AIF1 _ IBA1 (isoform 3) Antibody
- Known as:
- AIF1 _ IBA1 (isoform 3) Antibody
- Catalog number:
- AF1039b
- Product Quantity:
- 0.1mg
- Category:
- -
- Supplier:
- Abgen
- Gene target:
- AIF1 _ IBA1 (isoform 3) Antibody
Related genes to: AIF1 _ IBA1 (isoform 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 (isoform 3) Antibody
Related articles to: AIF1 _ IBA1 (isoform 3) Antibody
- Demyelination is a hallmark of various neurodegenerative diseases, including multiple sclerosis (MS), leading to impaired neural transmission and motor deficits. The Lysophosphatidylcholine (LPC)-induced demyelination model is widely used because it reflects many aspects of demyelinating pathology. This study examined how non-invasive 4 Hz visual theta oscillation entrainment affects LPC-induced demyelination in the optic chiasm of male C57BL/6J mice. Mice received daily one-hour sessions of 4 Hz stimulation for two weeks post-LPC injection. The analysis of the VEPs showed that the latency of P1 waves was shorter in the theta stimulation group and significantly different from the LPC group on days 7 and 14. IBA1 immunostaining showed reduced IBA1 immunoreactivity at early post-lesion time points, while qPCR analysis showed lower Aif-1 1 and Gfap transcript levels in the theta-stimulated group. Luxol Fast Blue (LFB) and FluoroMyelin staining suggested greater preservation of myelin staining in the theta group at day 14. In parallel, molecular analyses revealed increased expression of oligodendrocyte-lineage markers, including Pdfgra at days 3 and 7 and Olig2 and Plp1 at day 14. Taken together, these findings suggest that theta oscillation entrainment modulates the molecular, cellular and electrophysiological responses that follow demyelinating injury, and that it may also influence the processes associated with myelin repair. Further studies are needed to clarify the mechanisms underlying these effects and to assess the therapeutic relevance of this non-invasive approach for demyelinating disorders. - Source: PubMed
Publication date: 2026/09/15
Dehghan SamanehDehdar KolsoumAhmadirad NooshinMehrizi Sarina Sadat AboeiRaoufy Mohammad RezaJavan Mohammad - Canine macrophages are increasingly recognized as important regulators of tumor immunity; however, in vitro culture systems that minimize serum-derived variability remain limited. In this study, we established a serum-reduced culture system for canine peripheral blood mononuclear cell (PBMC)-derived macrophages and characterized their phenotypic, transcriptional, and functional properties. PBMCs from healthy Beagle dogs (n = 3) were differentiated into M0, M1, and M2 macrophages using Macrophage Base Medium supplemented with canine serum or recombinant cytokines. Morphology was assessed by phase-contrast microscopy, macrophage identity was evaluated by Iba1 immunostaining and AIF1 expression, and exploratory transcriptomic profiles were examined by RNA sequencing (n = 1). Phagocytic activity was assessed using FITC-labeled latex beads and flow cytometry, and macrophage-tumor cell interactions were evaluated by co-culture with canine urothelial carcinoma cells. M0, M1, and M2 macrophages exhibited distinct morphologies and transcriptional patterns. M1 macrophages showed increased expression of inflammatory genes, including IL1B and IFNG, whereas M2 macrophages showed increased expression of genes associated with alternative activation and immune regulation, including CD209, CD5L, and IL33. Phagocytic activity was observed in all subsets. In co-culture experiments, macrophages exhibited polarization-dependent interaction patterns with tumor cells, with M2 macrophages exhibiting features reminiscent of tumor-associated macrophages. These findings provide a pilot evaluation of this serum-reduced culture system, which generates phenotypically distinct canine macrophage subsets and may serve as a useful in vitro platform for future studies of canine macrophage polarization and tumor-associated immune responses. - Source: PubMed
Publication date: 2026/09/10
