A mutation in a CD44 variant of inflammatory cells enhances the mitogenic interaction of FGF with its receptor
J. Clin. Invest. Shlomo Nedvetzki, et al. 111:1211 doi:10.1172/JCI17100 [Go to this article.]

Figure 1
Schematic diagram of the CD44 molecule and the trinculeotide CAG insertion in the CD44v3-v10 sequence of RA patients. A schematic of the CD44 genomic map is shown at the top of the figure. The black squares represent the constant exons (designated C1, C2, etc.) at the two ends of the molecule. The white squares represent the variant exons (designated v2, v3, etc.) subjected to alternative splicing. Differential use of the variant exons generates the different CD44 isoforms, e.g., use of exons v3 to v10 in tandem forms the CD44v3-v10. Note that exon v1 is not included in human CD44. The gap between exon v4 and exon v5 indicates the insertion site of CAG, the extra trinucleotide detected in the CD44 variant of synovial fluid cells (CD44vRA), isolated using RT-PCR from cells removed from the joints of RA patients. Arrows mark the positions and directions of Ex1 sense and Ex20 antisense primers (for sequence, see Methods) used in the above-mentioned RT-PCR. Magnification of the CAG insertion site is shown at the bottom of the figure, indicating the nucleotide sequence at the 3′ end of exon v4 and the 5′ end of exon v5 and its alignment with the published sequence (shown in the boxes) in the same region (29). The drawing in the middle of the figure illustrates the single chain of CD44 proteoglycan, emphasizing the position of the variable region. The HS associated with exon v3 marks the attachment site of a heparan sulfate moiety, the GAG chain that binds to FGF-2 in the CD44 variant.