RAC2 functions as a molecular switch, cycling between an active GTP-bound state and an inactive GDP-bound state. This cycle is tightly regulated by guanine nucleotide exchange factors (GEFs), GTPase-activating proteins (GAPs), and guanine nucleotide dissociation inhibitors (GDIs) . When in its active state, RAC2 interacts with various effector proteins to regulate actin cytoskeleton remodeling, cell adhesion, migration, and other cellular behaviors .
RAC2 is predominantly expressed in immune cells, such as neutrophils, macrophages, and T lymphocytes. It is essential for the proper functioning of these cells, including their ability to migrate to sites of infection, produce reactive oxygen species, and phagocytose pathogens . Mutations in the RAC2 gene can lead to immunodeficiency disorders, highlighting its importance in maintaining immune system integrity .
Research has shown that RAC2 is involved in various pathological conditions, including cancer and immune disorders. For instance, RAC2 overexpression has been linked to the progression of certain cancers, making it a potential target for cancer therapy . Additionally, RAC2 mutations can cause primary immunodeficiency, leading to increased susceptibility to infections .
Mouse anti-human RAC2 antibodies are commonly used in research to study the expression and function of RAC2 in human cells. These antibodies are generated by immunizing mice with human RAC2 protein, leading to the production of specific antibodies that can be harvested and purified. These antibodies are valuable tools for various applications, including Western blotting, immunoprecipitation, and flow cytometry, allowing researchers to investigate RAC2’s role in different cellular contexts.