BID & RHOA Protein Protein Interaction Antibody Pair
- Known as:
- BID & RHOA Protein Protein Interaction Antibody Pair
- Catalog number:
- DI0472
- Product Quantity:
- 1 Set
- Category:
- -
- Supplier:
- Abno
- Gene target:
- BID & RHOA Protein Interaction Antibody Pair
Related genes to: BID & RHOA Protein Protein Interaction Antibody Pair
- 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: BID & RHOA Protein Protein Interaction Antibody Pair
Related articles to: BID & RHOA Protein Protein Interaction Antibody Pair
- Megakaryocytes (MKs) are polyploid cells that maintain bone marrow homeostasis by secreting cytokines, including transforming growth factor β1 (TGFβ1). During neoplastic transformation, MKs accumulate in the bone marrow, promoting fibrotic remodeling that leads to myelofibrosis. However, the therapeutic potential of targeting MK cytokine secretion remains poorly understood. Because unconventional secretion of TGFβ1 and interleukin 1β (IL1β) via secretory autophagy occurs in other cell types, we investigated whether MKs may utilize the same mechanism. Disrupting secretory autophagy, or inhibiting the small GTPase RhoA or its downstream effector Rho-associated kinase (ROCK), markedly reduced TGFβ1 and IL1β secretion in vitro. Conditional deletion of the autophagy gene Atg5 in the hematopoietic system limited megakaryocytosis and aberrant cytokine secretion in an MPL-driven transplant model, while MK-specific deletion of Rhoa protected mice from fibrosis. Ultimately, ROCK inhibition, alone or combined with a JAK2 inhibitor, also attenuated disease hallmarks, identifying the RhoA-secretory autophagy axis as a promising therapeutic target in myelofibrosis. - Source: PubMed
Publication date: 2026/08/13
Becker Isabelle CBranfield SiobhanBarrachina Maria NCamacho VirginiaLykins JoshuaStone Andrew PWalsey EthanBennani MuhammadChua Bernadette ASigner Robert A JMachlus Kellie RWhiteheart Sidney WRoweth Harvey GItaliano Joseph E - Shenqi Yanshen Decoction (SQYSD) is a traditional Chinese herbal formula that is used for treating chronic kidney disorders and kidney-related bone complications in the clinical setting under the traditional concept that "the kidney governs the bone". However, experimental evidence for its coordinated protective effects on renal and skeletal injury in chronic kidney disease-mineral and bone disorder (CKD-MBD) is limited. - Source: PubMed
Publication date: 2026/09/12
Zhang XiaoqiongLi TingLiu JinkunGao HongyanYe JinyinLi YanhuiLi YingChen YiMeng XianliWang Qin - Postmenopausal osteoporosis is driven by estrogen-deficiency-associated uncoupling of bone formation and resorption. This study quantified the independent and interactive effects of Zuogui Pill Yin-nourishing subformulations in an ovariectomized rat model and examined associations with the EphB4/ephrinB2/RhoA/alkaline phosphatase pathway. In accordance with ARRIVE 2.0, 130 specific pathogen-free female Sprague-Dawley rats were randomized to 13 groups (n=10/group), including nine groups in a three-by-three factorial design. Endpoints included P1NP, CTX-1, femoral bone mineral density measured by dual-energy X-ray absorptiometry (DXA), trabecular histology, and messenger ribonucleic acid and protein expression measured by reverse transcription quantitative polymerase chain reaction and Western blotting. The full formula (I2A2) was associated with higher P1NP, lower CTX-1, and higher BMD than the model group. Factorial analysis identified a Yin-Yang interaction between P1NP and BMD, supporting pharmacological synergy. Molecular changes were associated with increased EphB4/ephrinB2/ALP expression and reduced RhoA expression. These findings support an association between Zuogui Pill treatment, improved bone phenotypes, and modulation of pathway markers; causal pathway dependence requires inhibitor, knockdown, and co-culture validation. - Source: PubMed
Publication date: 2026/09/11
Dong ChongyangZhang XueliWang XiongyaoChen JianjunZhang ZengliangGao Xiaoming - Erectile dysfunction (ED) is a multifactorial condition with diverse underlying etiologies, including neurogenic, metabolic, vascular, hormonal, and psychogenic factors. Traditional animal models are often classified by induction technique (e.g., surgical, chemical) rather than by pathophysiological driver, limiting their translational relevance to specific clinical subtypes. This review proposes an etiology-oriented framework for rodent ED models, aiming to categorize models according to clinical causes and to summarize modeling strategies, key molecular mechanisms, and functional assessment methods for each category. - Source: PubMed
Publication date: 2026/08/27
Yin FengChen HongmingTu HongtaiZhong HaoMo YunqiXie TianxiangLai ZhubinyunZou JunrongXiao Rihai - This study investigated estrogen receptor (ER) subtype-specific effects on vascular hyporeactivity in cirrhotic portal hypertension (PHT), focusing on RhoA/ROCK signaling and β-arrestin-2. - Source: PubMed
Publication date: 2026/06/30
Sun Long-CiJi Lin-HuaZhang BinWu Zhi-Yong