|1.||Higashi, Hideyoshi: 2 articles (05/2012 - 02/2011)|
|2.||Watanabe, Shun: 2 articles (05/2012 - 02/2011)|
|3.||Yamamoto, Hiro-aki: 2 articles (06/2003 - 02/2003)|
|4.||Mohanan, Parayanthala V: 2 articles (06/2003 - 02/2003)|
|5.||Saha, S: 2 articles (03/2001 - 12/2000)|
|6.||Mondal, S: 2 articles (03/2001 - 12/2000)|
|7.||Sung, Jung-Suk: 1 article (01/2014)|
|8.||Kim, Jung Min: 1 article (01/2014)|
|9.||Lee, Seung-Hoon: 1 article (01/2014)|
|10.||Chung, Young-Ho: 1 article (01/2014)|
|1.||Lung Neoplasms (Lung Cancer)
01/01/2014 - "In this study, we show that the ganglioside GT1b induces proapoptotic signaling through two uPAR-ERK signaling pathways in A549 lung cancer cells. "
01/01/2014 - "Caveolin-1-dependent and -independent uPAR signaling pathways contribute to ganglioside GT1b induced early apoptosis in A549 lung cancer cells."
|2.||Alzheimer Disease (Alzheimer's Disease)
09/06/2002 - "Ganglioside GT1b was found to support BoNT/A activity significantly more effectively than GD1a, which was far more effective than GM1 when added to ganglioside-deficient murine cholinergic Neuro 2a or to human adrenergic SK-N-SH neuroblastoma cells. "
05/31/2012 - "Involvement of ganglioside GT1b in glutamate release from neuroblastoma cells."
12/01/2010 - "The binding domain end binds to mammalian nerve terminals at neuromuscular junctions, ganglioside GT1b (a target of botulinum toxin), and a variety of neuronal cells including primary chick embryo motor neurons, N2A neuroblastoma cells, NG108-15 cells, but not to NG CR72 cells, which lack complex gangliosides. "
12/01/2000 - "Ehrlich tumor expresses the ganglioside GT1b. "
03/01/2001 - "Suppression of Ehrlich subcutaneous solid tumor growth by immunization with ganglioside GT1b of its origin, its IgM antibody or anti-idiotype antibody."
01/01/1997 - "The experiments reported here make a contribution to the assessment of the nature of this angiogenic modulation, by demonstrating that a) GM3 gangliosides can block the proliferation of endothelium induced by neoplastic cells from human tumors of five different origins; b) this block also occurs when the endothelial cells are preincubated with GM3 and disappears when the cells are returned to a medium poor in GM3; c) in the presence of GM3 the capacity of the endothelial cells to bind to fibronectin and to collagen types I and IV was sharply reduced; d) concentrations of GM3 able to block endothelial cell growth are counteracted by addition to the medium of GT1b ganglioside. "
02/21/2003 - "These seizures were completely abolished by an intracerebroventricular (i.c.v.) injection of ganglioside GT1b (90 nmol/brain), a potent inhibitor of glutamate receptor mediated activation and translocation of protein kinase C and lipid peroxidation, or an i.p. "
02/21/2003 - "The effects of ganglioside GT1b or melatonin on damage to brain mitochondrial DNA (mtDNA) and seizures induced by kainic acid were investigated both in vivo and in vitro. "
02/21/2003 - "Ganglioside GT1B and melatonin inhibit brain mitochondrial DNA damage and seizures induced by kainic acid in mice."
02/21/2003 - "We conclude that the preventive effect of melatonin or ganglioside GT1b against kainic acid-induced mtDNA damage or seizures may be due to its scavenging of reactive oxygen species including the *OH."
06/01/2003 - "Therefore, we concluded that *OH scavengers, such as the pineal hormone melatonin and ganglioside GT1b, can protect against brain mtDNA damage, seizures, and lipid peroxidation induced by reactive oxygen species producers such as L-cysteine."
|2.||asialo GM1 ganglioside
|3.||Immunoglobulin M (IgM)
|4.||Glutamic Acid (Glutamate)
|5.||Glutamate Receptors (Glutamate Receptor)
|6.||Reactive Oxygen Species (Oxygen Radicals)
|9.||Mitochondrial DNA (mtDNA)