AIF1_BOVIN AIF-1 ELISA tesk kit
- Known as:
- AIF1_BOVIN AIF-1 Enzyme-linked immunosorbent assay test tesk reagent
- Catalog number:
- gen16108
- Product Quantity:
- 1
- Category:
- Peptides
- Supplier:
- Other suppliers
- Gene target:
- AIF1_BOVIN AIF-1 ELISA tesk kit
Ask about this productRelated genes to: AIF1_BOVIN AIF-1 ELISA tesk kit
- Gene:
- AIF1 NIH gene
- Name:
- allograft inflammatory factor 1
- Previous symbol:
- -
- Synonyms:
- IRT-1, AIF-1, Em:AF129756.17, IBA1
- Chromosome:
- 6p21.33
- Locus Type:
- gene with protein product
- Date approved:
- 1997-07-01
- Date modifiied:
- 2016-10-05
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- Bisphenol A (BPA) is a widespread plasticizer widely used in the food industry worldwide. However, a consensus on the safe level of its daily intake does not currently exist, while there are numerous data pointing to a link between prenatal exposure to BPA and early neuropsychiatric disorders, such as autism spectrum disorder (ASD) and attention deficit hyperactivity disorder (ADHD). The global average human-equivalent dose of BPA is estimated at 30 ng/kg body weight/day. Thus, the research herein was conducted on newborn and juvenile rat offspring of both sexes delivered from rats treated with 30 ng/kg body weight/day orally from day 6 to 21 of pregnancy and for a further 21 days during lactation. Our data indicate that prenatal exposure to 30 ng/kg/day from gestation day 6 to delivery induced sexually dimorphic, region-specific alterations in the neonatal (PD1) rat brains, impacting inflammatory reactions, estrogen receptor signaling, and neural progenitor dynamics. Prenatally BPA-treated males exhibited a pro-inflammatory state characterized by an increased total number of ramified Iba1+ microglia cells in the hippocampus alongside upregulation of , , , , and . Conversely, prenatally BPA-treated females showed only an increased total number of hippocampal Iba1+ cells and displayed inflammatory resilience, lacking upregulation of these markers. Both sexes exhibited a pro-inflammatory state in the prefrontal cortex via upregulation of , , , and . While both sexes showed decreased in the prefrontal cortex, they deployed distinct compensatory responses: males upregulated the neuroprotector only in the hippocampus, whereas in females, it was upregulated in both the hippocampus and the prefrontal cortex. Estrogen receptor expression was also highly dimorphic. In the hippocampus, males displayed an imbalance via upregulation and downregulation, while females showed downregulation alone. In the prefrontal cortex, these transcriptional profiles were the opposite. Finally, neural progenitor markers were altered. In the prefrontal cortex, BPA drove the upregulation of and in males but in females; in the hippocampus, only was upregulated, and only in males. The PAX6 protein level in the hippocampus was significantly increased in males but decreased in females. In juvenile offspring (PD21), behavioral patterns characterized by hyper-exploration, increased environmental investigation, and heightened emotional reactivity during social exposure were more pronounced in female offspring. These baseline neonatal disparities followed by behavioral changes underscore the necessity of sex-specific approaches when evaluating early-life neurodevelopment and subsequent adult behavioral and biological vulnerabilities. - Source: PubMed
Publication date: 2026/09/14
Gerasimov Andrey DSentyabreva Alexandra VGantsova Elena AMelnikova Ekaterina AKosyreva Anna M - This study integrates epidemiological analysis and computational toxicology approaches to systematically investigate the association between cadmium (Cd) exposure and osteoarthritis (OA), as well as the underlying molecular mechanisms. Based on the data from the 2013-2018 National Health and Nutrition Examination Survey (NHANES), multivariate logistic regression models and forest plot analyses revealed that elevated blood cadmium levels were significantly associated with an increased risk of OA, with particularly pronounced effects observed among individuals with diabetes, hypertension, vitamin D deficiency, low income, and smokers. Further, potential cadmium-related targets were identified through network toxicology, and by integrating differentially expressed genes (DEGs) in OA, weighted gene co-expression network analysis (WGCNA), and protein-protein interaction (PPI) networks (STRING), a total of 113 intersection genes were obtained. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses indicated that cadmium may promote OA progression by regulating pathways, such as cellular senescence, FOXO signaling, and TNF signaling. Through Cytoscape MCC algorithm, forest plot, and Lasso regression analysis, six key hub genes-MYC, FOXO1, FOXO3, ZFP36, AIF1, and KLF4-were identified. Molecular docking simulations further validated the strong binding affinity between cadmium nitrate and these core targets. Overall, this study comprehensively delineates the molecular network by which cadmium exposure may contribute to OA, providing novel insights into the environmental heavy metal toxicity mechanisms and potential therapeutic interventions. - Source: PubMed
