Disease relevance of AKT1S1

• Face Memory in MRI-Positive and MRI-Negative Temporal Lobe Epilepsy [1].
• HELLP Syndrome Complicated Bile Duct Injury and Subsequent Left Hepatic Lobe Atrophy [2].
• In the breast cancer model (MCF10A/MCF7) and lung cancer model (BEAS/H1198/H1170) we also found the same result: PRAS40 was constitutively active in H1198/H1170 and MCF7 pre-malignant and malignant cancer cells, but weakly expressed in MCF10A and BEAS normal cell [3].

Psychiatry related information on AKT1S1

• Frontal Lobe Metabolic Decreases with Sleep Deprivation not Totally Reversed by Recovery Sleep [4].
• Blood-Brain Barrier Permeability Correlates with Medial Temporal Lobe Atrophy but Not with Amyloid-beta Protein Transport across the Blood-Brain Barrier in Alzheimer's Disease [5].
• Eighteen patients with AD and 18 patients with PD, matched on age and education, were administered the Mattis Dementia Rating Scale and Frontal Systems Behavior Scale (formally Frontal Lobe Personality Scale) [6].

High impact information on AKT1S1

• Insulin stimulates Akt/PKB-mediated phosphorylation of PRAS40, which prevents its inhibition of mTORC1 in cells and in vitro [7].
• PRAS40 inhibits cell growth, S6K1 phosphorylation, and rheb-induced activation of the mTORC1 pathway, and in vitro it prevents the great increase in mTORC1 kinase activity induced by rheb1-GTP [7].
• We identify PRAS40 as a raptor-interacting protein that binds to mTORC1 in insulin-deprived cells and whose in vitro interaction with mTORC1 is disrupted by high salt concentrations [7].
• PRAS40 Is an Insulin-Regulated Inhibitor of the mTORC1 Protein Kinase [7].
• Phosphorylation of PRAS40 is increased by insulin in human, rat, and mouse insulin target tissues [8].

Biological context of AKT1S1

• METHODS: The effects of three key kinase inhibitors on PRAS40 activity in the cell survival pathway, serum withdrawal, H(2)O(2) and overexpression of Akt were tested [3].
• 14-3-3 is a PRAS40 binding protein, and the expression of 14-3-3, like that of PRAS40, was higher in HeLa cells than in HEK293 cells; PRAS40 had a stronger phosphorylation activity in A549 and HeLa cancer cells than in HEK293 normal cells [3].

Anatomical context of AKT1S1

• In cultured cell lines, insulin-mediated PRAS40 phosphorylation was prevented by the PI3K inhibitors wortmannin and LY294002 [8].
• Predicting Biliary Complications in Right Lobe Liver Transplant Recipients according to Distance between Donor's Bile Duct and Corresponding Hepatic Artery [9].
• CONCLUSION: The Frontal Lobe Score is a useful screening instrument for the clinical detection of effects of frontal lobe damage [10].
• RESULTS: Lobe-shape intestinal villi in duodenum were already developed at the twelfth week [11].
• We also discussed PRAS40 activity in other NSCLC cell lines [3].

Associations of AKT1S1 with chemical compounds

• Insulin-Mediated Phosphorylation of the Proline-Rich Akt Substrate PRAS40 Is Impaired in Insulin Target Tissues of High-Fat Diet-Fed Rats [8].
• Appendix II: Conceptual Foundations of Studies of Patients Undergoing Temporal Lobe Surgery for Seizure Control* [12].

Regulatory relationships of AKT1S1

• Small interfering RNA-mediated knockdown of PRAS40 impairs both the amino acid- and insulin-stimulated phosphorylation of 4E-BP1 and the phosphorylation of S6 [13].

Other interactions of AKT1S1

• Expression of proline-rich Akt-substrate PRAS40 in cell survival pathway and carcinogenesis [3].

Analytical, diagnostic and therapeutic context of AKT1S1

• Immunohistochemical and immunofluorescence studies showed that phosphorylated PRAS40 is predominantly localized to the nucleus [8].
• Temporal Lobe Perfusion in the Deaf: MR Measurement with Pulsed Arterial Spin Labeling (FAIR) [14].
• The expression of PRAS40, Akt, Raf and 14-3-3 in normal cells and cancer cell lines was determined by Western blot [3].
• The phosphorylation level of Akt decreased after serum withdrawal and treatment with the MEK inhibitor Uo126, but increased after treatment with H(2)O(2) at low concentration, whereas none of these treatments changed PRAS40 activity [3].

References