|1.||Bergo, Martin O: 6 articles (02/2013 - 05/2007)|
|2.||Young, Stephen G: 5 articles (02/2013 - 05/2007)|
|3.||Karlsson, Christin: 4 articles (02/2013 - 05/2007)|
|4.||Kwon, Ohyun: 3 articles (01/2015 - 05/2009)|
|5.||Lu, Jie: 3 articles (01/2015 - 05/2009)|
|6.||Tamanoi, Fuyuhiko: 3 articles (01/2015 - 05/2009)|
|7.||Liu, Meng: 3 articles (02/2011 - 05/2007)|
|8.||Sjogren, Anna-Karin M: 3 articles (02/2011 - 05/2007)|
|9.||Casey, Patrick J: 3 articles (07/2009 - 05/2007)|
|10.||Sebti, Saïd M: 3 articles (04/2009 - 12/2003)|
05/01/2007 - "Moreover, the absence of GGTase-I activity reduced lung tumor formation, eliminated myeloproliferative phenotypes, and increased survival of mice in which expression of oncogenic K-RAS was switched on in lung cells and myeloid cells. "
11/01/2007 - "Geranylgeranyltransferase I inhibitors (GGTIs) are presently undergoing advanced preclinical studies and have been shown to disrupt oncogenic and tumor survival pathways, to inhibit anchorage-dependent and -independent growth, and to induce apoptosis. "
05/01/2007 - "In this study, we determined the effects of GGTase-I deficiency on cell viability and K-RAS-induced cancer development in mice. "
03/01/2002 - "Some of these inhibitors show remarkable inhibition potency against PFTase at subnanomolar concentrations and >1000-fold selectivity compared to the related enzyme geranylgeranyltransferase-I. Certain of these compounds are highly effective at blocking the growth of human tumors in animal models and are now undergoing clinical trials. "
01/01/2015 - "Small molecule inhibitors against protein geranylgeranyltransferase-I such as P61A6 have been shown to inhibit proliferation of a variety of human cancer cells and exhibit antitumor activity in mouse models. "
|2.||Lung Neoplasms (Lung Cancer)
04/06/2010 - "FTase inactivation in mice with K-RAS-induced lung cancer reduced tumor growth and improved survival, similar to results obtained previously with inactivation of GGTase-I. Simultaneous inactivation of FTase and GGTase-I markedly reduced lung tumors and improved survival without apparent pulmonary toxicity. "
05/01/2007 - "GGTase-I deficiency reduces tumor formation and improves survival in mice with K-RAS-induced lung cancer."
01/01/2010 - "The GGTase I inhibitor GGTI-298 induced apoptosis and augmented tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-induced apoptosis in human lung cancer cells. "
|3.||Breast Neoplasms (Breast Cancer)
01/01/2004 - "The present studies confirm that gliotoxin is a dual inhibitor of farnesyltransferase and geranylgeranyltransferase I with pronounced antitumor activity and favorable toxicity profile against breast cancer in vitro and in vivo."
01/01/2015 - "Importantly, atorvastatin or the geranylgeranyltransferase I inhibitor GGTI-298 inhibited breast cancer cell proliferation through inactivation of YAP signaling and down-regulation of PBK. "
01/01/2004 - "Gliotoxin is a dual inhibitor of farnesyltransferase and geranylgeranyltransferase I with antitumor activity against breast cancer in vivo."
03/01/2002 - "Taken together, these data suggest that DN FTase/GGTase I alpha-subunit can assuage the mitogenic effects of IGF-1 and insulin on MCF-7 breast cancer cells."
10/12/2001 - "We recently demonstrated that in MCF-7 breast cancer cells, insulin promoted the phosphorylation and activation of geranylgeranyltransferase I (GGTI-I), increased the amounts of geranylgeranylated Rho-A and potentiated the transactivating activity of lysophosphatidic acid (LPA) (Chappell, J., Golovchenko, I., Wall, K., Stjernholm, R., Leitner, J., Goalstone, M., and Draznin, B. "
06/01/2015 - "These findings suggest that RalB might be one of the targets for facilitating the invasive phenotype of malignant gliomas induced by GGTase-I."
06/01/2015 - "We found that knockdown of GGTase-I or RalB both significantly decreased the migratory and invasive abilities of glioma cells. "
06/01/2015 - "Involvement of RalB in the effect of geranylgeranyltransferase I on glioma cell migration and invasion."
01/01/2013 - "Importantly, overexpressing dominant-negative Rac1 or Rac1 with the prenylation site deleted or mutated abrogated GGTase-I-induced proliferation in glioma cells. "
01/01/2013 - "Furthermore, overexpressing wild type or constitutively active Rac1 stimulated glioma cell growth, similar to the effect of GGTase-I overexpression. "
02/19/2013 - "In this study, we asked whether the increased inflammatory signaling of GGTase-I-deficient macrophages would influence the development of atherosclerosis in low-density lipoprotein receptor-deficient mice. "
02/19/2013 - "Targeting GGTase-I activates RHOA, increases macrophage reverse cholesterol transport, and reduces atherosclerosis in mice."
02/19/2013 - "Targeting GGTase-I activates RHOA and leads to increased macrophage reverse cholesterol transport and reduced atherosclerosis development despite a significant increase in inflammation."
07/23/2009 - "Geranylgeranyltransferase type I (GGTase-I) inhibitors (GGTIs) have therapeutic potential to treat inflammation, multiple sclerosis, atherosclerosis, and many other diseases. "
|1.||geranylgeranyltransferase type-I (protein geranylgeranyltransferase)
|3.||GTP Phosphohydrolases (GTPases)
|4.||LDL Receptors (LDL Receptor)
|9.||Proteins (Proteins, Gene)
|2.||Heterologous Transplantation (Xenotransplantation)