AIF1 _ IBA1 (isoform 3)
- Known as:
- AIF1 _ IBA1 (isoform 3)
- Catalog number:
- Y213515
- Product Quantity:
- 200ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- AIF1 _ IBA1 (isoform 3)
Ask about this productRelated genes to: AIF1 _ IBA1 (isoform 3)
- 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 (isoform 3)
(Biotin Conjugates) Phospho-Slingshot 1 isoform 1 antibodies Immunogen: peptide Host: Rabbit(FITC-conjugates) Phospho-Slingshot 1 isoform 1 antibodies Immunogen: peptide Host: Rabbit14-3-3 Isoform Panel, Rabbit anti-;14-3-3 protein c-isoform antibody Host rabbit14-3-3 protein c-isoform antibody Ab host: Rabbit14_3_3 Isoform Panel, Rabbit anti_;20 kDa myosin light chain,Homo sapiens,Human,LC20,MLC2,MLC-2C,MRLC1,MYL9,Myosin regulatory light chain 2, smooth muscle isoform,Myosin regulatory light chain 9,Myosin regulatory light chain MRLC1,Myos20 kDa myosin light chain,LC20,MYL9,Myosin regulatory light chain 2, smooth muscle isoform,Myosin regulatory light chain 9,Myosin regulatory light polypeptide 9,MYRL2,Pig,Sus scrofa3_hydroxyisobutyryl_Coenzyme A hydrolase isoform 24-alpha-hydroxy-tetrahydropterin dehydratase 2,Chicken,DCoH-alpha,DcoH-like protein DCoHm,DCOHM,Gallus gallus,Hepatocyte nuclear factor 1a dimerization cofactor isoform,PCBD2,PHS 2,Pterin-4-alpha-carb40S ribosomal protein S4, X isoform,CCG2,Homo sapiens,Human,RPS4,RPS4X,SCAR,SCR10,Single copy abundant mRNA protein40S ribosomal protein S4, X isoform,Mouse,Mus musculus,Rps4,Rps4x40S ribosomal protein S4, X isoform,Rat,Rattus norvegicus,Rps4,Rps4x40S ribosomal protein S4, Y isoform 1,Homo sapiens,Human,PRO2646,RPS4Y,RPS4Y140S ribosomal protein S4, Y isoform 2,Homo sapiens,Human,RPS4Y2,RPS4Y2P Related articles to: AIF1 _ IBA1 (isoform 3)
- Sugar-induced cell death (SICD) is a phenomenon observed in whereby cells rapidly lose viability in glucose-only solutions. One theory suggests that SICD occurs due to an imbalance in nitrogen and carbon, however, limited studies are available to support this. When stationary phase cells are transferred to glucose-only solutions, cell death resembles that of apoptosis, while exponential phase cells show hallmarks of primary necrosis. Apoptosis in stationary phase cells is independent of the yeast metacaspase, , however, it remains unknown if SICD occurs through a caspase-independent pathway. Using stationary phase BY4741, we showed that SICD can be induced to the same degree with 10 mM or 110 mM glucose. Interestingly, SICD induced by 10 mM of glucose can be protected by supplementation with low concentrations of highly preferred organic nitrogen sources, namely glutamate, glutamine, and arginine, as well as high concentrations of non-preferred organic nitrogen sources. Additionally, cell death can be rescued by deletion of and genes involved in caspase-independent apoptosis- or . On the other hand, when BY4741 is challenged with 110 mM glucose, SICD can only be rescued by supplementation with the same preferred organic nitrogen sources or deletion of or In all cases, protection is associated with a decrease in intracellular ROS and preservation of membrane integrity. Taken together, 110 mM glucose results in a catastrophic cell death phenotype that is more difficult to rescue, and nuclear localization of Aif1p and Nma111p is important for cell death in response to glucose. - Source: PubMed
Publication date: 2026/05/11
