AIF1 Antibody
- Known as:
- AIF1 Antibody
- Catalog number:
- csb-pa00667a0rb
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- CusAb
- Gene target:
- AIF1 Antibody
Related genes to: AIF1 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 Antibody
Related articles to: AIF1 Antibody
- As an important aquaculture bivalve, the Pacific oyster Crassostrea gigas faces severe constraints in artificial reproduction, where low sperm motility often leads to fertilization failure and limits the sustainable development of the oyster aquaculture industry. In the present study, the variation of sperm from different oyster individuals was observed, and high-quality sperm possessed intact, elongated flagella with no structural abnormalities, while low-quality sperm showed shortened flagella with frequent tangling or coiling defects. Transcriptomic analysis comparing high- and low-quality sperm revealed significantly reduced expression of genes associated with sperm motility and release (CgAIF1, CgAchR, CgSEX), sperm quality and development (CgEP4, CgIFi2b), and cryoprotection (CgISPs) in low-quality sperm. Notably, an allograft inflammatory factor (designed as CgAIF1) encoding EF-hand domain, known as Ca binding activity, was among the most significantly downregulated in low-motility sperm. CgAIF1 is highly expressed in haemocytes, ganglia, and gonads of oysters. Incubation with the recombinant AIF1 protein (rCgAIF1) significantly improved sperm curvilinear velocity, thereby enhancing the overall motility of C. gigas sperm. Furthermore, rCgAIF1 incubation increased intracellular Ca levels (2.13-fold at 30 min, 2.71-fold at 60 min) and superoxide dismutase (SOD) activity (1.44-fold at 30 min, 1.24-fold at 60 min) in sperm, suggesting potential roles in calcium homeostasis regulation and antioxidant defense. In conclusion, this study demonstrates that CgAIF1 significantly enhances motility of oyster sperm, providing a scientific basis for artificial breeding and seed production in oyster aquaculture. - Source: PubMed
Publication date: 2026/06/24
Shen LunyuGong WenhuiXiong ChunmeiWang WeilinSong LingyuanWang JiadiZhou XiaoxuWang LinglingSong Linsheng - : Observational studies have reported comorbidity between diabetic retinopathy (DR) and physical frailty, but their genetic interplay remains incompletely understood. This study evaluated shared genetic architecture and potential causal relationships between DR severity and frailty-related phenotypes (FRPs). : GWAS summary statistics were analyzed for four DR phenotypes (broad DR, background DR [BDR], severe non-proliferative DR, and proliferative DR [PDR]) and six FRPs, including frailty index (FI), appendicular lean mass, handgrip strength (HGS), and walking pace (UWP). Global and local genetic correlations were estimated using LDSC, HDL, and LAVA. Causality was assessed using bidirectional Mendelian randomization (MR) and latent causal variable (LCV) analyses. Biological mechanisms were investigated using partitioned heritability, cross-trait meta-analysis, Bayesian colocalization, tissue and cell enrichment, prioritization (MAGMA/TWAS), and 3D chromatin annotation. : BDR and PDR showed positive genetic correlations with FI and negative correlations with UWP. Local genetic correlation analyses identified 82 significant regions, including signals on chromosome 6. MR supported a directional effect in which genetic liability to DR was associated with higher FI and lower HGS, with no evidence of reverse causation. LCV indicated partial genetic causality within a shared polygenic architecture. Cross-trait meta-analysis and colocalization highlighted the MHC region, prioritizing , , , and . Additional non-MHC loci included the gene cluster and . : DR and frailty share genetic determinants involving neurovascular, metabolic, and immune-inflammatory pathways, supporting an association between DR liability and frailty-related decline. Future longitudinal and functional studies are needed to validate these findings and assess candidate pleiotropic genes. - Source: PubMed
Publication date: 2026/05/31
Luo RenxinYu XiaotongHuang ChenTan ShumeiTseng YulinFeng YueLi Xuemin - Chronic inflammation and macrophage activation are hallmarks of diabetic kidney disease (DKD). Allograft inflammatory factor-1 (AIF-1), a macrophage-associated inflammatory protein, aggravates high glucose-induced inflammation and oxidative stress in glomerular endothelial cells. However, its pathogenic role in macrophages remains unclear. In the present study, knockdown of AIF-1 by adeno-associated virus (AAV) in db/db mice improved renal function and ameliorated renal histopathological changes, with restored E-cadherin expression and reduced α-SMA expression. Double immunofluorescence staining demonstrated that AIF-1 was predominantly localized in infiltrating macrophages in diabetic kidneys. To explore the underlying mechanisms, THP-1-derived macrophages and a macrophage-tubular epithelial cell coculture system were employed. Under high-glucose conditions, AIF-1 knockdown inhibited NF-κB activation and reduced interleukin-1β (IL-1β) secretion in macrophages, whereas AIF-1 overexpression enhanced both responses. In coculture experiments, AIF-1 overexpression in macrophages promoted epithelial-mesenchymal transition (EMT)-related changes in HK-2 cells, as evidenced by decreased E-cadherin expression and increased α-SMA expression. Neutralization of IL-1β with canakinumab partially reversed the EMT changes induced by AIF-1 overexpression, indicating that IL-1β is a key mediator of macrophage-tubular epithelial cell communication. In conclusion, AIF-1 in macrophages promotes EMT of renal tubular epithelial cells through the NF-κB/IL-1β axis and may represent a potential therapeutic target for DKD. - Source: PubMed
