ArrayExpress Uploaderarrayexpress_sid3733epilepsynone0epilepsydexamethosone2epilepsydexamethosone6epilepsydexamethosone24epilepsynone0epilepsydexamethosone2epilepsydexamethosone6epilepsydexamethosone24epilepsynone0epilepsydexamethosone2epilepsydexamethosone6epilepsydexamethosone24normalnone0normaldexamethosone2normaldexamethosone6normaldexamethosone2404Article title: Expression, regulation and function of phosphofructo-kinase/fructose-biphosphatases (PFKFBs) in glucocorticoid-induced...21092265E-GEOD-22779/profile/8773/arrayexpressuploader316acute lymphoblastic leukemiacellcentralepilepsyglucoseleukemialymphoblastic leukemiaperipheralDec.12, 2014FalseE-GEOD-22779_A-AFFY-44transcription-profiling-by-array-of-human-perip-13Transcription profiling by array of human peripheral blood mononuclear cells from patients with epilepsy over a time course of dexamethasone treatmentSep.15, 2014Article title: Expression, regulation and function of phosphofructo-kinase/fructose-biphosphatases (PFKFBs) in glucocorticoid-induced apoptosis of acute lymphoblastic leukemia cells. Glucocorticoids (GCs) cause apoptosis and cell cycle arrest in lymphoid cells and constitute a central component in the therapy of lymphoid malignancies, most notably childhood acute lymphoblastic leukemia (ALL). PFKFB2 (6-phosphofructo-2-kinase/fructose-2,6-biphosphatase-2), a kinase controlling glucose metabolism, was identified by us previously as a GC response gene in expression profiling analyses performed in children with ALL during initial systemic GC mono-therapy. Since deregulation of glucose metabolism has been implicated in apoptosis induction, this gene and its relatives PFKFB1, 3, and 4 were further analyzed. Expression analyses in additional ALL children, non-leukemic individuals and leukemic cell lines confirmed frequent PFKFB2 induction by GC in most systems sensitive to GC-induced apoptosis, particularly in T-ALL cells. The 3 other family members, in contrast, were not or weakly expressed (PFKFB1 and 4) or not induced by GC (PFKFB3). Conditional PFKFB2 over-expression in the CCRF-CEM T-ALL in vitro model revealed that its 2 splice variants (15A and 15B) did not have any detectable effect on survival or cell cycle progression. Moreover, neither PFKFB2 splice variant significantly affected sensitivity to, or kinetics of, GC-induced apoptosis. Our data suggest that, at least in the model system investigated, PFKFB2 is not an essential upstream regulator of the anti-leukemic effects of GC. Gene expression profiles of 4 non-leukemic individuals (1 healthy and 3 with epilepsy) were generated from mononuclear cells isolated from peripheral blood samples before, and after 2, 6, and 24 hours of in-vivo glucocorticoid treatment.http://www.ebi.ac.uk/arrayexpress/experiments/E-GEOD-22779humanhttp://www.ebi.ac.uk/arrayexpress/experiments/E-GEOD-22779/samples/