BNIP3L antibody
- Known as:
- BNIP3L (anti-)
- Catalog number:
- orb101642
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Biorbyt biorb
- Gene target:
- BNIP3L antibody
Related genes to: BNIP3L antibody
- Gene:
- BNIP3L NIH gene
- Name:
- BCL2 interacting protein 3 like
- Previous symbol:
- -
- Synonyms:
- Nix, BNIP3a
- Chromosome:
- 8p21.2
- Locus Type:
- gene with protein product
- Date approved:
- 1997-07-01
- Date modifiied:
- 2018-04-18
Related products to: BNIP3L antibody
Related articles to: BNIP3L antibody
- Oxidative stress is a major contributor to neuronal apoptosis and subsequent neurofunctional deficits. This study investigates the dual role of the mitochondrial membrane-anchored protein NIX in PC12 cells, a model for mature neurons. We demonstrate that both overexpression and knockdown of NIX attenuate apoptosis under oxidative stress, albeit through distinct mechanisms. Overexpression of NIX promotes cell survival by activating NIX-mediated mitophagy, which clears damaged mitochondria and intracellular reactive oxygen species (ROS), thereby maintaining redox homeostasis. Conversely, knockdown of NIX reduces apoptosis primarily by diminishing the intrinsic pro-apoptotic function of the protein. Collectively, these findings reveal that NIX expression levels critically gate PC12 cell fate under oxidative stress by differentially activating pro-survival or anti-apoptotic pathways. - Source: PubMed
Publication date: 2026/05/31
Ge FanghuiShu JingxuanLiu ZiqianMa HaixiangCai MinghongDeng XinyanZhang HongWang Jiandong - : ASD is a class of neurodevelopmental disorders with onset in early childhood, whereas AD is a common chronic inflammatory skin disease. An increasing number of studies suggest that immune dysregulation and inflammatory responses play important roles in the onset and progression of both conditions; however, their shared molecular mechanisms remain unclear. : First, ASD-related and AD-related datasets were obtained from the GEO database. After removal of batch effects, the common DEGs between the two diseases were identified. Subsequently, 107 machine learning-based model configurations were employed to screen for key genes. Functional enrichment analyses and PPI network construction were performed to systematically explore their potential functions. Finally, the CIBERSORT was applied to analyze immune cell infiltration and to assess the correlation between hub gene expression and immune cell infiltration. : 164 common genes between ASD and AD were identified. GO and KEGG enrichment analyses revealed that these shared differentially expressed genes were mainly enriched in pathways related to immune regulation and inflammatory responses, suggesting that immuno-inflammatory processes may constitute an important biological basis linking ASD and AD. Further screening and validation using machine learning identified , , , , , , and as hub genes serving as common potential biomarkers for both diseases. Among them, , , and may represent key shared genes and demonstrated good diagnostic value in ROC curve and nomogram analyses. In addition, immune infiltration analysis indicated that these key genes were significantly correlated with the infiltration levels of multiple immune cell types, further supporting their potential roles in immune regulation. : This study reveals potential shared immuno-inflammatory molecular mechanisms between ASD and AD. Genes screened based on 107 machine learning models were verified as potential diagnostic biomarkers for both diseases after integrated analysis, providing a theoretical basis for further investigation of their immune-related pathogenesis and early clinical diagnosis. - Source: PubMed
Publication date: 2026/05/12
Yang RuilingZhang FushenHuang Jufang - Diabetic cardiomyopathy (DbCM) is a major complication of type 2 diabetes whose molecular basis in human hearts remains poorly understood. This study aimed to define the multi-omics landscape of DbCM in the human myocardium. - Source: PubMed
Publication date: 2026/05/18
Lu QiuhanTang ShulinFang SijiaWu YuwenChen LiangLiang MintongChen JiaqiWen PengjuJin LeigangYu JiansheJiao FengWu YuehengJiang Guozhi - Allergic rhinitis (AR) is a type 2 inflammation-related disease, potentially associated with innate lymphoid cells (ILC2s), nasal microbiota, and autophagy. Mice were divided into control, AR, AR + IL-33, and AR + antibiotic groups(n = 5). ELISA was used to measure IL-4, IL-5, and IL-13, Masson staining to evaluate tissue remodeling, flow cytometry to detect ILC2s and memory ILC2s, 16S rRNA sequencing to analyze nasal microbiota, and Western blot to assess autophagy and mitophagy proteins. Compared with controls, mice in each AR group exhibited more nasal symptoms, enhanced tissue remodeling, and altered microbiota diversity with reduced Proteobacteria and increased Firmicutes. IL-33 further elevated type 2 cytokines in serum and nasal lavage fluid, increased nasal ILC2s and miR-155 expression, but did not affect memory ILC2s. All treatment groups showed increased p62 and LC3II/LC3I ratio, along with decreased FUNDC1 and BNIP3L levels. These findings suggest that AR is characterized by type 2 inflammation, tissue remodeling, and microbial dysbiosis, with IL-33 aggravation. Autophagy and mitophagy dysfunction may contribute to AR pathogenesis. - Source: PubMed
Publication date: 2026/05/04
Wang ChenZhang Yi-MingZhou Min-LiLi MinCheng Ke-Jia - Mitochondrial quality control is a crucial factor governing self-renewal capacity, maintenance of metabolic balance, and cellular longevity in stem cells. Impaired mitophagy significantly contributes to cellular senescence, causing accumulation of damaged mitochondria and impaired proliferative capacity of cells, leading to reduced therapeutic efficiency. This study explores mitophagy's role in regulating senescence in human adipose-derived mesenchymal stem cells (HADMSCs) and evaluates the therapeutic potentiality of antioxidants-melatonin and coenzyme Q10 (CoQ10) targeting mitochondria. It also examines the impact of antioxidant intervention aimed at improving the fate and survival, thereby establishing a connection between metabolic reprogramming and mitophagy. Our study found that stress-induced HADMSCs have reduced Mitochondrial Membrane potential (MMP), increased ROS, and increased senescence-associated β-galactosidase activity as observed through fluorescence-based imaging and biochemical assays. It was observed that antioxidant intervention has prevented the damage caused by the stress and reduced mitochondrial ROS and lipid peroxidation and has significantly restored mitophagy markers like Parkin, NDP52, BNIP3, BNIP3L/Nix, and LC3B. Our findings suggest that antioxidants induced pharmacological stimulation of mitophagy could potentially reverse stem cell aging and prevent functional decline, thereby improving regeneration and offering new insights and perspectives on mitochondrial health for improved efficiency of stem cell transplantation, maintenance and longevity of HADMSCs. - Source: PubMed
Publication date: 2026/04/29
Vikraman AleenaRavi LogeswariKandasamy NaveenaDhanasekaran Anuradha