2004
DOI: 10.1038/sj.leu.2403241
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JAK/STAT, Raf/MEK/ERK, PI3K/Akt and BCR-ABL in cell cycle progression and leukemogenesis

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Cited by 624 publications
(538 citation statements)
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References 423 publications
(536 reference statements)
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“…These observations suggest that alternative mechanisms of activation exist for these signaling molecules in HA-CML cells. 33 In addition to the phosphorylation status of Bcr-Abl, the sensitivity to antileukemic agents depends on the balance of pro-and antiapoptotic molecules. 8 Akt pro-survival effects have been reported to be dependent on the first step in glycolysis.…”
Section: Discussionmentioning
confidence: 99%
“…These observations suggest that alternative mechanisms of activation exist for these signaling molecules in HA-CML cells. 33 In addition to the phosphorylation status of Bcr-Abl, the sensitivity to antileukemic agents depends on the balance of pro-and antiapoptotic molecules. 8 Akt pro-survival effects have been reported to be dependent on the first step in glycolysis.…”
Section: Discussionmentioning
confidence: 99%
“…These data indicated that BCR/ABL could upregulate SPK1 expression and increase its cellular activity in CML cells. It is known that BCR/ABL activates several signals, including mitogen-activated protein kinase, Janus kinase 2 (JAK2) and phosphoinositide 3-kinase (PI3K) in CML cells (Cortez et al, 1996;Skorski et al, 1997;Sillaber et al, 2000;Steelman et al, 2004;Samanta et al, 2006). To examine the roles of these signals in SPK1 expression induced by BCR/ABL in CML cells, the bcr-abl-transformed BaF3 cells, BaF3/pLXSN and K562 cells were pretreated with PD98059, Wortmannin and AG490, specific inhibitors of extracellular signal-regulated kinase 1/2, PI3K and JAK2, respectively, and then the BCR/ABL-induced SPK1 activity and expression were assayed.…”
mentioning
confidence: 99%
“…Such a tyrosine kinase activates the Ras/Raf/MEK/ERK and JAK/STAT signal transduction pathways, and this results in an amplified proliferative state [22]. Bcr-Abl causes hyperactivity of Ras, Raf and JAK/STAT, which can occur by multiple mechanisms; i.e., by Bcr-Abl activating these pathways directly, or by the induction of autocrine cytokines, which in turn activate these pathways [23].…”
Section: Proliferationmentioning
confidence: 99%
“…Two other adapter molecules, Shc and Crkl, can also activate Ras [9,24]. Ras activates Raf, and finally, Raf initiates a signaling cascade through the serine-threonine kinases Mek1/ Mek2 and Erk, which ultimately leads to the transcription of genes involved in cell proliferation and survival (Figure 1), such as c-Myc, Cyclin D, Cyclin A, Bcl-2, cytokines, etc [22].…”
Section: Proliferationmentioning
confidence: 99%