Results 11 to 20 of about 164,611 (306)
Catalysis by the Tumor-Suppressor Enzymes PTEN and PTEN-L [PDF]
PLOS ONE, 2015 Phosphatase and tensin homologue deleted from chromosome ten (PTEN) is a lipid phosphatase tumor suppressor that is lost or inactivated in most human tumors. The enzyme catalyzes the hydrolysis of phosphatidylinositol-(3,4,5)-trisphosphate (PIP3) to form phosphatidylinositol-(4,5)-bisphosphate (PIP2) and inorganic phosphate.
Sean B Johnston, Ronald T Raines
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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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Arresting times for PTEN [PDF]
The EMBO Journal, 2011 EMBO J 30 13, 2557–2568 (2011); published online June032011 [PMC free article] [PubMed] The tumour suppressor PTEN (phosphatase and tensin deleted on chromosome 10) is an important regulator of cell proliferation and migration. In this issue of The EMBO Journal, Lima-Fernandes and colleagues show that the universal signalling scaffold protein, β ...
Miles D Houslay, Houslay, M.D.
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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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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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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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PTEN and Gynecological Cancers [PDF]
Cancers, 2019 PTEN is a tumour suppressor gene, and its loss of function is frequently observed in both heritable and sporadic cancers. It is involved in a great variety of biological processes, including maintenance of genomic stability, cell survival, migration, proliferation and metabolism.
Nero C. +3 more
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Threonine 348 regulates the subcellular localization of PTEN. [PDF]
FEBS Open BioThr348 in the C2 domain is a key contributor to PTEN subcellular localization. The PTEN350 fragment and PTENA4 accumulated in the nucleus, whereas PTENK13R,A4 predominantly localized to the plasma membrane. In contrast, substitution of Thr348 with Asp (T348D) disrupted these characteristic localization patterns, resulting in predominant cytoplasmic ...
Kato T, Tanaka S, Ohashi M.
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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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Is PTEN loss associated with clinical outcome measures in human prostate cancer? [PDF]
, 2008 Inactivating PTEN mutations are commonly found in prostate cancer, resulting in an increased activation of Akt. In this study, we investigate the role of PTEN deletion and protein expression in the development of hormone-refractory prostate cancer using ...
S Grimsley +9 more
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