AIF1 _ IBA1 (isoforms 1 + 3) Antibody
- Known as:
- AIF1 _ IBA1 (isoforms 1 + 3) Antibody
- Catalog number:
- AF1039c
- Product Quantity:
- 0.1mg
- Category:
- -
- Supplier:
- Abgen
- Gene target:
- AIF1 _ IBA1 (isoforms 1 + 3) Antibody
Related genes to: AIF1 _ IBA1 (isoforms 1 + 3) Antibody
- 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 _ IBA1 (isoforms 1 + 3) Antibody
Related articles to: AIF1 _ IBA1 (isoforms 1 + 3) Antibody
- Studies on the effects of γ-radiation on nonhuman primate (NHP) brains are limited, despite the critical need to understand the impact of radiation exposure on the brain from various sources like radiotherapy equipment, space travel, and potential nuclear events. We investigated molecular and neuropathological changes in rhesus macaque brains after a single 5.8 Gy total-body γ-radiation exposure. We analyzed samples dissected from frontal cortex (FCtx), hippocampus (Hippo), and cerebellum (CRB) of irradiated (RAD) vs. unirradiated/control (CTRL) animals. Western blotting and digital PCR (dPCR) analyses were used to measure different phosphorylated-Tau (pTau) forms and neurodegeneration markers (i.e., amyloid protein precursor [APP], neurofilament-light chain [NFL], glial fibrillary acidic protein [GFAP], ionized calcium-binding adapter molecule 1 [IBA1/AIF1], and myelin basic protein [MBP]). We detected lower levels of different forms of soluble pTau species (pTau181, and pTau217, among others) in RAD vs. CTRL animals across all three examined brain regions. While APP and GFAP levels were unchanged in the FCtx, increased IBA1 and NFL levels were detected alongside decreased MBP levels. Moreover, dPCR data identified decreased expression of GFAP and MBP in the FCtx. Importantly, the molecular changes observed were not accompanied by overt signs of neurodegeneration or cellular abnormalities upon neuropathological assessment. These findings in irradiated NHPs' brains are novel and indicate that a single total-body γ-radiation exposure significantly alters soluble pTau levels after a few weeks from irradiation without causing obvious neurohistological damage. These results open intriguing new possibilities of exploring γ-radiation-based strategies to modulate the progression of tauopathies, including Alzheimer's disease. - Source: PubMed
Publication date: 2026/04/02
Murphy Erin KHatch KathleenWise Stephen YFatanmi OluseyiPetrus Sarah ABhomia ManishLecca DanielaKnollmann-Ritschel Barbara E CPerl DanielSingh Vijay KIacono Diego - CDKL5 Deficiency Disorder (CDD) is a severe neurodevelopmental encephalopathy characterized by early disruptions of synaptic maturation and network stability, leading to persistent motor, cognitive, and behavioral impairments. Given the role of the endocannabinoid system in synaptic development, neuroinflammation, and neuronal resilience, we investigated whether the sustained enhancement of endogenous 2-arachidonoylglycerol (2-AG) signaling via monoacylglycerol lipase (MAGL) inhibition could mitigate key pathological features in adult knockout (KO) mice. Using an intermittent 6-week treatment, the MAGL inhibitor JZL184 robustly increased plasma 2-AG levels, reduced MAGL protein levels, and activated CB1-AKT signaling without evidence of receptor desensitization. Despite this clear pharmacodynamic efficacy, behavioral effects were domain-specific: neither dose ameliorated core behavioral deficits, although the higher dose selectively reduced stereotypic jumping and modestly improved cue-dependent associative memory. At the cellular level, JZL184 induced biologically meaningful effects, partially restoring dendritic spine maturation in the primary somatosensory cortex and increasing neuronal survival in the vulnerable CA1 hippocampal region. In contrast, microglial responses were dose-dependent and divergent, with the lower dose exerting anti-inflammatory effects, while the higher dose increased cortical microglial density and Allograft Inflammatory Factor-1 (AIF-1) expression, suggesting engagement of compensatory or off-target mechanisms. Overall, these findings show that MAGL inhibition activates neuroprotective pathways and ameliorates select structural deficits in adult KO mice, but is insufficient to produce broad behavioral recovery, highlighting the domain-specific effects of selective 2-AG enhancement via MAGL inhibition and the need for developmentally informed or multimodal therapeutic strategies in CDD. - Source: PubMed
