scholarly journals Cloning and characterization of a complementary DNA for a thyroid hormone-responsive protein in mature rat cerebral tissue

1997 ◽  
Vol 327 (2) ◽  
pp. 617-623 ◽  
Author(s):  
N. Gul SHAH ◽  
Jianping LI ◽  
Patricia SCHNEIDERJOHN ◽  
D. Arshag MOORADIAN
Keyword(s):  
Thyroid Hormone ◽  
Rat Brain ◽  
Molecular Mechanisms ◽  
Sequence Similarity ◽  
Cdna Probe ◽  
Northern Analysis ◽  
Adrenergic System ◽  
Rat Tissues ◽  
Cerebral Tissue ◽  
Western Analysis

A gene responsive to thyroid hormone (TH) has been identified in the adult rat brain cerebral tissue. A cDNA probe differentially expressed in euthyroid, hypothyroid and hyperthyroid rat cerebral tissue, generated by reverse transcriptase-PCR differential display of mRNA, was used to screen the rat brain cDNA library. A 3.4 kb positive clone hybridized in Northern blots with a 3.8 kb mRNA that proved to be TH responsive (THR). The remaining coding sequence and a part of the 5ʹ untranslated region of this cDNA were obtained by 5ʹ rapid amplification of cDNA ends. The deduced amino acid sequence revealed that THR protein (THRP), a 68 kDa moiety, has 83% sequence similarity with c-Abl interactor protein (Abi-2), which is a substrate for tyrosine kinase activity of c-Abl. The extensive similarity between the two proteins suggests a potential role for THRP as a substrate for c-Abl. Northern analysis showed that the expression of THR mRNA in hyperthyroid rats is 6-fold that in euthyroid rats. There is also a 4-6-fold increase in the concentration of THRP, as analysed by Western analysis. Owing to the extensive similarity between rat THRP and human Abi-2, a polyclonal anti- (human Abi-2) antibody was successfully used for Western analysis of proteins from the rat tissues. The observed increase in both the mRNA and the protein did not decline after β-adrenergic system blockade with propranolol, suggesting that the action of TH on the expression of this gene is not mediated through the β-adrenergic system. Immunohistochemical studies revealed that neuronal cells were particularly rich in THRP. Both THR mRNA and THRP are rapidly induced in vivo after intravenous administration of thyroxine. Tissue distribution studies indicated that the cerebral tissue was particularly enriched with THR mRNA and 68 kDa THRP. A cDNA clone for a THR gene could provide a useful tool to study the molecular mechanisms of TH effects on cerebral tissue in adult animals.

Glucose-regulated protein-78 expression in the rat adrenal cortex

1993 ◽  
Vol 10 (1) ◽  
pp. 33-42 ◽  
Author(s):  
J Gregoire ◽  
L M Mertz ◽  
R C Pedersen
Keyword(s):  
Steady State ◽  
Sequence Similarity ◽  
Cdna Probe ◽  
The Other ◽  
Northern Analysis ◽  
Intracellular Accumulation ◽  
Adrenocortical Cells ◽  
Steady State Levels ◽  
Carboxyl Terminal ◽  
Glucose Regulated Protein

ABSTRACT We have postulated that steroidogenesis activator polypeptide (SAP) is a product of glucose-regulated protein-78 (grp78) proteolysis on the basis of a number of considerations, including a striking sequence similarity between the carboxyl-terminal region of grp78 and SAP. Since ACTH stimulates the rapid intracellular accumulation of SAP, experiments were conducted to determine whether ACTH might also regulate levels of grp78 mRNA and/or protein. Using a grp78 cDNA probe, Northern analysis of total RNA isolated from hypophysectomized or dexamethasone-suppressed rats revealed that neither treatment had a measurable influence on steady-state levels of grp78 mRNA over a 4-day period. Moreover, immunoblotting with an antiserum directed against a shared grp78/SAP sequence failed to detect a significant change in the grp78 content of adrenal homogenates from dexamethasone-suppressed rats as compared with untreated controls. On the other hand, grp78 in cultured rat adrenocortical cells fell to 50% of that in time-zero controls after 72 h in the absence of ACTH, whereas inclusion of ACTH in the medium blocked this decline. We conclude that while adrenocortical grp78 may be under some measure of trophic ACTH control, the rapid fluctuations reported for SAP are not likely to be driven by large changes in the size of the grp78 pool.

