Ask about this productRelated genes to: PTGES2 antibody
- Gene:
- PTGES2 NIH gene
- Name:
- prostaglandin E synthase 2
- Previous symbol:
- C9orf15
- Synonyms:
- FLJ14038
- Chromosome:
- 9q34.11
- Locus Type:
- gene with protein product
- Date approved:
- 2002-01-29
- Date modifiied:
- 2016-10-05
Related products to: PTGES2 antibody
Related articles to: PTGES2 antibody
- Benjakul (BJK) remedy, traditionally used to balance the four elements, has demonstrated clinical efficacy in relieving inflammation and allergic rhinitis (AR) symptoms. This study investigated differential serum peptide expression in AR patients treated with BJK remedy compared to loratadine using MALDI-TOF MS and LC-MS/MS. MALDI-TOF MS revealed four shared mass peptide patterns that were significantly upregulated ( < 0.05) after 3 and 6 weeks of both treatments. Identifying the peptides, 17β-hydroxysteroid dehydrogenase (17β-HSD) and microtubule-actin cross-linking factor 1 (MACF1) were linked to inflammatory suppression and hormonal balance, while zinc finger CCCH-type containing 4 (ZC3H4) and transducin beta-like protein 3 (TBL3) were associated with the relief of pulmonary fibrosis. Conversely, zinc finger homeobox 3 (ZFHX3) and transformation/transcription domain-associated protein (TRRAP) remained elevated after treatment, potentially promoting persistent inflammation via E2F transcription factor 1- (E2F1-) and E2F transcription factor 4- (E2F4-) mediated transcription. Among 1113 peptides identified by LC-MS/MS (selected using a significance threshold of < 0.05, without a fixed fold-change cutoff), 6-week treatment with BJK remedy significantly downregulated UBQLN1 (4.562-fold; = 0.016), suppressing toll-like receptor (TLR) activation and B-cell proliferation. It also upregulated Prostaglandin E synthase 2 (PTGES2) and PDZ and LIM domain protein 2 (PDLIM2) (7.841-fold and 8.697-fold, respectively; = 0.004 and 0.002), while enhancing antioxidant and immunoregulatory responses via ATP-binding cassette subfamily B member 8 (ABCB8) and ADP-ribosylation factor GTPase-activating protein 3 (ARFGAP3). By comparison, 3 weeks loratadine treatment significantly downregulated E2F transcription factor 3 (E2F3) and general transcription factor IIIC subunit 6 (GTF3C6) ( = 0.034 and 0.017) and upregulated CTD small phosphatase like 2 (CTDSPL2), suggesting a distinct but complementary anti-inflammatory mechanism. Together, these findings enhance the understanding of AR pathophysiology and may help to elucidate the mechanisms of BJK remedy and loratadine in treatment, supporting the further development of targeted therapies and biomarkers. - Source: PubMed
Publication date: 2026/08/18
Tiyao VilailakRoytrakul SittirukJaresitthikunchai JanthimaCharoenlappanit SawanyaPhaonakrop NarumonHoungiam KatanchaleeMukkasombut NichamonKuropakornpong PranpornMakchuchit SunitaChanvimalueng WaipojDavies Neal MItharat Arunporn - Microarray and Next Generation Sequencing studies offer insight into gene regulation in Parkinson's disease (PD). However, analysing vast numbers of genes can make the interpretation of data difficult when considering the platforms and techniques used across different studies. In this study, transcript expression, restricted to genes related to G-protein coupled receptors, activating agonists, agonist precursors, synthesis enzymes and transduction processes, as well as stress-related chaperones and solute carriers, was assessed across nine microarray platforms and two RNAseq studies of the substantia nigra (nigral volume). Changes in gene expression associated with PD were assessed by differential expression analysis while RNAseq studies were also used to calculate transcript per million values for each of the genes within the nigral volume. This analysis showed extensive changes in nigral volume signalling for several robustly expressed signal-related transcripts including tyrosine hydroxylase (TH), WNT signalling components (SFRP1, RSPO2 and DKK3), Kallikrein Related Peptidase 6 (KLK6), neurexins (NRXN1, NRXN3), prostaglandin synthases (PTGES2, PTGES3) and fractalkine (CX3CL1). The nigral volume signalling ligand data was then cross-referenced to the most abundant G-protein coupled receptor and signal transduction transcripts in the pigmented neurons using two RNAseq and two microarray studies. There were 32 significant changes in G-protein coupled receptor and associated signalling genes in pigmented neurons from PD tissue. Of these, 30 genes were upregulated. Analysis of the transcription factors likely regulating the 30 upregulated genes indicates a stimulation of cell stress pathways, particularly the JNK-MAP kinase pathway. Following this pathway back to changes in nigral signalling transcripts indicates that deficits in at least two autocrine/paracrine signalling systems; dopamine, via Gαo-coupled dopamine D2 receptors and Dickkopf-3 (DKK3) appear likely to contribute to pigmented neuron stress in PD. - Source: PubMed
