PARP7 Assay kit
- Known as:
- PARP7 Assay reagent
- Catalog number:
- 80557
- Product Quantity:
- 96 reactions
- Category:
- Peptides
- Supplier:
- BPS Bioscience
- Gene target:
- PARP7 Assay kit
Related genes to: PARP7 Assay kit
- Gene:
- TIPARP NIH gene
- Name:
- TCDD inducible poly(ADP-ribose) polymerase
- Previous symbol:
- -
- Synonyms:
- DKFZP434J214, DKFZp686N0351, DDF1, PARP7, PARP-7, PARP-1, pART14, RM1
- Chromosome:
- 3q25.31
- Locus Type:
- gene with protein product
- Date approved:
- 2003-12-02
- Date modifiied:
- 2016-04-04
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- Aryl hydrocarbon receptor (AHR) ligands are known to suppress antibody production. However, it remains unclear whether this suppression translates into altered antibody-mediated Fcγ receptor signaling in human cells. This study aimed to investigate the effects and mechanisms by which AHR ligands regulate antibody production and antibody-triggered responses in human peripheral blood mononuclear cells (PBMCs). - Source: PubMed
Publication date: 2026/08/04
Deb ArpitaKaplan Barbara L F - Prolonged cold exposure imposes substantial physiological and operational demands; however, the molecular mechanisms supporting human adaptation to sustained cold remain poorly defined. In this first-in-human study, we conducted genome-wide transcriptomic profiling of peripheral blood leukocytes from eight healthy adult males during a 24-h whole-body cold survival simulation (7.5 °C). Blood samples were collected at four standardized time points to characterize the dynamics of gene expression during continuous cold stress. Despite the clear physiological strain, the global leukocyte transcriptome remained remarkably stable. Differential expression analyses revealed a focused, transient induction of immediate-early genes-including , , and -primarily associated with standardized exercise bouts performed immediately before and after cold exposure, with expression returning to baseline thereafter. KEGG pathway enrichment indicated activation of immune and stress response signaling pathways (e.g., Toll-like receptor, MAPK, and B-cell receptor signaling) following pre-cold exercise, whereas post-cold sampling was enriched for metabolic pathways, including oxidative phosphorylation and glycolysis/gluconeogenesis, consistent with sustained thermogenic demand and metabolic flexibility. Notably, prolonged cold exposure was not associated with broad inflammatory activation, suggesting that humans maintain transcriptomic homeostasis under sustained cold stress through targeted, energetically efficient immunometabolic regulation. These findings establish peripheral blood as a viable biosampling matrix for monitoring gene-environment interactions during prolonged cold exposure and demonstrate the feasibility of transcriptomic surveillance in extreme environments. Collectively, this study provides foundational systems-level insights into early molecular signatures of human cold resilience and informs the development of blood-based biomarkers, predictive models, and precision countermeasures to support health and performance in Arctic, military, and expeditionary settings. - Source: PubMed
Publication date: 2026/07/09
Zhang JingRhind Shawn GDucharme Michel BShiu Maria YSelkirk Glen ATaber MichaelMcGarr Gregory WBasset Fabien AHaman FrançoisCheung Stephen S - Glioblastoma multiforme (GBM) is the most aggressive primary brain malignancy with limited treatment options and poor clinical outcomes. There is growing interest in using Zika virus as a treatment for GBM due to its selectivity in finding and killing rapidly proliferating neural cells. Several studies reproducibly show that Zika can effectively kill GBM cells. We sought to uncover the molecular mechanisms driving this cytotoxic effect by performing a meta-analysis of transcriptomic studies in which Zika virus was used to kill GBM cells. We integrated four datasets from studies on GBM and added neuroblastoma (NBM) studies as an outgroup comparator. Our analysis identified a shared molecular signature of the Zika-infected GBM cell. Interestingly, GBM cells killed by the Zika virus showed dysregulation of pathways commonly implicated in proliferation and metastasis, including TNF, NF-κB, and p53 signaling. Using a hypothesis-free design, we found several long non-coding RNAs (lncRNAs) that were consistently dysregulated in Zika-infected GBMs, many of which have previously unrecognized roles in cancer cell death. Among this group, we validated four lncRNAs for a role in Zika-mediated oncolysis. We functionally tested , , , and in adult GBM cell lines using siRNA-mediated knockdown. Silencing of augmented Zika-induced cell death, while knockdown of , , and attenuated oncolysis, identifying lncRNAs whose modulation is associated with altered Zika-mediated cytotoxicity. These findings elucidate candidate mechanisms of Zika oncolysis in GBM cell lines, highlight novel lncRNA targets, and support further exploration of lncRNA modulation as a strategy to enhance oncolytic virotherapy for GBM and related malignancies. - Source: PubMed
