Relevant bibliographies by topics / Stanniocalcina-2

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Academic literature on the topic 'Stanniocalcina-2'

Author: Grafiati
Published: 4 June 2021
Last updated: 5 February 2022

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Journal articles on the topic "Stanniocalcina-2"

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Luo, Ching-Wei, Margareta D. Pisarska, and Aaron J. W. Hsueh. "Identification of a Stanniocalcin Paralog, Stanniocalcin-2, in Fish and the Paracrine Actions of Stanniocalcin-2 in the Mammalian Ovary." Endocrinology 146, no. 1 (January 1, 2005): 469–76. http://dx.doi.org/10.1210/en.2004-1197.

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Chang, A. C. M., and Roger R. Reddel. "Identification of a second stanniocalcin cDNA in mouse and human: Stanniocalcin 2." Molecular and Cellular Endocrinology 141, no. 1-2 (June 1998): 95–99. http://dx.doi.org/10.1016/s0303-7207(98)00097-5.

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Gagliardi, Anthony D., Evan Y. W. Kuo, Sanda Raulic, Graham F. Wagner, and Gabriel E. DiMattia. "Human stanniocalcin-2 exhibits potent growth-suppressive properties in transgenic mice independently of growth hormone and IGFs." American Journal of Physiology-Endocrinology and Metabolism 288, no. 1 (January 2005): E92—E105. http://dx.doi.org/10.1152/ajpendo.00268.2004.

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Stanniocalcin (STC)-2 was discovered by its primary amino acid sequence identity to the hormone STC-1. The function of STC-2 has not been examined; thus we generated two lines of transgenic mice overexpressing human (h)STC-2 to gain insight into its potential functions through identification of overt phenotypes. Analysis of mouse Stc2 gene expression indicates that, unlike Stc1, it is not highly expressed during development but exhibits overlapping expression with Stc1 in adult mice, with heart and skeletal muscle exhibiting highest steady-state levels of Stc2 mRNA. Constitutive overexpression of hSTC-2 resulted in pre- and postnatal growth restriction as early as embryonic day 12.5, progressing such that mature hSTC-2-transgenic mice are ∼45% smaller than wild-type littermates. hSTC-2 overexpression is sometimes lethal; we observed 26–34% neonatal morbidity without obvious dysmorphology. hSTC-2-induced growth retardation is associated with developmental delay, most notably cranial suture formation. Organ allometry studies show that hSTC-2-induced dwarfism is associated with testicular organomegaly and a significant reduction in skeletal muscle mass likely contributing to the dwarf phenotype. hSTC-2-transgenic mice are also hyperphagic, but this does not result in obesity. Serum Ca2+ and PO4 were unchanged in hSTC-2-transgenic mice, although STC-1 can regulate intra- and extracellular Ca2+ in mammals. Interestingly, severe growth retardation induced by hSTC-2 is not associated with a decrease in GH or IGF expression. Consequently, similar to STC-1, STC-2 can act as a potent growth inhibitor and reduce intramembranous and endochondral bone development and skeletal muscle growth, implying that these tissues are specific physiological targets of stanniocalcins.
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Steffensen, Lasse B., Cheryl A. Conover, Martin M. Bjørklund, Thomas Ledet, Jacob F. Bentzon, and Claus Oxvig. "Stanniocalcin-2 overexpression reduces atherosclerosis in hypercholesterolemic mice." Atherosclerosis 248 (May 2016): 36–43. http://dx.doi.org/10.1016/j.atherosclerosis.2016.02.026.

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Sarapio, Elaine, Samir K. De Souza, Jorge F. A. Model, Marcia Trapp, and Roselis S. M. Da Silva. "Stanniocalcin-1 and -2 effects on glucose and lipid metabolism in white adipose tissue from fed and fasted rats." Canadian Journal of Physiology and Pharmacology 97, no. 10 (October 2019): 916–23. http://dx.doi.org/10.1139/cjpp-2019-0023.