Parbhudayal RaveenaCheng Hai-Ping - The human dorsal root ganglia (DRG) are increasingly recognized as immunologically active sites within the peripheral nervous system. While single-cell transcriptomics has recently identified myeloid populations with microglia-like profiles in DRG across species, an in-depth, spatially resolved protein-level characterization in human tissue is lacking. Here, we used highly multiplexed Imaging Mass Cytometry (IMC) to map and phenotype myeloid cells in human DRG at subcellular resolution. A 41-marker panel enabled in-depth profiling of immune and neural cell types in situ. We identified a subset of Iba1 myeloid cells co-expressing canonical microglial markers such as P2RY12, TMEM119, and SLC2A5, located in close spatial proximity to neuronal somata. Unsupervised clustering (FlowSOM) of >6000 Iba1 cells identified eight distinct clusters. Among them, distinct myeloid cell subsets exhibited a clear microglial-like signature and were localized near neurofilament neurons. In contrast, Iba1 clusters expressing CD68, HLA-DR, and other activation markers were spatially segregated. These findings provide a spatially resolved, protein‑level atlas of Iba1 myeloid subsets in human DRG and offer a resource for dissecting neuroimmune niches relevant to chronic pain and peripheral neuropathies. - Source: PubMed
Schwabenland MariusOeztuerk BusranurBlank ThomasBeck JuergenBengsch BertramPrinz Marco - The study explored the mechanism of Dan'e-fukang soft extract in treating endometriosis (EMs) through network pharmacology. The main active ingredients of Dan'e-fukang soft extract were analyzed based on the traditional Chinese medicine systems pharmacology database and analysis platform (TCMSP). Drug target genes were mined by PubChem, and differential genes were analyzed based on Gene Expression Omnibus (GEO) database microarrays GSE7305, GSE11691, and GSE12768. A total of 101 differential drug target genes were screened. Gene Ontology (GO) analysis revealed that the 101 differential drug target genes were mainly enriched in the regulation of cell migration, inflammatory response, and cytokine-mediated signaling pathways; among them, factors associated with both inflammatory response and negative regulation of cell migration were allograft inflammatory factor 1 (AIF-1), C-C motif chemokine ligand 2 (CCL2), and Cadherin-1 (CDH1), of which CCL2 was upregulated in all three endometriosis-related GEO datasets. CCL2 was also upregulated in endometriosis patient tissues as well as in ectopic endometrial stromal cells (ESCs). The overexpression of CCL2 in normal ESCs promoted cell proliferation, migration, invasion, and expression levels of inflammatory factors (TNF-α, IL-1β, and IL-6). However, the silencing of CCL2 in ectopic ESCs had the opposite result. Liquiritin was identified as a potential key active monomer of Dan'e-fukang soft extract based on network pharmacology prediction. Liquiritin inhibited CCL2 expression and inhibited proliferation, migration, invasion, and inflammation in ectopic ESCs, while overexpression of CCL2 partially reversed these functions of liquiritin. Liquiritin inhibits ectopic ESC proliferation, migration, and inflammation by inhibiting CCL2 and thereby alleviating endometriosis. - Source: PubMed
Publication date: 2026/05/07
Yang XiLi JiWang ChenHe SiliLi Lijie - Polycystic ovary syndrome (PCOS) is associated with an increased risk of type 2 diabetes mellitus (T2DM), and the risk of PCOS increases in patients with T2DM of reproductive age. The bidirectional link between PCOS and T2DM has been confirmed through experimental and epidemiological evidence; however, the genetic factors that contribute to deeper insights into the shared pathogenesis of these two diseases remain unclear. We aimed to identify shared immune- and inflammation-related genes and pathways in PCOS and T2DM, further explore the molecular mechanisms in developing this comorbidity, and predict drugs with potential effects to develop novel therapeutic strategies. - Source: PubMed
Publication date: 2026/04/16
Liu XuemengWang YanleiBi QiuhanZhang YingWang ShuminYang PanPei JieZhu WeixiChen YijingZhang ZhiguoChen BeiliZhang QiuZhang YiJiang Tian - Microglia remodel neuronal circuits in pathological conditions; however, the molecular requirements for these responses and their consequences for motoneuron survival remain unclear. - Source: PubMed
Publication date: 2026/05/07
Sekiguchi KojiShoji HirotakaShindo TomokoSasabe JumpeiTokuyasu DaikiNakahara JinMiyakawa TsuyoshiIto Daisuke