Results 11 to 20 of about 147,647 (257)

Catalysis by the Tumor-Suppressor Enzymes PTEN and PTEN-L

open access: yesPLOS 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
openaire   +5 more sources

Targeting human apurinic/apyrimidinic endonuclease 1 (APE1) in phosphatase and tensin homolog (PTEN) deficient melanoma cells for personalized therapy [PDF]

open access: yes, 2014
Phosphatase and tensin homolog (PTEN) loss is associated with genomic instability. APE1 is a key player in DNA base excision repair (BER) and an emerging drug target in cancer.
Seedhouse, C   +32 more
core   +1 more source

Is PTEN loss associated with clinical outcome measures in human prostate cancer? [PDF]

open access: yes, 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
core   +1 more source

Phosphoinositide-dependent kinase 1 controls migration and malignant transformation but not cell growth and proliferation in PTEN-null lymphocytes [PDF]

open access: yes, 2009
In normal T cell progenitors, phosphoinositide-dependent kinase l (PDK1)-mediated phosphorylation and activation of protein kinase B (PKB) is essential for the phosphorylation and inactivation of Foxo family transcription factors, and also controls T ...
Feijoo, C.   +20 more
core   +1 more source

Leptin-dependent Phosphorylation of PTEN Mediates Actin Restructuring and Activation of ATP-sensitive K+ Channels [PDF]

open access: yes, 2009
Leptin activates multiple signaling pathways in cells, including the phosphatidylinositol 3-kinase pathway, indicating a degree of cross-talk with insulin signaling. The exact mechanisms by which leptin alters this signaling pathway and how it relates to
Miller, L.C.   +15 more
core   +1 more source

Molecular characterisation of ERG, ETV1 and PTEN gene loci identifies patients at low and high risk of death from prostate cancer. [PDF]

open access: yes, 2010
BACKGROUND: The discovery of ERG/ETV1 gene rearrangements and PTEN gene loss warrants investigation in a mechanism-based prognostic classification of prostate cancer (PCa).
P T Scardino   +65 more
core   +1 more source

Phenotype selection reveals coevolution of muscle glycogen and protein and PTEN as a gate keeper for the accretion of muscle mass in adult female mice. [PDF]

open access: yes, 2012
We have investigated molecular mechanisms for muscle mass accretion in a non-inbred mouse model (DU6P mice) characterized by extreme muscle mass. This extreme muscle mass was developed during 138 generations of phenotype selection for high protein ...
Hammon Harald M.   +53 more
core   +1 more source

The role of systemically perturbed PTEN and PKBß/AKT2 signaling in accumulation of hepatic lipids [PDF]

open access: yes, 2013
Non-alcoholic fatty liver disease (NAFLD) is a major health problem and occurs frequently in the context of obesity and type 2 diabetes mellitus (T2D).
Schultze, Simon Manuel
core   +1 more source

Fos co-operation with PTEN loss elicits keratoacanthoma not carcinoma due to p53/p21WAF-induced differentiation triggered by GSK3b inactivation and reduced AKT activity [PDF]

open access: yes, 2008
To investigate gene synergism in multistage skin carcinogenesis, the RU486-inducible cre/lox system was employed to ablate PTEN function [K14.cre/D5PTENflx] in mouse epidermis expressing activated v-fos [HK1.fos].
Chan, W-C.   +11 more
core   +1 more source

DataSheet_1_TP53-PTEN-NF1 depletion in human brain organoids produces a glioma phenotype in vitro.zip

open access: yes, 2023
Glioblastoma (GBM) is fatal and the study of therapeutic resistance, disease progression, and drug discovery in GBM or glioma stem cells is often hindered by limited resources.
N. U. Farrukh Hameed (10001728)   +15 more
core   +1 more source

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