Publication date: 2026/03/19
Loi ManuelaMottolese NicolaMedici GiorgioIannibelli FelicianaInterino NicolòCandini GiuliaTrebbi FedericaBove Angelica MarinaFiori JessicaTrazzi StefaniaCiani Elisabetta - was to evaluate the possibilities and limitations of using the immunohistochemical detection of Iba-1 protein for morphofunctional analysis of microglia under different conditions. - Source: PubMed
Publication date: 2026/02/27
Guselnikova V VKirik O VSufieva D ARazenkova V ABeketova A AKorzhevskii D E - BACKGROUND In chronic alcohol consumers, immune cells may drive the progression from mild liver injury to more severe alcohol-associated liver diseases (ALD), including alcohol-associated hepatitis (AAH) and cancer. Liver macrophages, both resident and infiltrating, express Allograft Inflammatory Factor 1 (AIF1), which is upregulated during inflammation and enhances immune activation. METHODS Using serum and urine samples from 868 individuals classified as having alcohol use disorder or not based on DSM-IV/V criteria, along with serum and liver biopsy tissue from a second cohort of 27 patients diagnosed with AAH, we evaluated the impact of the AIF1 promoter single nucleotide polymorphism (SNP) (rs3132451; C/C, C/G, G/G) on liver function markers and immune cell profiles. RESULTS AIF1 transcript levels were genotype-dependent: C/C homozygotes expressed 5.2% of the levels observed in G/G individuals, while C/G heterozygotes expressed 46%. Unlike most SNPs associated with harmful effects, the G/G genotype is highly prevalent, present in ~70% of patients. Among chronic alcohol users, G/G individuals exhibited elevated markers of liver injury and a more than threefold increase in hepatic immune cells, including infiltrating AIF1⁺ macrophages and neutrophils. Despite similar durations of alcohol misuse, G/G individuals had higher Model for End-Stage Liver Disease scores compared to C/G individuals, indicating a significantly greater 90-day mortality risk. Notably, some immune abnormalities, such as elevated neutrophils, persisted in G/G males even after alcohol abstinence. CONCLUSION These findings suggest that functional genetic variation in AIF1 may contribute to the severity and persistence of ALD. TRIAL REGISTRATION ClinicalTrials.gov NCT02231840. FUNDING Research support was provided from the National Institute on Alcohol Abuse and Alcoholism (NIAAA) of the National Institutes of Health (NIH) under grant 1ZIAAA000440-02 and R24AA025017. - Source: PubMed
Publication date: 2026/03/10
Antonello Priscila CHodgkinson Colin AFeng DechunMarietta CherylMohana Krishnan BaskarParra Maria ASun ZhaoliGao BinGoldman DavidAntoine Michelle W - The biological activities of fucoidan from brown algae have attracted considerable attention. Degradation to low-molecular-weight fucoidan reduces viscosity and improves bioavailability, enhancing antioxidant and anti-inflammatory effects. Fucoidan was degraded using acetic acid combined with Co γ-ray irradiation and fractionated by Bio-Gel P10 chromatography to obtain four fractions (AIF1-AIF4). The fractions were structurally characterized and assessed for in vitro radical-scavenging activity and modulation of oxidative stress markers in HO-induced RAW264.7 macrophages. Compared with the model group, all fractions significantly increased catalase (CAT) and superoxide dismutase (SOD) activities, with the highest increase of approximately 1.33 U/mgprot for CAT and 20.32 U/mgprot for SOD, while decreasing malondialdehyde (MDA) and intracellular reactive oxygen species (ROS) levels. Among the four fractions, AIF4, with the lowest molecular weight, exhibited the highest antioxidant activity. LMWF treatment also upregulated the expression of antioxidant-related genes (, , ) and signaling molecules ( and ), accompanied by increased protein levels of nuclear factor erythroid 2-related factor 2 () and PI3K/Akt pathway components. These findings indicate that LMWF is closely associated with the regulation of the /- signaling axis under oxidative conditions and support its potential application as a dietary antioxidant ingredient. - Source: PubMed
Publication date: 2026/03/09
Meng YuanWei TuantuanZhao JinwenWu ShuangshuangMa YichaoLiu ShuHe YunhaiRen DandanWang Qiukuan