The Experts below are selected from a list of 291 Experts worldwide ranked by ideXlab platform
James L Sherley - One of the best experts on this subject based on the ideXlab platform.
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inosine 5 monophosphate dehydrogenase is a rate determining factor for p53 dependent Growth Regulation
Molecular Biology of the Cell, 1998Co-Authors: Shirley A Bohn, James L SherleyAbstract:We have proposed that reduced activity of inosine-5′-monophosphate dehydrogenase (IMPD; IMP:NAD oxidoreductase, EC 1.2.1.14), the rate-limiting enzyme for guanine nucleotide biosynthesis, in response to wild-type p53 expression, is essential for p53-dependent Growth suppression. A gene transfer strategy was used to demonstrate that under physiological conditions constitutive IMPD expression prevents p53-dependent Growth suppression. In these studies, expression of bax and waf1, genes implicated in p53-dependent Growth suppression in response to DNA damage, remains elevated in response to p53. These findings indicate that under physiological conditions IMPD is a rate-determining factor for p53-dependent Growth Regulation. In addition, they suggest that the impd gene may be epistatic to bax and waf1 in Growth suppression. Because of the role of IMPD in the production and balance of GTP and ATP, essential nucleotides for signal transduction, these results suggest that p53 controls cell division signals by regulating purine ribonucleotide metabolism.
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Inosine-5*-Monophosphate Dehydrogenase Is a Rate- determining Factor for p53-dependent Growth Regulation
Molecular biology of the cell, 1998Co-Authors: Yuan Liu, Shirley A Bohn, James L SherleyAbstract:We have proposed that reduced activity of inosine-5'-monophosphate dehydrogenase (IMPD; IMP:NAD oxidoreductase, EC 1.2.1.14), the rate-limiting enzyme for guanine nucleotide biosynthesis, in response to wild-type p53 expression, is essential for p53-dependent Growth suppression. A gene transfer strategy was used to demonstrate that under physiological conditions constitutive IMPD expression prevents p53-dependent Growth suppression. In these studies, expression of bax and waf1, genes implicated in p53-dependent Growth suppression in response to DNA damage, remains elevated in response to p53. These findings indicate that under physiological conditions IMPD is a rate-determining factor for p53-dependent Growth Regulation. In addition, they suggest that the impd gene may be epistatic to bax and waf1 in Growth suppression. Because of the role of IMPD in the production and balance of GTP and ATP, essential nucleotides for signal transduction, these results suggest that p53 controls cell division signals by regulating purine ribonucleotide metabolism.
Shirley A Bohn - One of the best experts on this subject based on the ideXlab platform.
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inosine 5 monophosphate dehydrogenase is a rate determining factor for p53 dependent Growth Regulation
Molecular Biology of the Cell, 1998Co-Authors: Shirley A Bohn, James L SherleyAbstract:We have proposed that reduced activity of inosine-5′-monophosphate dehydrogenase (IMPD; IMP:NAD oxidoreductase, EC 1.2.1.14), the rate-limiting enzyme for guanine nucleotide biosynthesis, in response to wild-type p53 expression, is essential for p53-dependent Growth suppression. A gene transfer strategy was used to demonstrate that under physiological conditions constitutive IMPD expression prevents p53-dependent Growth suppression. In these studies, expression of bax and waf1, genes implicated in p53-dependent Growth suppression in response to DNA damage, remains elevated in response to p53. These findings indicate that under physiological conditions IMPD is a rate-determining factor for p53-dependent Growth Regulation. In addition, they suggest that the impd gene may be epistatic to bax and waf1 in Growth suppression. Because of the role of IMPD in the production and balance of GTP and ATP, essential nucleotides for signal transduction, these results suggest that p53 controls cell division signals by regulating purine ribonucleotide metabolism.
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Inosine-5*-Monophosphate Dehydrogenase Is a Rate- determining Factor for p53-dependent Growth Regulation
Molecular biology of the cell, 1998Co-Authors: Yuan Liu, Shirley A Bohn, James L SherleyAbstract:We have proposed that reduced activity of inosine-5'-monophosphate dehydrogenase (IMPD; IMP:NAD oxidoreductase, EC 1.2.1.14), the rate-limiting enzyme for guanine nucleotide biosynthesis, in response to wild-type p53 expression, is essential for p53-dependent Growth suppression. A gene transfer strategy was used to demonstrate that under physiological conditions constitutive IMPD expression prevents p53-dependent Growth suppression. In these studies, expression of bax and waf1, genes implicated in p53-dependent Growth suppression in response to DNA damage, remains elevated in response to p53. These findings indicate that under physiological conditions IMPD is a rate-determining factor for p53-dependent Growth Regulation. In addition, they suggest that the impd gene may be epistatic to bax and waf1 in Growth suppression. Because of the role of IMPD in the production and balance of GTP and ATP, essential nucleotides for signal transduction, these results suggest that p53 controls cell division signals by regulating purine ribonucleotide metabolism.
