Results 1 to 10 of about 147,647 (257)
Annual Review of Biochemistry, 2014 The importance of PTEN in cellular function is underscored by the frequency of its deregulation in cancer. PTEN tumor-suppressor activity depends largely on its lipid phosphatase activity, which opposes PI3K/AKT activation. As such, PTEN regulates many cellular processes, including proliferation, survival, energy metabolism, cellular architecture, and ...
Carolyn A, Worby, Jack E, Dixon
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Focus on PTEN regulation [PDF]
Frontiers in Oncology, 2015 The role of phosphatase and tensin homolog on chromosome 10 (PTEN) as a tumor suppressor has been for a long time attributed to its lipid phosphatase activity against PI(3,4,5)P3, the phospholipid product of the class I PI3Ks. Besides its traditional role as a lipid phosphatase at the plasma membrane, a wealth of data has shown that PTEN can function ...
Bermúdez Brito, Miriam +2 more
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The PTEN Conundrum: How to Target PTEN-Deficient Prostate Cancer [PDF]
Cells, 2020 Loss of the tumor suppressor phosphatase and tensin homologue deleted on chromosome 10 (PTEN), which negatively regulates the PI3K–AKT–mTOR pathway, is strongly linked to advanced prostate cancer progression and poor clinical outcome. Accordingly, several therapeutic approaches are currently being explored to combat PTEN-deficient tumors. These include
Daniel J. Turnham +4 more
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Archives of Pathology & Laboratory Medicine, 2022 Context.— Intestinal neuronal dysplasia type B (IND B) is a complex entity involving the enteric nervous system, clinically manifested with constipation in infancy. Diagnosis has been established by histopathologic analysis of rectal biopsies.
Simone Antunes, Terra +2 more
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Cold Spring Harbor Perspectives in Medicine, 2019 Although tremendous progress has been made in understanding the functions of Phosphatase and tensin homolog deleted on chromosome 10 (PTEN) in tumor cells, only recently have tumor cell-non-autonomous PTEN actions within the tumor microenvironment (TME) been appreciated.
Katie A, Thies +3 more
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p85 Associates with Unphosphorylated PTEN and the PTEN-Associated Complex [PDF]
Molecular and Cellular Biology, 2009 The lipid phosphatase PTEN functions as a tumor suppressor by dephosphorylating the D3 position of phosphoinositide-3,4,5-trisphosphate, thereby negatively regulating the phosphoinositide 3-kinase (PI3K)/AKT signaling pathway. In mammalian cells, PTEN exists either as a monomer or as a part of a >600-kDa complex (the PTEN-associated complex [PAC ...
Rosalia, Rabinovsky +6 more
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Journal of Cell Science, 2012 Since its discovery in 1997 ([Li and Sun, 1997][1]; [Li et al., 1997][2]; [Steck et al., 1997][3]), the phosphatidylinositol (3,4,5)-trisphosphate [PtdIns(3,4,5) P 3] phosphatase and tensin homolog (PTEN) has been established as one of the most frequently mutated tumor suppressor genes in ...
Yuji, Shi +3 more
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PTEN regulation by Akt–EGR1–ARF–PTEN axis [PDF]
The EMBO Journal, 2008 The PTEN tumour suppressor gene is induced by the early growth response 1 (EGR1) transcription factor, which also transactivates p53, p73, and p300/CBP as well as other proapoptotic and anti-cancer genes. Here, we describe a novel Akt-EGR1-alternate reading frame (ARF)-PTEN axis, in which PTEN activation in vivo requires p14ARF-mediated sumoylation of ...
Jianxiu, Yu +11 more
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The nuclear affairs of PTEN [PDF]
Journal of Cell Science, 2008 PTEN encodes a major tumor-suppressor protein that is a dual-specificity phosphatase. Inactivation of PTEN has been shown to be involved in heritable and sporadic cancers. Mutation or deletion of PTEN, historically the most commonly identified mechanisms of inactivation of tumor suppressors, is found only in the minority of sporadic non-cultured ...
Sarah M, Planchon +2 more
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The perfect PTEN – transcriptional regulation by PTEN dictates sarcoma identity [PDF]
Molecular & Cellular Oncology, 2021 Fusion-negative rhabdomyosarcoma (FN-RMS) is molecularly heterogeneous with few universal alterations except for Phosphatase and tensin homolog (PTEN) promoter hypermethylation. We demonstrate that losing Pten in FN-RMS engages an aberrant transcriptional program key in tumor maintenance and cell identity. These results highlight the importance between
Casey G. Langdon, Mark E. Hatley
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