Publication: Localization and functions of steroid hormone receptors
Authors
Yamashita, S.
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Publisher
Murcia : F. Hernández
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DOI
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info:eu-repo/semantics/article
Description
Abstract
This review focuses on the subcellular
localization of steroid hormone receptors (SHRs), taking
into account the technical problems of immunohistochemistry
and the characteristics of nuclear localization
signals (NLSs) of each receptor, on the interaction
between SHKs and cellular components, and on the
possible roles of sex SHRs in the reproductive organs. It
is concluded that SHRs are basically localized in the
nucleus, regardless of hormonal status, and that
considerable amounts of unliganded SHRs may be
present in the cytoplasm of target cells in exceptional
cases. Most immunohistochemical results that
demonstrate nuclear translocation of liganded SHRs
seem to be responsible for insufficient fixation.
Immunoelectron microscopy shows that SHRs associate
with the chromatin in absence or presence of hormones
and that intranuclear translocation of liganded SHRs
from the condensed chromatin to euchromatin which
observed in some cell types, may be a passive process
caused by a consequence of conformational changes in
the chromatin binding receptors. Histochemical data
suggest that the nuclear matrix (NM) is not a main
binding site of liganded SHRs in the nucleus. The
artificial formation of intermolecular disulfide bonds
during NM preparation presumably causes the
entrapment of liganded SHRs into the fraction. It seems
that heat shock protein 90 (hsp90) does not form stable
complexes with unliganded receptors in vivo, and it
interacts with SHRs transiently cooperating with other
heat shock proteins as a chaperone that helps folding of newly synthesized and refolding of denatured receptors.
Estrogens transiently induce a number of nuclear
protooncogenes, such as c-fos and c-jun family proteins,
which act as transcription factors through estrogen
receptor (ER) system in the endometrial epithelium of
mature and immature rodents. Therefore, it is suggested
that the changes in concentrations of these gene products
trigger the proliferation and differentiation of uterine
epithelium. In addition, ER system, not only in stroma
cells but in the epithelia1 cells appears to participate in
the growth response and abnormalities of epithelium
elicited by the exogenous estrogen treatment at the neonatal period.
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