Guinea pig Fibronection related antigen ELISA kit
- Known as:
- Guinea pig Fibronection related antigenic Enzyme-linked immunosorbent assay test reagent
- Catalog number:
- e05f0245
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Blue gene shanghai
- Gene target:
- Guinea pig Fibronection related antigen ELISA kit
Related genes to: Guinea pig Fibronection related antigen ELISA kit
- Gene:
- MAPK4 NIH gene
- Name:
- mitogen-activated protein kinase 4
- Previous symbol:
- PRKM4
- Synonyms:
- Erk3-related, Erk4
- Chromosome:
- 18q21.1-q21.2
- Locus Type:
- gene with protein product
- Date approved:
- 1993-11-08
- Date modifiied:
- 2018-02-13
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- Wheat germ glycoprotein (WGPII) exhibits immunomodulatory activity; however, its protective mechanisms against intestinal injury remain unclear. This study investigated WGPII effects in cyclophosphamide (CTX)-induced intestinal injury mice. WGPII significantly reversed immunosuppression by increasing serum cytokines and immunoglobulins and mitigated intestinal damage by upregulating SIgA and tight junction proteins. 16S rDNA sequencing and metabolomics revealed that WGPII enriched beneficial taxa (Lachnospiraceae_NK4A136_group, Roseburia) and decreased Bacteroides, correlating with TCA cycle activation and key metabolite enrichment (α-ketoglutarate, pyruvate, and N-acetyl-l-glutamate). WGPII also upregulated colonic miR-217-5p, miR-769-x, and miR-654-3p, while suppressing their predicted targets (Cxcl12, Mapk4, IL-17F). Correlation analysis suggested a potential "miRNA-gut microbiota-metabolite" regulatory network that may contribute to WGPII's protective effects. These correlational findings provide a theoretical basis for developing WGPII-based functional products for intestinal health, though direct mechanistic validation is warranted. - Source: PubMed
Zhang JinpengZhao TiantianZhang FanXu FeiranYun LiyuanSiriwattananon LalitaZhang Min - Adenoma malignum-like (AM-L) pattern is the least common invasion type in endometrioid carcinoma of the uterus and is characterized by a bland morphologic appearance in accordance with International Federation of Gynecology and Obstetrics Grade 1 endometrioid carcinoma. However, the biological behavior of the AM-L pattern is not always indolent, and it may present at an advanced tumor stage. Although several studies have described the clinicopathological features of this pattern, the molecular alterations have not yet been explored. Here, we report a case of endometrioid carcinoma with AM-L invasion pattern and analyzed its genetic alterations using a next-generation sequencing panel that included 571 genes. Six single nucleotide variations or insertion/deletion alterations were detected, including ARID1A exon 4 c.1848dup p.(S617Lfs*6), CTNNB1 exon 3 c.101G>A p.(G34E), PTEN exon 5 c.332G>A p.(W111*), PTEN exon 6 c.548dup p.(N184Efs*6), BCOR exon 10 c.4376A>G p.(N1459S), and MAPK4 exon 6 c.1594G>A p.(G532S). Neither POLE nor TP53 alteration was detected. No copy number variations or gene fusions were observed. The microsatellite status was stable, and the tumor mutational burden was low. The molecular features demonstrate the endometrioid nature of the AM-L pattern. Further studies are needed to explore the significance of these genetic alterations in this particular pattern and to clarify their oncogenic mechanism. - Source: PubMed
Publication date: 2026/07/15
Jia MengYu Shi-LiSun Ping-Li - Alzheimer's disease (AD) is characterized by neuroinflammation, yet the impact of concurrent systemic infections on the AD brain remains poorly understood. We investigated the molecular mechanisms underlying the central nervous system response to systemic infections in AD by analyzing RNA sequencing data generated in the prefrontal cortex from 202 post-mortem donors (113 AD, 89 controls), where we stratified by the presence of a respiratory infection at the time of death. We identified 763 significant differentially expressed genes (DEGs) between AD and controls without infection, which were enriched for oxidative phosphorylation and neurodegenerative pathways. In contrast, 122 DEGs distinguished AD from controls during infection, with 57 genes uniquely altered in AD in the presence of infection, including MAPK4, VAV3, and POU3F4, implicating infection-dependent mechanisms of vascular and immune regulation. Pathway activity analysis revealed that infection in AD suppresses some immune and vascular pathways, while enhancing transcriptional and