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Stanniocalcin-1 and -2 belong to a family of molecules that exhibit both paracrine and autocrine effects in mammalian cells. Human stanniocalcin-1 (hSTC-1) is expressed in a wide range of tissues, including white adipose tissue. In fed rats, hSTC-1 increases carbon flux from glucose to lipids in retroperitoneal white adipose tissue. Human stanniocalcin-2 (hSTC-2) is expressed in almost all tissues and regulates various biological processes. The aim of this work was to study the action of hSTC-1 and hSTC-2 in the lipid and glucose metabolism of epididymal white adipose tissue (eWAT) in rats in different nutritional states. This study shows for the first time an opposite effect of hSTC-1 and hSTC-2 on glyceride-glycerol generation from glucose in eWAT of fed rats. hSTC-1 stimulated the storage of triacylglycerol in eWAT in the postprandial period, increasing glucose uptake and glyceride-glycerol generation from 14C-glucose. hSTC-2 decreased triacylglycerol synthesis, reducing glyceride-glycerol generation from 14C-glucose, direct phosphorylation of glycerol, and fatty acid synthesis from 14C-glucose in eWAT of fed rats. However, both hormones increased glucose uptake in fed and fasting states. These findings provide evidence for a direct role of hSTC-1 and hSTC-2 in the regulation of lipid and glucose metabolism in eWAT of rats.
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Zhou, Juan, Yinghua Li, Lina Yang, Yougen Wu, Yunjiao Zhou, Yunqing Cui, Gong Yang, and Yang Hong. "Stanniocalcin 2 improved osteoblast differentiation via phosphorylation of ERK." Molecular Medicine Reports 14, no. 6 (November 16, 2016): 5653–59. http://dx.doi.org/10.3892/mmr.2016.5951.

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ZHANG, ZHEN-HAI, YA-GUANG WU, CHENG-KUN QIN, ZHONG-HOU RONG, ZHONG-XUE SU, and GUO-ZHE XIAN. "Stanniocalcin 2 expression predicts poor prognosis of hepatocellular carcinoma." Oncology Letters 8, no. 5 (September 10, 2014): 2160–64. http://dx.doi.org/10.3892/ol.2014.2520.

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Zhou, Han, Ying-Ying Li, Wei-Qiang Zhang, Dan Lin, Wei-Ming Zhang, and Wei-Da Dong. "Expression of Stanniocalcin-1 and Stanniocalcin-2 in Laryngeal Squamous Cell Carcinoma and Correlations with Clinical and Pathological Parameters." PLoS ONE 9, no. 4 (April 17, 2014): e95466. http://dx.doi.org/10.1371/journal.pone.0095466.

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Hu, Lixia, Yanyan Zha, Fanliang Kong, and Yueyin Pan. "Prognostic value of high stanniocalcin 2 expression in solid cancers." Medicine 98, no. 43 (October 2019): e17432. http://dx.doi.org/10.1097/md.0000000000017432.

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Meyer, Hellmuth-A., Angelika Tölle, Monika Jung, Florian R. Fritzsche, Bernard Haendler, Ilka Kristiansen, Ariana Gaspert, Manfred Johannsen, Klaus Jung, and Glen Kristiansen. "Identification of Stanniocalcin 2 as Prognostic Marker in Renal Cell Carcinoma." European Urology 55, no. 3 (March 2009): 669–78. http://dx.doi.org/10.1016/j.eururo.2008.04.001.

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Dissertations / Theses on the topic "Stanniocalcina-2"

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Rossetti, Camila Lüdke. "Ação dos hormônios Stanniocalcina-1 e Stanniocalcina-2 sobre o metabolismo de aminoácidos em ratos." reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2013. http://hdl.handle.net/10183/72425.

