预约演示

更新于：2025-01-23

RHOB

更新于：2025-01-23

基本信息

别名

ARH6、ARHB、h6

+ [9]

简介

Mediates apoptosis in neoplastically transformed cells after DNA damage. Not essential for development but affects cell adhesion and growth factor signaling in transformed cells. Plays a negative role in tumorigenesis as deletion causes tumor formation. Involved in intracellular protein trafficking of a number of proteins. Targets PKN1 to endosomes and is involved in trafficking of the EGF receptor from late endosomes to lysosomes. Also required for stability and nuclear trafficking of AKT1/AKT which promotes endothelial cell survival during vascular development. Serves as a microtubule-dependent signal that is required for the myosin contractile ring formation during cell cycle cytokinesis. Required for genotoxic stress-induced cell death in breast cancer cells.

关联

项与 RHOB 相关的药物

BA-240

靶点

RHOB

作用机制

RHOB抑制剂

在研机构-

原研机构

BioAxone Therapeutic, Inc.

在研适应症-

非在研适应症

青光眼 [+1]

最高研发阶段无进展

首次获批国家/地区-

首次获批日期1800-01-20

100 项与 RHOB 相关的临床结果

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100 项与 RHOB 相关的转化医学

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0 项与 RHOB 相关的专利（医药）

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930

项与 RHOB 相关的文献（医药）

2025-01-14·Proceedings of the National Academy of Sciences

Exome sequencing identifies genes for socioeconomic status in 350,770 individuals

Article

作者: Dong, Qiang ; Wu, Bang-Sheng ; Cheng, Wei ; Yu, Jin-Tai ; Kang, Ju-Jiao ; Liu, Wei-Shi ; Yang, Liu ; Sahakian, Barbara J. ; Wu, Xin-Rui ; Feng, Jian-Feng ; Deng, Yue-Ting

Socioeconomic status (SES) is a critical factor in determining health outcomes and is influenced by genetic and environmental factors. However, our understanding of the genetic structure of SES remains incomplete. Here, we conducted a large-scale exome study of SES markers (household income, occupational status, educational attainment, and social deprivation) in 350,770 individuals. For rare coding variants, we identified 56 significant associations by gene-based collapsing tests, unveiling 7 additional SES-associated genes ( NRN1 , CCDC36 , RHOB , EP400 , NCAM1, TPTEP2-CSNK1E , and LINC02881 ). Exome-wide single common variant analysis revealed nine lead single-nucleotide polymorphisms (SNPs) associated with household income and 34 lead SNPs associated with EduYears, replicating previous GWAS findings. The gene–environment correlations had a substantial impact on the genetic associations with SES, as indicated by the significantly increased P values in several associations after controlling for geographic regions. Furthermore, we observed the pleiotropic effects of SES-associated genetic factors on a wide range of health outcomes, such as cognitive function, psychosocial status, and diabetes. This study highlights the contribution of coding variants to SES and their associations with health phenotypes.

2025-01-01·Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease

Thioredoxin-1 protein interactions in neuronal survival and neurodegeneration

Article

作者: Rashid, Mahmud-ur ; Sultana, Shakila ; Padmanabhan, Nirmala ; Siddiqui, Tabrez J. ; Eftekharpour, Eftekhar ; Vitiello, Peter F. ; Siddiqui, Tabrez J ; Islam, Md Imamul ; Vitiello, Peter F ; Rashid, Mahamud-Ur ; Karimi-Abdolrezaee, Soheila ; Coombs, Kevin M. ; Coombs, Kevin M

Neuronal cell death remains the principal pathophysiologic hallmark of neurodegenerative diseases and the main challenge for treatment strategies. Thioredoxin1 (Trx1) is a major cytoplasmic thiol oxidoreductase protein involved in redox signaling, hence a crucial player in maintaining neuronal health. Trx1 levels are notably reduced in neurodegenerative diseases including Alzheimer's and Parkinson's diseases, however, the impact of this decrease on neuronal physiology remains largely unexplored. This is mainly due to the nature of Trx1 redox regulatory role which is afforded by a rapid electron transfer to its oxidized protein substrates. During this reaction, Trx1 forms a transient bond with the oxidized disulfide bond in the substrate. This is a highly fast reaction which makes the identification of Trx1 substrates a technically challenging task. In this project, we utilized a transgenic mouse model expressing a Flag-tagged mutant form of Trx1 that can form stable disulfide bonds with its substrates, hence allowing identification of the Trx1 target proteins. Autophagy is a vital housekeeping process in neurons that is critical for degradation of damaged proteins under oxidative stress conditions and is interrupted in neurodegenerative diseases. Given Trx1's suggested involvement in autophagy, we aimed to identify potential Trx1 substrates following pharmacologic induction of autophagy in primary cortical neurons. Treatment with rapamycin, an autophagy inducer, significantly reduced neurite outgrowth and caused cytoskeletal alterations. Using immunoprecipitation and mass spectrometry, we have identified 77 Trx1 target proteins associated with a wide range of cellular functions including cytoskeletal organization and neurodegenerative diseases. Focusing on neuronal cytoskeleton organization, we identified a novel interaction between Trx1 and RhoB which was confirmed in genetic models of Trx1 downregulation in primary neuronal cultures and HT22 mouse immortalized hippocampal neurons. The applicability of these findings was also tested against the publicly available proteomic data from Alzheimer's patients. Our study uncovers a novel role for Trx1 in regulating neuronal cytoskeleton organization and provides a mechanistic explanation for its multifaceted role in the physiology and pathology of the nervous system, offering new insights into the molecular mechanisms underlying neurodegeneration.

2024-12-01·Molecular Biology Reports

MiR-21-5p knockdown inhibits epithelial to mesenchymal transition in A549 lung adenocarcinoma cells by upregulating RhoB

Article

作者: Khair, Hiba Hussein A ; Karagöz, Işık Didem

BACKGROUNDMiR-21-5p is a highly expressed microRNA that plays an important role in various cancer-promoting processes, including anchorage-independent growth, invasion, migration metastasis, and drug resistance in lung cancer. Studies indicate that miR-21-5p may contribute to these processes by promoting epithelial-mesenchymal transition (EMT). Ras homolog gene family member B (RhoB), a gene downregulated by miR-21-5p, has also been linked to EMT in lung cancer. However, the role of the miR-21-5p/RhoB axis in EMT regulation in lung adenocarcinoma remains unclear. In this study, we aimed to investigate the regulatory role of the miR-21-5p/RhoB axis in EMT and related in vitro functional characteristics such as migration, invasion, cisplatin resistance, and the formation of tumor spheroids.METHODS AND RESULTSA549 cells were transfected with the miR-21-5p inhibitor, RhoB siRNA, and their corresponding negative controls. Wound healing, transwell invasion, Methyl thiazole tetrazolium (MTT), and sphere formation assays were also performed to evaluate the migration, invasion, cisplatin resistance, and anchorage-independent growth of A549 cells. RT-qPCR was used to determine the mRNA expression levels of EMT markers. MiR-21-5p knockdown inhibited migration, invasion, cisplatin resistance, and sphere formation while upregulating E-cadherin and downregulating Slug. Furthermore, RhoB silencing restored EMT and related in vitro functional characteristics in A549 cells.CONCLUSIONSKnockdown of miR-21-5p inhibits EMT and related in vitro functional characteristics by upregulating RhoB, suggesting that miR-21-5p may promote EMT through downregulation of RhoB.

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