RHOA Mouse Monoclonal Antibody
- Known as:
- RHOA Mouse Monoclonal Antibody
- Catalog number:
- APO-000387-M05
- Product Quantity:
- 0.1mg
- Category:
- -
- Supplier:
- Zyagen
- Gene target:
- RHOA Mouse Monoclonal Antibody
Related genes to: RHOA Mouse Monoclonal Antibody
- 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 Mouse Monoclonal Antibody
Related articles to: RHOA Mouse Monoclonal Antibody
- Erlotinib, an epidermal growth factor receptor (EGFR) inhibitor, is widely used in cancer therapy but frequently causes cutaneous adverse effects that suggest impairment of the epidermal barrier. To better understand the underlying mechanisms, we examined how erlotinib affects barrier integrity, with a focus on tight junctions (TJs) and their relation with the actin cytoskeleton. Using human and mouse ex vivo epidermis as well as cultured keratinocytes, we assessed junctional assembly and stability under pharmacological inhibition of EGFR and Src. Erlotinib treatment disrupted the epithelial barrier, as demonstrated by enhanced biotin tracer penetration and a marked reduction in transepithelial electrical resistance. In line with functional impairment, erlotinib reduced EGFR and Src activity disturbing maturation of junctions, as evidenced by discontinuous claudin-1 and ZO-1 localization. Furthermore, erlotinib induced a loss of the apically localized tension-sensitive conformation of α-catenin in the stratum granulosum and in cultured keratinocytes. This was accompanied by disorganization of cortical actin and increased presence of stress fibers, in parallel with elevated activation of RhoA and phosphorylation of MLC2. Inhibition of Src with PP2 led to similar effects on barrier integrity. However, this detrimental outcome could be rescued by EGF treatment. Together, these findings indicate that erlotinib impairs epidermal barrier function by affecting junctional maturation via disrupted α-catenin membrane distribution, and ultimately, TJ stability involving intracellular contraction and tension. Thus, strategies focused on targeting tension‑related mechanisms downstream of EGFR/Src might help prevent or alleviate the cutaneous toxicities associated with EGFR inhibitory therapies. - Source: PubMed
Publication date: 2026/07/13
Imafuku KeisukeGarcia-Ponce AlexanderWaschke Jens - [This corrects the article DOI: 10.1016/j.isci.2023.107292.]. - Source: PubMed
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Ueda YoshihiroHigasa KoichiroKamioka YujiKondo NaoyukiHoritani ShunsukeIkeda YoshikiBergmeier WolfgangFukui YoshinoriKinashi Tatsuo - Hyperuricaemia (HUA) is associated with hypertension, but the mechanisms remain unclear. This study investigated whether the RhoA/ROCK pathway mediates HUA-induced vascular remodeling and hypertension. - Source: PubMed
Publication date: 2026/07/11
Zhang YanWang ZhongchaoXu YinliWang NanXu ZihuaRen TianshuZhao QingchunMeng Weihong - Neuroinflammation in the trigeminal nucleus caudalis (TNC) plays an important role in the pathological process of chronic migraine (CM). The Paeoniae Radix Alba (Baishao, BS)-Chuanxiong Rhizoma (Chuanxiong, CX) herb pair (BSCX) is widely used in the treatment of migraine, but its mechanism of action and representative candidate constituents remain unclear. - Source: PubMed
Publication date: 2026/07/10
Liu LirongFeng MenghanLiu JieCai ShengnanCong ShiyuXu YifanLi YuetingGao JialeXiao Hongbin - Exercise is widely recommended in oncology; however, its role in orthopedic oncology remains insufficiently defined within a clinical context where tumor biology, skeletal fragility, muscle loss, systemic therapy, and reconstructive biomechanics converge. Existing rehabilitation frameworks primarily emphasize functional recovery, while the biological integration between mechanical loading and tumor-host systems remains incompletely characterized in clinical decision-making contexts. This narrative review synthesizes mechanistic evidence across tumor mechanobiology and its integration with bone-muscle endocrine crosstalk, marrow niche regulation, immunometabolism, and vascular-metabolic adaptation. Key pathways, including integrin-FAK/Src signaling, RhoA/ROCK dynamics, YAP/TAZ and β-catenin transcriptional regulation, Piezo-mediated mechanosensing, and load-sensitive RANKL/OPG balance, are examined within hybrid movement strategies that integrate aerobic, resistance, neuromotor, isometric, eccentric, and blood flow-restricted modalities. Emerging evidence indicates that mechanical stimuli may be associated with coordinated changes in extracellular matrix organization, perfusion dynamics, and immune cell trafficking, with secondary effects on mitochondrial function and marrow adiposity. These effects appear to remain context-dependent, with implications for fracture risk, cachexia, neuropathy, and treatment tolerance. However, the boundary between adaptive remodeling and pro-invasive signaling remains incompletely defined, supporting a threshold-dependent rather than linear dose-response relationship. Accordingly, this review proposes a safety-calibrated, phase-sensitive framework for translational movement dosing in orthopedic oncology. Future research should prioritize biomarker-driven clinical trials and temporally resolved dosing strategies to clarify how structured movement may support musculoskeletal integrity while remaining aligned with oncologic treatment constraints. - Source: PubMed
Publication date: 2026/06/13
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