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As Stanniocalcinas (STC1 e STC2) são hormônios glicoproteicos originalmente encontrados em peixes teleósteos. Em mamíferos, esses hormônios são expressos em uma variedade de tecidos e estão envolvidos em processos como o transporte de cálcio e fosfato pelos rins e intestino, a carcinogênese, a reprodução e o crescimento. Recentemente, foram encontrados efeitos da STC1 e da STC2 no metabolismo intermediário. Sítios de ligação para a STC1 já foram identificados na membrana mitocondrial e resultados preliminares do nosso laboratório demonstraram que a STC1 possui um efeito inibitório sobre a gliconeogênese renal e tanto a STC1 quanto a STC2 diminuem a incorporação de 14C-glicose em 14CO2 no fígado e no músculo gastrocnêmio, respectivamente, de ratos. No entanto, o papel desses hormônios no metabolismo de aminoácidos permanece desconhecido. No presente trabalho, as ações da STC1 e da STC2 foram avaliadas no fígado e no músculo gastrocnêmio excisados de ratos machos (Rattus norvegicus, n=48 animais) de 300±50g, alimentados ad libitum. Os resultados obtidos mostram que a STC1, no fígado, diminuiu a captação do ácido 2-(metilamino)isobutírico, aumentou a atividade da bomba Na+/K+-ATPase, diminuiu a atividade da enzima malato desidrogenase mitocondrial e estimulou a síntese de glicogênio a partir da alanina. A STC2, no fígado, diminuiu a atividade da enzima malato desidrogenase mitocondrial, estimulou a síntese de proteínas a partir de leucina, e estimulou a síntese de glicogênio a partir de alanina. Já, no músculo, a STC2 estimulou a oxidação de leucina e a incorporação desse aminoácido em proteínas. Esses resultados confirmam a existência de ações das STC1 e STC2 no metabolismo de aminoácidos e sugerem, com exceção da ação da STC2 sobre a enzima malato desidrogenase, um papel anabólico para a STC2 em ambos os tecidos. A mesma afirmação não pode ser feita para a STC1, que apresentou efeitos antagônicos no tecido hepático. Por fim, o trabalho mostrou que as ações da STC1 e da STC2 sobre as vias metabólicas dos aminoácidos ocorrem com a utilização de doses muito baixas desses hormônios.
Stanniocalcins (STC) are glycoprotein hormones that were first discovered in teleostean fishes. In mammals, these hormones are expressed in a variety of tissues. Besides its role on the calcium and phosphate transport by the kidneys and intestine, they are involved in processes such as carcinogenesis, reproduction and growth. Recently it has been shown that STC1 and STC2 affect the control of intermediary metabolism. Binding sites for STC1 have been already identified in the mitochondrial membrane. Preliminary results of our laboratory showed that STC1 has an inhibitory effect on renal gluconeogenesis in rats and both STC1 and STC2 decrease the 14C-glicose incorporation into 14CO2 in the liver and the gastrocnemius muscle, respectively. Despite these evidences that STC1 and STC2 have a role in the control of glucose and lipids metabolism, the function of these hormones in amino acids metabolism remains unknown. In the present study, the STC1 and STC2 actions were evaluated in livers and gastrocnemius muscles excised from male rats (Rattus norvegicus, n=48 animals). The rats weighted 300±50g and were fed ad libitum. The results show that STC1 decreased 2-(metilamine)isobutyric acid uptake, increased Na+/K+-ATPase activity, decreased mitochondrial malate dehydrogenase activity and stimulated glycogen synthesis from alanine. All actions of STC1 were shown in the hepatic tissue and this hormone did not affect any parameter in muscular tissue. In the liver, STC2, decreased the mitochondrial malate dehydrogenase activity, stimulated protein synthesis from leucine and stimulated glycogen synthesis from alanine. In muscle, STC2 stimulated leucine incorporation into CO2 and proteins. These results confirm the regulatory role of STC1 and STC2 on amino acid metabolism in muscle and liver of rats. They suggest, with exception to the STC2 action into the hepatic malate dehydrogenase, an anabolic role for STC2 in both tissues. However this cannot be stated for STC1, which show antagonistic effects in the hepatic tissue. Lastly, another important finding of this study is that STC1 and STC2 actions on amino acid metabolism occur with low hormone concentrations.
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ARAÚJO, Juliana Gusmão De. "Identificação de potenciais biomarcadores No colesteatoma adquirido." Universidade Federal De Pernambuco, 2012. https://repositorio.ufpe.br/handle/123456789/18385.

