AAG11, DRAL, FHL-2, SLIM-3, SLIM3, Four and a half LIM domains protein 2, LIM domain protein DRAL, Skeletal muscle LIM-protein 3, FHL2, RNA Binding Motif Protein 18, RNA-Binding Motif Protein 18, RBM18.
AAG11, DRAL, FHL-2, SLIM-3, SLIM3, Four and a half LIM domains protein 2, LIM domain protein DRAL, Skeletal muscle LIM-protein 3, FHL2, RNA Binding Motif Protein 18, RNA-Binding Motif Protein 18, RBM18.
FHL2 antibody was purified from mouse ascitic fluids by protein-A affinity chromatography.
PAT21D11AT.
Anti-human FHL2 mAb, is derived from hybridization of mouse F0 myeloma cells with spleen cells from BALB/c mice immunized with a recombinant human FHL2 protein 1-279 amino acids purified from E. coli.
Mouse IgG1 heavy chain and k light chain.
The Four And A Half LIM Domains 2 (FHL2) protein, also known as DRAL (Down-Regulated in Rhabdomyosarcoma LIM Protein), is a member of the LIM-only protein family. This family is characterized by the presence of LIM domains, which are double zinc finger motifs that facilitate protein-protein interactions .
The FHL2 gene is located on chromosome 2 in humans and chromosome 1 in mice . The protein encoded by this gene contains four and a half LIM domains, which are essential for its role in cellular signaling and transcriptional regulation . The LIM domains are highly conserved and are involved in binding zinc atoms, which is crucial for the protein’s structural integrity and function .
FHL2 is predominantly expressed in cardiac and skeletal muscle cells, although it is also found in other tissues at lower levels . The protein plays a significant role in the assembly of extracellular membranes and acts as a molecular transmitter linking various signaling pathways to transcriptional regulation . It negatively regulates the transcriptional repressor E4F1 and inhibits the transcriptional activity of FOXO1, thereby influencing cell growth and apoptosis .
FHL2 has been implicated in several diseases, including familial isolated dilated cardiomyopathy and familial hypertrophic cardiomyopathy . It is also down-regulated during the transformation of normal myoblasts to rhabdomyosarcoma cells, suggesting a potential role in cancer biology . In FHL2-deficient mice, studies have shown that the protein acts as a negative regulator of adrenergic-mediated signaling and cardiac hypertrophy .
The study of FHL2 has significant implications for understanding muscle biology and disease. Mouse models, particularly those involving anti-human FHL2 antibodies, are crucial for investigating the protein’s function and its role in various signaling pathways. These models help in elucidating the mechanisms by which FHL2 contributes to cellular processes and disease development .