Cystin, a novel cilia-associated protein, is disrupted in the cpk mouse model of polycystic kidney disease
J. Clin. Invest. Xiaoying Hou, et al. 109:533 doi:10.1172/JCI14099 [Go to this article.]

Figure 3
Expression pattern of the cpk transcript and characterization of the predicted protein product. (a) The tissue distribution of the 2.2-kb cpk transcript is shown in adult mouse tissues. The size of the polyadenylated transcript is consistent with the 1,856-bp full-length cDNA. The size markers are indicated on the left and expressed as kilobases. (b) Northern blot analysis of mouse fetal poly(A⁺) RNA revealed a 2.2-kb transcript in the fetal kidney. (c) Northern blot analysis of human fetal poly(A⁺) RNA revealed a 2.4-kb transcript in the fetal kidney. (d) The relative expression of the 2.2-kb cpk transcript is shown in kidney and liver poly(A⁺) RNA from 2-week-old B6-WT (n = 5 mice) and B6-cpk/cpk (n = 5 mice) (top panel). Rehybridization with Gapdh cDNA served as a loading control (middle panel). RT-PCR was performed using the deletion-flanking primer pairs on the same poly(A⁺) RNAs (bottom panel). (e) Amino acid sequence of the predicted 145-AA protein product. Two potential myristoylation sites (residues 2–7, 43–48, indicated by asterisks) are predicted, the first of which is coupled to a polybasic domain (underlined).