Bhlhe41 antibody - N-terminal region (ARP33575_P050)
- Known as:
- Bhlhe41 (anti-) - N-terminal region (ARP33575_P050)
- Catalog number:
- arp33575_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- Bhlhe41 antibody - N-terminal region (ARP33575_P050)
Related genes to: Bhlhe41 antibody - N-terminal region (ARP33575_P050)
- Gene:
- BHLHE41 NIH gene
- Name:
- basic helix-loop-helix family member e41
- Previous symbol:
- BHLHB3
- Synonyms:
- DEC2, SHARP-1, SHARP1, bHLHe41
- Chromosome:
- 12p12.1
- Locus Type:
- gene with protein product
- Date approved:
- 2001-09-26
- Date modifiied:
- 2015-11-18
Related products to: Bhlhe41 antibody - N-terminal region (ARP33575_P050)
Related articles to: Bhlhe41 antibody - N-terminal region (ARP33575_P050)
- Osteoporosis (OP) is characterized by impaired bone homeostasis in which bone resorption exceeds bone formation. Disulfidptosis, a recently described disulfide stress-induced cell death program linked to cytoskeletal collapse, has been suggested to contribute to OP, yet its cell-type-specific relevance within the bone marrow mesenchymal stem cell (BM-MSC) osteogenic lineage-and the upstream upstream transcriptional and epigenetic programs shaping this stress response-remain unclear. - Source: PubMed
Publication date: 2026/04/02
Zhao XiaomingXue WenyaGao JunZhang YileiChen JinghongZhang YingangLong Song - Aging accelerates central nervous system remyelination failure and neurodegeneration. Microglia promote remyelination by phagocytosing myelin debris, but this function is impaired by aging-related CD22 upregulation. However, the molecular mechanisms counteracting premature aging-related microglial dysfunction and remyelination impairment remain unclear. Here, we report that Aurka-Bhlhe41 axis prevents premature aging-like microglial dysfunction and promotes remyelination by restraining progressive CD22 upregulation. We identified that microglia-enriched Bhlhe41 was negatively autoregulated and inhibited by Aurka loss. Bhlhe41- or Aurka-deficient young mice exhibited aging-like microglial morphology, phagocytic deficits, progressive CD22 upregulation, and remyelination impairment in cuprizone-induced demyelination model. Conversely, ectopic Bhlhe41 expression induced hypertrophic microglia, and counteracted phagocytic deficits and CD22 upregulation in Aurka-deficient microglia. CD22 blockade restored phagocytic function and remyelination in Bhlhe41-deficient mice. Notably, a conserved pattern of CD22 upregulation was observed in human PCDH9 microglia subsets with BHLHE41 downregulation. These findings offer insights into potential therapeutic strategies to combat aging-related neurodegeneration and central nervous system functional decline. - Source: PubMed
Publication date: 2026/03/27
Yan WeixingZhao YelinLi HuiHong LiJia QiZhu DiXiang DongDu LiHu LangBai RuixueXu MeizhenTang YangyangChen XinzhuCao YiweiJia WenyuWang SiyuLiu YutingRen JinfengPan ShuaiShi YanbiaoGao SijiaDong FuxingShi JianhongLi JinghuaZheng KuiyangYang JingZhao ShuliWang Hui - Lineage-committed precursors are essential yet rarely identified in mammalian organogenesis, as they lack definitive molecular signatures required for conventional marker-based approaches. Herein, we developed iCommitted, an integrated multi-omics computational pipeline for precise identification of these precursors. iCommitted first reconstructs in vivo organogenesis by modeling the in vitro differentiation trajectory spanning naïve to terminally differentiated cells. It then integrates epigenomic (ATAC-seq/DNase-seq) and transcriptomic (RNA-seq) data to achieve standardized developmental staging and precursor identification. Applied to mammalian hematopoiesis, iCommitted robustly identified hematopoietic progenitors as the hematopoietic lineage-committed precursors. Subsequent cis-regulatory annotation generated a high-confidence atlas of 16 774 hematopoietic cis-regulatory elements. Functional analysis of the atlas further pinpointed a 218-bp hematopoietic enhancer (chr6:145 855 899-145 856 116) that regulates Bhlhe41 expression during lineage commitment. This study establishes a valuable approach for identifying lineage-committed precursors and elucidating regulatory mechanisms in mammalian organogenesis, offering broad utility in developmental biology. - Source: PubMed
