|1.||Inokuchi, Jin-ichi: 4 articles (05/2015 - 07/2006)|
|2.||Igarashi, Yasuyuki: 4 articles (10/2007 - 02/2002)|
|3.||Kabayama, Kazuya: 4 articles (10/2007 - 02/2002)|
|4.||Yamashita, Tadashi: 3 articles (02/2014 - 01/2012)|
|5.||Noguchi, Mariko: 3 articles (10/2007 - 03/2003)|
|6.||Choi, Hee-Jung: 3 articles (04/2007 - 01/2004)|
|7.||Kim, Cheorl-Ho: 3 articles (04/2007 - 01/2004)|
|8.||Saito, Masaki: 3 articles (07/2006 - 02/2002)|
|9.||Uemura, Satoshi: 3 articles (07/2006 - 02/2002)|
|10.||Fujiwara, Michihiro: 2 articles (05/2015 - 02/2012)|
|1.||Polycystic Kidney Diseases (Polycystic Kidney Disease)
04/30/2007 - "Our results demonstrate that induction of GM3 synthase during megakaryocytic differentiation in PMA-stimulated human leukemia K562 cells depends upon the PKC/ERK/CREB pathway."
01/02/2004 - "Involvement of CREB in the transcriptional regulation of the human GM3 synthase (hST3Gal V) gene during megakaryocytoid differentiation of human leukemia K562 cells."
03/01/2005 - "Previous studies have demonstrated that the activity of GM3 synthase and GM3 content are increased during the differentiation of human promyelocytic leukemia HL-60 cells into the monocyte/macrophage lineage after phorbol 12-myristate 13-acetate (PMA) treatment. "
04/30/2007 - "Previously we showed that the human GM3 synthase gene was expressed during the induction of megakaryocytic differentiation in human leukemia K562 cells by phorbol 12-myristate 13-acetate (PMA). "
02/01/1989 - "Effects of inducers of differentiation on protein kinase C and CMP-N-acetylneuraminic acid:lactosylceramide sialyltransferase activities of HL-60 leukemia cells."
|3.||Breast Neoplasms (Breast Cancer)
01/01/2008 - "The findings suggest that GM3 synthase may be of value as a therapeutic target in breast cancer."
01/01/2008 - "Our findings indicate that GM3 synthase silencing suppressed lung metastasis in murine breast cancer cells. "
01/01/2008 - "Silencing of GM3 synthase suppresses lung metastasis of murine breast cancer cells."
01/01/2008 - "Further studies indicated that activation of the phosphoinositide-3 kinase/Akt pathway, and consequently inhibition of nuclear factor of activated T cell (NFAT)1 expression, could be the mechanism underlying the suppression of breast cancer migration/invasion induced by GM3 synthase silencing. "
01/01/2008 - "To investigate the roles of gangliosides in breast tumor development, GM3 synthase was silenced in the highly metastatic 4T1 cells and over-expressed in the non-metastatic 67NR cells. "
05/01/2006 - "To investigate their role in tumor formation and angiogenesis, we sought to develop an inhibitory model targeting human GM3 synthase, an essential enzyme in the ganglioside synthesis pathway, by antisense transfection. "
11/01/2001 - "It was suggested that the marked GM3 accumulation in superficial tumors was caused not only by upregulated GM3 synthase but also by downregulated activities of Gb3 and GD3 synthase. "
04/03/1995 - "Taken together, our results suggest that the human melanoma cells which are able to escape from the primary tumor and invade the lungs have an impaired ganglioside biosynthesis with a deficient GM3 synthase."
11/01/2001 - "The activities of glycosyltransferases responsible for GM3 synthesis (GM3 synthase, Gb3 synthase and GD3 synthase) were consistent with upregulated expression of GM3 in superficial tumors. "
11/25/2011 - "These data suggest a role for gangliosides in regulating tumor cell motility by affecting the function of a signaling complex organized by caveolin-1, responsible for Src inactivation downstream to integrin receptors, and imply that GM3 synthase is a key target for the regulation of cell motility in human ovarian carcinoma."
05/01/2013 - "We show for the first time that GM3 synthase deficiency, responsible for early-onset epilepsy syndrome, leads to a secondary RC dysfunction. "
05/01/2013 - "Refractory epilepsy and mitochondrial dysfunction due to GM3 synthase deficiency."
08/01/2008 - "Infantile-onset symptomatic epilepsy syndrome caused by a homozygous loss-of-function mutation of GM3 synthase. "
10/09/2006 - "Although diseases in the pathway of sphingolipid degradation have been known for decades, the first disease in the biosynthetic pathway was only reported in 2004, when a form of infantile-onset symptomatic epilepsy was described as a genetic defect in GM3 synthase. "
11/01/2004 - "Infantile-onset symptomatic epilepsy syndrome caused by a homozygous loss-of-function mutation of GM3 synthase."
|5.||Complementary DNA (cDNA)
|6.||Messenger RNA (mRNA)
|9.||Tumor Necrosis Factor-alpha (Tumor Necrosis Factor)
|10.||Cytidine Monophosphate (CMP)