DRAP1 antibody - N-terminal region (ARP31488_P050)
- Known as:
- DRAP1 (anti-) - N-terminal region (ARP31488_P050)
- Catalog number:
- arp31488_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- DRAP1 antibody - N-terminal region (ARP31488_P050)
Related genes to: DRAP1 antibody - N-terminal region (ARP31488_P050)
- Gene:
- DRAP1 NIH gene
- Name:
- DR1 associated protein 1
- Previous symbol:
- -
- Synonyms:
- NC2-alpha
- Chromosome:
- 11q13.1
- Locus Type:
- gene with protein product
- Date approved:
- 1998-09-22
- Date modifiied:
- 2016-10-05
Related products to: DRAP1 antibody - N-terminal region (ARP31488_P050)
Related articles to: DRAP1 antibody - N-terminal region (ARP31488_P050)
- Hepatocellular carcinoma (HCC) is a prevalent type of cancer with high incidence and mortality rates. It is the third most common cause of cancer-related deaths. CD8 T cell exhaustion (TEX) is a progressive decline in T cell function due to sustained T cell receptor stimulation from continuous antigen exposure. Studies have shown that CD8 TEX plays an important role in the anti-tumor immune process and is significantly correlated with patient prognosis. The aim of the research is to establish a reliable CD8 TEX-based signature using single-cell RNA sequencing (scRNA-seq) and high-throughput RNA sequencing (RNA-seq), providing a new approach to evaluate HCC patient prognosis and immune microenvironment. - Source: PubMed
Publication date: 2024/11/20
Fan JianhuiZhang QinghuaHuang TiancongLi HaitaoFang Guoxu - Triple-negative breast cancer (TNBC) is the most aggressive subtype of breast cancer. Transcriptional dysregulation is a hallmark of cancer, and several transcriptional regulators have been demonstrated to contribute to cancer progression. In this study, we identified an upregulation of the transcriptional corepressor downregulator of transcription 1-associated protein 1 (DRAP1) in TNBC, which was closely associated with poor recurrence-free survival in patients with TNBC. DRAP1 promoted TNBC proliferation, migration, and invasion in vitro and tumor growth and metastasis in vivo. Mechanistically, the downregulator of transcription 1 (DR1)/DRAP1 heterodimer complex inhibited expression of the cytosolic arginine sensor for mTORC1 subunit 1 (CASTOR1) and thereby increased activation of mTOR, which sensitized TNBC to treatment with the mTOR inhibitor everolimus. DRAP1 and DR1 also formed a positive feedback loop. DRAP1 enhanced the stability of DR1 by recruiting the deubiquitinase USP7 to inhibit its proteasomal degradation; in turn, DR1 directly promoted DRAP1 transcription. Collectively, this study uncovered a DRAP1-DR1 bidirectional regulatory pathway that promotes TNBC progression, suggesting that targeting the DRAP1/DR1 complex might be a potential therapeutic strategy to treat TNBC. Significance: DR1 and DRAP1 form a positive feedback loop and a repressor complex to cooperatively inhibit cytosolic arginine sensor for mTORC1 subunit 1 transcription and stimulate mTOR signaling, leading to progression and increased everolimus sensitivity in triple-negative breast cancer. - Source: PubMed
Huang Min-YingHu Shu-YuanDong JiaDeng LingAndriani LisaMa Xiao-YanZhang Yin-LingZhang Fang-LinShao Zhi-MingLi Da-Qiang - HIV-1 antagonizes SERINC5 by redundant mechanisms, primarily through Nef and additionally via envelope glycoprotein. Paradoxically, HIV-1 preserves Nef function to ensure the exclusion of SERINC5 from virion incorporation regardless of the availability of envelope that can confer resistance, suggesting additional roles of the virion-incorporated host factor. Here, we report an unusual mode of SERINC5 action in inhibiting viral gene expression. This inhibition is observed only in the myeloid lineage cells but not in the cells of epithelial or lymphoid origin. We found that SERINC5-bearing viruses induce the expression of RPL35 and DRAP1 in macrophages, and these host proteins intercept HIV-1 Tat from binding to and recruiting a mammalian capping enzyme (MCE1) to the HIV-1 transcriptional complex. As a result, uncapped viral