ. Given the small sample size, these findings are preliminary and validation in larger studies is warranted. - Source: PubMed
Publication date: 2025/11/20
Alshammari Raed AwadhTantawy MarwaWang DanxinCastro-Hall ElysseAbreu MariaVilla AlessandroKatz JosephHolliday Lexie ShannonGong Yan - The liver served as a primary target organ for cadmium (Cd)-induced toxicity. Maternal Cd exposure during gestation and lactation heightened susceptibility to hepatic injury in male offspring, although the underlying mechanisms remained incompletely understood. Through integrated approaches utilizing rat models and in vitro hepatic stellate cells (HSCs) analyses, we demonstrated that maternal Cd exposure induced persistent lactate accumulation and hepatic fibrosis in male offspring. Mechanistically, Cd directly bound to lactate dehydrogenase A (LDHA), enhancing its enzymatic activity without altering protein expression and consequently promoting lactate production. The accumulated lactate specifically drove lactylation at lysine 18 of histone H3 (H3K18la), an epigenetic modification that increases phosphodiesterase 8 A (PDE8A) transcription. This activation suppressed the cAMP/CREB signaling pathway and ultimately triggered HSCs activation. Our findings identify the Lactate→H3K18la→PDE8A→cAMP/CREB cascade as a novel metabolome-epigenome signaling pathway driving persistent liver injury in male offspring following maternal Cd exposure. - Source: PubMed
Publication date: 2025/10/24
Wang YoujinLiu XiaojuLi PeiyuLan QiqiFan KeweiLi CongcongHuang XuanchengYu ZhijianWen Zewen - Although immune responses to bacillus Calmette-Guerin (BCG)-vaccination and susceptibility to pediatric tuberculosis (TB) vary across individuals, the underlying cellular mechanism regulating this heterogeneity is poorly understood. We used a nested case-control study with a 2-yr prospective observation period to examine whether genetic variation is associated with BCG-induced innate immune responses and susceptibility to pediatric TB (N = 134 cases, 516 controls) in BCG-vaccinated infants. Whole blood collected at 10 wk of age from 189 control infants was stimulated with BCG or media and examined with flow cytometry to measure BCG-induced PDL1, CD40, and cytokine expression in myeloid (mDC) and plasmacytoid (pDC) dendritic cells, monocytes, and neutrophils. We used a cellular and clinical GWAS to assess for associations between genetic variants, BCG-induced innate immune responses, and susceptibility to TB. We identified 11 lead genetic variants at genome-wide level significance associated with BCG-induced cytokine and surface expression markers including PDL1 (5 pDCs, 3 mDCs, 1 monocytes), CD40 (1 mDCs), and IL-6 (1 monocytes). An IGLL1 variant (rs2096522) was associated with mDC CD40 expression (P = 1.6e-08) and was also discovered as a significant variant using a gene-based method. In the clinical GWAS, we identified 39 lead variants mapping to 74 genes suggestive of an association with susceptibility to pediatric TB (P < 1e-05), but no variant reached genome-wide significance. One clinical lead variant in the PDE8A region (rs1023844, P = 9.6e-07) was also an eQTL and associated with BCG-induced monocyte PDL1 expression. In summary, we identified genetic variants associated with heterogeneity in infant BCG-induced innate immune responses with potential immunoregulatory mechanisms. - Source: PubMed
Anterasian ChristineGela AneleMwambene Temwa-DangoShah Javeed AIvie JoshDill-McFarland Kimberly AHanekom Willem AKiritsy Michael CSassetti Christopher MMusvosvi MunyaradziHatherill MarkScriba Thomas JHawn Thomas R