GSK3β-ЗАВИСИМОЕ ФОСФОРИЛИРОВАНИЕ РИКТОРА ПО Ser1235 РЕГУЛИРУЕТ КЛЕТОЧНУЮ ПРОЛИФЕРАЦИЮ И ОПУХОЛЕВЫЙ РОСТ

Authors

  • Ч. Х. Чен 1Department of Molecular and Cellular Oncology, University of Texas M. D. Anderson Cancer Center, Houston, TX 77030, USA; 2The University of Texas Graduate School of Biomedical Sciences at Houston, Houston, TX 77030, USA; 3Whitehead Institute for Biomedical Research, Cambridge, MA 02142, USA; 4Howard Hughes Medical Institute, Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02142, USA; 5Кафедра генетики и молекулярной биологии, Казахский национальный университет им. аль-Фараби, Алматы, Казахстан)
  • Т. Ш. Шайкенов 1Department of Molecular and Cellular Oncology, University of Texas M. D. Anderson Cancer Center, Houston, TX 77030, USA; 2The University of Texas Graduate School of Biomedical Sciences at Houston, Houston, TX 77030, USA; 3Whitehead Institute for Biomedical Research, Cambridge, MA 02142, USA; 4Howard Hughes Medical Institute, Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02142, USA; 5Кафедра генетики и молекулярной биологии, Казахский национальный университет им. аль-Фараби, Алматы, Казахстан)
  • Т. Р. Петерсон 1Department of Molecular and Cellular Oncology, University of Texas M. D. Anderson Cancer Center, Houston, TX 77030, USA; 2The University of Texas Graduate School of Biomedical Sciences at Houston, Houston, TX 77030, USA; 3Whitehead Institute for Biomedical Research, Cambridge, MA 02142, USA; 4Howard Hughes Medical Institute, Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02142, USA; 5Кафедра генетики и молекулярной биологии, Казахский национальный университет им. аль-Фараби, Алматы, Казахстан)
  • Р. А. Аимбетов 1Department of Molecular and Cellular Oncology, University of Texas M. D. Anderson Cancer Center, Houston, TX 77030, USA; 2The University of Texas Graduate School of Biomedical Sciences at Houston, Houston, TX 77030, USA; 3Whitehead Institute for Biomedical Research, Cambridge, MA 02142, USA; 4Howard Hughes Medical Institute, Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02142, USA; 5Кафедра генетики и молекулярной биологии, Казахский национальный университет им. аль-Фараби, Алматы, Казахстан)
  • С. В. Ли 1Department of Molecular and Cellular Oncology, University of Texas M. D. Anderson Cancer Center, Houston, TX 77030, USA; 2The University of Texas Graduate School of Biomedical Sciences at Houston, Houston, TX 77030, USA; 3Whitehead Institute for Biomedical Research, Cambridge, MA 02142, USA; 4Howard Hughes Medical Institute, Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02142, USA; 5Кафедра генетики и молекулярной биологии, Казахский национальный университет им. аль-Фараби, Алматы, Казахстан)
  • Ч. В Ву 1Department of Molecular and Cellular Oncology, University of Texas M. D. Anderson Cancer Center, Houston, TX 77030, USA; 2The University of Texas Graduate School of Biomedical Sciences at Houston, Houston, TX 77030, USA; 3Whitehead Institute for Biomedical Research, Cambridge, MA 02142, USA; 4Howard Hughes Medical Institute, Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02142, USA; 5Кафедра генетики и молекулярной биологии, Казахский национальный университет им. аль-Фараби, Алматы, Казахстан)
  • Х. К. Лин 1Department of Molecular and Cellular Oncology, University of Texas M. D. Anderson Cancer Center, Houston, TX 77030, USA; 2The University of Texas Graduate School of Biomedical Sciences at Houston, Houston, TX 77030, USA; 3Whitehead Institute for Biomedical Research, Cambridge, MA 02142, USA; 4Howard Hughes Medical Institute, Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02142, USA; 5Кафедра генетики и молекулярной биологии, Казахский национальный университет им. аль-Фараби, Алматы, Казахстан)
  • А. К. Бисенбаев 1Department of Molecular and Cellular Oncology, University of Texas M. D. Anderson Cancer Center, Houston, TX 77030, USA; 2The University of Texas Graduate School of Biomedical Sciences at Houston, Houston, TX 77030, USA; 3Whitehead Institute for Biomedical Research, Cambridge, MA 02142, USA; 4Howard Hughes Medical Institute, Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02142, USA; 5Кафедра генетики и молекулярной биологии, Казахский национальный университет им. аль-Фараби, Алматы, Казахстан)
  • Д. Д. Сарбасов 1Department of Molecular and Cellular Oncology, University of Texas M. D. Anderson Cancer Center, Houston, TX 77030, USA; 2The University of Texas Graduate School of Biomedical Sciences at Houston, Houston, TX 77030, USA; 3Whitehead Institute for Biomedical Research, Cambridge, MA 02142, USA; 4Howard Hughes Medical Institute, Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02142, USA; 5Кафедра генетики и молекулярной биологии, Казахский национальный университет им. аль-Фараби, Алматы, Казахстан)
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Keywords:

mammalian target of rapamycin complex 2 (mTORC2,

Abstract

Growth factor signaling promotes anabolic processes and stimulates cell growth, proliferation, and survival by activation of the phosphoinositide 3-kinase (PI3K)/Akt pathway. Akt phosphorylation of GSK3β inhibits its enzymatic activity and stimulates glycogen synthesis. GSK3β itself is a negative regulator of Akt that acts by controlling mammalian target of rapamycin complex 2 (mTORC2), one of the activating kinases of Akt. Under stress conditions the mTORC2 component rictor is highly phosphorylated by GSK3β on its Ser-1235 site. This phosphorylation event caused inhibition of the mTORC2 kinase activity. In this paper we show that this phosphorylation site is important for cell proliferation and tumor growth.

References

1 Shaw R.J., Cantley L.C., Ras, PI(3)K and mTOR signalling controls tumour cell growth. Nature 441, 424–430 (2006).

2 Sarbassov D.D., Guertin D.A., Ali S.M., Sabatini D.M. Phosphorylation and regulation of Akt/PKB by the rictor-mTOR complex. Science 307, 1098–1101 (2005).

3 Sarbassov D.D., Guertin D.A., Ali S.M., Sabatini D.M. Phosphorylation and regulation of Akt/PKB by the rictor-mTOR complex. Science 307, 1098–1101 (2005).

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How to Cite

Чен, Ч. Х., Шайкенов, Т. Ш., Петерсон, Т. Р., Аимбетов, Р. А., Ли, С. В., Ву, Ч. В., Лин, Х. К., Бисенбаев, А. К., & Сарбасов, Д. Д. (2015). GSK3β-ЗАВИСИМОЕ ФОСФОРИЛИРОВАНИЕ РИКТОРА ПО Ser1235 РЕГУЛИРУЕТ КЛЕТОЧНУЮ ПРОЛИФЕРАЦИЮ И ОПУХОЛЕВЫЙ РОСТ. Experimental Biology, 49(3), 162–164. Retrieved from https://bb.kaznu.kz/index.php/biology/article/view/519

Issue

Vol. 49 No. 3 (2011): KazNU Bulletin. Biology series

Section

BIOLOGY

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