Rac2 Activation Assay
- Known as:
- Rac2 Activation Assay
- Catalog number:
- STA-401-2
- Product Quantity:
- 20 assays
- Category:
- Peptides
- Supplier:
- Cell Biolabs
- Gene target:
- Rac2 Activation Assay
Related genes to: Rac2 Activation Assay
- Gene:
- RAC2 NIH gene
- Name:
- Rac family small GTPase 2
- Previous symbol:
- -
- Synonyms:
- EN-7
- Chromosome:
- 22q13.1
- Locus Type:
- gene with protein product
- Date approved:
- 1993-11-05
- Date modifiied:
- 2019-04-23
Related products to: Rac2 Activation Assay
Related articles to: Rac2 Activation Assay
- The phagocyte respiratory burst is an effector mechanism of immunity by which granulocytes, monocytes, and other myeloid cells generate reactive oxygen species (ROS). Inborn errors of core phagocyte NADPH oxidase components (gp91phox, p22phox, p47phox, and p67phox) underlie most cases of chronic granulomatous disease, characterized by severe, recurrent bacterial and fungal infections. An expanding spectrum of inborn errors of immunity (IEIs) has been identified that affect molecules that trigger (IFN-γ, TNF, and their signaling pathways) or control NADPH oxidase assembly and activation (EROS, p40phox, PKCδ, RAC2, and DOCK2), thereby impairing ROS production. Studies of these genetic disorders, which include infection, autoinflammation, and autoimmunity, have identified crucial pathways governing the induction, regulation, assembly, priming, activation, and function of the phagocyte NADPH oxidase complex. We review here the diverse IEIs affecting phagocyte ROS production, highlighting disorders in which ROS generation is absent, reduced, or subset-specific, and the corresponding cellular, immunological, and clinical phenotypes. - Source: PubMed
Publication date: 2026/09/18
Neehus Anna-LenaSankaran Vijay GCasanova Jean-LaurentBustamante Jacinta - Wound repair requires tight control of immune cell behavior, yet the mechanisms that restrain immune-driven wound repair responses remain poorly defined. Here, we demonstrate that rhomboid intramembrane serine protease Rhbdl2 influences wound repair in zebrafish. We generated rhbdl2 mutants using CRISPR-Cas9 and found that, although Rhbdl2 is dispensable for normal development, its loss triggers enhanced wound repair following injury. This regenerative phenotype is accompanied by increased macrophage migration speed and accumulation at the wound site, as well as elevated early apoptosis and cell proliferation. Proteomic analyses reveal increased Rac2 protein levels in rhbdl2 mutants, which was previously identified as a regulator of leukocyte motility. Functionally, Rac2 morpholino-mediated knockdown in rhbdl2 mutant larvae suppresses the elevated macrophage recruitment and enhanced tissue repair phenotype. Together, these findings identify Rhbdl2 as a modulator of macrophage recruitment to the wound site during tissue repair, with implications for inflammatory disease, fibrosis, and tumor-immune interactions. - Source: PubMed
Publication date: 2026/09/11
Gourkanti SarojRamakrishnan GayathriCheung JacquelineSchoen Taylor JMunoz YazminChavez Rosa MDohnálek JanMartin KatieLovett-Barron MatthewWhisenant ThomasStrisovsky KvidoNeal Sonya E - Chronic rhinosinusitis with nasal polyps (CRSwNP) is a chronic inflammatory disease of the upper airway driven by diverse inflammatory cells and mediators. This study aimed to characterize the inflammatory landscape of CRSwNP and to identify and validate oxidative stress-related key genes in CRSwNP. - Source: PubMed
Publication date: 2026/08/26
Gu YuelongTang RuLiu ZhihanZhou JiayaoZhu YingMao SongLi ZhipengZhang WeitianLin Hai - Glioblastoma multiforme (GBM), the most lethal type of primary brain tumor, exhibits profound metabolic plasticity driven by glioma stem cells (GSCs), which sustain therapeutic resistance and tumor recurrence. Here, we elucidate a novel epigenetic-metabolic axis mediated by the histone acetyltransferase KAT7 that orchestrates oxidative phosphorylation (OXPHOS) dominance in GSCs. Through a multi-omics analysis, we demonstrated that KAT7 is preferentially upregulated in GBM, particularly in the classical subtype and in GSC-enriched populations, where it activates Rac family samll GTPase 2 (RAC2) expression via H3K14 acetylation of its promoter. Mechanistically, KAT7-mediated RAC2 upregulation triggers PAK1/2/3 phosphorylation, increasing tricarboxylic acid cycle (TCA) and ATP production. Genetic ablation of KAT7 impairs GSCs self-renewal, induces apoptosis, and suppresses tumor growth in orthotopic xenograft models. Conversely, KAT7 overexpression or pharmacological activation of the KAT7-RAC2 axis restores metabolic fitness and malignant phenotypes. Notably, the small-molecule inhibitor WM-3835, which targets KAT7, exhibits potent anti-GBM efficacy by disrupting H3K14ac and mitochondrial respiration, leading to prolonged survival in mice. Our study identifies KAT7 as a master regulator of GSCs metabolism, revealing an actionable therapeutic target in GBM progression. Targeting the KAT7-RAC2-PAK axis may represent a precise strategy to overcome metabolic plasticity-driven therapeutic resistance in this recalcitrant malignancy. - Source: PubMed
Publication date: 2026/09/08
Liu JilongSun YanfeiZhu YuehuaMu GuangjingWang JiazhengWang LiangliangZhao FeihuZhao ZhiminWang JianHe YingJiang ZhengLi XingangHan MingzhiHuang Bin - In this review, we comprehensively summarize how RAC2+ innate immune cells contribute to a spectrum of immune dysregulation and disease states across multiple organ systems in humans. Our lab has recently identified critical role in immune cell biology in the context of human and murine wound healing and fibrosis, induced by aberrant mechanical signaling. Thus, we sought to investigate the role of RAC2 in human immune cells. Here, we summarize the effects of gain-of-function (GOF), loss-of-function (LOF), and null mutations on neutrophil phenotypes. As such, we propose a novel mechanism for RAC2-dependent biphasic neutrophil migration, critical for these cells in migrating to sites of injury across many disease states, including wound healing and fibrosis. Innate immune cells circulate and home to injury sites during the initial healing phases in all organs, therefore, understanding RAC2 regulation of neutrophil functions may reveal new avenues for systemic immunomodulatory therapies to treat immune dysregulation, and to better characterize mechanisms of wound healing and fibrosis. - Source: PubMed
Publication date: 2026/08/20
Berthiaume Fox Kayleigh AGalvin Emily RGurtner Geoffrey CChen Kellen