Ask about this productRelated genes to: Rhebl1 antibody
- Gene:
- RHEBL1 NIH gene
- Name:
- RHEB like 1
- Previous symbol:
- -
- Synonyms:
- MGC34869, FLJ25797, RHEB2
- Chromosome:
- 12q13.12
- Locus Type:
- gene with protein product
- Date approved:
- 2003-05-22
- Date modifiied:
- 2017-08-07
Related products to: Rhebl1 antibody
Related articles to: Rhebl1 antibody
- RHEBL1 is the Rheb branch of the GTPase proteins that are members of the Ras superfamily. However, it remains unclear how it is relevant to the tumour immune microenvironment. This research evaluates the expression of RHEBL1 employing data from the Cancer Genome Atlas (TCGA) and Genotypic Tissue Expression (GTEx) databases. TCGA cohort was employed to identify the clinical characteristics and prognostic effect of RHEBL1. R Package clusterProfiler was employed to execute Gene Set enrichment analysis (GSEA) on RHEBL1. The association between RHEBL1 and immune cell infiltration (ICI) score was analyzed by employing TCGA samples copied from the public platform and TIMER2 database. Correlation analysis of IC50 values of 192 anti-cancer medicine copied from the Genomics of Drug Sensitivity in Cancer (GDSC) database. In the end, real-time fluorescence quantitative polymerase chain reaction (RT-qPCR) was employed to assessing RHEBL1 expression level in tumours and paracancerous tissues of colon cancer patients. It was found that the overall survival (OS), disease-specific survival (DSS), disease-free interval (DFI), and progression free interval (PFI) progression of colon adenocarcinoma (COAD) are highly related with high expression of RHEBL1 (p < 0.05). In addition, pathways related to immune regulation were closely involved in RHEBL1 expression. Furthermore, the levels of tumour-associated macrophage (TAM) and CD8 + T-cell infiltration were positively correlated with the expression of RHEBL1 in TCGA Pan-cancer samples. Patients with high RHEBL1 expression may be more sensitive to treatment with 5-FU, ABT737, Afuresertib, AGI-5198, AGI-6780, and Alisertib (p < 0.05) and could benefit from these chemotherapeutic agents. In vitro experimental results showed that RHEBL1 was significantly increased in COAD (p < 0.05). These findings indicate that RHEBL1 is an oncogene for multiple tumours and an important factor affecting tumour prognosis. Pan-cancer samples suggested that high RHEBL1 expression facilitates TAM infiltration and is correlated with tumour immunosuppressive status (TCGA). High expression of RHEBL1 may benefit from the therapy of 5-FU, ABT737, Afuresertib, AGI-5198, AGI-6780, and Alisertib. - Source: PubMed
Publication date: 2025/05/14
Chen YueFeng XiaoYin XindongYi NanZhao YaWang QianXing WenyaMa ChaoqunChen Dexuan - Glucocorticoid therapy has a beneficial effect in several diseases, but chronic treatment has adverse effects, including muscle atrophy, which refers to the gradual decrease in muscle mass, size and strength. It is important to know how the muscle atrophy occurs, but the underlying mechanism is not yet fully understood. This study shows that dexamethasone decreases levels of the transcriptional co-activator with PDZ binding motif (TAZ), which facilitates dexamethasone-induced muscle atrophy. - Source: PubMed
Kim Kyung MinOh Ho TaekDo YoujinYoo Gi DonHeo WoongPark JeekeonYang HyejinYoon Suh JinByun Mi RanHwang Eun SookHong Jeong-Ho - Cardiac fibroblasts (CFs) play roles in the maintenance of myocardial tissue structure. Cellular senescence is a state of stable cell cycle arrest. We previously reported that extracellular vesicles (EV) secreted by doxorubicin (DOX, 1000 nM)-induced senescent CFs (D10-EV) caused autophagy in CFs. EV mediate cell-to-cell communication through the transfer of microRNA (miRNA). In this study, we focused on miRNA contained in EV and aimed to elucidate mechanisms underlying the autophagy induction by D10-EV