AIF1_HUMAN AIF1 ELISA tesk kit
- Known as:
- AIF1_HUMAN AIF1 Enzyme-linked immunosorbent assay test tesk reagent
- Catalog number:
- gen16110
- Product Quantity:
- 1
- Category:
- Peptides
- Supplier:
- Other suppliers
- Gene target:
- AIF1_HUMAN AIF1 ELISA tesk kit
Related genes to: AIF1_HUMAN AIF1 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
Related products to: AIF1_HUMAN AIF1 ELISA tesk kit
Related articles to: AIF1_HUMAN AIF1 ELISA tesk kit
- Clostridioides difficile infection (CDI) remains a leading cause of healthcare-associated diarrhea and is characterized by high recurrence rates and inadequate predictive tools despite available therapeutic options. Current toxin- or nucleic acid-based assays do not fully capture host inflammatory dynamics, highlighting the need for mechanistically informed host-response studies that may complement existing microbiological approaches. This study aims to clarify the molecular mechanisms through which Clostridioides difficile (C. difficile) toxins toxin A (TcdA) and toxin B (TcdB) induce CDI and establish the theoretical foundation for more targeted interventions. We systematically identified core candidate genes associated with CDI using differential expression analysis of multiple datasets, weighted gene co-expression network analysis (WGCNA), and integration of TcdA/TcdB-related gene sets derived from multiple databases. We further integrated machine learning algorithms, protein-protein interaction (PPI) network analysis, and immune infiltration analysis to investigate the relationships between TcdA/TcdB-associated host responses and immune microenvironment remodeling, defined here as inferred changes in immune-cell composition. We identified 66 candidate genes located at the intersection of CDI-associated differential expression, WGCNA-derived genes, and TcdA/TcdB-related gene sets. Machine learning algorithms further narrowed these to nine core genes: Areg, Ptgs2, Cd40, Tlr7, Aif1, Cxcl10, Il6, Cybb, and Nos2. These genes occupy key positions within inflammatory and immune-related molecular networks associated with CDI. In addition, immune infiltration analysis suggested that dysregulation of the host immune microenvironment contributes substantially to disease progression. TcdA and TcdB may contribute to the onset and progression of CDI through host transcriptional and immune programs associated with specific inflammatory signaling pathways. The nine core genes identified through machine learning, together with immune infiltration and functional enrichment analyses, support the relevance of TcdA/TcdB-associated host-response networks in CDI. These findings provide a useful foundation for future mechanistic and experimental studies aimed at clarifying the molecular basis of TcdA/TcdB-associated CDI. - Source: PubMed
Publication date: 2026/06/03
Zhao WenhuaLi HuiHu MaolingBu Tiansheng - Acute ischemic stroke is a major cause of death and disability, yet many patients cannot engage in early rehabilitation due to severe motor deficits. Resulting immobility accelerates muscle atrophy and systemic inflammation, highlighting muscle-brain interactions as potential therapeutic targets. Electrical muscle stimulation (EMS) provides a non-volitional means of activating skeletal muscle and may mimic key neuroprotective features of exercise. We tested whether hyperacute EMS modulates muscle-to-brain signaling to improve stroke outcomes. Transient middle cerebral artery occlusion was induced in male and female C57BL/6 mice, followed by daily neurological assessments and 4 Hz lower-limb EMS for three days. Myofiber morphology, infarct size, blood lactate, and muscle and brain gene expression were subsequently analyzed. EMS preserved myofiber size and reduced stress-response gene expression (Hsp25, Hspb8, Atf4) in skeletal muscle. In the brain, EMS decreased infarct volume, limited necrosis, and improved neurological function. Stroke-associated inflammation was attenuated, evidenced by reduced Tnf, Nlrp3 and Aif1 expression. EMS elevated circulating lactate, while stroke groups showed increased expression of the monocarboxylate transporter Mct-1, supporting a lactate-dependent metabolic coupling mechanism. These findings identify hyperacute EMS as a feasible, noninvasive intervention that confers neuroprotective and anti-inflammatory benefits after stroke, potentially via lactate-mediated muscle-to-brain signaling. EMS may represent a valuable adjunct for patients unable to mobilize during the critical early phase of stroke recovery. - Source: PubMed
Publication date: 2026/06/02