Molecular mechanisms of sex-dependent thyroid hormone action on target tissues

2014 ◽  
Vol 122 (03) ◽  
Author(s):  
H Rakov ◽  
K Engels ◽  
D Zwanziger ◽  
M Renders ◽  
K Brix ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Molecular Mechanisms ◽  
Hormone Action ◽  
Thyroid Hormone Action

scholarly journals Thyroid hormone up-regulates NGFI-A gene expression in rat brain during development.

1992 ◽  
Vol 267 (1) ◽  
pp. 21-23
Author(s):  
C Pipaon ◽  
A Santos ◽  
A Perez-Castillo
Keyword(s):  
Gene Expression ◽  
Thyroid Hormone ◽  
Rat Brain

scholarly journals Plant Morphological, Physiological and Anatomical Adaption to Flooding Stress and the Underlying Molecular Mechanisms

2021 ◽  
Vol 22 (3) ◽  
pp. 1088
Author(s):  
Weitao Jia ◽  
Maohua Ma ◽  
Jilong Chen ◽  
Shengjun Wu
Keyword(s):  
Molecular Mechanisms ◽  
Sequence Similarity ◽  
Survival Strategies ◽  
Ethylene Response Factor ◽  
Flooding Tolerance ◽  
Plant Tolerance ◽  
Flooding Stress ◽  
Crop Varieties ◽  
The Future ◽  
Plant Acclimation

Globally, flooding is a major threat causing substantial yield decline of cereal crops, and is expected to be even more serious in many parts of the world due to climatic anomaly in the future. Understanding the mechanisms of plants coping with unanticipated flooding will be crucial for developing new flooding-tolerance crop varieties. Here we describe survival strategies of plants adaptation to flooding stress at the morphological, physiological and anatomical scale systemically, such as the formation of adventitious roots (ARs), aerenchyma and radial O2 loss (ROL) barriers. Then molecular mechanisms underlying the adaptive strategies are summarized, and more than thirty identified functional genes or proteins associated with flooding-tolerance are searched out and expounded. Moreover, we elaborated the regulatory roles of phytohormones in plant against flooding stress, especially ethylene and its relevant transcription factors from the group VII Ethylene Response Factor (ERF-VII) family. ERF-VIIs of main crops and several reported ERF-VIIs involving plant tolerance to flooding stress were collected and analyzed according to sequence similarity, which can provide references for screening flooding-tolerant genes more precisely. Finally, the potential research directions in the future were summarized and discussed. Through this review, we aim to provide references for the studies of plant acclimation to flooding stress and breeding new flooding-resistant crops in the future.

scholarly journals Polychlorinated biphenyls (PCBs) exert thyroid hormone-like effects in the fetal rat brain but do not bind to thyroid hormone receptors.

2004 ◽  
Vol 112 (5) ◽  
pp. 516-523 ◽  
Author(s):  
Kelly J Gauger ◽  
Yoshihisa Kato ◽  
Koichi Haraguchi ◽  
Hans-Joachim Lehmler ◽  
Larry W Robertson ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Polychlorinated Biphenyls ◽  
Rat Brain ◽  
Hormone Receptors ◽  
Thyroid Hormone Receptors ◽  
Fetal Rat ◽  
Fetal Rat Brain

Immunocytochemical Localization of Thyroid Hormone Receptors in the Adult Rat Brain

Thyroid ◽  
1991 ◽  
Vol 1 (2) ◽  
pp. 173-184 ◽  
Author(s):  
J. PUYMIRAT ◽  
M. MIEHE ◽  
R. MARCHAND ◽  
L. SARLIEVE ◽  
J.H. DUSSAULT
Keyword(s):  
Thyroid Hormone ◽  
Rat Brain ◽  
Hormone Receptors ◽  
Thyroid Hormone Receptors ◽  
Immunocytochemical Localization ◽  
Adult Rat ◽  
Adult Rat Brain

Thyroid hormones regulate phosphate homoeostasis through transcriptional control of the renal type IIa sodium-dependent phosphate co-transporter (Npt2a) gene

