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1 skeletal defects resulting from mutations in GDF-5.
2 cells, and may do so by acting downstream of GDF-5.
4 on, comparative in situ localizations of the GDF-5, 6, and 7 mRNAs suggest that these molecules are i
8 ngth and shortened propeptides), BMP-10, and GDF-5 allowed us to conclude that all, except for BMP-2
11 lopmental program of forming joints, we used GDF-5 and Autotaxin (Atx) as joint tissue specific marke
12 een prodomains of BMP-2, -4, -7, and -10 and GDF-5 and fibrillins, raising the possibility that laten
14 he propeptides of BMP-2, -4, -7, and -10 and GDF-5, but not GDF-8, and located the BMP/GDF binding si
15 ifferent stages of development, we show that GDF-5 can increase both the size of the early cartilage
18 -5 controls skeletogenesis, we overexpressed GDF-5 during chick limb development using the retrovirus
20 we found that DAN was able to interact with GDF-5 in a frog embryo assay, suggesting that DAN may re
21 early steps of chondrogenesis, we show that GDF-5 increases chondrogenesis in a dose-dependent manne
22 In contrast, pulse labelling experiments of GDF-5-infected limbs showed that at later stages of skel
24 owever, cell suspension cultures showed that GDF-5 might act at these stages by increasing cell adhes
25 ated with the joint master regulator protein GDF-5 were implanted close to incipient joints in mouse
26 ubfamily, including BMP-2, BMP-4, BMP-7, and GDF-5, with similar kinetics and ligand binding domains
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