Tania Weber Furlanetto - One of the best experts on this subject based on the ideXlab platform.
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role of estrogen in thyroid function and Growth Regulation
Journal of Thyroid Research, 2011Co-Authors: Ana Paula Santin, Tania Weber FurlanettoAbstract:Thyroid diseases are more prevalent in women, particularly between puberty and menopause. It is wellknown that estrogen (E) has indirect effects on the thyroid economy. Direct effects of this steroid hormone on thyroid cells have been described more recently; so, the aim of the present paper was to review the evidences of these effects on thyroid function and Growth Regulation, and its mechanisms. The expression and ratios of the two E receptors, α and β, that mediate the genomic effects of E on normal and abnormal thyroid tissue were also reviewed, as well as nongenomic, distinct molecular pathways. Several evidences support the hypothesis that E has a direct role in thyroid follicular cells; understanding its influence on the Growth and function of the thyroid in normal and abnormal conditions can potentially provide new targets for the treatment of thyroid diseases.
Mario A. Pisarev - One of the best experts on this subject based on the ideXlab platform.
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Thyroid Function and Growth Regulation under Normal and Abnormal Conditions.
Journal of thyroid research, 2011Co-Authors: Guillermo Juvenal, Daniel Christophe, Pierre P. Roger, Mario A. PisarevAbstract:The thyroid gland exerts a major control on the physiology of the whole body, and it raises fundamental questions about molecular physiological processes. Moreover, an increased proliferation of thyroid cells is associated with several pathologies, and several mechanisms may be involved. Thyroid disorders are very common, affecting millions of people. These include hypothyroidism, hyperthyroidism, thyroid nodules, thyroid cancer, and so forth, but they are also associated with other nonthyroid disorders. This special issue is devoted to illustrate the particular richness of current investigations in the field of thyroid function and Growth Regulation under normal and abnormal conditions. Although thyroid gland function is mainly under the control of pituitary TSH in normal conditions, other factors may also play a role in this process. Thyroid disease is more common in women than in men. Tania Weber Furlanetto and Ana Paula Santin reviewed the direct effects of estrogens on thyroid function and Growth Regulation in the paper titled “Role of estrogen in thyroid function and Growth Regulation.” Thyroid cancer is the most common endocrine malignancy, and its incidence has significantly risen in the last decades in the world. The knowledge how thyroid cancer develops is expanding rapidly. The sequential acquisition of mutations which arise as a consequence of damage to the genome is required in order to transform a normal cell into a malignant one. The understanding of the process of thyroid carcinogenesis at the molecular level will improve not only the diagnostic but also the treatment of this pathology. Ioannis Legakis and Konstantinos Syrigos describe the molecular events associated with the progression and dedifferentiation of thyroid carcinoma in the paper titled “Recent advances in molecular diagnosis of thyroid cancer.” Thyroid-specific transcription factors regulate thyroid-specific gene expression and organogenesis. Their possible role in thyroid cancer as well as in the maintenance and/or activity of stem cells is discussed by Shioko Kimura in the paper titled “Thyroid-specific transcription factors and their roles in thyroid cancer.” MicroRNAs (miRNAs) are short ribonucleic acid molecules (around 22 nucleotides) found in eukaryotic cells. miRNAs are posttranscriptional regulators that bind to complementary sequences on messenger RNA transcripts inducing the translational repression or messenger RNA degradation. Several miRNAs have been found to have links with some types of cancer. Francesca Marini, Ettore Luzi, and Maria Luisa Brandi reviewed the role of miRNAs in thyroid cancer development in the paper titled “MicroRNA role in thyroid cancer development.” Growth factors play a role in thyroid proliferation and function, while EGF acts as a mitogen for thyroid cells inhibiting also thyroid differentiation. TGF-β is a potent inhibitor of thyroid cell Growth. However, in some transformed thyroid cells this inhibition is lost. The role of TGF-β and EGF on thyroid carcinogenesis and the crosstalk between these Growth factors are discussed by Gabriella Mincione Maria Carmela Di Marcantonio, Chiara Tarantelli, Sonia D'Inzeo, Arianna Nicolussi, Francesco Nardi, Caterina Francesca Donini, and Anna Coppa in the paper titled “EGF and TGF-β1 effects on thyroid function.” Grave's disease and Hashimoto's thyroiditis are the two main types of autoimmune thyroid disease. Occasionally they are also associated with other autoimmune diseases. Emina Kasumagic-Halilovic, Asja Prohic, Begler Begovic, and Nermina Ovcina-Kurtovic bring additional support to the existence of a significant association between vitiligo and thyroid autoimmunity in the paper titled “Association between vitiligo and thyroid autoimmunity.” Although some authors have found an association between an abnormal thyroid condition and bipolar disorder, little is known about the implication of the hypothalamo-pituitary-thyroid in neuropsychological deficits. Subho Chakrabarti review the last findings on this topic including genetic and neuroimaging investigations (Thyroid Functions and Bipolar Affective Disorder). Guillermo Juvenal Daniel Christophe Pierre Roger Mario Pisarev
Kazuhiko Takehara - One of the best experts on this subject based on the ideXlab platform.