2010 ◽  
Vol 427 (1) ◽  
pp. 161-169 ◽  
Author(s):  
Mariko Ishiguro ◽  
Hironori Yamamoto ◽  
Masashi Masuda ◽  
Mina Kozai ◽  
Yuichiro Takei ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Hormones ◽  
Molecular Mechanisms ◽  
Hormone Receptors ◽  
Critical Role ◽  
Serum Phosphate ◽  
Luciferase Assay ◽  
Mobility Shift ◽  
Intron 1 ◽  
Sodium Dependent

The type IIa renal sodium-dependent phosphate (Na/Pi) co-transporter Npt2a is implicated in the control of serum phosphate levels. It has been demonstrated previously that renal Npt2a protein and its mRNA expression are both up-regulated by the thyroid hormone T3 (3,3′,5-tri-iodothyronine) in rats. However, it has never been established whether the induction was mediated by a direct effect of thyroid hormones on the Npt2a promoter. To address the role of Npt2a in T3-dependent regulation of phosphate homoeostasis and to identify the molecular mechanisms by which thyroid hormones modulate Npt2a gene expression, mice were rendered pharmacologically hypo- and hyper-thyroid. Hypothyroid mice showed low levels of serum phosphate and a marked decrease in renal Npt2a protein abundance. Importantly, we also showed that Npt2a-deficient mice had impaired serum phosphate responsiveness to T3 compared with wild-type mice. Promoter analysis with a luciferase assay revealed that the transcriptional activity of a reporter gene containing the Npt2a promoter and intron 1 was dependent upon TRs (thyroid hormone receptors) and specifically increased by T3 in renal cells. Deletion analysis and EMSAs (electrophoretic mobility-shift assays) determined that there were unique TREs (thyroid-hormone-responsive elements) within intron 1 of the Npt2a gene. These results suggest that Npt2a plays a critical role as a T3-target gene, to control phosphate homoeostasis, and that T3 transcriptionally activates the Npt2a gene via TRs in a renal cell-specific manner.

Thyroid hormone specifically regulates skeletal muscle Na(+)-K(+)-ATPase alpha 2- and beta 2-isoforms

1993 ◽  
Vol 265 (3) ◽  
pp. C680-C687 ◽  
Author(s):  
K. K. Azuma ◽  
C. B. Hensley ◽  
M. J. Tang ◽  
A. A. McDonough
Keyword(s):  
Skeletal Muscle ◽  
Thyroid Hormone ◽  
State Level ◽  
Mrna Abundance ◽  
Northern Analysis ◽  
Protein Abundance ◽  
Constant Amount ◽  
Protein Levels ◽  
Subunit Expression ◽  
Beta 2

The purpose of this study was to determine the pattern of thyroid hormone (triiodothyronine, T3) regulation of the Na(+)-K(+)-adenosinetriphosphatase (Na(+)-K(+)-ATPase) alpha- and beta-subunit expression in skeletal muscle, which expresses alpha 1-, alpha 2-, beta 1-, and beta 2-subunits, and compare it with that seen in kidney, which expresses only alpha 1 and beta 1. Three steady states were studied: hypothyroid, euthyroid, and hyperthyroid (hypothyroids injected daily with 1 microgram T3/g body wt for 2-16 days). Protein and mRNA abundance, determined by Western and Northern analysis, were normalized to a constant amount of homogenate protein and total RNA, respectively. In skeletal muscle, there was no change in alpha 1- or beta 1-mRNA or protein levels in the transition from hypothyroid to hyperthyroid. However, alpha 2 was highly regulated; mRNA reached a new steady-state level of fivefold over hypothyroid by 8 days of T3 treatment and protein abundance increased threefold. In addition, beta 2-mRNA and protein were detected in skeletal muscle and were also highly regulated by T3; beta 2-mRNA increased nearly fourfold over hypothyroid level, and beta 2-protein abundance increased over twofold. In kidney in the transition from hypothyroid to hyperthyroid, there were coordinate 1.6-fold increases in both alpha 1- and beta 1-mRNA abundance that predicted the observed changes in alpha 1- and beta 1-protein levels and Na(+)-K(+)-ATPase activity.(ABSTRACT TRUNCATED AT 250 WORDS)

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