Correlation between synaptogenesis and the PTEN phosphatase expression in dendrites during postnatal brain development

Perandones, Claudia; Costanzo, Roxana V.; Kowaljow, Valeria; Pivetta, Omar H.; Carminatti, Héctor; Radrizzani, Martı́n

doi:10.1016/j.molbrainres.2004.05.021

Cited by 40 publications

(41 citation statements)

References 34 publications

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“…b After PTEN immunoprecipitation note the presence of Hsp27. The antibody used for PTEN IP was a rabbit polyclonal antibody (Perandones et al 2004). This antibody recognizes PTEN and the ubiquitinated forms of PTEN.…”

Section: Resultsmentioning

confidence: 99%

Downregulation of Hsp27 (HSPB1) in MCF-7 human breast cancer cells induces upregulation of PTEN

Cayado-Gutiérrez

Moncalero

Rosales

et al. 2013

Cell Stress and Chaperones

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Section: Resultsmentioning

confidence: 99%

Downregulation of Hsp27 (HSPB1) in MCF-7 human breast cancer cells induces upregulation of PTEN

Cayado-Gutiérrez

Moncalero

Rosales

et al. 2013

Cell Stress and Chaperones

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“…The first report placing Pten at the synapse came in 2004, when Peradones et al [79] described PTEN localization in dendrites and their spines during developmental periods of synaptic stabilization. Linking canonical functions of PTEN with synaptic activity, turnover of the PIP 2 /PIP 3 pool is critical for neurotransmitter vesicle cycling and PI3K activity is essential for long-term potentiation (LTP) [80].…”

Section: Pten Loss In Mice Leads To Cytoarchitecture and Synaptic Altmentioning

confidence: 99%

Balancing Proliferation and Connectivity in PTEN-associated Autism Spectrum Disorder

2015

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Germline mutations in PTEN, which encodes a widely expressed phosphatase, was mapped to 10q23 and identified as the susceptibility gene for Cowden syndrome, characterized by macrocephaly and high risks of breast, thyroid, and other cancers. The phenotypic spectrum of PTEN mutations expanded to include autism with macrocephaly only 10 years ago. Neurological studies of patients with PTENassociated autism spectrum disorder (ASD) show increases in cortical white matter and a distinctive cognitive profile, including delayed language development with poor working memory and processing speed. Once a germline PTEN mutation is found, and a diagnosis of phosphatase and tensin homolog (PTEN) hamartoma tumor syndrome made, the clinical outlook broadens to include higher lifetime risks for multiple cancers, beginning in childhood with thyroid cancer. First described as a tumor suppressor, PTEN is a major negative regulator of the phosphatidylinositol 3-kinase/protein kinase B/mammalian target of rapamycin (mTOR) signaling pathway-controlling growth, protein synthesis, and proliferation. This canonical function combines with less well-understood mechanisms to influence synaptic plasticity and neuronal cytoarchitecture. Several excellent mouse models of Pten loss or dysfunction link these neural functions to autism-like behavioral abnormalities, such as altered sociability, repetitive behaviors, and phenotypes like anxiety that are often associated with ASD in humans. These models also show the promise of mTOR inhibitors as therapeutic agents capable of reversing phenotypes ranging from overgrowth to low social behavior. Based on these findings, therapeutic options for patients with PTEN hamartoma tumor syndrome and ASD are coming into view, even as new discoveries in PTEN biology add complexity to our understanding of this master regulator.

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Section: Our Team Has Recently Reported That Ptenmentioning

confidence: 99%

“…One study demonstrated that a 34 kDa fragment of PTEN was localised to the mouse neuronal dendrites [65]. In the weaver mouse model, PTEN was absent in Purkinje dendrites where there is defective synaptogenesis [65]. Moreover transgenic mice with conditional deletion of PTEN in the brain had enlarged dendrites and axons with defective synaptic transmission indicating a role for PTEN in synaptic plasticity [66].…”

Section: Our Team Has Recently Reported That Ptenmentioning

confidence: 99%

PTEN: A molecular target for neurodegenerative disorders

Ismail

Ning

Al-Hayani

et al. 2012

Translational Neuroscience

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PTEN: a molecular target for neurodegeneratIve dIsorders abstract PTEN (phosphatase and tensin homologue deleted in chromosome 10) was first identified as a candidate tumour suppressor gene located on chromosome 10q23. It is considered as one of the most frequently mutated genes in human malignancies. Emerging evidence shows that the biological function of PTEN extends beyond its tumour suppressor activity. In the central nervous system PTEN is a crucial regulator of neuronal development, neuronal survival, axonal regeneration and synaptic plasticity. Furthermore, PTEN has been linked to the pathogenesis of neurodegenerative disorders such as Alzheimer's disease, Parkinson's disease and amyotrophic lateral sclerosis. Recently increased attention has been focused on PTEN as a potential target for the treatment of brain injury and neurodegeneration. In this review we discuss the essential functions of PTEN in the central nervous system and its involvement in neurodegeneration.

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Correlation between synaptogenesis and the PTEN phosphatase expression in dendrites during postnatal brain development

Cited by 40 publications

References 34 publications

Downregulation of Hsp27 (HSPB1) in MCF-7 human breast cancer cells induces upregulation of PTEN

Downregulation of Hsp27 (HSPB1) in MCF-7 human breast cancer cells induces upregulation of PTEN

Balancing Proliferation and Connectivity in PTEN-associated Autism Spectrum Disorder

PTEN: A molecular target for neurodegenerative disorders

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