Ask about this productRelated genes to: RHOA Blocking Peptide
- Gene:
- RHOA NIH gene
- Name:
- ras homolog family member A
- Previous symbol:
- ARH12, ARHA
- Synonyms:
- RhoA, Rho12, RHOH12
- Chromosome:
- 3p21.31
- Locus Type:
- gene with protein product
- Date approved:
- 1990-03-19
- Date modifiied:
- 2019-04-23
Related products to: RHOA Blocking Peptide
Related articles to: RHOA Blocking Peptide
- The mechano-sensitivity of bone marrow-derived macrophages (BMDMs) is crucial for bone remodeling. In addition to force strength, BMDMs also showed a force-direction-dependent response. However, how anisotropic force regulates the function and differentiation of BMDMs is still under debate. Herein, a single-cell-level force-application system was developed to manipulate cells in a noncontact model based on biospecific magnetic microbeads. By adjusting the magnetic field parameters, the microbeads attached to the cell surface can generate controllable forces with specific directions. BMDMs exhibited differential responses to tensile and compressive forces regarding cell spreading. Surprisingly, although less potent than tensile force, compressive force demonstrated a significant suppressive effect on the osteoclast differentiation of BMDMs. The results suggest that this cellular behavior results from distinct pathways through which BMDMs sense and transduce tensile and compressive forces. BMDMs sense tensile force signals through α5β1 integrin and transduce them via the Rac-pPAK pathway. Compressive force, however, initially activates αvβ3 integrin on BMDMs, leading to signal transduction through the RhoA/ROCK-pMLC signaling axis that regulates BMDM differentiation. Furthermore, both in vitro coculture and in vivo subcutaneous ectopic osteogenesis studies suggest that tensile and compressive forces not only individually regulate the fate specification of BMDMs and BMSCs but also simultaneously mediate the crosstalk between these cell types. These findings provide novel insight into the mechanoresponsive mechanisms of BMDMs, deepening our understanding of mechanically induced bone remodeling. - Source: PubMed
Publication date: 2026/05/20
Xiao LiLi JiaLi QunWu DanCao ShuqinWang YuanYu Leixiao - Quantitative real-time PCR (RT-qPCR) is a powerful method for gene expression analysis, but its accuracy critically depends on the selection of stable reference genes for normalization. In non-model organisms such as sponges (phylum Porifera), this task is complicated with high biological variability, seasonal fluctuations, and limited molecular resources. In this study, we first identified and validated candidate reference genes in the calcareous sponge Leucosolenia corallorrhiza. Seven commonly used housekeeping genes (ACT1, GAPDH, RPL13A, HPRT1, RPS3A, TBP, LMN1) were selected based on available transcriptomic and genomic data, and their expression stability was evaluated using geNorm, NormFinder, BestKeeper, and RefFinder under physiological conditions and during tissue regeneration. RPL13A, ACT1, and GAPDH were identified as the most stable reference genes in L. corallorrhiza. To assess whether reference genes identified in L. corallorrhiza can be applied more broadly, we extended the analysis to three phylogenetically and ecologically distinct sponge species: Halisarca dujardinii (marine demosponge), Ephydatia fluviatilis (freshwater demosponge), and Lycopodina hypogea (carnivorous marine demosponge). The same panel of candidate genes was evaluated in all species using the same analytical approaches. Although similar subsets of genes (including RPL13A, ACT1, and GAPDH) consistently ranked among the most stable candidates, no single gene exhibited universal stability across all species. Pairwise variation analysis indicated that the use of two reference genes is sufficient for accurate normalization, while the geometric mean of three top-ranked genes further improves reproducibility and reduces the risk of false-positive results, as demonstrated performing RHOA normalization. Overall, our results demonstrate that reference gene stability in sponges is species-specific and cannot be reliably predicted based on ecological or phylogenetic grouping alone. At the same time, we define a robust panel of candidate reference genes that can serve as a starting point for RT-qPCR studies in Porifera, provided that species- and condition-specific validation is performed. Our study also highlights that technical challenges inherent to research on non-model organisms must be carefully considered in the design of future studies. - Source: PubMed
Publication date: 2026/05/20
