Ask about this productRelated genes to: ARHGAP30 Blocking Peptide
- Gene:
- ARHGAP30 NIH gene
- Name:
- Rho GTPase activating protein 30
- Previous symbol:
- -
- Synonyms:
- FLJ00267
- Chromosome:
- 1q23.3
- Locus Type:
- gene with protein product
- Date approved:
- 2005-06-16
- Date modifiied:
- 2014-11-19
Related products to: ARHGAP30 Blocking Peptide
Related articles to: ARHGAP30 Blocking Peptide
- With survival rates for osteosarcoma largely unchanged for 40 years-especially in metastatic/recurrent cases. While the immune microenvironment is believed to play a crucial role, the heterogeneity of immune cell infiltration (ICI) and its precise impact on prognosis and therapeutic response remain poorly characterized. There is a lack of a robust, ICI-based scoring system to stratify patients and identify novel therapeutic targets. This study aimed to identify the characteristics of ICI subtypes for evaluating prognosis and therapeutic benefits. - Source: PubMed
Wang YuerongLiu XueniXie GuojinLi Zheqian - Endometrial cancer (EC) is one of the few malignancies with increasing incidence and mortality rates. Targeted therapy and immunotherapy have become pivotal treatment strategies for EC patients. However, the current methods and biomarkers for predicting immunotherapy responses and prognosis are remain limited. Programmed cell death (PCD) pathways play a crucial role in cancer development and progression and may serve as prognostic markers and indicators of drug sensitivity in EC. In our study, we integrated multiple PCD pathways and comprehensive multi-omics datasets from TCGA-EC and GEO databases. By analyzing distinct PCD signatures, we discovered two major EC subgroups with distinctive prognoses, tumor microenvironment (TME) profiles, and responses to immunotherapy. To further investigate the cellular basis of these PCD patterns, single-cell RNA sequencing analysis was conducted to explore tumor heterogeneity in PCD characteristics across EC subpopulations. Further investigation revealed seven key PCD-associated genes (HIF3A, ACTL8, SIRPG, FBN3, ARHGAP30, CD6, and P2RY13) that formed the basis for a novel prognostic scoring system-risk score (RS). Our findings showed that patients with lower risk scores had better survival rates and improved immunotherapy outcomes. Conversely, patients with higher risk scores experienced poor clinical outcomes and reduced immunotherapy efficacy, although alternative therapies such as docetaxel and olaparib demonstrated potential therapeutic benefits. Overall, the RS provides a valuable tool for early prognosis prediction and for identifying patients who may benefit from immunotherapy. - Source: PubMed
Publication date: 2025/07/01
Lu ShanWei YiyunChen LiuyanCheng JinlianQin LiuyanLu XuemeiPang Lihong - T cells are central to adaptive immunity, with proper thymic development and egress critical for T cell homeostasis in peripheral tissues. The molecular mechanisms governing thymic egress remain poorly understood. Here, we identify Rho GTPase-activating protein 30 (ARHGAP30), predominantly expressed in lymphoid organs and previously uncharacterized in immunity, as a key regulator of thymocyte migration and egress. Loss of ARHGAP30 leads to impaired thymic development and severe T cell lymphopenia. Notably, Arhgap30-deficient mice exhibit a reduced number of immature single-positive (SP) thymocytes but a normal number of mature SP thymocytes, indicating a blockade in thymic egress. Mechanistically, ARHGAP30 deficiency lowers GTP-bound active RAC1 independent of its GAP activity, impairing actin polarization and thymocyte motility. ARHGAP30 selectively binds and stabilizes active RAC1, preventing its proteasomal degradation via K48-linked ubiquitination. These findings establish ARHGAP30 as a critical checkpoint for thymic egress and underscore its essential role in maintaining peripheral T cell homeostasis. - Source: PubMed
Publication date: 2025/05/22
Zhang HuilingGuo ZhihanYi JingjingWu JiayingWang YihanRen TingrongZhang YuqiZhao HaipingWu NanaWei GaigaiZhang Duanwu - - Source: PubMed
Publication date: 2025/02/27
Zhou YongpingHua ZhiyuanZhu YeWang LiyingChen FangmingShan TingZhou YunhaiDai Tu - In recent years, as more and more lung-cancer patients have been treated with immunotherapeutic agents, their survival has been prolonged compared to before. It is well known that BTK (Bruton's tyrosine kinase) is predominantly found in cells of the hematopoietic system. However, there is a distinct lack of literature on BTK expression in lung adenocarcinoma (LUAD) patients and its effect on the immune microenvironment. Consequently, the main goal of this investigation was to analyze how BTK expression in lung adenocarcinoma affects its progression, along with its prognostic significance, through the utilization of bioinformatics online resources and publicly available databases. Data on the sequencing results and clinical records of lung adenocarcinoma patients were gathered from The Cancer Genome Atlas (TCGA) database. Based on the expression level of BKT, TCGA categorized lung adenocarcinoma patients into BTK high-expression and low-expression groups. We investigated the effects of BKT on clinicopathologic, genomic, and immunologic characteristics of lung adenocarcinoma patients. We analyzed BTK mRNA expression in tumors and normal tissues using two key resources: Tumor Immuno Estimation Resource 2.0 (TIMER 2.0) and Gene Expression Profiling Interactive Analysis 2 (GEPIA 2). We analyzed the prognosis of the patients using GEPIA2 and validated the results using univariate and multivariate analyses. In addition, we assessed BTK protein expression by Human Protein Atlas (HPA). We sought to elucidate the clinical prognostic significance of BTK in The TCGA using the online tool GEPIA 2. Furthermore, to clarify the biologic roles and pathways linked to BTK, we conducted a genomic enrichment analysis of the information. To predict the proportion of various immune cell infiltrations in the immune microenvironment of lung adenocarcinoma patients diagnosed in the TCGA database, we performed an analysis using the TIMER online tool. Using TIMER and CIBERSORT, the correlation between genes co-expressed with BTK and the corresponding tumor-infiltrating immune cells was explored; finally, the relationship between BTK expression and immune infiltration and immune checkpoints in the TMB group and the high and low groups was analyzed by R language analysis using the TCGA database. The expression of BTK provides some hints about the prognosis of the patients. The high expression of BTK is involved in immune response regulation signaling pathways, leukocyte-mediated immunity, leukocyte intercellular adhesion, graft rejection, and complement. Analysis of the GEPIA 2 database showed that BTK was co-expressed with the genes FGD2, SASH3, NCKAP1L, CD53, ARHGAP30 and LPXN. Increased expression of the above-mentioned genes resulted in increased proportions of CD8 + T cells, memory CD4 + T cells, B cells, macrophages, and dendritic cells, and decreased proportions of Treg cells and TH2 cells. In addition, our study revealed a strong positive correlation between various key immune checkpoints (e.g., PDCD1, CD274, PDCD1LG2, CTLA4, HAVCR2, LAG3, TIGIT, and SIGLEC15) and BTK expression. In conclusion, increased BTK expression in lung adenocarcinoma is closely associated with prolonged survival of lung-cancer patients. Moreover, the genes classified under the BTK high-expression group exhibit significant enrichment in immune-related pathways, suggesting a potential impact on the tumor microenvironment. We investigated the potential of BTK as a tumor suppressor gene in predicting prolonged patient survival. In addition, we further investigated the possibility that BTK further affects the immunotherapeutic response of patients by influencing the microenvironment of tumor immune infiltration, but the relevant mechanisms remain to be further studied. - Source: PubMed
Publication date: 2024/08/28
Jiao LijunTao YujianDing HuizhenWu FengLiu YantongLi ChuangLi Feifei