Skip to main content
. Author manuscript; available in PMC: 2009 Jan 8.
Published in final edited form as: Biochemistry. 2007 Dec 15;47(1):479–489. doi: 10.1021/bi7013882

Fig 7. Natural expression of ΔS2 PRLRs.

Fig 7

(A) Amplicons resulting from the expression of both intact and ΔS2 PRLR were observed in human LNCaP (LN), DU145 (DU), PC3 (PC) and microvessel human endothelial (Hm) cells and their identities were confirmed by sequencing. (B) Use of form-specific reverse primers demonstrated the presence of a ΔS2 variant of each receptor in all cells, and PC3 cells are illustrated by way of example. Again, the identities of the amplicons were verified by sequencing. Note that different numbers of cycles were required to demonstrate this for each receptor isoform and so the panels cannot be compared in terms of relative abundance (LF and SF1a, 35 cycles; SF1b, 40 cycles). (C) After immunoprecipitation, ΔS2 versions of SF1b are illustrated (closed arrow) as detected by Western blot (using the same anti-ECD antibody) in PC3, LNCaP and T47D (T) cells. Also illustrated is co-migration of immunoprecipitated ΔS2SF1b stably expressed under the control of tetracycline in T47D cells (TΔS2). M, molecular mass markers; IP, immunoprecipitated with control isotype-matched antibody (IgG) or antibody against the extracellular domain (ECD); open arrow marks a LF of the receptor. The vertical line separates samples run on different gels. The sample from normal T47D cells (T) was run on the same gel, but the lane was cut and pasted to be next to the TΔS2 cells to eliminate distracting additional experiments.