transcripts are synthesized, leading to the inhibition of viral protein synthesis and subsequent progeny virion biogenesis. Cell-type-specific inhibition of HIV-1 gene expression thus exemplifies a novel antiviral function of virion-incorporated SERINC5. In addition to Nef, HIV-1 envelope glycoprotein has been shown to modulate SERINC5-mediated inhibition. Counterintuitively, Nef from the same isolates preserves the ability to prevent SERINC5 incorporation into virions, implying additional functions of the host protein. We identify that virion-associated SERINC5 can manifest an antiviral mechanism independent of the envelope glycoprotein to regulate HIV-1 gene expression in macrophages. This mechanism is exhibited by affecting the viral RNA capping and is plausibly adopted by the host to overcome the envelope glycoprotein-mediated resistance to SERINC5 restriction. - Source: PubMed
Publication date: 2023/03/28
Ramdas PavitraChande Ajit - Mutations in superoxide dismutase 1 (SOD1) result in misfolding and aggregation of the protein, causing neurodegenerative amyotrophic lateral sclerosis (ALS). In recent years, several new SOD1 variants that trigger ALS have been identified, making it increasingly crucial to understand the SOD1 toxicity pathway in ALS. Here we used an integrated bioinformatics approach, including the Ingenuity Pathway Analysis (IPA) tool to analyze signaling pathways, regulators, functions, and network molecules of SOD1 with an emphasis on ALS. IPA toxicity analysis of SOD1 identified superoxide radicals' degradation, apelin adipocyte, ALS, NRF2-mediated oxidative stress response, and sirtuin signaling as the key signaling pathways, while the toxicity of SOD1 is exerted via mitochondrial swelling and oxidative stress. IPA listed CNR1, APLN, BTG2, MAPK, DRAP1, NFE2L2, SNCA, and CG as the upstream regulators of SOD1. IPA further revealed that mutation in SOD1 results in hereditary disorders, including ALS. The exploration of the relationship between SOD1 and ALS using IPA unveiled SOD1-ALS pathway molecules. The gene ontology (GO) analysis of SOD1-ALS pathway molecules with ShinyGO reaffirmed that SOD1 toxicity results in ALS and neurodegeneration. The GO analysis further identified enriched biological processes, molecular functions, and cellular components for SOD1-ALS pathway molecules. The construction of a protein-protein interaction network of SOD1-ALS pathway molecules using STRING and further analysis of that network with Cytoscape identified ACTB followed by TP53, IL6, CASP3, SOD1, IL1B, APP, APOE, and VEGFA as the major network hubs. Taken together, our study provides insight into the molecular underpinning of SOD1's toxicity in ALS. - Source: PubMed
Publication date: 2023/01/15
Suthar Sharad KumarLee Sang-Yoon - Clear cell renal cell carcinoma (ccRCC) usually affects multiple organs (e.g., bone and brain), and patient prognosis is usually poor. Although it is known that CD8+ T cell infiltration can potentially alleviate ccRCC progression, few studies have concentrated on the correlation between CD8+ T cell infiltration and ccRCC prognosis. In this study, ten genes expressed by infiltrated CD8+ T cells (i.e., , and ) were suggested as potential ccRCC prognostic biomarkers, by using next-generation sequencing (i.e. bulk sequencing and single-cell sequencing) of ccRCC, papillary renal cell carcinoma (papRCC), and control kidney biopsies. Specifically, we identified four genes (i.e., , and ) as potential novel prognostic biomarkers for ccRCC. It is noteworthy that derived from CD8+ T cells negatively correlates to Atg7+ neutrophils in ccRCC, compared with papRCC, indicating a potential decreased neutrophil metabolic function in autophagy and fatty acids. This study elucidated the protective role of infiltrated CD8+ T cells in ccRCC and identified ten candidate genes related to an improved prognosis in patients with ccRCC. - Source: PubMed
Publication date: 2022/06/24
Wang JieHuang FeifanZhao JingjieHuang PengTan JunhuaHuang MeiyingMa RuiyingXiao YuHe SiyuanWang ZechenShen JiajiaLu HemingMeng Lingzhang