PARP14 Chemiluminescent Assay Kit
- Known as:
- PARP14 Chemiluminescent Assay Kit
- Catalog number:
- 80568
- Product Quantity:
- 32 reactions
- Category:
- -
- Supplier:
- BPS Bioscience
- Gene target:
- PARP14 Chemiluminescent Assay Kit
Related genes to: PARP14 Chemiluminescent Assay Kit
- Gene:
- PARP14 NIH gene
- Name:
- poly(ADP-ribose) polymerase family member 14
- Previous symbol:
- -
- Synonyms:
- KIAA1268, pART8
- Chromosome:
- 3q21.1
- Locus Type:
- gene with protein product
- Date approved:
- 2004-08-25
- Date modifiied:
- 2016-10-05
Related products to: PARP14 Chemiluminescent Assay Kit
Human ELC ELISA KIT 96 TEST
OxiSelect Hydroxyl Radical Antioxidant Capacity (HORAC) Activity Assay, Trial Size
OxiSelect In Vitro ROS/RNS Assay Kit (Green Fluorescence), Trial Size
OxiSelect Methylglyoxal (MG) Competitive ELISA Kit
OxiSelect Methylglyoxal (MG) Competitive ELISA Kit
OxiSelect TBARS Assay Kit (MDA Quantitation), Trial Size
OxiSelect Total Antioxidant Capacity (TAC) Assay Kit, Trial Size
OxiSelect™ In Vitro ROS RNS Assay Kit (Green Fluorescence), Trial Size(1-Kit )11,12-EET DHET Immunoassay Kit(1-Kit )11,12-EET_DHET Immunoassay Kit(1-Kit) 11,12-DHET Immunoassay Kit(1-Kit) 14,15-DHET Human Urine ELISA Kit(1-Kit) 14,15-DHET Hypertension ELISA Kit(1-Kit) 14,15-DHET sEH activity ELISA Kit(1-Kit) 14,15-EET DHET Hypertension ELISA Kit Related articles to: PARP14 Chemiluminescent Assay Kit
- Human adenovirus type 7 (HAdV-7) can cause severe pneumonia and sepsis in children, but the associated host epigenetic and immune alterations remain poorly defined. We profiled peripheral-blood DNA methylation in 11 children with HAdV-7-associated sepsis (6 survivors and 5 non-survivors) and 5 pediatric controls without clinically detectable HAdV-7 infection using reduced representation bisulfite sequencing. Differentially methylated genes were integrated with pediatric septic shock transcriptomic modules from GSE26440, and their cellular distribution and predicted regulatory effects were explored using the single-cell dataset GSE167363 and scTenifoldKnk. We identified 106 genes showing differential methylation across all three pairwise comparisons. Cross-cohort integration prioritized 19 candidate genes, among which TP53INP1 showed preferential expression in B cells in the external sepsis single-cell dataset. In silico perturbation of TP53INP1 was associated with changes in interferon-stimulated and antiviral genes, including TRIM22, IFI44L, and PARP14. These findings identify TP53INP1 as a hypothesis-generating candidate linking HAdV-7-associated whole-blood methylation changes with B-cell regulatory networks observed in an external sepsis dataset. Given the small discovery cohort and absence of experimental validation, the findings are exploratory and require confirmation in independent cohorts. - Source: PubMed
Publication date: 2026/09/17
Hu PeidanHuang BolunYang WenminZhang ChunminHuang JindaYang YiyuChen Feiyan - ADP-ribosylation is a highly dynamic process that is increasingly linked to a diverse set of cellular functions and pathophysiological outcomes. The modification of target substrates (e.g., proteins, DNA, RNA) involves ligation to an array of different chemical moieties. Recent work has shown that the ester bonds formed between ribose and Asp/Glu residues are particularly labile. A common strategy to overcome this lability is the replacement of the ADP-ribose (ADPr) by hydroxylamine. Attachment of hydroxamic acid (HA) permanently shifts the mass of labeled Asp/Glu residues by +15 Da. However, this method suffers from two notable limitations: HA treatment for long periods of time will label Asp/Glu sites that are solvent exposed, but not modified by ADPr; and the competing hydrolysis reaction still occurs in the conditions routinely used for HA labeling. Herein, we optimize a mass spectrometry (MS) workflow that overcomes these drawbacks. As a proof-of-principle, a truncated form of PARP14 was assessed for its ability to ADP-ribosylate peptides and itself. Conditions that prioritize HA attack over the background rate of hydrolysis were determined using an ultrathin matrix-assisted laser-desorption/ionization (TLC-MALDI) time-of-flight (TOF) method with ADPr-peptides. These efforts doubled HA labeling efficiency and completely removed ADPr within an hour. Next, a series of MS experiments identified the sites of PARP14 automodification using both standard HA labeling conditions (overnight, pH 7.0, 25 °C) and the optimized conditions. Of the identified 9 ADPr sites on PARP14, 5 are unique to the optimized conditions and 6 are newly identified. Mutagenesis revealed a set of sites that down-regulated PARP14 and another set that appears to activate PARP14. Taken together, these efforts have improved the true positive site identification rate using HA and have revealed a novel role for several automodification sites in PARP14 regulation. - Source: PubMed
Publication date: 2026/09/21