Törteli AnnaKozák PéterUno HiroyukiHősi RajmundRuppert ZsófiaGáspár EszterBari FerencTörök ZsoltFarkas EszterTóth Melinda EMenyhárt Ákos - Multiple sclerosis (MS) is a chronic inflammatory disorder characterized by demyelination within the central nervous system. Emerging evidence suggests that plasma proteins may serve as genetically supported candidate targets, yet their underlying mechanisms in MS remain poorly understood. In this study, we applied proteome-wide Mendelian randomization (MR) to systematically identify plasma proteins that are causally associated with MS risk and to explore their potential biological roles and treatment implications. - Source: PubMed
Publication date: 2026/05/19
Wang ZheyiSun YizeBai ZetaiLi MeiKong DeyuanWu Guanzhao - Hemorrhagic shock (HS) is a life-threatening condition that leads to multiple organ failure due to centralization of blood flow and impaired blood clotting. In this study, we investigated the acute and delayed effects of HS on the brain, kidneys, and liver of rats to identify molecular targets for therapy of the consequences of shock. Blood acid-base balance and electrocardiography (ECG) parameters were studied in rats in the acute phase of HS. Gene expression of antioxidant enzymes (Gpx1, Sod1, Cat, Nfe2l2) and inflammatory markers (Ptprc, Cxcl1, Cd86, Itgal, Il1b, Il6, Tnf, Tlr2, Cox2, Cst7, Ccl3, Il10) in brain, kidney, and liver tissues was analyzed, as well as the amount of protein markers for kidney damage (NGAL, KIM-1) in urine 24 h after HS. In addition, markers for the activation of astrocytes (Gfap) and microglia (Aif1) as well as neuronal markers (Eno2, Tubb3) in brain tissue were analyzed. Biochemical markers for liver and kidney damage and total antioxidant activity were determined in blood serum. Acute HS caused decompensated lactic acidosis, arterial hypotension and characteristic changes in the ECG. Although no pronounced inflammatory response was detected in brain, kidney and liver tissue in the late phase after acute blood loss, the brain and liver tissue were more susceptible to the adverse effects of acute blood loss than the kidneys according to a number of indicators. This points to the need to develop targeted strategies to protect organs in the postresuscitation period by targeting specific molecular targets in specific tissues. - Source: PubMed
Andrianova N VLapin K NBrezgunova A ABocharnikov A DPevzner I BBuyan M IRemneva E SKirpicheva D AKalabushev S NRyzhkov I APlotnikov E Y - Epilepsy is a severe chronic condition that remains pharmacoresistant in approximately 30% of the patients, which necessitates the search for new treatment approaches. Epileptogenesis involves disruption in the interaction between metabolic pathways and neuronal signaling. A promising therapeutic target is the peroxisome proliferator-activated receptors (PPARs), which integrate metabolic and anti-inflammatory signals. The aim of this work was to evaluate effects of the PPARγ agonist pioglitazone on the complex of epileptogenesis manifestations: behavior and expression of the genes encoding glial markers, cytokines, neurotrophic factors, and glutamate receptor subunits during the latent phase of the lithium-pilocarpine model in rats. The study was conducted with 8-week-old male Wistar rats divided into control and experimental groups. Pioglitazone was administered at low doses (7 mg/kg after status epilepticus, followed by 1 mg/kg/day for 7 days). On the days 8-9, locomotor and social activities were assessed using the Open Field and Social Interaction tests. On the day 10, expression of the genes encoding markers for activation and various states of astro- and microglia, cytokines, neurotrophic factors, and glutamate receptor subunits was analyzed in the dorsal hippocampus and temporal cortex using RT-qPCR. It was shown that pioglitazone partially alleviated the pilocarpine-induced social deficit. In the brain of rats with the epilepsy model, increased expression of the glial activation markers (, ) and cytokines (, ) was found, which was weakly affected by administration of pioglitazone. At the same time, the drug completely prevented the pilocarpine-induced decrease in the expression of the glutamate receptor subunit gene . The obtained data suggest that, at the applied doses, pioglitazone primarily modulates expression of the genes related to synaptic plasticity and does not exert a significant effect on expression of the genes associated with glial activation and inflammation. Thus, activation of PPARγ as a metabolic sensor during epileptogenesis could stabilize transcriptional programs that are important for maintaining synaptic homeostasis, which opens the possibilities for targeted modulation of metabolic pathways in epilepsy therapy. - Source: PubMed
Kharisova Adeliya RZubareva Olga EKovalenko Anna ASinyak Denis SZaitsev Aleksey V