A CK2-dependent mechanism for degradation of the PML tumor suppressor

Article Abstract:

A mouse model of lung cancer is used to show that Pml inactivation leads to increased tumorigenesis in addition to the casein kinase 2 (CK2) pharmocological inhibition enhancing the PML tumor-suppressive property in vivo. Therapy with specific CK2 inhibitors or proteasome inhibitors like bortezomib, used in the treatment of several human cancers, may be effective in tumors that display aberrant CK2 activity and loss of PML protein.

author: Pandolfi, Pier Paolo, Erdjument-Bromage, Hediye, Scaglioni, Pier Paolo, Teruya-Feldstein, Julie, Thomas M. Yung, Lu Fan Cai, Kaufman, Andrew J., Singh, Bhuvanesh
Protein kinases, Tumor suppressor genes, Genetic research, Tumour suppressor genes

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Hematopoiesis controlled by distinct TIF1[gama] and Smad4 branches of the TGF[beta] pathway

Article Abstract:

Studies reveal that formation of transcription regulatory complexes by the association of Smad4 with receptor-phosphorylated Smads 2 and 3 is a central event in the canonical TGF[beta] pathway. Evidence is provided for a branching of this pathway, where the ubiquitious nuclear protein Transcriptional Intermediary Factor 1 [gama] selectively binds receptor-phosphorylated Smad2/3 in competition with Smad4.

author: Massague, Joan, Moore, Malcolm A.S., Erdjument-Bromage, Hediye, Tempst, Paul, Wei He; Dorn, David C.
Hematopoiesis, Binding proteins

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Phosphorylation and functional inactivation of TSC2 by Erk: Implications for tuberous sclerosis and cancer pathogenesis

Article Abstract:

A study conducted shows that extracellular signal-regulated kinase (Erk) play a critical role in tuberous sclerosis (TSC) progression through posttranslational inactivation of TSC2. The findings suggest that Erk may modulate mTOR signaling and contribute to disease progression through phosphorylation and inactivation of TSC2.

author: Pandolfi, Pier Paolo, Erdjument-Bromage, Hediye, Tempst, Paul, Li Ma, Zhenbang Chen
Tuberous sclerosis

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subjects list: Research, Oncogenes, Phosphorylation
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