Ask about this productRelated genes to: ARHGDIA antibody
- Gene:
- ARHGDIA NIH gene
- Name:
- Rho GDP dissociation inhibitor alpha
- Previous symbol:
- GDIA1
- Synonyms:
- RHOGDI
- Chromosome:
- 17q25.3
- Locus Type:
- gene with protein product
- Date approved:
- 1996-04-30
- Date modifiied:
- 2018-03-20
Related products to: ARHGDIA antibody
Related articles to: ARHGDIA antibody
- The global incidence of metabolic dysfunction-associated steatotic liver disease (MASLD) is rising alongside epidemics of diabetes and obesity. Rho GDP-dissociation inhibitor (RhoGDI) is now recognized to play dual regulatory roles in disease. A deeper understanding of its mechanistic contributions in MASLD could offer critical insights for developing novel therapies against this growing health burden. Immunohistochemical staining was used to examine RhoGDI expression in liver tissues from patients with MASLD. Hepatocyte-specific deletion of Arhgdia (the gene encodes RhoGDI) was generated in mice, and they subjected to NASH diets to induce hepatic steatosis. Transcriptomic sequencing was carried out to identify altered pathways in the Arhgdia-deficient mice, followed by functional investigations of downstream signaling and mitochondrial performance. Finally, the therapeutic potential of a candidate compound was evaluated in the MASLD model. The expression level of RhoGDI was significantly upregulated, and hepatocyte-specific deletion of Arhgdia (the gene encodes RhoGDI) attenuated hepatic lipid accumulation and fibrotic progression. The RNA sequencing analysis revealed that RhoGDI deficiency suppressed the hepatic steroid hormone biosynthesis pathway. It was demonstrated that RhoGDI plays a crucial role in maintaining mitochondrial function, since hepatocyte-specific knockout of Arhgdia significantly reversed mitochondrial dysfunction in mice. Furthermore, a natural compound was found to alleviate hepatic steatosis and inflammation in MASLD mice by targeting RhoGDI. This finding demonstrates that Arhgdia deletion confers protection against the progression of MASLD by reducing hepatic lipid accumulation and enhances mitochondrial β-oxidation in hepatocytes establishing RhoGDI as a critical regulator of MASLD pathogenesis and highlighting its potential as a therapeutic target for metabolic liver diseases. - Source: PubMed
Publication date: 2026/01/23
Wang YongzhiZhou YuanqiXu YifanWang ChenMeng ShuoLi HonglinTang HuifangZhang Jian - Rhesus macaques (Macaca mulatta) are the most common non-human primates living in captivity. The use of rhesus macaques as model objects is determined, first of all, by their phylogenetic and physiological closeness to humans, and, as a consequence, the possibility of extrapolating the obtained results to humans. Currently, it is known that a number of biochemical changes occur under various physiological conditions, including at the transcriptomic level. The real-time polymerase chain reaction is a widely used universal method for gene expression analysis. Carrying out such studies always requires a preliminary selection of "housekeeping genes" (HKGs) - genes necessary for the implementation of basic functions in the cell and stably expressed in different cell types and under different conditions. At present, there are only two systematic studies on the search for HKGs in the rhesus macaque brain, and therefore in this work a search and systematization of HKGs for this species were carried out. As a result, two panels of promising HKGs for M. mulatta were formed: an extended panel, consisting of 56 genes, and a small panel, consisting of 8 genes: ARHGDIA, CYB5R1, NDUFA7, RRAGA, TTC1, UBA6, VPS72, and YWHAH. Both panels of potential HKGs do not have pseudogenes in macaques or humans, are characterized by stable and sufficient expression in the brain of rhesus macaques and can be used to analyze expression not only in the brain but also in peripheral blood. However, it should be noted that the data have not been experimentally verified and require verification in laboratory conditions. - Source: PubMed
Shulskaya M VAlieva A KhKumakov I RShadrina M ISlominsky P A - Demethylase fat mass and obesity-related protein (FTO), which belongs to the AlkB homologous (ABH) family, is associated with various neurological diseases, cancer, and obesity. This protein, which contains many structurally and functionally different regions, contains a COOH-terminal domain whose function, unlike other ABH members, is not fully understood. This study aimed to investigate the effects of the exonic V493F mutation in this region of FTO on the soluble proteome. - Source: PubMed
Kanli Aylin - The RhoA (Ras homolog family member A) signaling pathway is pivotal in regulating vascular smooth muscle cells (VSMCs) function and blood pressure homeostasis. Current inhibitors of the RhoA signaling pathway are limited in hypertension treatment, suffering from poor efficacy, insufficient specificity, and developmental challenges. - Source: PubMed
Publication date: 2025/06/16
Wang JiawenYuan ZhenYu NaJiao QianZhou HongleiLiao WenjieShan JiweiRuan ShanshanZhao YiMo YaQi LuyaoLi TiejunFu JianjunKe BowenXu YufangQian XuhongZhang JianZhao ZhenjiangLi ShiliangWang RuiLi Honglin - Genetic testing in nephrotic syndrome may identify heterozygous predicted-pathogenic variants (HPPVs) in autosomal recessive (AR) genes that are known to cause disease in the homozygous or compound heterozygous state. In such cases, it can be difficult to define the variant's true significance and questions remain about whether a second pathogenic variant has been missed during analysis or whether the variant is an incidental finding. There are now known to be over 70 genes associated with nephrotic syndrome, the majority inherited as an AR trait. Knowledge of whether such HPPVs occur with equal frequency in patients compared to the general population would assist interpretation of their significance. Exome sequencing was performed on 187 Steroid-Resistant Nephrotic Syndrome (SRNS) paediatric patients recruited to a UK rare disease registry plus originating from clinics at Evelina, London. 59 AR podocytopathy linked genes were analysed in each patient and a list of HPPVs created. We compared the frequency of detected HPPVs with a 'control' population from the gnomAD database containing exome data from approximately 50,000 individuals. A bespoke filtering process was used for both patients and controls to predict 'likely pathogenicity' of variants. In total 130 Caucasian SRNS patients were screened across 59 AR genes and 201 rare heterozygous variants were identified. 17/201 (8.5%) were assigned as 'likely pathogenic' (HPPV) using our bespoke filtering method. Comparing each gene in turn, for SRNS patients with a confirmed genetic diagnosis, in 57 of the 59 genes we found no statistically significant difference in the frequency of these HPPVs between patients and controls (In genes ARHGDIA and TP53RK, we identified a significantly higher number of HPPVs in the control population compared with the patients when filtering was performed with 'high stringency' settings only). In the SRNS patients without a genetics diagnosis confirmed, there was no statistically significant difference identified in any gene between patient and control. In children with SRNS, we propose that identification of HPPV in AR podocytopathy linked genes is not necessarily representative of pathogenicity, given that the frequency is similar to that seen in controls for the majority. Whilst this may not exclude the presence of genetic kidney disease, this type of heterozygous variant is unlikely to be causal and each result must be interpreted in its clinical context. - Source: PubMed
Publication date: 2024/08/10
Platt C JBierzynska ADing WSaleem S AKoziell ASaleem M A