Publication date: 2026/06/23
Wu QiHou DonghuaWang XingzhiFu YutingXing YingJi HengyuanSui ManshuHao Lirong - Traumatic brain injury (TBI) remains a leading cause of neurological morbidity and mortality, characterized by complex pathophysiological cascades. Here, we investigate the role of the transcription factor EGR1 (early growth response 1) in modulating mitochondrial homeostasis via the HIF1A (hypoxia inducible factor 1, alpha subunit)-BNIP3 (BCL2/adenovirus E1B interacting protein 3) axis following TBI. Using integrated transcriptomic and epigenomic analyses, we identified EGR1 as a critical regulator of TBI pathology, with its expression acutely upregulated in neurons post-injury. Genetic ablation of in mice significantly reduced neuronal apoptosis, preserved dendritic integrity, and ameliorated cognitive and sensorimotor deficits. Mechanistically, chromatin immunoprecipitation and luciferase assays revealed that EGR1 directly binds to the promoter, repressing its transcription. Loss of EGR1 enhanced HIF1A-BNIP3-mediated mitophagy, reducing mitochondrial dysfunction and oxidative stress both and . Conversely, silencing HIF1A or BNIP3 abrogated the neuroprotective effects of EGR1 deficiency. These findings establish a novel EGR1-HIF1A-mitophagy signaling axis as a key determinant of TBI outcomes, highlighting EGR1 as a potential therapeutic target.: AAV: adeno-associated virus; ACTB/β-actin: actin, beta; AIF1/IBA1: allograft inflammatory factor 1; BAF: bafilomycin A1; BNIP3: BCL2/adenovirus E1B interacting protein 3; CCI: controlled cortical impact; COX8: cytochrome c oxidase subunit 8; CUT&Tag: cleavage under targets and tagmentation; DAPI: 4,'6-diamidino-2-phenylindole; DEGs: differentially expressed genes; eGFP: enhanced green fluorescent protein; EGR1: early growth response 1; GFAP: glial fibrillary acidic protein; GO: gene ontology; GSEA: gene set enrichment analysis; HCQ: hydroxychloroquine; HIF1A/HIF-1α: hypoxia inducible factor 1, alpha subunit; IGV: integrative genomics viewer; KEGG: Kyoto encyclopedia of genes and genomes; KO: knockout; LAMP1: lysosomal-associated membrane protein 1; MAP1LC3/LC3: microtubule-associated protein 1 light chain 3; Lv: lentivirus; MAP2: microtubule-associated protein 2; mCherry: monomeric cherry fluorescent protein; mRFP: monomeric red fluorescent protein; MTOR: mechanistic target of rapamycin kinase; MUT: mutant; MWM: Morris water maze; NAB1: Ngfi-A binding protein 1; NAB2: Ngfi-A binding protein 2; RBFOX3/NeuN: RNA binding protein, fox-1 homolog (C. elegans) 3; OGD: oxygen-glucose deprivation; OLIG2: oligodendrocyte transcription factor 2; PBS: phosphate-buffered saline; PECAM1/CD31: platelet/endothelial cell adhesion molecule 1; PFA: paraformaldehyde; PPI: protein-protein interaction; Puro: puromycin; ROI: region of interest; ROS: reactive oxygen species; SEM: standard error of the mean; SQSTM1/p62: sequestosome 1; TBI: traumatic brain injury; TOMM20: translocase of outer mitochondrial membrane 20; TSA: tyramide signal amplification; TUNEL: terminal deoxynucleotidyl transferase dUTP nick end labeling; VDAC1: voltage-dependent anion channel 1; WT: wild-type. - Source: PubMed
Publication date: 2026/06/28
Hou XiaoxiangZhang DanfengSang XianzhengPeng ChaoguiChen WenXu JingYe YichaoGuo YanguShi HantongYang ChengziCai HanziWang YijianChu GuangxinXu HaoxiangLv LiquanJin HaiWang ChunhuiQu Xiaolin - Cycloleucine, a non-proteinogenic amino acid, has been identified as a potent inhibitor of fungal growth; however, its molecular mechanisms of action against the edible mushroom remain inadequately understood. In this study, we integrated transcriptomic and m6A methylome analyses to elucidate the inhibitory effects of cycloleucine on . Our findings demonstrate that cycloleucine treatment suppresses hyphal growth and biomass accumulation in , which are associated with a significant reduction in global RNA m6A levels. Through meRIP-seq analysis, we identified 67 differentially m6A-modified genes, including (apoptosis-inducing factor 1) and (major facilitator superfamily transporter 1), suggesting their involvement in growth regulation. Genome-wide screening and expression detection revealed that EVM0008471-mediated m6A demethylation plays a potential role in controlling hyphal growth dynamics. This study provides the first evidence of m6A-dependent growth regulation in , advancing the understanding of fungal epitranscriptomics and offering potential targets for optimizing industrial mushroom cultivation. - Source: PubMed
Publication date: 2026/02/28
Yang ChiWu DandanXiao DonglaiJiang XiaolingLin HuiWang XinLin YanquanMa Lu