Hoshino YukiAnzai RihoKobayashi SaoriUchida NaohiroIshiguro-Oonuma ToshinaNaito IkunoriYamada ShinjiMotegi TomokiYamamoto Yoshio - Diabetic retinopathy (DR) is a common late-stage complication of diabetes and a leading cause of vision loss. Oxidative stress plays a crucial role in DR progression by activating stress pathways and altering gene expression. This study investigated the effect of Tempol (4-hydroxy-2,2,6,6-tetramethylpiperidine-1-oxyl), a ROS scavenger, on diabetes-induced transcriptomic changes in the neural retina of Wistar rats. Twelve-week-old male Wistar rats (n = 5 per group) were divided into four groups: control, control with Tempol (25 mg/kg/day), streptozotocin-induced diabetic (STZ 50 mg/kg), and diabetic with Tempol. Animals were maintained for 12 weeks with weekly monitoring of body weight and blood glucose. Neural retinas were dissected and preserved in RNAlater. Total RNA was extracted, and microarray analysis was used to assess expression of over 22,000 genes. Selected genes (Stat1, Txnip, Aif1, Gfap, and Opn1sw) were validated using quantitative real-time PCR. Diabetic retinas exhibited 494 differentially expressed genes. Upregulated genes were primarily linked to oxidative stress, immune activation, and inflammatory pathways, whereas downregulated ones were associated with retinal structure and function. Tempol-treated diabetic rats exhibited substantially fewer transcriptomic alterations when compared to diabetic rats, indicating attenuation of diabetes-induced oxidative stress and glial activation. The number of altered genes from control were lower by 73% in the diabetic Tempol-treated group compared with untreated diabetic rats, indicating a normalizing effect. Tempol attenuates diabetes-induced oxidative and inflammatory stress, supporting its potential as an intervention in diabetic retinopathy. - Source: PubMed
Publication date: 2026/09/07
Al-Hussaini HebaD'Souza LeoraHasan Sonia MAl-Onaizi MohammedAbed Baha SJahanbani ImanMadhyastha Sampath - Complement Factor H (FH) regulates the alternative complement pathway, and FH deficiency promotes complement activation, macrophage recruitment, and renal injury. Extracellular vesicles (EVs) mediate intercellular communication and may provide molecular signatures of tissue inflammation. We examined complement- and macrophage-associated transcriptional signatures in renal tissue and serum-, kidney-, and urine-derived EVs using a FH-deficient murine model of chronic serum sickness. Pilot kidney microarray analysis was combined with qRT-PCR and EV transcript profiling. FH deficiency increased renal expression of macrophage-associated inflammatory genes, including AIF1, MMP9, S100A10, and CD44, and the complement receptor C3aR1. EVs from FH-deficient mice lacked FH transcripts and exhibited increased complement- and macrophage-associated transcripts across serum-, kidney-, and urine-derived EV populations. EV transcriptional profiles paralleled inflammatory gene expression observed in renal tissue. FH deficiency-associated complement dysregulation produces coordinated inflammatory transcriptional signatures detectable in both kidney tissue and EVs. The concordance between intrarenal inflammatory programs and EV cargo suggests that EVs may reflect complement-mediated renal immune activity. In particular, urinary EVs may provide a non-invasive source of molecular information and potential biomarkers of complement-mediated kidney inflammation. - Source: PubMed
Publication date: 2026/09/07
Campanieri AumFraher ShaneSatheeshkumar Poolakkad SReynolds JessicaQuigg Richard JAlexander Jessy J - The combination of ethyl acetate fractions from Uncaria sp. and Selaginella doederleinii (EAF-BC) holds potential as an anticancer agent; however, its underlying molecular mechanism remains unclear. This study aimed to determine the anticancer potential of these combinations by evaluating the hallmarks of apoptosis using a Saccharomyces cerevisiae model. - Source: PubMed
Publication date: 2026/09/05
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