Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P20020 (adenosine triphosphatase)
 3,299 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To evaluate a possible role of ovarian sex hormones in the Ca2+ responsiveness of cardiac myofilament activation, the relations of pCa (-log Ca2+ molar concentration) to actomyosin adenosine triphosphatase (ATPase) activity of isolated myofibrillar preparations from 8-10 week ovariectomized (Ovx) rat hearts were compared with those from sham-operated hearts. Deficiency of ovarian sex hormones in plasma of ovariectomized rats was indirectly verified by a significant reduction in uterine weights. Body weights of the ovariectomized rats were significantly greater than those of sham-operated controls. Despite a significant increase in heart weight of 10 week ovariectomized animals, the percent of heart weight-to-body weight ratio was not different from control group. The maximum myofibrillar ATPase activity at pH 7.0 was significantly suppressed after ovariectomy in both eight and ten week groups. However, the maximum ATPase activity at pH 6.5 was significantly suppressed only in 10 week ovariectomized hearts. Surprisingly, in every condition with depressed maximum myofibrillar ATPase activity, the pCa-actomyosin ATPase relationships of ovariectomized cardiac myofilaments demonstrated a significant leftward shift in pCa50 (-log half-maximally Ca2+ activation) from those of sham-operated controls. There was, however, no change in the Hill-coefficient of these cardiac myofilaments after ovariectomy. Analysis of myofilament proteins using gel electrophoresis demonstrated neither change nor loss of any thin filament proteins. These results indicate a possible modulating effect of ovarian sex hormone deficiency on the Ca2+ responsiveness of cardiac myofilament activation by induction of myofilament Ca2+ hypersensitivity but suppression of maximum myofibrillar ATPase activity.
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PMID:Increase in calcium responsiveness of cardiac myofilament activation in ovariectomized rats. 974 96

Thyroid hormone exerts its biological effect by binding to a TR. Both liganded and unliganded TRs regulate the transcription of T(3)-responsive genes. Cofactors with activating or repressing function modulate the transcriptional regulation by TRs. We showed that steroid receptor coactivator 1 (SRC-1)-deficient mice (SRC-1(-/-)) exhibit partial resistance to thyroid hormone at the level of the pituitary thyrotrophs. To determine whether SRC-1 deficiency affects globally T(3)-dependent transcriptional regulation, we studied the effects of thyroid hormone deprivation and replacement on the expression of several genes in different tissues of SRC-1(-/-) and wild-type mice (SRC-1(+/+)). Thyroid hormone deficiency was induced by a low iodine diet (LoI) supplemented with propylthiouracil (PTU) for 2 wk. L-T(3) was injected ip for the last 4 d in one group (PTU+T(3) group), and another group (PTU group) received only vehicle. Levels of mRNAs for T(3)-responsive genes were determined by Northern blotting: GH and TSH beta in pituitary; type 1 iodothyronine 5'-deiodinase, spot 14 (S14), and malic enzyme in liver; and sarcoplasmic reticulum calcium adenosine triphosphatase 2 and myosin heavy chain alpha and beta in heart. Serum parameters, TSH, total cholesterol, creatine kinase, and alkaline phosphatase (AP), were also measured. Hypothyroidism produced a comparable increase in TSH beta mRNA in both genotypes, but its suppression by L-T(3) was attenuated in SRC-1(-/-) mice. In contrast, hypothyroidism failed to reduce S14 mRNA levels in SRC-1(-/-) mice. As a consequence, the response to L-T(3) was not observed in these mice. SRC-1 deficiency had no effect on the expression of the rest of the T(3)-responsive genes examined. Of the four serum parameters, the T(3)-mediated decrease in TSH and changes in AP were attenuated in SRC-1(-/-) mice. We conclude that SRC-1 deficiency altered the expression of only some of the T(3)-responsive genes. SRC-1 appears to be involved not only in transcriptional activation by liganded TRs, but also in the suppression by liganded or unliganded TRs. Some of the effects of SRC-1 may be TR isoform specific.
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PMID:Steroid receptor coactivator-1 deficiency causes variable alterations in the modulation of T(3)-regulated transcription of genes in vivo. 1189 91