RAC1: Target/Biomarker Introduction, products summarized (antibody/ADC/bispecific/antigen/ORF vector/VLP) and disease/indication/condition/MOA for drug discovery and IVD
It's the GeneMedi's summary page for Target/Biomarker Introduction of RAC1. The page also collects GeneMedi's different modalities and formats products for RAC1 in therapeutics/drug discovery and IVD diagnostics, which is including antibody, ADC, bispecific, antigen, ORF vector, VLP, etc. With GeneMedi's target-insight database-GM ITD database, the RAC1 target is also connected to human indications/diseases/conditions/MOA.
Target sublocation: Introcelluar Protein.
The protein encoded by this gene is a GTPase which belongs to the RAS superfamily of small GTP-binding proteins. Members of this superfamily appear to regulate a diverse array of cellular events, including the control of cell growth, cytoskeletal reorganization, and the activation of protein kinases. Two transcript variants encoding different isoforms have been found for this gene. [provided by RefSeq, Mar 2009]
|Gene Official Name||RAC1|
|Gene Alias||MIG5, MRD48, Rac-1, TC-25, p21-Rac1|
|Protein Sub-location||Introcelluar Protein|
Pre-made anti-RAC1 monoclonal antibody(mab)-benchmark antibody for ELISA, affinity binding assay, drug discovery and mechanism of action (MOA) research.
Pre-made anti-RAC1 monoclonal antibody(mab) is expressed by mammalian cell line as a benchmark antibody for cell culture, ELISA or other affinity binding assay or functional assay development, animal model development, PK/PD model development (Pharmacokinetics & Pharmacodynamic). The anti-RAC1 mab is expressed and produced by mammalian cell line as a benchmark reference therapeutic antibody for biological drug discovery items including cell culture, assay development, animal model development, PK/PD model development (Pharmacokinetics & Pharmacodynamic) and mechanism of action (MOA) research.
|Cat No.||Antibody Name||Format||Classified by tag||Order|
|GM-Tg-hg-T65721-Ab||Anti-RAC1 monoclonal antibody||mab||null|