A mathematical model of phosphorylation AKT in Acute myeloid leukemia

Adi, Yudi and Adi-Kusumo, Fajar and Aryati, Lina and Hardianti, Mardiah (2016) A mathematical model of phosphorylation AKT in Acute myeloid leukemia. [Artikel Dosen]

Text 2016-AIP Proceeding symomath 2015.pdf Download (326kB)

Abstract

In this paper we consider a mathematical model of PI3K/AKT signaling pathways in phosphorylation AKT. PI3K/AKT pathway is an important mediator of cytokine signaling implicated in regulation of hematopoiesis. Constitutive activation of PI3K/AKT signaling pathway has been observed in Acute Meyloid Leukemia (AML) it caused by the mutation of Fms-like Tyrosine Kinase 3 in internal tandem duplication (FLT3-ITD), the most common molecular abnormality associated with AML. Depending upon its phosphorylation status, protein interaction, substrate availability, and localization, AKT can phosphorylate or inhibite numerous substrates in its downstream pathways that promote protein synthesis, survival, proliferation, and metabolism. Firstly, we present a mass action ordinary differential equation model describing AKT double phosphorylation (AKTpp) in a system with 11 equations. Finally, under the asumtion enzyme catalyst constant and steady state equilibrium, we reduce the system in 4 equation included Michaelis Menten constant. Simulation result suggested that a high concentration of PI3K and/or a low concentration of phospatase increased AKTpp activation. This result also indicates that PI3K is a potential target theraphy in AML.

Item Type:	Artikel Dosen
Subjects:	Q Science > QA Mathematics
Divisi / Prodi:	Faculty of Applied Science and Technology (Fakultas Sains Dan Teknologi Terapan)
Depositing User:	Dr. Yudi Ari Adi
Date Deposited:	15 Apr 2021 02:50
Last Modified:	15 Apr 2021 02:50
URI:	http://eprints.uad.ac.id/id/eprint/24317

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