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B16F10黑色素瘤转基因小鼠模型中STAT3和AKT在左心室表达的数据。

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

作者信息

Pietzsch Stefan, Ricke-Hoch Melanie, Stapel Britta, Hilfiker-Kleiner Denise

机构信息

Department of Cardiology and Angiology, Hannover Medical School, Hannover, Germany.

Department of Psychiatry, Social Psychiatry and Psychotherapy, Hannover Medical School, Hannover, Germany.

出版信息

Data Brief. 2019 Sep 18;26:104508. doi: 10.1016/j.dib.2019.104508. eCollection 2019 Oct.

DOI:10.1016/j.dib.2019.104508
PMID:31667271
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6811954/
Abstract

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).

摘要

该数据集描述了在健康野生型(WT)小鼠、携带B16F10黑色素瘤肿瘤的(B16F10-TM)野生型小鼠、具有心肌细胞特异性组成型活性AKT转基因的小鼠(AKTtg)以及心肌细胞限制性缺失STAT3的小鼠(CKO)的左心室组织(LV)中,磷酸化和总信号转导子及转录激活子3(STAT3)、蛋白激酶B(AKT)和细胞因子信号转导抑制因子3(SOCS3)的蛋白质表达情况,这些是通过蛋白质印迹法和/或荧光显微镜实验进行分析的。本文所呈现的数据与发表在《生物化学与生物物理学报:分子细胞研究》(1)上的题为“临床前癌症模型中心脏AKT和STAT3信号传导的调节及其对心脏的影响”的研究论文相关。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/507f/6811954/b1667767ffc7/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/507f/6811954/280305e9cf31/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/507f/6811954/b1667767ffc7/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/507f/6811954/280305e9cf31/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/507f/6811954/b1667767ffc7/gr2.jpg

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本文引用的文献

1
Modulation of cardiac AKT and STAT3 signalling in preclinical cancer models and their impact on the heart.心脏 AKT 和 STAT3 信号转导在临床前癌症模型中的调节及其对心脏的影响。
Biochim Biophys Acta Mol Cell Res. 2020 Mar;1867(3):118519. doi: 10.1016/j.bbamcr.2019.07.014. Epub 2019 Jul 31.
2
Insulin supplementation attenuates cancer-induced cardiomyopathy and slows tumor disease progression.补充胰岛素可减轻癌症诱发的心肌病,并减缓肿瘤疾病进展。
JCI Insight. 2017 May 18;2(10). doi: 10.1172/jci.insight.93098.
3
Opposing roles of Akt and STAT3 in the protection of the maternal heart from peripartum stress.
Akt 和 STAT3 在保护产妇心脏免受围产期应激中的作用相反。
Cardiovasc Res. 2014 Mar 15;101(4):587-96. doi: 10.1093/cvr/cvu010. Epub 2014 Jan 20.
4
Erythropoietin preserves the endothelial differentiation capacity of cardiac progenitor cells and reduces heart failure during anticancer therapies.促红细胞生成素可保持心脏祖细胞的内皮细胞分化能力,并减少抗癌治疗期间的心力衰竭。
Cell Stem Cell. 2011 Aug 5;9(2):131-43. doi: 10.1016/j.stem.2011.07.001.
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STAT3 and cardiac remodeling.STAT3 与心脏重构。
Heart Fail Rev. 2011 Jan;16(1):35-47. doi: 10.1007/s10741-010-9170-x.
6
Survival pathways in hypertrophy and heart failure: the gp130-STAT axis.肥大与心力衰竭中的生存途径:gp130-STAT轴
Basic Res Cardiol. 2007 Sep;102(5):393-411. doi: 10.1007/s00395-007-0674-z.
7
A cathepsin D-cleaved 16 kDa form of prolactin mediates postpartum cardiomyopathy.组织蛋白酶D切割产生的16 kDa催乳素形式介导产后心肌病。
Cell. 2007 Feb 9;128(3):589-600. doi: 10.1016/j.cell.2006.12.036.
8
Signal transducer and activator of transcription 3 is required for myocardial capillary growth, control of interstitial matrix deposition, and heart protection from ischemic injury.心肌毛细血管生长、间质基质沉积的控制以及心脏免受缺血性损伤需要信号转导和转录激活因子3。
Circ Res. 2004 Jul 23;95(2):187-95. doi: 10.1161/01.RES.0000134921.50377.61. Epub 2004 Jun 10.
9
Akt induces enhanced myocardial contractility and cell size in vivo in transgenic mice.在转基因小鼠体内,Akt可诱导心肌收缩力增强和细胞大小增加。
Proc Natl Acad Sci U S A. 2002 Sep 17;99(19):12333-8. doi: 10.1073/pnas.172376399.
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Signal transducer and activator of transcription 3 in the heart transduces not only a hypertrophic signal but a protective signal against doxorubicin-induced cardiomyopathy.心脏中的信号转导和转录激活因子3不仅能转导肥厚信号,还能转导针对阿霉素诱导的心肌病的保护信号。
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