Skorentseva Kseniia VMelnikov Nikolai PEreskovsky Alexander VLavrov Andrey ISaidova Aleena A - Microtubules are dynamic cytoskeletal filaments that have important organizing roles in all eukaryotic cells. Early studies on the effect of pH on microtubule stability focused on microtubules isolated from whole cell lysates, which can only replicate changes in intracellular pH. However, how extracellular pH can affect microtubule dynamics remains unclear. Here, we report that acidosis activates β1 integrin by increasing its affinity for RGD-containing ligands through the displacement of divalent ions in the metal-ion-binding sites of β1 integrin extracellular domain via protonation of Asp138. This induces the activation of RhoA and its downstream effector ROCK, which, via phosphorylation of Collapsin Response Mediator Protein-2 (CRMP-2), negatively regulates microtubules stability and changes the positioning and architecture of the Golgi apparatus. Thereby, extracellular pH modulates microtubule dynamics, which could have important consequences for intracellular organization, cell polarization, vesicular trafficking, nucleocytoplasmic shuttling, and cell division. There are multiple processes in human physiology associated with acidosis. The presented mechanochemical mechanism that links low extracellular pH and microtubule stability may serve as a blueprint for advancing our knowledge of cellular transport and exploring potential targets for drug development. - Source: PubMed
Publication date: 2026/05/20
Lachowski DariuszCortes ErnestoMykuliak VasylFernandez-de la Torre MiguelBastida Urkiza AnderMuñoz-Barrutia ArrateGarcia-Gonzalez DanielHytönen VesaDel Rio Hernandez Armando - Exosomes, as key mediators of intercellular communication, play a central regulatory role in cellular physiological and pathological processes through their dynamic interaction with the cytoskeleton. The cytoskeleton is a dynamic network composed of microtubules, microfilaments, and intermediate filaments. Microtubules provide track support for the directional transport of MVBs. Microfilament rearrangement generates contractile forces that promote MVB fusion with the plasma membrane. Therefore, the cytoskeleton directly participates in the biogenesis, intracellular transport, and secretion of exosomes. Moreover, cytoskeletal dynamics, coordinated by molecules such as Rab GTPases, affect exosome secretion efficiency. Conversely, exosomes carry bioactive molecules such as proteins, nucleic acids, and lipids. These molecules can regulate cytoskeletal rearrangement in recipient cells by modulating signaling pathways like the TGF-β/Smad signaling pathway and the RhoA/ROCK signaling pathway. Consequently, they influence target cell functions like morphology maintenance, migration, and proliferation. Dysregulation of this interaction is closely related to the progression of various diseases, including tumors and neurodegenerative diseases. For instance, disrupting the dynamic structure of the cytoskeleton or blocking the cytoskeletal remodeling process can significantly reduce exosome secretion, while abnormal exosome transfer disrupts cytoskeletal homeostasis. Current research still faces challenges, such as unresolved details of the molecular regulatory network and a lack of in-depth mechanistic validation in in vivo models. Future studies need to explore in depth novel regulatory factors and signaling pathways and investigate disease diagnosis and treatment strategies based on this interaction. This will provide a theoretical basis and innovative ideas for the prevention and treatment of related diseases. - Source: PubMed
Publication date: 2026/05/04
Yang ShiliZhang XinyanChen BoKou HaiyangLai LingyanLiu HuaiquanXu YunlingSun Yu - Estrogen plays pivotal roles in regulating bone formation and mineralization via estrogen receptors. Although the expression of G protein-coupled estrogen receptor-1 (GPER-1) is widespread in eukaryotic cells like bone marrow-derived mesenchymal stem cells (BMSCs), the precise mechanism by which this membrane receptor dictates BMSC differentiation has not been thoroughly established. In this study, we investigated whether GPER-1 regulates BMSC osteogenesis by modulating cytoskeletal dynamics and cellular rigidity via the Ras homolog family member A (RhoA) signaling pathway. Murine BMSCs were treated with the GPER-1 agonist G1, antagonist G15, or GPER-1-targeted siRNA, and changes in cell morphology, F-actin organization, focal adhesion, and stiffness were assessed using confocal and atomic force microscopy. RhoA activity was measured using pull-down assays, and osteogenic differentiation was evaluated based on Alizarin Red S (ARS) staining and osteogenic gene expression. Treatment with G1 significantly suppressed RhoA activation in BMSCs, reduced the thickness of actin filaments and number of focal adhesions, and diminished cellular tension. Importantly, GPER-1 activation reduced mineralization and osteogenic gene expression. Furthermore, treatment with G15 attenuated the inhibitory effects of G1. These findings indicate that GPER-1 negatively regulates the osteogenic differentiation of murine BMSCs by inhibiting RhoA-mediated cytoskeletal remodeling, associated with the RhoA/actin/cell rigidity axis. Collectively, our findings in this study reveal a previously unrecognized regulatory role of GPER-1 in bone biology and identify this receptor as a potential therapeutic target for modulating stem cell differentiation during skeletal regeneration and osteoporosis. - Source: PubMed
Publication date: 2026/05/18
Chou Ya-ShuanChuang Shu-ChunWu Che WeiTsao Yun-YaChen Chung-HwanHo Mei-LingChang Je-Ken