Ask about this productRelated genes to: SELENBP1 antibody
- Gene:
- SELENBP1 NIH gene
- Name:
- selenium binding protein 1
- Previous symbol:
- -
- Synonyms:
- hSP56, hSBP, LPSB
- Chromosome:
- 1q21.3
- Locus Type:
- gene with protein product
- Date approved:
- 1999-01-15
- Date modifiied:
- 2018-07-27
Related products to: SELENBP1 antibody
Related articles to: SELENBP1 antibody
- Although immune dysregulation is implicated in both autoimmune diseases and cancer, comparative pathogenesis and immune response mechanisms between systemic lupus erythematosus (SLE) and colorectal cancer (CRC) remain elusive. This study identifies common molecular biomarkers and pathogenic pathways shared between SLE and CRC via multi-omics analysis. - Source: PubMed
Publication date: 2026/02/26
Guan HuiTian ChengziZhong MingZhang LihuanWang WenjingHuang MingchengChen Duo - Although a range of glomerular diseases profoundly affect glomerulus-associated cells, a comprehensive understanding of their molecular alterations is still lacking. Here, we performed in-depth analysis of glomerular data from mouse models of primary and secondary glomerulopathies and constructed a multi-disease cellular landscape of glomerular cells. We identified a putative subset of proliferative glomerular endothelial cells(gECs) that highly expresses genetic susceptibility genes associated with multiple glomerular diseases. Podocytes exhibited shared injury-associated cell types across different disease models. A podocyte subset highly expressing , , , , , and was predominantly derived from ob/ob mice, whereas another podocyte subset with high expression of , , , , and was mainly observed in adriamycin-induced mice. Mesangial cells shared common injury-related alterations across diseases (high expression of , , , and ), while ob/ob mice exhibited a distinct mesangial cell subset (high expression of and ). In contrast, the gECs displayed similar molecular changes across different diseases without giving rise to disease-specific subtypes. Intercellular ligand-receptor analysis underpins the recruitment of immune cells by injured mesangial cells and podocytes via specific engagement of pairs such as CXCL and MIF, respectively. Our study systematically elucidates the molecular alterations of glomerulus-associated cells across various diseases, providing a foundation and strategic insights for future targeted therapies tailored to specific glomerular disease contexts. - Source: PubMed
Publication date: 2026/02/24
Huang YanLi ShuoLi ShuyingDuan ShuzhongHuang LanWang JingMa LiangyanLiu CeChen Qilin - [This corrects the article DOI: 10.1155/2019/5294105.]. - Source: PubMed
Publication date: 2026/02/25
- Selenium-binding protein 1 (SELENBP1) may act as a tumor suppressor gene in colorectal cancer (CRC). However, it remains unclear whether SELENBP1 regulates cell cycle progression governed by cyclin-dependent kinase 2 (CDK2). Herein, we validated the intracellular binding of SELENBP1 to CDK2, based on our previous observations. We investigated the regulatory effects of SELENBP1 on retinoblastoma protein (RB) signaling pathway activation and CDK2-mediated cell cycle progression. Finally, we explored the molecular mechanism through which SELENBP1 inhibited CDK2 expression. Both ectopically induced and endogenously expressed SELENBP1 bound to CDK2 in cultured CRC cells. SELENBP1 inhibited the expression of CDK2 and activated RB signaling. Studies have indicated that SELENBP1 inhibits the cell cycle and suppresses tumor growth. Mechanistic studies showed that SELENBP1 might suppress cancer cell growth by causing CDK2 breakdown via ubiquitination. We conclude that SELENBP1 plays a distinct role as a potential tumor suppressor-associated gene that blocks the interphase and mitosis continuum and suppresses tumor growth in CRC by inducing the ubiquitination-mediated degradation of CDK2. - Source: PubMed
Publication date: 2025/12/04
Zhang XiaotianZhang DongLiu QichangCao ZhipengYang JuLi LiangHong RunqiHu ZhiqingZhu JiankangChen RuiNiu GengmingHan ShanliangKe ChongweiChen Liang - How does first-line chemotherapy alter follicular survival and the ovarian microenvironment? - Source: PubMed
Grosbois JohanneBisteau XavierImbault VirginieConrard LouiseCondorelli MargheritaFindikli NecatiLybaert PascaleDemeestere Isabelle