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Growth Regulation of skin fibroblasts.
Journal of Dermatological Science, 2000Co-Authors: Kazuhiko TakeharaAbstract:Abstract The Growth of skin fibroblasts is regulated in a complex manner by various Growth factors. Representative Growth factors are platelet-derived Growth factor (PDGF), basic fibroblast Growth factor (b-FGF), transforming Growth factor-β (TGF-β), and connective tissue Growth factor (CTGF). These Growth factors have various biological activities besides Growth Regulation of skin fibroblasts, and are involved in wound healing and in the pathogenesis of various disorders. For example, PDGF and CTGF stimulate chemotaxis of skin fibroblasts, b-FGF stimulates angiogenesis, and TGF-β stimulates production of matrix proteins. First, the properties of these Growth factors are reviewed briefly. Our skin fibrosis model in newborn mice are also described here. In 1986, Roberts et al. reported that subcutaneous injection of TGF-β in newborn mice caused granulation tissue formation followed by fibrosis (Roberts et al. Proc Natl Acad Sci USA 1986;83:4167–71). We conducted similar experiments, and found that TGF-β1, β2 or β3 caused skin fibrosis after 3 consecutive days of injection; this change was transient and disappeared after 7 consecutive days of injection. In contrast, irreversible fibrosis was observed upon stimultaneous injection of TGF-β and b-FGF or TGF-β and CTGF, or TGF-β injection for the first 3 days and b-FGF or CTGF injection for the next 4 days (Shinozaki et al. Biochem Biophys Res Commun 1997;237:292–7; Mori et al. J Cell Physiol 1999;181:153–9). These observations suggest that TGF-β induces skin fibrosis and b-FGF or CTGF maintains it in various skin fibrotic disorders. In the 21st century, we speculate that cocktails of various Growth factors may permit subtle Growth Regulation of skin fibroblasts; such technology would have applications in the treatment of many skin diseases.
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Growth Regulation of skin fibroblasts.
Journal of dermatological science, 2000Co-Authors: Kazuhiko TakeharaAbstract:The Growth of skin fibroblasts is regulated in a complex manner by various Growth factors. Representative Growth factors are platelet-derived Growth factor (PDGF), basic fibroblast Growth factor (b-FGF), transforming Growth factor-beta (TGF-beta), and connective tissue Growth factor (CTGF). These Growth factors have various biological activities besides Growth Regulation of skin fibroblasts, and are involved in wound healing and in the pathogenesis of various disorders. For example, PDGF and CTGF stimulate chemotaxis of skin fibroblasts, b-FGF stimulates angiogenesis, and TGF-beta stimulates production of matrix proteins. First, the properties of these Growth factors are reviewed briefly. Our skin fibrosis model in newborn mice are also described here. In 1986, Roberts et al. reported that subcutaneous injection of TGF-beta in newborn mice caused granulation tissue formation followed by fibrosis (Roberts et al. Proc Natl Acad Sci USA 1986;83:4167-71). We conducted similar experiments, and found that TGF-beta1, beta2 or beta3 caused skin fibrosis after 3 consecutive days of injection; this change was transient and disappeared after 7 consecutive days of injection. In contrast, irreversible fibrosis was observed upon stimultaneous injection of TGF-beta and b-FGF or TGF-beta and CTGF, or TGF-beta injection for the first 3 days and b-FGF or CTGF injection for the next 4 days (Shinozaki et al. Biochem Biophys Res Commun 1997;237:292-7; Mori et al. J Cell Physiol 1999;181:153-9). These observations suggest that TGF-beta induces skin fibrosis and b-FGF or CTGF maintains it in various skin fibrotic disorders. In the 21st century, we speculate that cocktails of various Growth factors may permit subtle Growth Regulation of skin fibroblasts; such technology would have applications in the treatment of many skin diseases.
