Pten regulates neuronal arborization and social interaction in mice.

By C. Kwon, Bryan W. Luikart, Craig M. Powell, Jing Zhou, Sharon A. Matheny, Wei Zhang, Yanjiao Li, Suzanne J. Baker, L. Parada. Neuron, 2006

937 citations recorded by the source corpus.

Subfields: Cell Biology, Genetics, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/c17558708c984d639fb33dbe8622020c78433303

How researchers see this paper

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

In Cell Biology

1. Mark F. Bear
2. T. Franke

In Genetics

1. Thomas Bourgeron
2. R. J. Kelleher
3. Mark F. Bear
4. Mu Yang
5. T. Franke

In Molecular Biology

1. R. J. Kelleher
2. A. Holmgren
3. Mark F. Bear
4. Thomas Bourgeron
5. T. Franke

Citations in the corpus

• A synaptic trek to autism. (2009, background): “However, studies in mice showing that loss of Tsc1/Tsc2 or Pten results in neuronal hypertrophy have led to the hypothesis that susceptibility to ASD was not because of the tubers, but to an abnormal shape and size of the neurons [8 ,9].”
• Absence of CNTNAP2 leads to epilepsy, neuronal migration abnormalities and core autism-related deficits (2011, neutral): “Nest building has also been shown to be related to the dopaminergic pathway (Szczypka et al., 2001) and has been reported as disrupted in mice with hyperactivity (Kwon et al., 2006; Zhou et al., 2010).”
• DISC1 regulates new neuron development in the adult brain via modulation of AKT-mTOR signaling through KIAA1212 (2009, neutral): “AKT signaling is a major pathway in response to these growth factors, and recent studies have implicated its role in morphogenesis and dendritic development of postmitotic dentate granule cells in the adult hippocampus (Kwon et al., 2006; Zhou et al., 2009).”
• GSK3 signaling in neural development (2010, background): “These proteins include phosphatase and tensin homologue ( PTEN”
• PI3K/Akt: getting it right matters (2008, methodology): “Additional experimental support for a possible involvement of PTEN/Akt in ASD is provided by data from the Parada laboratory examining the morphology and behavior of mutant mice with neuron-specific knockout of PTEN (Kwon et al., 2006).”
• The Neurology of mTOR (2014, neutral): “Increased mTOR signaling due to loss of either TSC1/2 or PTEN results in profound changes in neuronal architecture and differentiation (Kwon et al., 2006; Tavazoie et al., 2005).”
• Molecular and Structural Basis for Redox Regulation of β-Actin (2007, background): “PTEN, discussed above in connection with it being the link between oxidation by H2O2 and Rac, is implicated in the etiology of autism and would appear to exert its influence on brain development via the actin microfilament system.(81) The relevance of ROS action on the actin system in vivo remains t”
• Autism‐like behavioral phenotypes in BTBR T+tf/J mice (2008, background): “…and targeted mutations in candidate genes (reverse genetics) (Bolivar et al. 2007; Brodkin et al. 2004; Brodkin 2007; Cheh et al. 2006; Crawley 2004; Insel & Young 2001; Kuemerle et al. 2007; Kwon et al. 2006; Levitt 2005; Mineur et al. 2006; Moy et al. 2004, 2007; Nadler et al. 2004; Zoghbi 2005).”
• Dendritic spine pathology in neuropsychiatric disorders (2011, background): “PTEN deficiency results in dendritic hypertrophy and elevated spine densit”
• The autistic neuron: troubled translation? (2008, background): “Further evidence that excessive translation can compromise cognitive function comes from mouse models deficient in PTEN and TSC1/2 function, in which elevated mTORC1 activity is associated with impaired hippocampal memory (Kwon et al., 2006; Goorden et al., 2007; Ehninger et al., 2008).”