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Volumn 19, Issue 6, 2008, Pages 620-621

Lipid metabolism: Sphingolipids- from membrane constituents to signaling molecules that control cell-to-cell communications

Author keywords

[No Author keywords available]

Indexed keywords

CERAMIDE; CYCLOOXYGENASE 2; SPHINGOLIPID; SPHINGOSINE 1 PHOSPHATE;

EID: 56549099592     PISSN: 09579672     EISSN: None     Source Type: Journal    
DOI: 10.1097/MOL.0b013e328316c01a     Document Type: Editorial
Times cited : (3)

References (20)
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    • Gude DR, Alvarez SE, Spiegel S, et al. Apoptosis induces expression of sphingosine kinase 1 to release sphingosine-1-phosphate as a 'come-and-get-me' signal. FASEB J 2008; 22:2629-2638. In this work, the sphingosine kinase inhibitor, N,N-dimethylsphingosine was used in Jurkat cells. This inhibitor promoted apoptosis but unexpectedly induced the expression of SK1 but not of SK2, The resulting S1P secretion attracted monocytes. The augmentation in SK1 levels appears to be a consequence of apoptotic stress because caspase inhibitors efficiently blocked SK1 expression induced by the anticancer drug, doxorubicin. Earlier studies had already indicated that S1P, in response to different apoptotic stimuli, can be secreted by apoptotic Jurkat cells but this was reported to be SK2-dependent. It is, therefore, possible that distinct death stimuli will rely on different sphingosine kinase isoforms to produce and release S1P
    • Gude DR, Alvarez SE, Spiegel S, et al. Apoptosis induces expression of sphingosine kinase 1 to release sphingosine-1-phosphate as a 'come-and-get-me' signal. FASEB J 2008; 22:2629-2638. In this work, the sphingosine kinase inhibitor, N,N-dimethylsphingosine was used in Jurkat cells. This inhibitor promoted apoptosis but unexpectedly induced the expression of SK1 (but not of SK2). The resulting S1P secretion attracted monocytes. The augmentation in SK1 levels appears to be a consequence of apoptotic stress because caspase inhibitors efficiently blocked SK1 expression induced by the anticancer drug, doxorubicin. Earlier studies had already indicated that S1P, in response to different apoptotic stimuli, can be secreted by apoptotic Jurkat cells but this was reported to be SK2-dependent. It is, therefore, possible that distinct death stimuli will rely on different sphingosine kinase isoforms to produce and release S1P.


* 이 정보는 Elsevier사의 SCOPUS DB에서 KISTI가 분석하여 추출한 것입니다.