Publication date: 2026/06/15
Singh ShriyaGerlein MartinHorvath Allison RHenderson LisaHwang Eugene IPacker Roger JShao ChunboKousa Youssef AMansour Tamer A - There are few studies on the genomics of heat stress response and the molecular mechanisms of thermoregulation. In this experimental model, Sprague-Dawley rats were subjected to temperatures of 22 ± 1 °C (control group; CT) and 42 °C for varying durations (30, 60, and 120 min, H30, H60, and H120, respectively). Significantly high rectal body temperatures were recorded post-heat stress across all treatment groups. Adrenal corticosterone levels increased significantly, especially in H120 group. Heat stress predictive accuracies of adrenal corticosterone at H60 and H120 were higher with relatively high sensitivity and AUC greater than 0.85. RNA-sequencing of adrenal gland tissue from CT vs. H30, CT vs. H60, and CT vs. H120 identified 4, 8 and 8 known; and 72, 305 and 160 de novo differentially expressed lncRNA (DElncRNAs), respectively. A total of 61, 208, and 124 genes were found to interact with DElncRNAs in the three comparisons, of which 1, 24, and 20 were differentially expressed transcripts (DETs), respectively. Among these known DElncRNAs, Gng 2-202, MAFK-203, Rab32-201, AABR07048992.1-201 were enriched in all three comparisons. Functional enrichment and interaction network analysis of DETs interacting with DElncRNAs indicated their enrichment in pathways related to inflammation-metabolism nexus determined by DETs like Jun, Map3k5, Cyp1b1, Tiparp, Ezh2, and Cbx4. This study will supplement our understanding of the transcriptome level response mechanism of rat adrenal tissue under heat stress and provide theoretical reference for the study of mammalian body response to heat stress stimulation. - Source: PubMed
Publication date: 2026/05/16
Gu JingyiSammad AbdulGuo RenyunKang ShuaiMuniz Maria Malane MagalhãesXu YaxiSheng XihuiDou Jinhuan - BackgroundAxillary lymph node metastasis (ALNM) serves as a critical prognostic determinant in breast cancer, yet the molecular drivers governing lymphatic dissemination remain poorly characterized. Integrating single-cell transcriptomic profiling with Mendelian-randomization (MR)-based genetic prioritization may help reveal cell type-specific mechanisms underlying metastatic progression.MethodsWe analyzed the GSE195861 single-cell RNA sequencing dataset encompassing six invasive ductal carcinoma (IDC) samples and paired ALNM specimens. t-distributed Stochastic Neighbor Embedding-based clustering and SingleR annotation delineated cellular heterogeneity, while differential expression analysis identified metastasis-associated genes in epithelial compartments. MR analysis employing five robust methods (inverse variance-weighted, weighted median, MR-Egger, simple/weighted mode) integrated genome-wide association study data (GCST90018799) to establish causal gene-breast cancer associations. CellChat reconstructed ligand-receptor networks across nine annotated cell types.ResultsUnsupervised clustering resolved 27 cell clusters into nine lineages, revealing ALNM-specific expansion of monocytes, pre-B cells, and CD34+ hematopoietic stem cells (HSCs). Epithelial cells exhibited 2421 differentially expressed genes (DEGs) between IDC and ALNM, including 12 genes whose genetically predicted expression showed significant associations with breast cancer risk in MR analysis (P < 0.05). CD53 (odds ratio (OR) = 1.110, 95% confidence interval (CI) = 1.019-1.209, P = 0.017) and TCDD-inducible poly-ADP-ribose polymerase (TIPARP) (OR = 1.153, 95% CI = 1.032-1.288, P = 0.012) were prioritized as candidate genes, as their genetically predicted expression was associated with increased breast cancer risk in weighted median MR. Cell-cell communication analysis implicated macrophage-derived midkine-nucleolin signaling and B-cell-orchestrated macrophage migration inhibitory factor-(CD74 + CXCR4) axis in metastatic crosstalk. Functional enrichment linked DEGs to extracellular matrix remodeling and MAPK/PI3K-Akt activation.ConclusionThis multi-omics integration prioritizes CD53 and TIPARP as ALNM-associated candidate genes with genetically supported associations with breast cancer risk, with macrophage-epithelial and B-cell-HSC interactions serving as potential therapeutic targets. Our findings provide a roadmap for developing metastasis-interceptive strategies through precision targeting of the ALNM-associated tumor microenvironment. - Source: PubMed
Publication date: 2026/05/12
Qu LimengLi JinyangDing ShirongLong QianYi Wenjun