AIF1_PIG AIF1 ELISA tesk kit
- Known as:
- AIF1_PIG AIF1 Enzyme-linked immunosorbent assay test tesk reagent
- Catalog number:
- gen16122
- Product Quantity:
- 1
- Category:
- Peptides
- Supplier:
- Other suppliers
- Gene target:
- AIF1_PIG AIF1 ELISA tesk kit
Related genes to: AIF1_PIG 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
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- Membrane-bound organelles undergo extensive remodeling during environmental stress, yet systematic side-by-side comparisons of organelle responses in budding yeast remain limited. Here, a panel of fluorescent markers was used to examine multiple organelles in exposed to heat, hydrogen peroxide, acetic acid, or ethanol. Across all conditions, mitochondria consistently shifted from tubular networks to fragmented puncta, representing a common stress response. Quantitative scoring showed that heat stress induced mitochondrial fragmentation in more than 90% of cells within 20 min, and GFP-HDEL redistribution was detected in a substantial fraction of cells under all four stress conditions, with the strongest effect under heat stress. In contrast, overall endoplasmic reticulum (ER) morphology remained largely preserved, although redistribution of GFP-HDEL indicated altered ER retention and/or endomembrane homeostasis. Heat and oxidative stress also induced Ire1 puncta. Several nuclear proteins exhibited stress-dependent redistribution from the nucleus, indicating dynamic remodeling of nuclear protein localization. Vacuoles generally appeared enlarged and fused, whereas acetic acid induced a distinct phenotype with Ybh3 enrichment at the vacuolar membrane and redistribution of Prc1 and Pep4 to cytoplasmic puncta. Markers of the early and late Golgi and the late endosome showed stress-specific loss, clustering, or relocalization. Lipid droplets, peroxisomes, and autophagy-related structures were also altered. Additionally, Yca1, Aif1, and Mmi1 formed puncta under heat and ethanol stress. Together, these findings provide a comparative imaging framework defining shared and stress-specific features of organelle remodeling in budding yeast. - Source: PubMed
Publication date: 2026/07/28
Sheng PengSun MengnaWang XinyueBai LizheCao HongLi Dan - Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection causes an immune-mediated neurological syndrome, which persists long after infection. Mechanisms for SARS-CoV-2-associated neurological complications are multifactorial, with an increased risk of drug abuse such as methamphetamine (meth). SARS-CoV-2 infection and its viral proteins play pivotal roles in coronavirus disease 2019 (COVID-19)-associated neuroinflammation, which can lead to long COVID. We hypothesize that meth augments activation of the microglial NOD-, leucine-rich repeat, and pyrin domain-containing protein 3 (NLRP3) inflammasome by the SARS-CoV-2 nucleocapsid (N) protein, resulting in neuroinflammation. To test this hypothesis, we investigated the effect of N-protein and meth on NLRP3 inflammasome activation in primary rat microglial cultures using enzyme-linked immunosorbent assay (ELISA), Reverse Transcription quantitative Polymerase Chain reaction (RT-qPCR), western blot (WB), and immunofluorescence assay (IFA). Our results showed that meth augmented N-protein-induced microglial activation, as evidenced by increased ionized calcium-binding adapter 1 (Iba-1) expression. The addition of meth to the microglial cultures treated with N-protein increased proinflammatory cytokine production. Meth augmentation of N-protein-induced neuroinflammation was further supported by increased inducible nitric oxide synthase (iNOS)-mediated nitric oxide (NO) production. The effects of meth on N-protein-associated inflammatory responses were significantly attenuated by MCC950, a specific NLRP3 inhibitor. Moreover, meth-associated NLRP3 activation was either blocked by the opioid sigma1-receptor (σ1R) inhibitor BD1047 or by σ1R siRNA knockdown. Taken together, these results demonstrated that meth augmented SARS-CoV-2 N-protein-induced neuroinflammation via microglial σ1R and the NLRP3 inflammasome, which may underlie the pathogenesis of neurological manifestations in COVID-19, such as long COVID with meth abuse. These results may also underscore the impact of drug abuse on long COVID and provide targets for the development of therapeutic strategies to control the neurological outcomes of long COVID. - Source: PubMed
Publication date: 2026/08/03