developmental programs. Weighted gene co-expression network analysis uncovered three key modules: one module strongly associated with AD, enriched for aging and signal transduction; one module linked to both AD and infection, highlighting cytoskeletal remodeling and host-pathogen interactions; and one module specific to infection, enriched in astrocytes, pericytes, and endothelial cells, implicating blood-brain barrier dysfunction. These findings suggest that systemic respiratory infections reshape transcriptional programs in the AD brain, dampening immune effector pathways and engaging vascular and host-pathogen processes in blood-brain-barrier-associated cell types. Our results highlight the complex interplay between systemic infection, neuroinflammation, and vascular responses in AD. - Source: PubMed
Publication date: 2026/06/26
Pegoraro GiuliaMacBean Lachlan FSmith Adam RSoanes Darren MSmith Rebecca GImm JenniferHarvey JoshuaKouhsar MortezaLaroche ValentinWeymouth LukeCastanho IsabelHide WinstonPalmer LauraLett Debra JRobinson Andrew CWoodman NatalieMcDade KarinaBoche DelphinePishva EhsanLunnon Katie - Genomic instability in high-grade serous tubo-ovarian carcinoma (HGSTOC) can generate fusion genes with potential roles in tumor evolution and clinical relevance. HGSTOCs commonly disseminate prior to diagnosis, but most studies analyze only one tumor sample per patient, limiting understanding of fusion gene dynamics. Here, RNA sequencing was performed on 108 tumor samples from multiple intra‑abdominal sites in 23 patients. A consensus approach involving three fusion callers identified 170 high-confidence fusion genes present in all samples from each patient, most of which were non‑recurrent and not in-frame. Protein kinases were significantly enriched among fusion partners, and commonly retained intact catalytic domains. Several of the kinase fusion genes may have oncogenic relevance, including AKAP8L::BRD4 (recurrent in three patients), GPBP1L1::MKNK1, SPAG16::ERBB4, UGP2::MAPK4, and STRN3::PRKD1. Four fusions involved homologous recombination-related genes, including FUT10::SPIDR, RAD54B::VIRMA, RAD54L::PLXNA2, and SMARCAD1::BOD1L1. Integration of these fusion genes with other somatic alterations in homologous recombination-related genes, deficiency signatures, and germline BRCA1/2 variants increased the involvement of the homologous recombination pathway to 15 HGSTOCs (65%). Overall, HGSTOC has a heterogeneous fusion gene landscape, and multi-site sampling with consensus calling offers a robust strategy for resolving fusion profiles. - Source: PubMed
Publication date: 2026/06/25
Panagopoulos IoannisStranger AneSveen AnitaJareid MieKidd Susanne GBischof KatharinaTaskén KjetilDørum AnneDavidson BenLothe Ragnhild ASkotheim Rolf IJohannessen Bjarne - Canine flank alopecia (CFA) is a recurrent, seasonal, non-inflammatory skin disorder of uncertain etiology that affects several breeds, including Rhodesian ridgebacks. While endocrine and environmental influences have been suggested, the genetic background remains unclear. This study aimed to identify candidate genes associated with CFA in Rhodesian ridgebacks using a genome-wide approach. Low-pass whole-genome sequencing with imputation was performed on 48 Rhodesian ridgebacks (24 cases, 24 controls), followed by genome-wide association analyses and evaluation of protein-coding variants. Filtering for variants with predicted functional impact revealed variants in , EPB41L1, and DPY19L1, which are involved in cytoskeletal function, cell adhesion, neural signaling, and pathways critical for hair follicle cycling, such as Wnt, BMP, MAPK, Notch, and Hedgehog signaling. Our findings demonstrate that CFA is likely a skin disorder with genetic heterogeneity, where multiple loci and possibly modifier variants influence disease susceptibility, rather than a simple monogenic disorder. These results align with the complex inheritance observed in atypical recurrent flank alopecia, supporting a complex multifactorial etiology involving both genetic and environmental factors. This study provides the first insights into the genetic background of CFA in Rhodesian ridgebacks and highlights candidate genes for further functional investigation. Broader genomic approaches are needed to elucidate the disorder's genetic basis, ultimately guiding CFA-preventative breeding strategies. - Source: PubMed
Publication date: 2026/04/21
Verschuuren-Tjoeng Millie U M YVree LiekeRozendom ClaudiaSchlotter YvetteGehring Ronettevan Steenbeek Frank G