Ask about this productRelated genes to: AIFM1 Blocking Peptide
- Gene:
- AIFM1 NIH gene
- Name:
- apoptosis inducing factor mitochondria associated 1
- Previous symbol:
- PDCD8, NAMSD
- Synonyms:
- AIF, CMTX4
- Chromosome:
- Xq26.1
- Locus Type:
- gene with protein product
- Date approved:
- 1999-05-28
- Date modifiied:
- 2017-01-12
Related products to: AIFM1 Blocking Peptide
Related articles to: AIFM1 Blocking Peptide
- Poststroke cognitive impairment (PSCI) frequently occurs after ischaemic stroke (IS). Despite its widespread clinical application in treating ischaemic cardio-cerebrovascular diseases, the effect of Shuxuening injection (SXNI) on PSCI is unknown. - Source: PubMed
Publication date: 2026/05/28
Lv JingTao XufengWu YuChen XuyangLv LinlinGuo FangyueZhang LuZhang XiaonanGan GuangshuoLu YanDong Deshi - X-chromosome inactivation (XCI) modifies disease severity in females with X-linked variants, but clinically applicable high-resolution assessment remains limited. We report a family with an AIFM1 variant showing marked intrafamilial phenotypic variability and evaluated whether haplotype-resolved nanopore sequencing can inform clinical interpretation. Targeted long-read sequencing was performed in a severely affected hemizygous male, his asymptomatic heterozygous mother, and a severely affected heterozygous sibling. In the hemizygous male, the sample served as a technical control, with all reads mapping to a single haplotype, consistent with a hemizygous X chromosome. Among heterozygous carriers with the identical variant (c.506C>T; p.Pro169Leu), XCI correlated with severity: the affected sibling showed 84% skew favoring activation of the pathogenic allele, whereas the mother showed preferential inactivation (20%). This family-based study shows that using nanopore sequencing for haplotype-resolved X-inactivation (XCI) analysis may provide a practical framework for selected X-linked disorders with variable expressivity. - Source: PubMed
Publication date: 2026/06/09
Nakamura KohtaOkazaki AtsukoMotooka DaisukeMatsumoto NaoyukiHasegawa YuikoFukuda SayakaYabe ManamiSugiura AyumuYatsuka YukikoFushimi TakuyaOnuki TakanoriAida YukoOhtake AkiraMurayama KeiOkazaki Yasushi - Ammonia accumulation is a major constraint in intensive Macrobrachium rosenbergii aquaculture, yet the mechanisms linking multi-organ injury to tissue deterioration remain unclear. Juvenile prawns were exposed for 7 days to 0, 2, and 50 mg L⁻¹ total ammonia nitrogen (TAN) to evaluate integrated physiological, histological, transcriptomic, and metabolomic responses in gill, hepatopancreas, and muscle. Survival decreased from 100% in controls to 89% and 75% at 2 and 50 mg L⁻¹, respectively, accompanied by gill lamellar disruption, hepatopancreatic tubule degeneration, and muscle fiber separation. RNA-seq identified 4,944 differentially expressed genes with strong organ-specific patterns. The hepatopancreas showed enhanced lysosomal activity and redox defenses, the gills exhibited disrupted nitrogen and lipid metabolism, and the muscle displayed impaired glycolysis and altered structural protein signaling. Changes in CD63, CssYP2J, GLUL, and AIFM1 expression, together with altered CAT, GS, and GDH activities, indicated adaptive detoxification at moderate TAN. However, high TAN overwhelmed these responses, leading to glutamine detoxification failure, lipid peroxidation, and malondialdehyde accumulation. Gill metabolomics revealed TAN-dependent alterations in carbon, amino acid, and phospholipid pathways, particularly glycerol-phosphocholine, citric acid, and citrulline metabolism, highlighting metabolite-gene interactions within nitrogen and membrane lipid networks. Overall, even sublethal TAN acted as a systemic stressor, reprogramming metabolic and antioxidant pathways across organs, with muscle emerging as the most vulnerable tissue. These findings refine ammonia toxicity thresholds and support maintaining TAN below 2 mg L⁻¹ to protect prawn health and aquaculture sustainability. - Source: PubMed
Publication date: 2026/06/06
Liaqat NusratLi XuenanRaza MohsanShahzadi KiranYou SiminArshad ShamoonaNissa Mehr UnKhan NaumanDai Xilin - This study aimed to develop a robust predictive model and nomogram for breast cancer (BC) based on genes associated with diverse cell death methods. A prognostic model was constructed using the LASSO Cox method, incorporating twelve genes (CREB3L1, SFRP1, SHARPIN, AIFM1, IL‑18, CD24, EDA2R, CRIP1, XBP1, BCL2A1, NKX3‑1, and NME5). BC patients were classified into high‑risk and low‑risk subgroups, with the low‑risk subgroup showing superior survival, and this prognostic value was validated in an independent external cohort. A nomogram was also developed and confirmed as a reliable independent predictor of outcome. Enrichment analyses suggested a link between patient risk and immune response. The low‑risk subgroup exhibited a higher tumor microenvironment (TME) score. Patients in the high‑risk group showed improved responses to lapatinib, BI‑2536, OSI‑027, and SB505124, whereas those in the low‑risk subgroup had better sensitivity to axitinib, epirubicin, fulvestrant, and olaparib. Additionally, CD24 overexpression in BC cell lines promoted proliferation and migration, and inhibited apoptosis. These findings contribute to personalized treatment strategies and help elucidate the tumor microenvironment characteristics of BC patients. - Source: PubMed
Wu RihanWang ZiruiBai YuanruiDong ChunhuiLiu YihuiChen Ling - Intervertebral disk degeneration (IDD) is the leading cause of chronic low back pain, yet its link to amino acid metabolic reprogramming remains unclear. - Source: PubMed
Publication date: 2026/05/13
Li XushengShuid Ahmad NazrunMiswan Mohd Fairudz MohdZhang XiaoGu WenboCao DonghuiWang JungangJiang ZiyangYuan Haifeng