Publication date: 2026/07/24
Haynes John M - Psoriasis is a chronic inflammatory autoimmune skin disease for which no standardised and reliable molecular biomarkers of disease course or activity are currently available. Here, we aimed to identify serum biomarkers of psoriasis. Serum samples from 40 patients with psoriasis and 40 healthy volunteers were analysed using ELISA and Proximity Extension Assay proteomics. ELISA revealed significantly increased serum levels of AGO2 and APOA1 in psoriatic patients versus controls, with a strong association between APOA1 and psoriasis (OR = 20.72, 95% CI of 4.57-93.87, = 0.000137). Targeted serum proteomics additionally identified 35 differentially expressed proteins, including well-known psoriasis drivers (e.g., top upregulated IL17A and SERPINB4). The most downregulated was adrenomedullin (ADM, FC = -10.12). For 14 altered proteins, no previous direct associations with psoriasis were reported. Among them, DEFB103A_DEFB103B and DSG3 showed the best discrimination between psoriasis and control samples, while SERPINB4 correlated with psoriasis severity. APOA1, DEFB103A_DEFB103B, and DSG3 emerge as novel candidate circulating psoriasis biomarkers, and SERPINB4 as a biomarker of psoriasis severity. The functional role of DSG3 and other newly identified proteins (ACRV1, HAO1, ADH4, GPD1, GFER, PTGES2, DSG3, AFAP1L1, GALNT3, RASGRP2, MAP2K6, LXN, NBEAL2, and VPS54) in psoriasis requires further studies. - Source: PubMed
Publication date: 2026/06/26
Dźwigała MonikaSys DorotaŻycka-Krzesińska JoannaRybicka BeataPopławski PiotrWalecka-Herniczek IrenaPiekiełko-Witkowska AgnieszkaBogusławska Joanna - Renal aging shortens healthspan and propagates organ dysfunction beyond the kidney, yet its molecular drivers remain incompletely defined. Here we identify microsomal prostaglandin E synthase-2 (mPGES-2) as a critical regulator of renal aging and its skeletal consequence. Genetic ablation of Ptges2 improved health indices in aged mice, prolonged median survival, and markedly alleviated glomerulosclerosis, podocyte injury, and renal senescence. Single-cell transcriptomic analysis, together with podocyte- and tubule-specific knockout models, showed that podocyte mPGES-2, rather than tubular mPGES-2, is the dominant intrarenal driver of aging-related kidney injury. Mechanistically, mPGES-2 promoted podocyte senescence through a PGE/EP1 signaling axis. Podocyte-specific Ptges2 deletion also mitigated age-related osteoporosis and restored renal calcitriol and α-klotho, supporting a kidney-bone mechanism secondary to impaired renal endocrine function. Consistent with the genetic models, pharmacological inhibition of mPGES-2 with SZ0232 attenuated renal aging and improved bone microarchitecture in aged mice. Both genetic deficiency and pharmacological inhibition of mPGES-2 were well tolerated, with no overt adverse effects on major organs. These findings identify podocyte mPGES-2 as a druggable determinant of renal aging and a potential therapeutic target for aging-associated osteoporosis. - Source: PubMed
Zhong DandanHao ChangLi MengyueLiu JingXu ZhengZhou JiantengZhao LuNi SiyuHu ZhenchaoSun YueZou YingyingSun DongGuo HaoJia ZhanjunGuo DongCao Jun-LiSun Ying - Cerebral malaria (CM) is a life-threatening neurological complication of infection characterized by excessive inflammation, blood-brain barrier (BBB) disruption, and immune dysregulation. Macrophage-mediated inflammatory responses play a central role in CM pathogenesis, where imbalanced activation contributes to disease progression and tissue damage. However, integrated analyses combining macrophage surface phenotyping with transcriptional profiling remain limited, restricting comprehensive understanding of immune modulation during CM. - Source: PubMed
Publication date: 2026/06/10
Gupta AartiSharan Thakur RevaOjha Rajesh KumarKhan TahseenKalkal MeenuDas Jyoti