Dutta DebashisLiu JianuoXiong Huangui - Traumatic optic nerve and retinal injuries can lead to severe visual impairment, with undetermined underlying molecular mechanism and few reliable molecular biomarkers. This study aims to identify dysregulated genes and signaling pathways potentially involved in these injuries. - Source: PubMed
Publication date: 2026/07/27
Li JinjunZhang YongZhou Shu - Alzheimer's disease (AD) is a multifactorial neurodegenerative disorder in which immune dysregulation has emerged as an important component of disease pathogenesis; however, the contribution of circulating proteins and their cellular context remains incompletely understood. Here, we performed an integrative multi-omics analysis combining Mendelian randomization (MR), bulk transcriptomics, single-cell RNA sequencing, and peripheral blood validation to systematically identify plasma proteins associated with AD. Proteome-wide MR analysis identified multiple circulating proteins associated with AD risk. Integration with transcriptomic data identified AIF1 (allograft inflammatory factor 1) as a shared candidate supported by both genetic prioritization and differential expression analysis. Although bulk transcriptomic data showed reduced AIF1 expression in AD, single-cell analysis revealed distinct cell type-specific expression patterns, with predominant enrichment in monocytes and other innate immune populations. PBMC-based qPCR further confirmed an overall reduction in AIF1 expression in AD. Further analyses suggested that AIF1-associated immune alterations were linked to changes in inflammatory signaling pathways, including STAT, IRF, and NF-κB-related activity, as well as differences in intercellular communication involving MIF, GALECTIN, ANNEXIN, and CypA-related signaling. Peripheral immune cell composition analysis indicated differences between AD and control samples, characterized by relative changes in innate immune cell proportions. Collectively, these findings identify AIF1 as an immune-associated factor linked to genetic and transcriptional alterations in AD and suggest its association with monocyte-related immune states and altered immune signaling patterns. This study provides a multi-layered framework for investigating peripheral immune involvement in AD and highlights potential directions for understanding immune-related alterations and biomarker discovery. - Source: PubMed
Publication date: 2026/08/08
Li QianLi MingjianHuang XiCao CongcongHu Yi - Glaucoma is a leading cause of irreversible blindness worldwide, yet available treatments fail to prevent disease progression for all patients. It is characterized by a progressive dysfunction and loss of retinal ganglion cells. Neuroinflammation has been recognized as an underlying neurodegenerative mechanism of glaucoma in animal models and human post-mortem samples, and targeting neuroinflammation may provide additional means to neuroprotection. Galectin-3, a pro-inflammatory mediator encoded by the LGALS3 gene in humans, holds promise as a treatable target as its pharmacological and genetic inhibition is neuroprotective in multiple models of experimental glaucoma. However, the role of Galectin-3 in glaucoma remains unclear, particularly whether its emergence is a consequence of degeneration, or occurs at earlier time points. To address these knowledge gaps, we labeled IBA1, GFAP, and Galectin-3 in retina sections at early glaucoma stages in the rat bead glaucoma model, and in human retina from glaucoma donors. In the rat, IBA1 volume, but not GFAP, increased at an early, pre-degenerative timepoint. Accompanying this, we identified a significant increase of Galectin-3/IBA1 colocalization compared to control at the same timepoint, supporting the upregulation of Galectin-3 in early inflammation, preceding retinal ganglion cell degeneration in experimental glaucoma. However, a significant increase in Galectin-3/GFAP colocalization compared to control at the same timepoint in the rat additionally associates Galectin-3 production with astrocytes and Müller glia. This Galectin-3 to Müller glia relationship was significantly pronounced in human glaucomatous retina, predominating over microglia co-labelling. We further demonstarted that human MIO-M1 Müller glia in vitro express Galectin-3, but this is not altered in response to glaucoma relevant stimuli (TNF-α or mild-metabolic stress from rotenone). Instead, Galectin-3 expression was altered in phagocytosing states from exposure to E. coli particles, brain synaptosomes, or apoptotic neuronal debris. These findings provide further insight into Galectin-3 and gross inflammatory responses in glaucoma pathology. - Source: PubMed
Publication date: 2026/08/04
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