Publication date: 2026/09/24
Luo YingjinZhou DaqianZhou MingminZheng Qianghua - Spinal cord injury (SCI)-associated neuropathic pain (NP) is a severely disabling complication with limited treatment options. Although spinal microglial activation is well documented in SCI-NP, the functional role of microglia in the primary motor cortex (M1) and their response to repetitive transcranial magnetic stimulation (rTMS) remain poorly understood. - Source: PubMed
Publication date: 2026/09/16
Zhang KunlongYang XinjiangHou RuibinZhao RuiLi DongjinLiao HanchengTian FeiSun XiaolongYuan Hua - Demyelination is a hallmark of various neurodegenerative diseases, including multiple sclerosis (MS), leading to impaired neural transmission and motor deficits. The Lysophosphatidylcholine (LPC)-induced demyelination model is widely used because it reflects many aspects of demyelinating pathology. This study examined how non-invasive 4 Hz visual theta oscillation entrainment affects LPC-induced demyelination in the optic chiasm of male C57BL/6J mice. Mice received daily one-hour sessions of 4 Hz stimulation for two weeks post-LPC injection. The analysis of the VEPs showed that the latency of P1 waves was shorter in the theta stimulation group and significantly different from the LPC group on days 7 and 14. IBA1 immunostaining showed reduced IBA1 immunoreactivity at early post-lesion time points, while qPCR analysis showed lower Aif-1 1 and Gfap transcript levels in the theta-stimulated group. Luxol Fast Blue (LFB) and FluoroMyelin staining suggested greater preservation of myelin staining in the theta group at day 14. In parallel, molecular analyses revealed increased expression of oligodendrocyte-lineage markers, including Pdfgra at days 3 and 7 and Olig2 and Plp1 at day 14. Taken together, these findings suggest that theta oscillation entrainment modulates the molecular, cellular and electrophysiological responses that follow demyelinating injury, and that it may also influence the processes associated with myelin repair. Further studies are needed to clarify the mechanisms underlying these effects and to assess the therapeutic relevance of this non-invasive approach for demyelinating disorders. - Source: PubMed
Publication date: 2026/09/15
Dehghan SamanehDehdar KolsoumAhmadirad NooshinMehrizi Sarina Sadat AboeiRaoufy Mohammad RezaJavan Mohammad - Canine macrophages are increasingly recognized as important regulators of tumor immunity; however, in vitro culture systems that minimize serum-derived variability remain limited. In this study, we established a serum-reduced culture system for canine peripheral blood mononuclear cell (PBMC)-derived macrophages and characterized their phenotypic, transcriptional, and functional properties. PBMCs from healthy Beagle dogs (n = 3) were differentiated into M0, M1, and M2 macrophages using Macrophage Base Medium supplemented with canine serum or recombinant cytokines. Morphology was assessed by phase-contrast microscopy, macrophage identity was evaluated by Iba1 immunostaining and AIF1 expression, and exploratory transcriptomic profiles were examined by RNA sequencing (n = 1). Phagocytic activity was assessed using FITC-labeled latex beads and flow cytometry, and macrophage-tumor cell interactions were evaluated by co-culture with canine urothelial carcinoma cells. M0, M1, and M2 macrophages exhibited distinct morphologies and transcriptional patterns. M1 macrophages showed increased expression of inflammatory genes, including IL1B and IFNG, whereas M2 macrophages showed increased expression of genes associated with alternative activation and immune regulation, including CD209, CD5L, and IL33. Phagocytic activity was observed in all subsets. In co-culture experiments, macrophages exhibited polarization-dependent interaction patterns with tumor cells, with M2 macrophages exhibiting features reminiscent of tumor-associated macrophages. These findings provide a pilot evaluation of this serum-reduced culture system, which generates phenotypically distinct canine macrophage subsets and may serve as a useful in vitro platform for future studies of canine macrophage polarization and tumor-associated immune responses. - Source: PubMed
Publication date: 2026/09/10
Hoshino YukiAnzai RihoKobayashi SaoriUchida NaohiroIshiguro-Oonuma ToshinaNaito IkunoriYamada ShinjiMotegi TomokiYamamoto Yoshio