Integration of Smad and forkhead pathways in the control of neuroepithelial and glioblastoma cell proliferation.
By J. Seoane, Hong-Van Le, Lijian Shen, S. Anderson, J. Massagué. Cell, 2004
1,088 citations recorded by the source corpus.
Subfields: Molecular Biology
View Paper: https://www.semanticscholar.org/paper/09807614f88ebec51d63efbab1c6bd146f5eb310
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Citations in the corpus
- FoxOs are critical mediators of hematopoietic stem cell resistance to physiologic oxidative stress. (2007, background): “…Elsevier Inc. arrest by activation of p27, p130, p21, and repression of Cyclin D expression (G1/S arrest) (Kops et al., 2002b; Medema et al., 2000; Seoane et al., 2004); activation of Cyclin G2 (G0/G1 arrest) (Martinez-Gac et al., 2004); and activation of Cyclin B and polo-like kinase (G2/M…”
- Non-Smad TGF-β signals (2005, neutral): “5) (Datto et al., 1995; Moustakas and Kardassis, 1998; Pardali et al., 2000; Cordenonsi et al., 2003; Seoane et al., 2004).”
- SPECIFICITY AND VERSATILITY IN TGF-β SIGNALING THROUGH SMADS (2005, background): “At the p21Cip1 promoter, the Smad3/4 complex interacts with FoxO, a target of the PI3 kinase/Akt pathway, to induce transcription of the p21Cip1 gene (Seoane et al. 2004).”
- The emerging roles of forkhead box (Fox) proteins in cancer (2007, background): “For example, in response to transforming growth factor-β ( TGFβ ), FOXO3A complexes with SMAD3 to transactivate CDKN1A expression, while FOXG1 is capable of binding to the FOXO3A–SMAD3 complex and preventing induction of CDKN1A , possibly through the recruitment of co-repressor”
- FOXO transcription factors at the interface between longevity and tumor suppression (2005, background): “In the presence of TGFb, FOXO factors also bind to the promoter of p21, a cell cycle inhibitor, and induce cell cycle arrest at the G1/S transition (Seoane et al., 2004).”
- RTK and TGF-β signaling pathways genes in the sea urchin genome (2006, background): “…1998) t9:12 Sp-FoxO Smad3 transcriptional partner for the activation of p21 cyclin -dependent inhibitors SPU-009179 Q12778: Forkhead box protein O1A (Seoane et al., 2004) t9:13 Sp-E2F Transcription activator SPU-006753 SPU-028828 NP-001940: E2F transcription factor 3 (Chen et al., 2002) t9:14…”
- The pan-ErbB negative regulator, Lrig1, is an intestinal stem cell marker that functions as a tumor suppressor (2012, positive): “Notably, Cdkna1, which is significantly up-regulated in the Lrig1+ cells, is a target of FoxO signaling (Seoane et al., 2004), suggesting its cell cycle repressive properties are linked to the damage response.”
- NF-κB is essential for epithelial-mesenchymal transition and metastasis in a model of breast cancer progression (2004, background): “TGF-β induces transcription of the cell cycle inhibitor p21CIP1 by a mechanism, in which Smad proteins cooperate with FoxO transcription factors (47).”
- The logic of TGFβ signaling (2006, background): “An activated Smad-FoxO transcriptional complex mediates p21CIP1 induction [52] whereas induction of p15INK4b requires a Smad-FoxO-C/EBPb transcriptional complex [49] (Fig.”
- Reversal of cancer cachexia and muscle wasting by ActRIIB antagonism leads to prolonged survival. (2010, background): “Smad and FOXO signal transduction systems can influence each other’s activity (Seoane et al., 2004), and in skeletal muscle, the myostatin-Smad pathway stimulates FOXO function (Sartori et al., 2009; Trendelenburg et al., 2009).”