BASP1 ELISA kit
- Known as:
- BASP1 Enzyme-linked immunosorbent assay test reagent
- Catalog number:
- DL-BASP1-Hu
- Product Quantity:
- 96T
- Category:
- Elisa Kits
- Supplier:
- WDSTD
- Gene target:
- BASP1 ELISA kit
Ask about this productRelated genes to: BASP1 ELISA kit
- Gene:
- BASP1 NIH gene
- Name:
- brain abundant membrane attached signal protein 1
- Previous symbol:
- -
- Synonyms:
- NAP-22, NAP22, CAP23, CAP-23
- Chromosome:
- 5p15.1
- Locus Type:
- gene with protein product
- Date approved:
- 1999-12-08
- Date modifiied:
- 2016-01-06
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- Myeloid-derived suppressor cells (MDSCs) are essential immunosuppressive elements found within the tumor microenvironment (TME) and significantly influence the development of breast cancer (BC). Given their critical role in cancer progression, identifying MDSC-related genes is urgently needed to develop more effective treatment strategies for BC patients. The integration of bulk RNA-seq data from the TCGA-BC cohort alongside scRNA-seq data from the GSE176078 dataset was performed for identifying MDSC-related genes through bioinformatic analysis. Subsequently, the potential of the hub gene BASP1 in predicting prognosis and immune infiltration in BC was evaluated. Furthermore, the functional role of BASP1 in BC was investigated both in vitro and in vivo. Notably, BASP1 levels were significantly higher in BC tissues than in adjacent normal tissues, and elevated BASP1 expression was closely associated with adverse clinical outcomes. Additionally, BC patients with increased BASP1 levels exhibited increased infiltration of immunosuppressive cells (M2 macrophages and Tregs) but reduced infiltration of CD8 + T cells. Functionally, downregulation of BASP1 was observed to suppress BC cell proliferation and migration in vitro through inactivation of AKT and ERK signalings. Mechanistically, BASP1 in 4T1 cells promoted MDSC migration, at least partially, via upregulating CXCL12 secretion, while BASP1 in MDSCs directly suppressed T cell function. In vivo experiments showed that BASP1 knockdown markedly inhibited tumor growth in mouse models bearing 4T1 tumors, accompanied by decreased MDSCs infiltration and increased Granzyme B + CD8 + T cell accumulation in tumor tissues. Collectively, BASP1 may serve as a potential prognostic biomarker and a therapeutic target for BC intervention, functioning both as a pro-tumorigenic gene and as an immunomodulatory molecule that shapes an immunosuppressive microenvironment. - Source: PubMed
Publication date: 2026/06/23
Hu HaijieFeng XiaominYan Zhi'anQi FuzhongLi DonghaiLuo Xuegang - Leptospirosis is a globally neglected zoonotic disease caused by pathogenic species and characterized by diverse clinical manifestations. However, the molecular immune responses occurring in circulating human immune cells during acute infection remain incompletely understood. Although several leptospiral virulence determinants have been investigated, a detailed characterization of host immune signaling during human infection is still limited. To characterize host molecular responses during acute leptospirosis, we performed integrated transcriptomic and proteomic profiling of peripheral blood mononuclear cells (PBMCs) from laboratory-confirmed leptospirosis patients and healthy controls. PBMCs were selected because they contain circulating immune cells involved in pathogen recognition and cytokine signaling, enabling focused analysis of host immune responses. Multi-omics network analysis was used to identify conserved immune pathways, and key host factors were further examined using human whole-blood infection models and infection of human macrophages and monocytes. Transcriptomic profiling identified over 5,800 differentially expressed genes, predominantly upregulated, and associated with inflammatory signaling, including tumor necrosis factor signaling, interferon responses, and cytokine-mediated immune activation. Proteomic analyses detected 362 differentially expressed proteins in clinical PBMC samples and 818 differentially expressed proteins in the experimental infection model, with overlapping proteins defining a conserved host response. Comparative analysis identified 16 consistently upregulated host factors enriched in pathways related to neutrophil activation, hemostasis, and cytokine signaling. Quantitative RT-PCR confirmed increased expression of and supporting their roles in inflammatory signaling and acute-phase immune responses. Together, these findings reveal conserved immune pathways activated during acute infection and provide molecular insights into host-pathogen interactions in human