The gene ras-related C3 botulinum toxin substrate 1 (RAC1), with 7 exons spanning 29 kb, is mapped to human chromosome 7p22. The encoded protein belongs to the Rho family of small GTPases. RAC1 is a maternal factor expressed in decidual cells.
Immunogen
The antiserum was produced against synthesized peptide derived from human Rac1/CDC42.
Immunogen Range: 38-87
Biochem/physiol Actions
Ras-related C3 botulinum toxin substrate 1 (RAC1), expressed in decidua, modulates uterine secretions that helps in maternal-fetal communication crucial for placental development and establishment of pregnancy. RAC1 regulates the secretory activity of human endometrial stromal cells during decidualization. Members of rho family of small GTPases, including RAC1, is associated with signal transduction pathways that regulate proliferation, adhesion, and migration of cells during embryonic development and invasiveness of tumor cells. RAC1 acts as a regulator of nuclear factor-κB (NF-κB) signaling pathway, and it is also associated with inflammation.Hindrance of RAC1 expression in lens epithelial cells can be a potential method for the treatment of cataract. Elevated expression of RAC1 promotes the proliferation, migration, and invasion of lens epithelial cells, and regulates the epithelial-mesenchymal transition (EMT) process, thus, RAC1 is associated with cataract. RAC1 functions as an oncogene in tumor cells. Deletion of RAC1 retards cell migration and wound healing of epidermal keratinocytes.
Features and Benefits
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Physical form
Rabbit IgG in phosphate buffered saline (without Mg2+ and Ca2+), pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol.
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Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.
International journal of molecular sciences, 21(16) (2020-08-23)
Increased platelet activation and apoptosis are characteristic of diabetic (DM) platelets, where a Parkin-dependent mitophagy serves a major endogenous protective role. We now demonstrate that Parkin is highly expressed in both healthy platelets and diabetic platelets, compared to other mitochondria-enriched
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