구강 편평세포암종 세포에서 코발트 이온이 Erk kinase를 활성화시키는
(주)코리아스칼라
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- 2016.04.02
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- 2009.04
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서지정보
ㆍ발행기관 : 대한구강악안면병리학회
ㆍ수록지정보 : 대한구강악안면병리학회지 / 33권 / 2호
ㆍ저자명 : 박정희, 박지은, 정진, 박봉수, 유미현, 박혜련
목차
I. INTRODUCTION
II. MATERIALS AND METHODS
1. Cell culture
2. Reagents
3. Western blot analysis
III. RESULTS
1. Identification of an Akt activator in OSCC cellsunder hypoxic condition induced by CoCl2
2. CoCl2 activates Erk in a Raf kinase-independentmechanism
3. Erk activation by CoCl2 treatment occurs throughEGFR
4. Activities of PTEN and PDK1 is independent onEGFR signaling
IV. DISCUSSION
V. REFERENCES
영어 초록
Tumor cells under hypoxic conditions are often found due to the rapid outgrowth of their vascular supply, and,in order to survive hypoxia, these cells induce numerous signaling factors. Erk is an important kinase in cell survival, and its activity is regulated by Raf kinases through numerous growth factor receptors. The authors investigated Erk activation and Raf/Erk signaling using the hypoxia-mimetic agent, cobalt chloride (CoCl2), in oral squamous cell carcinoma (OSCC) cells. CoCl2 increases Erk phosphorylation in both a dose- and time-dependent manner. In addition, blocking the activation of epidermal growth factor receptor (EGFR) using PD168393 abolished Erk activation in response to CoCl2, suggesting that Erk phosphorylation by CoCl2 is dependent on EGFR.
참고 자료
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