leptospirosis.IMPORTANCELeptospirosis is a globally important zoonotic disease caused by bacteria of the genus . It can lead to severe systemic complications such as kidney failure, lung injury, and multi-organ dysfunction in affected individuals. Accumulating evidence indicates that these severe clinical manifestations are closely associated with dysregulated host immune and inflammatory responses triggered during infection. However, the molecular mechanisms underlying these immune responses, particularly the transcriptional and proteomic alterations occurring in human immune cells during infection, remain incompletely understood. In this study, we analyzed immune cells from patients with leptospirosis and identified key host molecules and immune pathways activated during infection. Experiments using human blood and immune cell models confirmed the involvement of several inflammatory host factors. These findings improve our understanding of how the human immune system responds to infection and identify host-response molecules that may help guide future biomarker discovery and therapeutic strategies. - Source: PubMed
Publication date: 2026/06/15
Cp JusailVyas PallaviNoor HudaKavela SridharKodugade Mansoor AKammili NagamaniFaisal Syed M - Dedifferentiated liposarcoma (DDLPS) with rhabdomyosarcomatous differentiation is associated with a poorer prognosis compared to other DDLPS subtypes. This highlights the importance of exploring its clinicopathological, immune microenvironment, and molecular characteristics to inform personalized treatment strategies. In this study, we investigated five DDLPS patients with rhabdomyosarcomatous differentiation, summarizing their clinicopathological features, immune landscape through immunohistochemistry, and molecular alterations via next-generation sequencing (NGS) analysis, including both DNA and RNA sequencing. Additionally, we conducted a comparative analysis between the well-differentiated (WD) and dedifferentiated (DD) components within these tumors. Our findings identified recurrent HMGA2 fusions, including HMGA2-C12orf74, HMGA2-LPP, HMGA2-BASP1, HMGA2-NAV3, HMGA2-MYF6, and MYO10-HMGA2, which were mutually exclusive with MYC amplification. Notably, these HMGA2 fusions were associated with a more favorable prognosis, demonstrating a mean relapse-free time of 24.0 months, compared to only 2 months in patients without the fusion (P = 0.039). Chromosomal alterations were frequently observed, with 12q amplification being the most prevalent across all 10 tumor samples (5 DD and 5 WD components). Furthermore, DD components exhibited significantly higher levels of copy number variations (CNVs) than their WD counterparts (P = 0.01), with 15q loss exclusively detected in DD components (P < 0.01). In terms of the immune microenvironment, both DD and WD components showed significant infiltration of T cells and M2 macrophages. However, CD20 B cells were more abundant in WD components compared to DD components. Additionally, DD components harboring MYC amplification exhibited a more immunosuppressive state than those containing HMGA2 fusions, further underscoring the heterogeneity of these tumors. In conclusion, our multi-omics analysis identifies HMGA2 fusion as a promising diagnostic and prognostic biomarker for DDLPS with rhabdomyosarcomatous differentiation. The comprehensive molecular and immune landscape of this tumor subtype not only deepens our understanding of its pathophysiology but also provides critical insights for future precision medicine strategies. - Source: PubMed
Publication date: 2026/06/06
Zhang XinkeShen XiujiaoChen PingXian XinyiQu ChunhuaYang YuanzhongChen JierongChen JieweiLu ChenChen XiaocongZhang ZichenLi JingWang ZhouyuGe MinghuiHan TiantianChen DongshengHu Wanming - The central nervous system responds to acute injury with plastic remodeling of its network. However, the temporal and structural dynamics of this response in the denervated dentate gyrus remain poorly understood. Therefore, we examined the transcriptional programs activated after perforant path transection, focusing on the outer molecular layer (OML) and the granule cell layer (GCL). - Source: PubMed
Publication date: 2026/05/19
Schlaudraff JessicaDel Turco DomenicoKey JanaDeller ThomasAuburger Georg - Kidney stones are a globally prevalent condition, but their pathogenesis remains incompletely understood. This study aimed to identify and validate key genes implicated in kidney stone formation through sequencing data analysis, offering novel molecular targets for elucidating the underlying pathogenic mechanisms. - Source: PubMed
Jiang HuaJiang YanjiJi JieChou AnyangMao WeipuChen MingZheng Yang