|1.||Proud, Christopher G: 11 articles (12/2015 - 10/2002)|
|2.||van der Knaap, Marjo S: 8 articles (09/2011 - 02/2002)|
|3.||Schiffmann, Raphael: 7 articles (01/2009 - 06/2003)|
|4.||Elroy-Stein, Orna: 6 articles (08/2015 - 10/2005)|
|5.||Pavitt, Graham D: 6 articles (01/2014 - 03/2004)|
|6.||Fogli, Anne: 6 articles (01/2013 - 06/2003)|
|7.||Scheper, Gert C: 6 articles (01/2013 - 11/2003)|
|8.||Kimball, Scot R: 6 articles (10/2011 - 11/2002)|
|9.||Wortham, Noel C: 5 articles (12/2015 - 09/2011)|
|10.||Boespflug-Tanguy, Odile: 5 articles (08/2009 - 06/2003)|
10/01/2002 - "Thus, several different processes contributed to ischemia-induced suppression of the initiation of protein synthesis: a long-lasting dephosphorylation of eIF2B epsilon and p70 S6K starting during ischemia, a transient phosphorylation of eIF2alpha during early reperfusion, and a marked decrease of eIF2B epsilon, eIF4G1, and p70 S6K protein levels starting during vascular occlusion (eIF4G1). "
10/01/2002 - "eIF2B epsilon and p70 S6 kinase were completely dephosphorylated during ischemia and phosphorylation did not recover completely following reperfusion. "
10/01/2002 - "In this study, we investigated ischemia-induced changes in protein levels and phosphorylation states of the initiation factors eIF2alpha, eIF2B epsilon, and eIF4G1 and of p70 S6 kinase, proteins playing a central role in the control of the initiation of translation. "
08/01/2006 - "Activation of Akt stimulated signaling through the protein kinase mammalian target of rapamycin, as evidenced by increased phosphorylation of two of its effectors, the ribosomal protein S6 kinase and the eukaryotic initiation factor eIF4E binding protein 1. Ischemia and reperfusion also resulted in increased phosphorylation of eIF2 and eIF2B. "
|2.||Bipolar Disorder (Mania)
02/01/2007 - "For unknown reasons, oligodendrocytes appear to be particularly prone to defects in the translation initiation complex (EIF2B) and the convergence of these environmental and genomic signalling pathways on this area might well explain their vulnerability in bipolar disorder."
11/01/2007 - "eIF2B and oligodendrocyte survival: where nature and nurture meet in bipolar disorder and schizophrenia?"
07/12/2002 - "We used Western blot analysis to quantify the protein level of the catalytic epsilon (epsilon) subunit of eIF-2B in brains of rats fed lithium chloride (LiCl) for 6 weeks so as to produce a brain lithium concentration that is therapeutically effective in bipolar disorder. "
04/01/2014 - "The previous studies have shown that mutations in five subunits of eIF2B cause white matter disease of the brain and thus EIF2B is the main culprit in development of white matter disease. "
04/01/2010 - "[Advances in functional study of EIF2B mutations in leukoencephalopathy with vanishing white matter]."
07/01/2014 - "In 283, genetic mutation of EIF2B was confirmed with the onset of vanishing white matter disease reported as antenatal (seven), infantile (eight), early childhood (107), between infantile and early childhood (20), late childhood (25), between early and late childhood (three), adult (68), and between late childhood and adult (21). "
03/09/2012 - "In addition, inherited mutations in eIF2B cause a fatal leukoencephalopathy. "
01/01/2012 - "Poor cerebral inflammatory response in eIF2B knock-in mice: implications for the aetiology of vanishing white matter disease."
11/01/2000 - "Instead, on the basis of our previous studies, changes in eIF2B appear to be responsible for limiting protein synthesis in skeletal muscle during sepsis."
01/01/1996 - "In the present study, we investigated the expression of two subunits of eIF-2B, i.e., the beta- and epsilon-subunits during sepsis. "
08/01/2010 - "In an effort to restore a deficit in eIF2B activity, we utilized an established model of chronic sepsis in which skeletal muscle eIF2B activity is known to be impaired. "
01/01/1996 - "The expression of both beta- and epsilon-subunits of eIF-2B in gastrocnemius was decreased approximately 50% from control values during the first 5 days after induction of sepsis. "
01/01/1996 - "Sepsis causes an inhibition of protein synthesis in skeletal muscles composed of fast-twitch fibers, in part, as a result of a decreased activity of the eukaryotic initiation factor 2B (eIF-2B). "
|5.||Neurodegenerative Diseases (Neurodegenerative Disease)
01/01/2015 - "By modulating eIF2B function, ISRIB promises to be an invaluable tool in proof-of-principle studies aiming to ameliorate cognitive defects resulting from neurodegenerative diseases. "
01/01/2013 - "Recessive inherited mutations in any of five subunits of the general protein synthesis factor eIF2B are responsible for a white mater neurodegenerative disease with a large clinical spectrum. "
07/01/2012 - "Leukodystrophy with vanishing white matter (VWM) is a neurodegenerative disorder with autosomal recessive traits that is caused by alteration of the eukaryotic translation initiation factor-2B (EIF2B). "
08/01/2015 - "Vanishing white matter (VWM) is a recessive neurodegenerative disease caused by mutations in translation initiation factor eIF2B and leading to progressive brain myelin deterioration, secondary axonal damage, and death in early adolescence. "
01/01/2004 - "It has been discovered recently that mutations in subunits of eukaryotic initiation factor 2B (eIF2B) underlie the neurodegenerative disease termed 'vanishing white matter'."
|3.||Eukaryotic Initiation Factor-2B (Eukaryotic Initiation Factor 2B)
|4.||Peptide Initiation Factors (Initiation Factor)
|5.||Proteins (Proteins, Gene)
|6.||70-kDa Ribosomal Protein S6 Kinases (Ribosomal Protein S6 Kinases, 70 kDa)
|8.||Eukaryotic Initiation Factor-2 (EIF 2)
|10.||Guanine Nucleotide Exchange Factors (Guanine Nucleotide Exchange Factor)