Disease relevance of RCJMB04_38l20

• Ciliary neurotrophic factor stimulates the phosphorylation of two forms of STAT3 in chick ciliary ganglion neurons [1].

High impact information on RCJMB04_38l20

• Matrix-independent activation of phosphatidylinositol 3-kinase, Stat3, and cyclin A-associated Cdk2 Is essential for anchorage-independent growth of v-Ros-transformed chicken embryo fibroblasts [2].
• Finally, we found that overexpressing a constitutively active mutant of STAT3 (STAT3C) conferred a resistance to the inhibition of Ros-induced anchorage-independent growth by LY294002, suggesting a possible overlap of functions between PI3K and STAT3 signaling in mediating Ros-induced anchorage-independent growth [3].
• In addition, we identify a second, 100-kDa form of STAT3 that appears in response to CNTF [1].
• Here we show that CNTF induced the rapid tyrosine phosphorylation and nuclear accumulation of this protein and identify it as an avian form of the transcription factor, STAT3 [1].
• Unlike previous reports, utilizing mammalian cell lines that detected a slower migrating form of STAT3 resulting from H7-sensitive protein phosphorylation, H7 did not prevent the appearance of the 100-kDa form in ciliary neurons [1].

Biological context of RCJMB04_38l20

• BTK physically associated with and tyrosine phosphorylated STAT3; this association was promoted by pervanadate (PV)-induced oxidative stress [4].
• Bruton's tyrosine kinase prevents activation of the anti-apoptotic transcription factor STAT3 and promotes apoptosis in neoplastic B-cells and B-cell precursors exposed to oxidative stress [4].
• CNTFRalpha-mediated signal transduction was demonstrated in E7 and E11 DRG neuron cultures by CNTF-induced STAT3 phosphorylation [5].
• Mice with targeted deletion of STAT3 in the lens were generated by Cre/lox recombination and STAT1-/-, STAT3-/- deficient as well as normal lenses were characterized by histology [6].

Anatomical context of RCJMB04_38l20

• METHODS: Expression of STAT1 and STAT3 was analyzed in mouse lens and lens epithelial cells by RT-PCR and western blot analysis [6].

Regulatory relationships of RCJMB04_38l20

• In vivo activation of JAK2/STAT-3 pathway during angiogenesis induced by GM-CSF [7].

Other interactions of RCJMB04_38l20

• RESULTS: We show that PDGF and IGF1 induce proliferation in 1AMLE6 lens cells and couple their extracellular signals to gene transcription, in part through activation of STAT3 and to a lesser extent STAT1 signal transduction pathways [6].
• All-trans-retinoic acid induced as much as a 3-fold increase in CNTF receptor alpha subunit mRNA in a time and concentration dependent manner and resulted in an enhanced CNTF-induced tyrosine phosphorylation of the transcription factor, STAT3 [8].

Analytical, diagnostic and therapeutic context of RCJMB04_38l20

• The present study examined whether BTK mediates apoptosis during oxidative stress by interfering with the anti-apoptotic function of signal transducer and activator of transcription 3 (STAT3) [4].

References