Jin LihuiHan ZhenyuanHannah RebeccaShao HongyuHuang JunxinWang ShiyingZhang WeibinLin JiangSun KunYu Yu - Alcoholic Heart Disease (AHD) involves gut microbiota dysbiosis, metabolic disturbances, and circadian disruption, yet their interconnections remain unclear. Using a murine AHD model, we integrated echocardiography, metabolomics, cardiac transcriptomics, and 16S rRNA sequencing to investigate alcohol-induced pathology. It evaluated dietary fiber and acetate interventions for their potential to restore gut microbiota balance, lactate homeostasis, and circadian gene expression. Statistical analyses included correlation networks, receiver operating characteristic (ROC) curves, and pathway enrichment. Chronic alcohol consumption led to gut dysbiosis characterized by an overgrowth of Akkermansia muciniphila and a depletion of Lactobacillus intestinalisand and Bacteroides acidifaciens. This condition was associated with hyperlactatemia fraction, myocardial dysfunction, evidenced by a reduced revealed fraction and cardiac fibrosis. Transcriptomic analysis revealed strong dysregulation of circadian-related genes, including BHLHE41, NFIL3, and PER2. Interventions improved microbial diversity, reduced lactate levels, and successfully regulated cardiac related indicators through the lactate-circadian rhythm pathway. ROC analysis validated BHLHE41, NFIL3, and PER2 as high-accuracy biomarkers (AUC > 0.85). Our study reveals a gut‑heart axis in AHD where microbiota‑derived lactate links to circadian disruption, worsening disease. Dietary fiber and acetate are promising therapies that rebalance metabolites and modulate circadian networks, offering novel biomarkers and strategies for alcohol‑related cardiovascular disease. - Source: PubMed
Publication date: 2026/03/11
Siang WeiWenji LinYiji ZhaoYan FengRen Lai - The complex and dynamic relationship between plasticity and genetic adaptation in response to a changing environment represents a longstanding and controversial debate in evolutionary biology. In particular, the molecular and cellular mechanisms underlying this relationship have not been explored. Here, we conducted a plain-to-plateau animal translocation experiment using sheep as a model. We obtained brain, heart and lung tissues from normoxia-adapted, normoxia-to-hypoxia translocated and hypoxia-adapted sheep. We generated 27 scRNA-seq and 54 snRNA-seq datasets for tissues from 27 animals and analyzed gene expression in 236,805 cells and 906,315 nuclei. We revealed cell-specific gene expression plasticity, which is overwhelmingly reversed by genetic adaptation at the cellular level. We discovered a high level of reversing plasticity specifically in immune cells, which promotes genetic adaptation through strong selection on reversing genes to achieve the required level of fitness for adaptation. We revealed a correlative pattern of cellular expression plasticity underlying acclimatization to hypoxia via a common regulatory network (the activator protein 1 family (AP-1)→hypoxia-inducible factor (HIF)∣-BHLHE41 network) and cell plasticity (e.g., microglial activation in the brain and capillary endothelial cell to endothelial-to-mesenchymal transition cell (CEC-to-EndMT) transformation in the heart) in the three organs. Additionally, time-series cellular transcriptional analysis of hypoxia-related disease genes implied a greater contribution of high-scoring cell types (e.g., alveolar type 1 cells in the lung) and plastic disease genes to the incidence and progression of these diseases. Our study generates the first cellular transcriptomes of vital organs under hypoxia acclimatization and provides new insights into hypoxia adaptation and hypoxic diseases. - Source: PubMed
Publication date: 2026/03/03
Wei Wen-TianYan ZeWu HuiZhou Ming-LiangMo Dong-XinWan XingMa RuiWu Mei-MingHuang Jia-HuiLiu Ya-JingYang JiLi Meng-Hua