Nivaggioli StephNguyen Hannah HHarker Kiana KMohr Christian MWood JakeDupen MikaylaJaved ZeeshanKarjalainen NataliaYousefpor ViolettaReddy AshokCarter-O'Connell Ian - In Cell Press Blue, Carvalho et al. identify spatially organized tumor-macrophage niches, EMT-like CD44 cancer cells paired with SPP1/PARP14 macrophages, that drive chemoresistance in bladder cancer. PARP14 inhibition can flip this protective niche into an inflammatory, cisplatin-sensitizing state. - Source: PubMed
Publication date: 2026/08/20
Wang YuzhaoChen ZibinLiu ZhuoweiMa Zikun - Autoimmune myocarditis frequently progresses to inflammatory cardiomyopathy through dysregulated immune-stromal interactions. This study employs single-nuclei RNA-sequencing (snRNA-seq) to profile 46,233 cardiac nuclei from the experimental autoimmune myocarditis (EAM) mouse model at four timepoints: day 0 (healthy), day 14 (inflammation), day 21 (acute inflammation), and day 40 (late cardiac remodelling). Single-nuclei RNA profiling identified 18 transcriptionally distinct cell populations. Global cell-cell communication analysis revealed a dramatic peak of intercellular signalling at day 14 (5907 interactions), with fibroblast subpopulations and macrophages as dominant hubs, followed by partial resolution at day 21 (2264 interactions) and renewed remodelling at day 40 (4862 interactions). Subclustering of the macrophage compartment identified five subpopulations: Mac-TLF, Mac-MHCII, Mac-rMHCII, Mac-ResL, and Classical Monocytes. Tissue-resident macrophages (Mac-TLF, CCR2-) dominated at healthy state (~55%) but were rapidly depleted at day 14, coinciding with a dramatic influx of recruited CCR2 macrophages (Mac-rMHCII), which expanded to over 70% of the compartment and maintained dominance through day 40. At inflammation (day 14), the expanded Mac-rMHCII subpopulation displayed a strongly pro-inflammatory signature (, , , ), and the overall macrophage compartment was enriched for cytokine response, Fc-gamma receptor, and Notch signalling pathways, while downregulating homeostatic and mitochondrial metabolic programmes, potentially contributing to impaired efferocytosis and cardiomyocyte dysfunction. Macrophage-centred communication networks expanded markedly at day 14 (1047 interactions), with resting fibroblasts (FB-R) as the primary signalling partner, driving pro-inflammatory stromal activation marked by upregulation of , , and . Intra-macrophage subcluster communication also intensified at this timepoint (447 interactions). These findings delineate the temporal and functional heterogeneity of cardiac macrophages during EAM progression and identify key immune-stromal interactions driving pathological cardiac remodelling. The coexistence of pro-inflammatory and transitional reparative macrophage subsets highlights the limitations of broad immunosuppression and supports precision strategies targeting CCR2-mediated recruitment, the SPP1 signalling axis, and macrophage-fibroblast crosstalk as therapeutic avenues in myocarditis and its progression. - Source: PubMed
Publication date: 2026/06/19
Stefanska MonikaKot MartaKoterba DamianZeyland Joanna - Keloids are fibroproliferative dermal disorders characterized by excessive extracellular matrix deposition and a strong tendency to recur, yet the mechanistic links between inherited genetic variation, molecular phenotypes and disease risk remain incompletely understood. We integrated GTEx v8 skin expression quantitative trait loci (eQTL) data, pooled GWAS statistics for 338 cerebrospinal fluid (CSF) metabolites, and two independent European keloid GWAS datasets within a three-step Mendelian randomization (MR) framework to identify causal mediation pathways from skin gene expression through systemic metabolite levels to keloid susceptibility. Bulk RNA-seq, single-cell RNA-seq and in vitro fibroblast and smooth muscle cell experiments were then used to validate the functional roles of the prioritized genes and metabolites. Four CSF metabolites-sphingomyelin, 1-stearoyl-2-oleoyl-glycerophosphocholine (SOPC), N-acetylarginine and X-23593-were causally associated with increased keloid risk (OR > 1) and replicated across both GWAS datasets. PARP14 emerged as a reproducible upstream risk gene (OR = 1.17, 95% CI 1.02-1.34) coordinating effects across all four mediators, whereas ALDH2 was identified as a SOPC-mediated protective gene (OR < 1). Single-cell profiling localized elevated PARP14 expression to smooth muscle cells and reduced ALDH2 expression to a disease-expanded mesenchymal fibroblast subset, with both signals embedded within canonical pro-fibrotic signaling programs (TGF-β, Wnt, Hippo, PI3K-Akt/mTOR, ECM-receptor interaction and focal adhesion). In vitro, SOPC and sphingomyelin produced dose-dependent fibroblast proliferation and induction of COL1A1, COL3A1, POSTN, and FN1, while modulation of PARP14 and ALDH2 by siRNA and lentiviral overexpression confirmed their roles in regulating proliferation and fibrotic marker expression. Together, these findings delineate a skin eQTL → CSF metabolite → cell-state axis in keloid pathogenesis, nominating PARP14, ALDH2 and SOPC-linked lipid remodeling as candidates for mechanistic study and therapeutic targeting. - Source: PubMed
Xu JieBai MengqiLiu Tongyun