Aberrant accumulation of PTTG1 induced by a mutated thyroid hormone β receptor inhibits mitotic progression
J. Clin. Invest. Hao Ying, et al. 116:2972 doi:10.1172/JCI28598 [
Go to this article.]
Figure 4Colocalization of PTTG1 with TRβ1 or PV by confocal microscopy. (
A–
P) CV-1 cells (1–1.3 × 10
5) were transfected with expression plasmids F-TRβ1 or F-PV and cultured in the absence (
A–
D and
I–
L) or presence (
E–
H and
M–
P) of T3. Endogenous PTTG1 (
B,
F,
J, and
N; red) and the transfected F-TRβ1 (
A and
E; green) and F-PV (
I and
M; green) were visualized in cells at the interphase by fluorescence microscopy using anti-Flag antibody for F-TRβ1 and F-PV and anti-PTTG1 antibody for endogenous PTTG1.
D,
H,
L, and
P were stained with DAPI. Merged images are shown in
C,
G,
K, and
O. (
Q–
X) Colocalization of the endogenous PTTG1 with F-TRβ1 in FH-TRβ1 cells (
Q–
T) or F-PV in FH-PV cells (
U–
X) in the absence of T3 at the prometaphase/metaphase. Merged images are shown in
T and
X. Magnification, ×160. (
Y) Interaction of PTTG1 with TRβ1 determined by PTTG1-GAL4/UAS reporter system. The Gal4 report system is described in Methods. CV-1 cells were cotransfected with the expression plasmids of PTTG1-GAL4, UAS–luciferase reporter, and TRβ1 or PV (with or without 100 nM T3), and luciferase activity was determined. Data are mean ± SE (
n = 3). Td, T3 deficient.
