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Julie A. Semon Lauren H. Nagy Claire B. Llamas H. Alan Tucker Ryang Hwa Lee Darwin J. Prockop 《Cell and tissue research》2010,340(1):147-158
Estradiol (E2) stimulates not only secretion of prolactin (PRL) and proliferation of PRL-producing cells (PRL cells) in the
anterior pituitary, but also the expression of growth factors. In insulin-like growth factor-I (IGF-I) knockout (KO) mice,
the number of PRL cells is decreased and administration of IGF-I does not increase either the number of PRL cells or plasma
PRL levels, indicating that IGF-I plays a pivotal role in PRL cells. The effect of E2 on PRL cells in KO mice was investigated
by immunohistochemistry and real-time RT-PCR. The number of PRL cells in KO mice was significantly lower than in the wild-type
(WT) control mice. E2 increased the PRL mRNA in WT and KO mice; however, an increase of PRL mRNA in KO was less than that
in WT. In addition, no vasoactive intestinal peptide (VIP)-immunoreactive cells were found in KO mice, therefore IGF-I is
essential for VIP expression. To investigate the roles of IGF-I on PRL cells in the postnatal development, double-immunostaining
with PRL and BrdU was performed in WT and KO mice from days 5–20. The percentages of PRL cells and BrdU-labeled cells in the
anterior pituitary of KO mice were lower than in WT mice. Thus, IGF-I may be responsible for proliferation and differentiation
of PRL cells in this postnatal period. Differentiation and the proliferation of PRL cells are controlled by IGF-I during the
postnatal development, and IGF may be a mediator of E2 action through VIP induction in PRL cells of adults. 相似文献
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SCA8 RAN polySer protein preferentially accumulates in white matter regions and is regulated by eIF3F
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Hannah K Shorrock Tao Zu Monica Banez‐Coronel Tammy Reid Hirokazu Furuya H Brent Clark Juan C Troncoso Christopher A Ross SH Subramony Tetsuo Ashizawa Eric T Wang Anthony T Yachnis Laura PW Ranum 《The EMBO journal》2018,37(19)
Spinocerebellar ataxia type 8 (SCA8) is caused by a bidirectionally transcribed CTG·CAG expansion that results in the in vivo accumulation of CUG RNA foci, an ATG‐initiated polyGln and a polyAla protein expressed by repeat‐associated non‐ATG (RAN) translation. Although RAN proteins have been reported in a growing number of diseases, the mechanisms and role of RAN translation in disease are poorly understood. We report a novel toxic SCA8 polySer protein which accumulates in white matter (WM) regions as aggregates that increase with age and disease severity. WM regions with polySer aggregates show demyelination and axonal degeneration in SCA8 human and mouse brains. Additionally, knockdown of the eukaryotic translation initiation factor eIF3F in cells reduces steady‐state levels of SCA8 polySer and other RAN proteins. Taken together, these data show polySer and WM abnormalities contribute to SCA8 and identify eIF3F as a novel modulator of RAN protein accumulation. 相似文献