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Submitted by Irene Nascimento (irene.kessia@ufpe.br) on 2017-03-08T16:58:52Z No. of bitstreams: 2 license_rdf: 1232 bytes, checksum: 66e71c371cc565284e70f40736c94386 (MD5) Juliana Gusmão de Araujo.pdf: 5234646 bytes, checksum: 87f79f1087a57c64407eda5226cb557f (MD5)
Made available in DSpace on 2017-03-08T16:58:52Z (GMT). No. of bitstreams: 2 license_rdf: 1232 bytes, checksum: 66e71c371cc565284e70f40736c94386 (MD5) Juliana Gusmão de Araujo.pdf: 5234646 bytes, checksum: 87f79f1087a57c64407eda5226cb557f (MD5) Previous issue date: 2012-12-26
O colesteatoma adquirido, mesmo com os conhecimentos acumulados desde sua primeira descrição, ainda se mantém como um problema de saúde pública distante de ser solucionado. O entendimento mais profundo da patogênese do colesteatoma é de extrema importância visto que a natureza desta lesão é destrutiva e causadora de complicações potencialmente graves. Apesar das teorias propostas e das várias proteínas terem sido identificados no colesteatoma, a verdadeira etiopatogenia da doença ainda carece de investigações. Objetivo: Identificar biomarcadores do colesteatoma adquirido utilizando a plataforma proteômica. Casuística e Métodos: Foram coletadas amostras de colesteatoma e também fragmento de pele da região retroauricular de 12 indivíduos submetidos a cirurgia para remoção do colesteatoma. As amostras foram armazenadas em solução salina e mantidas a -20ºC até pesagem tecidual e extração das proteínas. Eletroforese bidimensional foi realizada, os géis foram corados com nitrato de prata e suas imagens digitalizadas. Todas as análises foram realizadas em triplicatas. Os peptídeos extraídos após a digestão do spots foram levados à espectrometria de massa e os espectros obtidos foram analisados usando o algoritmo Mascot utilizando os bancos de dados de proteína do NCBI e SwissProt. Resultados: Dos 393 spots identificados na análise do extrato proteico de colesteatoma adquirido, apenas 10 estavam dentro dos parâmetros estatísticos aceitáveis pelo algoritmo Mascot. As principais proteínas detectadas no colesteatoma adquirido foram a cadeia beta do fibrinogênio, proteína da matriz extracelular 2, actina citoplasmática 1, heparan sulfato glucosamina 3-O-sulfotransferase 3A1, fator de necrose tumoral alfa induzido proteína 8-like 1, Stanniocalcina-2, lisofosfolipase eosinofílica e OFUT1.Conclusão: Foram identificadas proteínas envolvidas com a migração celular, regulação da apoptose, vias de sinalização, hiperproliferação celular, cicatrização e processos inflamatórios. Pudemos, desta maneira, traçar um perfil proteômico do colesteatoma adquirido.
The acquired cholesteatoma, even with all the knowledge accumulated since its first description, still remains a public health problem, far from being solved. A deeper understanding of its pathogenesis is extremely important since it is a destructive lesion that might cause potentially serious complications. Several proteins have been identified in cholesteatoma and a few theories were described, however the true etiology of the disease still needs investigation. Objective: Identify acquired cholesteatoma biomarkers using proteomics platform. Patients and methods: Cholesteatoma samples were collected and also a skin fragment of the surgical incision of twelve patients undergoing surgery for cholesteatoma removal. The samples were stored in saline solution and kept at -20 ° C until weighing tissue and proteins extraction. Two-dimensional electrophoresis was conducted, the gels were stained with silver nitrate and their images were digitized. All analyzes were performed in triplicate. The peptides extracted after spots digestion were taken to mass spectrometry and the spectra obtained were analyzed using the Mascot algorithm comparing databases of the NCBI and SwissProt protein. Results: Of the 393 spots identified in the analysis of protein extracts of acquired cholesteatoma, only 10 were within acceptable statistical parameters by Mascot algorithm. The proteins detected in acquired cholesteatoma were fibrinogen beta chain, extracellular matrix protein 2, actin cytoplasmic 1, heparan sulfate glucosamine 3-O-sulfotransferase 3A1, tumor necrosis factor alpha 8 induced proteinlike 1, stanniocalcin-2, eosinophil lysophospholipase and OFUT1. Conclusion: Proteins involved in cell migration, regulation of apoptosis, signaling pathways, cellular proliferation, wound healing and inflammatory processes were identified. We were able to draw a proteomic profile of acquired cholesteatoma.
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Volland, Sonja. "Die Bedeutung von Stanniocalcin 2 im humanen Neuroblastom." Doctoral thesis, 2009. http://hdl.handle.net/11858/00-1735-0000-0006-AD54-E.

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Volland, Sonja Lena [Verfasser]. "Die Bedeutung von Stanniocalcin 2 im humanen Neuroblastom / vorgelegt von Sonja Lena Volland." 2008. http://d-nb.info/995939047/34.

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Conference papers on the topic "Stanniocalcina-2"

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Qie, Shuo, Lifeng Tian, Chenguang Wang, and Nianli Sang. "Abstract LB-135: Stanniocalcin 2 attenuates tumor cell proliferation but suppresses apoptosis in nutrient-deprived conditions." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-lb-135.

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Ohkouchi, Shinya, Masahiko Kanehira, Toshiaki Kikuchi, and Masahito Ebina. "Novel Functions Of Stanniocalcin-1(STC1) Through Uncoupling Protein 2 (UCP2) Up-Regulation; Promoting Survival Of Cancer Cells Under Oxidative Stress And Inducing The Uncoupling Respiration (Warburg Effect)." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a6374.

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Ohkouchi, Shinya, Ahmed M. Katsha, Masahiko Kanehira, Toshiaki Kikuchi, Masahito Ebina, and Toshihiro Nukiwa. "Multipotent Stromal Cell-Derived Stanniocalcin-1 Reduces Reactive Oxygen Species And Promotes Survival Of Injured A549 Lung Cancer Cells Through Upregulation Of Uncoupling-Protein 2 And Induction Of The Warburg Effect." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a4909.

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