Decreased nuclear β‐catenin, tau hyperphosphorylation and neurodegeneration in GSK‐3β conditional transgenic mice

By J. Lucas, F. Hernández, P. Gómez-Ramos, M. Morán, R. Hen, J. Ávila. 2001

829 citations recorded by the source corpus.

Subfields: Cellular and Molecular Neuroscience, Molecular Biology, Physiology

View Paper: https://www.semanticscholar.org/paper/e7f679aa6b65eaa27f4191b28c07d362f455a42c

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cellular and Molecular Neuroscience

1. Fei Liu
2. C. Gong
3. K. Iqbal
4. Li-Huei Tsai
5. M. Goedert
6. C. Zhong
7. Zhichun Chen
8. Michael J Frank

In Molecular Biology

1. Fei Liu
2. C. Gong
3. K. Iqbal
4. I. Grundke‐Iqbal
5. Eléonore Beurel
6. Paul Greengard
7. L. Meijer
8. M. Flajolet

In Physiology

1. Fei Liu
2. C. Gong
3. K. Iqbal
4. I. Grundke‐Iqbal
5. Li-Huei Tsai
6. M. Goedert
7. C. Zhong
8. Zhichun Chen

Citations in the corpus

• Decoding Alzheimer's disease from perturbed cerebral glucose metabolism: implications for diagnostic and therapeutic strategies. (2013, background): “…of expression or activity of GSK-3 (Blalock et al., 2004), and hence hyper-activation of GSK-3 could induce the apoptosis of cholinergic neurons (Hoshi et al., 1996), tau-hyperphosphoryaltion (Cho and Johnson, 2003; Lovestone et al., 1994), and subsequent NFTs formation (Lucas et al., 2001).”
• Pharmacological inhibitors of glycogen synthase kinase 3. (2004, background): “The first is that conditionaltransgenic mice that overexpress GSK-3 in brain during adulthood show signs of neurodegeneration and spatiallearning deficits [ 37 ].”
• Contributions of protein phosphatases PP1, PP2A, PP2B and PP5 to the regulation of tau phosphorylation (2005, background): “…hyperphosphorylation of tau is believed to be responsible for its loss of biological activity, for its gain of toxic activity and for its aggregation into PHFs (Iqbal et al., 1986; Alonso et al., 1994; 2001a,b; Lucas et al., 2001; Fath et al., 2002; Jackson et al., 2002; Perez et al., 2002).”
• β-Catenin signaling is required for neural differentiation of embryonic stem cells (2004, background): “Phosphorylation of β-catenin at residues Ser33/37;Thr41 targets it for ubiquitin-directed proteolysis (Brantjes et al., 2002) and inhibits nuclear β-catenin (Lucas et al., 2001), therefore suggesting that β-catenin signaling is more active when ES cells are differentiated at low density.”
• The GSK3 hypothesis of Alzheimer's disease (2008, background): “Consistent with this, GSK3b transgenic mice display tau hyper-phosphorylation and neurodegeneration (Lucas et al. 2001) and chronic lithium (GSK3 inhibitor) treatment prevents tau hyper-phosphorylation and NFT formation in double transgenic mice over-expressing GSK3b and tau (harboring a triple…”
• GSK3 inhibitors: development and therapeutic potential (2004, background): “Moreover, overexpression of GSK3 in transgenic mice does not seem to lead to the formation of tau filament”
• Glycogen Synthase Kinase-3 (GSK3): Inflammation, Diseases, and Therapeutics (2007, background): “Furthermore, tau phosphorylation is increased in transgenic mice overexpressing GSK3b [99, 100].”
• Aberrant Cdk5 activation by p25 triggers pathological events leading to neurodegeneration and neurofibrillary tangles. (2003, background): “Nonproline- in the formation of NFTs and neurodegeneration (Jackson et al., 2002; Lucas et al., 2001; Noble et al., 2003).directed sites of tau phosphorylated in p25 Tg mice include S198, S239, S400, and T403.”