Expression of the pro-apoptotic Bcl-2 family member Bim is regulated by the forkhead transcription factor FKHR-L1.

By P. Dijkers, R. Medema, J. Lammers, L. Koenderman, P. Coffer. Current Biology, 2000

1,082 citations recorded by the source corpus.

Subfields: Immunology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/1a3dc86b3f8aa68a3b6b5b2e5b60525fb2dd3a56

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In Immunology

1. Jerry M. Adams
2. Suzanne Cory
3. A. Strasser
4. X. Wang
5. C. Kenyon
6. H. Beere
7. Douglas R. Green
8. D. Godfrey

In Molecular Biology

1. Jerry M. Adams
2. A. Strasser
3. Suzanne Cory
4. Douglas R. Green
5. S. Manolagas
6. A. Brunet
7. X. Wang
8. F. Llambi

Citations in the corpus

• Cell Death Signaling. (2015, background): “protein Stimulus/input Type of regulation Signaling pathway Output References Bad Growth factors and cytokines Phosphorylation Akt Cell survival Datta et al. 1997, 2002; del Peso et al. 1997 Phosphorylation p70 S6K Cell survival Harada et al. 2001 Phosphorylation PKA Cell survival Harada et al. 1999”
• Keeping killers on a tight leash: transcriptional and post-translational control of the pro-apoptotic activity of BH3-only proteins (2002, background): “Growth factor withdrawal was shown to cause increased Bim expression in various populations of neuronal(42,43) and hematopoietic cell types.(44,46) Interestingly, in NGF-deprived neurons apparently only one isoform of Bim, BimEL, is upregulated.”
• FOXO transcription factors at the interface between longevity and tumor suppression (2005, background): “…growth factor I (IGF-I) (Brunet et al., 1999; Rena et al., 1999), insulin (Kops and Burgering, 1999; Nakae et al., 1999), interleukin 3 (Dijkers et al., 2000a), erythropoietin (Kashii et al., 2000), epidermal growth factor (Jackson et al., 2000), and nerve growth factor (Zheng et al.,…”
• Growth Hormone Receptor Deficiency is Associated With a Major Reduction in Pro-aging Signaling, Cancer and Diabetes in Humans (2011, positive): “are known to protect against oxidative stress as well as promote apoptosis (54, 57, 58), we hypothesize that increased FoxO activity could account, in part, for the protective effects observed in HMECs incubated in GHRD serum.”
• Glycogen synthase kinase-3 regulates mitochondrial outer membrane permeabilization and apoptosis by destabilization of MCL-1. (2006, background): “The proapoptotic BH3-only protein BIM is induced upon removal of IL-3 (Dijkers et al., 2000), stabilized in the absence of growth factor signaling (Luciano et al.”
• The Bcl-2 apoptotic switch in cancer development and therapy (2007, background): “Whereas bim can also be induced downstream of Akt by a Forkhead transcription factor (Dijkers et al., 2000), the Bim protein is subject to several types of post-translational regulation.”
• From estrogen-centric to aging and oxidative stress: a revised perspective of the pathogenesis of osteoporosis. (2010, background): “FoxOs can also induce apoptosis through FoxOmediated regulation of several proapoptotic genes (56, 71).”
• BH3-only Bcl-2 family member Bim is required for apoptosis of autoreactive thymocytes (2002, background): “PTEN might either enhance Bim expression through AKT/PKB kinase-mediated effects on forkhead transcription factors, which can activate the Bim promote”
• FOXO transcription factors directly activate bim gene expression and promote apoptosis in sympathetic neurons (2003, background): “…appears that this is significantly more complex than the comparable situation in hematopoietic cells where the PI3-K–mediated regulation of FOXO transcription factors alone might be responsible for full BIM induction after growth factor withdrawal (Dijkers et al., 2000, 2002; Stahl et al., 2002).”