|1.||Patti, Gary J: 2 articles (09/2015 - 03/2012)|
|2.||Siuzdak, Gary: 2 articles (09/2015 - 03/2012)|
|3.||Manchester, Marianne: 2 articles (09/2015 - 03/2012)|
|4.||Shriver, Leah P: 2 articles (09/2015 - 03/2012)|
|5.||Qin, Meng-Bin: 2 articles (02/2013 - 12/2012)|
|6.||Tang, Guo-Du: 2 articles (02/2013 - 12/2012)|
|7.||Liu, Shi-Quan: 2 articles (02/2013 - 12/2012)|
|8.||Su, Ying-Jie: 2 articles (02/2013 - 12/2012)|
|9.||Huang, Jie-An: 2 articles (02/2013 - 12/2012)|
|10.||Melendez, Alirio J: 2 articles (03/2008 - 05/2005)|
|1.||Squamous Cell Carcinoma (Epidermoid Carcinoma)
08/25/1991 - "The present studies compare effects of ceramide, sphingosine, and N,N-dimethylsphingosine on epidermal growth factor (EGF) receptor phosphorylation in A431 human epidermoid carcinoma cells. "
04/05/1990 - "Our previous study suggested that N,N-dimethylsphingosine, but not unsubstituted sphingosine, could be a modulator of protein kinase C in epidermoid carcinoma A431 cells, since N,N-dimethyl-D-erythrosphingenine showed a stronger stereospecific effect on protein kinase C activity in comparison with N,N-dimethyl-L-erythrosphingenine, unsubstituted D- or L-erythrosphingenine, and gangliosides (Igarashi, Y., Hakomori, S., Toyokuni, T., Dean, B., Fujita, S., Sugimoto, M., Ogawa, T., El-Ghendy, K., and Racker, E. "
|2.||Stomach Neoplasms (Stomach Cancer)
02/01/2012 - "To study the effect of the sphingosine kinase 1 (SphK1) inhibitor N,N-dimethylsphingosine (DMS) in combination with chemotherapeutic drugs (DDP, 5-Fu, MMC) on the proliferation of gastric cancer cells (SGC7901) in vitro, and to evaluate whether SphK1 inhibitors could be used as synergetic agents in chemotherapy. "
|3.||Colonic Neoplasms (Colon Cancer)
01/01/2008 - "N, N-dimethyl-D-erythro-sphingosine increases intracellular Ca2+ concentration via Na+-Ca2+-exchanger in HCT116 human colon cancer cells."
05/01/2013 - "Human colon cancer LoVo cells were divided into three groups: phorbol 12-myristate 13-acetate (PMA) was used to induce the activation of SphK1 in the PMA group, N,N-dimethylsphingosine (DMS) used to suppress the activity of SphK1 in DMS group, and the cells treated with equal amount of 0.9 % NaCl instead of drugs served as the control group. "
12/01/2012 - "SphK1 plasmid or SphK1 shRNA transfection and N,N-dimethylsphingosine (DMS) was used to regulate the expression and activity of SphK1 in colon cancer line LOVO. "
02/01/2013 - "In addition, N,N-dimethylsphingosine (DMS), SphK1 DNA and shRNA transfection were used to regulate the expression and activity of SphK1 in the LOVO colon cancer cell line. "
|4.||Neuralgia (Stump Neuralgia)
09/01/2015 - "Recently, metabolomics revealed that the concentration of the endogenous metabolite N,N-dimethylsphingosine (DMS) is increased in the spinal cord in a model of neuropathic pain. "
10/24/2014 - "We previously showed that an increased level of the endogenous metabolite N,N-dimethylsphingosine (DMS) in the central nervous system (CNS) is sufficient to induce neuropathic pain-like behavior in rats. "
03/01/2012 - "We show by using untargeted metabolomics that sphingomyelin-ceramide metabolism is altered in the dorsal horn of rats with neuropathic pain and that the upregulated, endogenous metabolite N,N-dimethylsphingosine induces mechanical hypersensitivity in vivo. "
05/03/1996 - "We report here that Sph and its methylated derivative N,N,-dimethylsphingosine (DMS) are able to induce apoptosis in cancer cells of both hematopoietic and carcinoma origin. "
05/03/1996 - "Sphingosine and its methylated derivative N,N-dimethylsphingosine (DMS) induce apoptosis in a variety of human cancer cell lines."
04/15/1994 - "We demonstrated previously that N,N,N-trimethylsphingosine (TMS) and N,N-dimethylsphingosine (DMS), but not unsubstituted sphingosine, produce significant inhibitory effects on in vivo growth of human tumor cells in nude mice (K. "
01/26/1993 - "N,N-Dimethylsphingosine and N,N,N-trimethylsphingosine, which inhibit the metastatic potential of human and murine tumor cells, were weak activators of PLC delta 1. It is postulated that HPC is more effective as an antineoplastic agent than lysophospholipids because HPC is metabolized slowly, while the lysophospholipids are metabolized rapidly in vivo."
|3.||Epidermal Growth Factor Receptor (EGF Receptor)
|4.||Protein Kinase C
|6.||Epidermal Growth Factor (EGF)
|8.||Small Interfering RNA (siRNA)
|1.||Drug Therapy (Chemotherapy)