Ask about this productRelated genes to: ARL11 antibody
- Gene:
- ARL11 NIH gene
- Name:
- ADP ribosylation factor like GTPase 11
- Previous symbol:
- -
- Synonyms:
- ARLTS1, FLJ33930
- Chromosome:
- 13q14.2
- Locus Type:
- gene with protein product
- Date approved:
- 2004-02-05
- Date modifiied:
- 2017-11-27
Related products to: ARL11 antibody
Related articles to: ARL11 antibody
- Prostate cancer (PCa) progression and therapeutic resistance are largely driven by aberrant oncogenic signaling and an immunosuppressive microenvironment. Ginsenoside Rg3, a natural saponin from Panax ginseng, exhibits antitumor and immunomodulatory activity, but its therapeutic efficacy is limited when used as a monotherapy. Here, we investigated the synergistic potential of combining Rg3 with near-infrared (NIR) exposure in PCa. In PC-3 and DU145 cells, co-treatment with Rg3 and NIR synergistically inhibited proliferation, migration, and angiogenesis, while promoting apoptosis and reversal of epithelial-mesenchymal transition. Bioinformatic and molecular analyses identified the RAS/RAF/ERK pathway as a key target, with Rg3 showing a strong potential to interact with RAS and suppressing downstream phosphorylation of RAF and ERK; pharmacologic RAS activation partially reversed these effects. Beyond direct tumor inhibition, the combination also enhanced macrophage ARL11 expression and reprogrammed tumor-associated macrophages from an M2 to M1 phenotype through suppression of tumor RAS signaling. In xenograft models, Rg3 and NIR co-treatment markedly reduced tumor growth without systemic toxicity and increased M1 infiltration within tumor tissues. Collectively, these findings demonstrate that Rg3 combined with NIR exerts potent and safe antitumor activity by concurrently targeting tumor-intrinsic RAS/RAF/ERK signaling and ARL11-mediated immune reprogramming, offering a promising multimodal strategy for PCa therapy. - Source: PubMed
Publication date: 2026/02/23
Zhang HaipingChang YingFu QiangJin TiefengZhang SongnanZhang Meihua - Resistance to poly-(ADP)-ribose polymerase inhibitors (PARPi) remains a significant challenge in clinical practice, leading to treatment failure in many patients. It is crucial to better understand the molecular mechanisms that underlie PARPi resistance. In this study, utilizing a genome-wide CRISPR activation screen with olaparib, we identified ARL11 as a potential modulator of PARPi treatment response in BRCA-wild-type MDA-MB-231 cells. Mechanistically, ARL11 interacts with STING to enhance innate immunity and forms positive feedback with type I interferon (IFN) induction, which induces ARL11 up-regulation and contributes to resistance to PARPi therapy. Additionally, we observed that ARL11 interacts with the RUVBL1 and RUVBL2 (RUVBL1/2) complex, the key DNA double-strand repair proteins, facilitating DNA homologous recombination (HR) repair and significantly reducing PARPi-induced DNA double-strand damages. Clinical sample analysis reveals that the expression levels of ARL11 and RUVBL1/2 are significantly elevated in breast cancer patients compared to healthy controls. Collectively, our findings suggested that ARL11 and RUVBL1/2 may be promising therapeutic targets to sensitize breast cancer cells to PARPi therapy. - Source: PubMed
Publication date: 2025/03/23
Zhang TengjiangZhang YuanWang XuxiangHu HaitianLin Christopher GXu YaruZheng Hanqiu - Atherosclerosis (AS), an arterial vasculature disease, is characterized by abnormal lipid accumulation and inflammatory response. ADP ribosylation factor like GTPase 11 (ARL11) is linked to multifarious processes in cells. This study aims to clarify the underlying mechanism of ARL11 in AS. - Source: PubMed
Publication date: 2024/09/05
Zhen YanhuaYang JiaqiSong JiXing ZeyuZheng Jiahe - Spinal cord injury (SCI) is a severe central nervous system injury and microglia are major participants in neuroinflammation after injury. ADP-ribosylation factor-like GTPase 11 (ARL11) is a GTP-binding protein. Whether ARL11 is involved in the SCI progression is unknown. In the impactor-induced moderate SCI mouse model, ARL11 protein and mRNA expression were significantly increased in the injury site. LPS (100 ng/mL) and IFN-γ (20 ng/mL) were incubated with BV2 cells (immortalized mouse microglial cell line) to drive them into an M1-like phenotype. ARL11 up-regulation was also observed in activated microglia in SCI mice and LPS and IFN-γ treated BV2 cells. Basso Mouse Scale scores and inclined plate test revealed that ARL11 deletion promoted motor function recovery in SCI mice. Pathological examination showed ARL11 knockdown reduced spinal cord tissue damage, increased neuron numbers, and inhibited neuronal apoptosis in SCI mice. ARL11 knockdown notably inhibited IL-1β and IL-6 production in vivo and in vitro. Furthermore, ARL11 deletion significantly inhibited iNOS protein and mRNA expression in vivo and in vitro, and COX-2 expression in vivo. Mechanism studies revealed that ARL11 silencing decreased phosphorylated ERK1/2 protein expression. Additionally, ELF1 knockdown significantly inhibited ARL11 protein and mRNA expression in vitro. ELF1 acted as a transcription activator in regulating ARL11 expression by binding to the promoter. In conclusion, ARL11 knockdown protects neurons by inhibiting M1 microglia-induced neuroinflammation, thereby promoting motor functional recovery in SCI mice. This may occur in part under the regulation of ELF1. Our study provides a new molecular target for SCI treatment. - Source: PubMed
Publication date: 2024/09/20
Zhang HaocongXiang LiangbiYuan HongYu Hailong - This study aimed to identify feature genes and explore the molecular mechanisms of keratoconus (KC). We downloaded data files from NCBI GEO public database. The Limma package was used for differential expression analysis of gene profiles. Lasso regression was used to identify the feature genes. The CIBERSORT algorithm was used to infer the proportion of immune-infiltrating cells and analyse the correlation between gene expression levels and immune cells. Related transcription factors and miRNAs of key genes were predicted using the Cistrome DB and Mircode databases. Analysis of expression differences in disease genes was based on the GeneCards database. The CMap was used to analyse targeted therapeutic drugs. IHC was performed to verify the expression levels of ATOH7 and MYRF in corneas. Exactly 593 upregulated and 473 downregulated genes were identified. Lasso regression analysis identified ATOH7, DBNDD1, RNF217-AS1, ARL11, MYRF and SNORA74B as feature genes for KC. All key genes were correlated with immune infiltration and the levels of activated memory CD4+ T cells and plasma cells were significantly increased. miRNA, IRF and STAT families were correlated to feature genes. The expression levels of key genes were significantly correlated to KC-related genes. Entinostat, ochratoxin-a, diphencyprone and GSK-3-inhibitor-II were predicted as potential KC medications. The expression of MYRF was significantly higher in the KC samples, contrary to the expression of ATOH7. KC is related to both immune infiltration and genetic factors. MYRF and ATOH7 were newly identified and verified feature genes of KC. - Source: PubMed
Lyu NingDai YiqinWu JiawenFan YidanLyu ZhaoyuanGu JiayuCheng JingyiXu Jianjiang