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Home › Dataset Library › Transcription profiling by array of human peripheral blood mononuclear cells from patients with epilepsy over a time course of...

Dataset: Transcription profiling by array of human peripheral blood mononuclear cells from patients with epilepsy over a time course of dexamethasone treatment

Article title: Expression, regulation and function of phosphofructo-kinase/fructose-biphosphatases (PFKFBs) in glucocorticoid-induced...

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Article 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.

Species:
human

Samples:
16

Source:
E-GEOD-22779

PubMed:
21092265

Updated:
Dec.12, 2014

Registered:
Sep.15, 2014


Factors: (via ArrayExpress)
Sample disease state clinical treatment time
GSM56324 epilepsy none 0
GSM563242 epilepsy dexamethosone 2
GSM563243 epilepsy dexamethosone 6
GSM563244 epilepsy dexamethosone 24
GSM56324 epilepsy none 0
GSM563242 epilepsy dexamethosone 2
GSM563243 epilepsy dexamethosone 6
GSM563244 epilepsy dexamethosone 24
GSM56324 epilepsy none 0
GSM563242 epilepsy dexamethosone 2
GSM563243 epilepsy dexamethosone 6
GSM563244 epilepsy dexamethosone 24
GSM563253 normal none 0
GSM563254 normal dexamethosone 2
GSM563255 normal dexamethosone 6
GSM563256 normal dexamethosone 24

Tags

  • acute lymphoblastic leukemia
  • cell
  • central
  • epilepsy
  • glucose
  • leukemia
  • lymphoblastic leukemia
  • peripheral

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