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Data on left ventricular expression of STAT3 and AKT in transgenic mouse models with B16F10 melanoma

The dataset describes protein expression of phosphorylated and total signal transducer and activator of transcription 3 (STAT3), protein kinase B (AKT) and suppressor of cytokine signalling 3 (SOCS3) in left ventricular tissue (LV) from healthy and B16F10 melanoma tumour-bearing (B16F10-TM) wildtype...

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Autores principales: Pietzsch, Stefan, Ricke-Hoch, Melanie, Stapel, Britta, Hilfiker-Kleiner, Denise
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Elsevier 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6811954/
https://www.ncbi.nlm.nih.gov/pubmed/31667271
http://dx.doi.org/10.1016/j.dib.2019.104508
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author Pietzsch, Stefan
Ricke-Hoch, Melanie
Stapel, Britta
Hilfiker-Kleiner, Denise
author_facet Pietzsch, Stefan
Ricke-Hoch, Melanie
Stapel, Britta
Hilfiker-Kleiner, Denise
author_sort Pietzsch, Stefan
collection PubMed
description The dataset describes protein expression of phosphorylated and total signal transducer and activator of transcription 3 (STAT3), protein kinase B (AKT) and suppressor of cytokine signalling 3 (SOCS3) in left ventricular tissue (LV) from healthy and B16F10 melanoma tumour-bearing (B16F10-TM) wildtype (WT) mice, mice with cardiomyocyte-specific constitutively active AKT transgene (AKTtg) and mice with cardiomyocyte-restricted deletion of STAT3 (CKO) analysed in Western blot and/or fluorescence microscopy experiments. The data presented in this article are related to the research paper entitled “Modulation of cardiac AKT and STAT3 signalling in preclinical cancer models and their impact on the heart”, available in Biochim. Biophys. Acta Mol. Cell Res. (1).
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spelling pubmed-68119542019-10-30 Data on left ventricular expression of STAT3 and AKT in transgenic mouse models with B16F10 melanoma Pietzsch, Stefan Ricke-Hoch, Melanie Stapel, Britta Hilfiker-Kleiner, Denise Data Brief Biochemistry, Genetics and Molecular Biology The dataset describes protein expression of phosphorylated and total signal transducer and activator of transcription 3 (STAT3), protein kinase B (AKT) and suppressor of cytokine signalling 3 (SOCS3) in left ventricular tissue (LV) from healthy and B16F10 melanoma tumour-bearing (B16F10-TM) wildtype (WT) mice, mice with cardiomyocyte-specific constitutively active AKT transgene (AKTtg) and mice with cardiomyocyte-restricted deletion of STAT3 (CKO) analysed in Western blot and/or fluorescence microscopy experiments. The data presented in this article are related to the research paper entitled “Modulation of cardiac AKT and STAT3 signalling in preclinical cancer models and their impact on the heart”, available in Biochim. Biophys. Acta Mol. Cell Res. (1). Elsevier 2019-09-18 /pmc/articles/PMC6811954/ /pubmed/31667271 http://dx.doi.org/10.1016/j.dib.2019.104508 Text en © 2019 The Author(s) http://creativecommons.org/licenses/by/4.0/ This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).
spellingShingle Biochemistry, Genetics and Molecular Biology
Pietzsch, Stefan
Ricke-Hoch, Melanie
Stapel, Britta
Hilfiker-Kleiner, Denise
Data on left ventricular expression of STAT3 and AKT in transgenic mouse models with B16F10 melanoma
title Data on left ventricular expression of STAT3 and AKT in transgenic mouse models with B16F10 melanoma
title_full Data on left ventricular expression of STAT3 and AKT in transgenic mouse models with B16F10 melanoma
title_fullStr Data on left ventricular expression of STAT3 and AKT in transgenic mouse models with B16F10 melanoma
title_full_unstemmed Data on left ventricular expression of STAT3 and AKT in transgenic mouse models with B16F10 melanoma
title_short Data on left ventricular expression of STAT3 and AKT in transgenic mouse models with B16F10 melanoma
title_sort data on left ventricular expression of stat3 and akt in transgenic mouse models with b16f10 melanoma
topic Biochemistry, Genetics and Molecular Biology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6811954/
https://www.ncbi.nlm.nih.gov/pubmed/31667271
http://dx.doi.org/10.1016/j.dib.2019.104508
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