in CFs. Neonatal rat CFs (NRCFs) were treated with DOX for the induction of cellular senescence. EV were isolated from culture media of NRCFs. miRNA was extracted from the EV and miRNA profiles were analyzed using miRNA-seq. Seven miRNAs were significantly decreased, whereas 14 miRNAs were significantly increased in D10-EV compared with the vehicle-treated NRCFs-derived EV. Among the target genes of 14 miRNAs, Rhebl1 was identified. D10-EV significantly increased microtubule-associated protein 1 light chain 3 (LC3)-II/LC3-I and decreased protein expression of Ras homolog enriched in brain like 1 (RHEBL1) in NRCFs. Small interfering RNA against Rhebl1 tended to increase LC3-II/LC3-I. In conclusion, we for the first time revealed that the senescent NRCFs-derived EV induced autophagy in NRCFs via the suppression of RHEBL1 protein. - Source: PubMed
Publication date: 2025/02/24
Fujioka YuseiOtani KosukeOkada MuneyoshiYamawaki Hideyuki - Mitophagy influences the progression and prognosis of ischemic stroke (IS). However, whether DNA methylation in the brain is associated with altered mitophagy in hypoxia-injured neurons remains unclear. Here, miR-138-5p was found to be highly expressed in exosomes secreted by astrocytes stimulated with oxygen and glucose deprivation/re-oxygenation (OGD/R), which could influence the recovery of OGD/R-injured neurons through autophagy. Mechanistically, miR-138-5p promotes the stable expression of Ras homolog enriched in brain like 1(Rhebl1) through DNA-methyltransferase-3a (DNMT3A), thereby enhancing ubiquitin-dependent mitophagy to maintain mitochondrial homeostasis. Furthermore, we employed glycosylation engineering and bioorthogonal click reactions to load mirna onto the surface of microglia and deliver them to injured region utilising the inflammatory chemotactic properties of microglia to achieve drug-targeted delivery to the central nervous system (CNS). Our findings demonstrate miR-138-5p improves mitochondrial function in neurons through the miR-138-5p/DNMT3A/Rhebl1 axis. Additionally, our engineered cell vector-targeted delivery system could be promising for treating IS. STATEMENT OF SIGNIFICANCE: In this study, we demonstrated that miR-138-5p in exosomes secreted by astrocytes under hypoxia plays a critical role in the treatment of hypoxia-injured neurons. And we find a new target of miR-138-5p, DNMT3A, which affects neuronal mitophagy and thus exerts a protective effect by regulating the methylation of Rbebl1. Furthermore, we have developed a carrier delivery system by combining miR-138-5p with the cell membrane of microglia and utilized the inflammatory chemotactic properties of microglia to deliver this system to the brain via intravenous injection. This groundbreaking study not only provides a novel therapeutic approach for ischemia-reperfusion treatment but also establishes a solid theoretical foundation for further research on targeted drug delivery for central nervous system diseases with promising clinical applications. - Source: PubMed
Publication date: 2024/08/08
Zhu XingjiaLiu QianqianZhu FengweiJiang RuiLu ZhichaoWang ChenxingGong PeipeiYao QiXia TianSun JieJu FeiWang DefengSun RuifanZhou YoulangYou BoShi Wei - The Mammalian Target of Rapamycin (mTOR) signaling pathway regulates protein phosphorylation and exerts control over major cellular processes. mTOR is activated by the small G-protein Ras Homolog Enriched in Brain (Rheb), which is encoded by the and () genes. There is currently a paucity of information on the role of RhebL1, and specifically its involvement in viral infection. In the present study we investigated the role of RhebL1 during human influenza A/NWS/33 (NWS/33) (H1N1) virus infection of rhesus monkey-kidney (LLC-MK2) cells and human type II alveolar epithelial (A549) cells. - Source: PubMed
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