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The state transition acetyltransferase GNAT2 interacts with GNAT1 and GNAT3 in independent complexes

ABSTRACT: The acetylation of amino groups within proteins is one of the major posttranslational modifications (PTMs) in all organisms. N-terminal acetyltransferases (NATs) or lysine acetyltransferases (KATs) catalyze the transfer of the acetyl group from the donor substrate acetyl coenzyme A (Ac-CoA) to the targeted amino group, which is either the α-amino groups of N-termini or the ε-amino group of internal lysine residues. In contrast to N-terminal acetylation (NTA), the acetylation of lysine residues (KA) is reversible, whereby lysine deacetylases (KDACs) are responsible for the removal of acetyl groups from proteins. Furthermore, KA occurs posttranslationally, whereas NTA is described mainly as a cotranslational modification with the exception for N-terminally processed proteins, which are imported to chloroplasts and mitochondria

ORGANISM(S): Arabidopsis Thaliana (mouse-ear Cress)

SUBMITTER: Iris Finkemeier

PROVIDER: PXD044167 | JPOST Repository | Mon Aug 19 00:00:00 BST 2024

REPOSITORIES: jPOST

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			Action	DRS
	190417_C19_008_QHF1_PTM_Rev01_%2319_016_ABR45_K1.raw	Raw
	190417_C19_008_QHF1_PTM_Rev01_%2319_016_ABR45_K2.raw	Raw
	190417_C19_008_QHF1_PTM_Rev01_%2319_016_ABR45_K3.raw	Raw
	190417_C19_008_QHF1_PTM_Rev01_%2319_016_ABR46_K1.raw	Raw
	190417_C19_008_QHF1_PTM_Rev01_%2319_016_ABR46_K2.raw	Raw

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Project description:Acute myeloid leukaemia (AML) is a highly heterogeneous entity of disorders in haematopoietic progenitors, characterised by an arrest in differentiation and an outgrowth of myeloid blasts in the bone marrow. AML is a disease of the aging, many patients are unable to withstand standard chemotherapy therefore novel approaches for anti-cancer agents has arisen in the understanding of epigenetic regulation in cancer cells, such as chromatin remodelling. Acetylation of histones is a reversible process, whereby acetyl groups are transferred on the ε-amino groups of specific lysine residues by a specific group of enzymes, histone acetyltransferases (HATs) and removed by histone deacetylase complexes (HDACs). HDACs are involved in regulating a number of processes in the cell, such as cell proliferation, differentiation as well as apoptosis. Deregulation of the activity of these enzymes is associated with cancer; therefore it is important that the HAT and HDAC equilibrium is regained. This equilibrium can be improved through the inhibition of HDAC enzymes using HDAC inhibitors. Vorinostat is a HDAC inhibitor, clinically approved for the treatment of CTCL, and is in phase II clinical trials for AML and a number of haematological malignancies. Studies have shown that some patients are non-responsive/resistant to Vorinostat; therefore a fuller characterisation of Vorinostat needs to be made so an adequate combination drug can be identified, as understanding of resistance is crucial to overcoming it. The purpose of this study was to provide a comprehensive analysis of Vorinostat in AML cell lines and to identify potential synergistic therapies that could be used in combination with Vorinostat to provide a better outlook in AML. The global identification of genes associated with Vorinostat induced histone H3 lysine 9 (H3K9) acetylation, investigated using chromatin immunoprecipitation coupled with next generation sequencing (ChIP-SEQ), was integrated with data from gene expression studies to provide a comprehensive approach to understanding Vorinostat. This study has identified the sonic hedgehog homolog (SHH) as a rational and potential therapeutic target for combination therapy with Vorinostat

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The state transition acetyltransferase GNAT2 interacts with GNAT1 and GNAT3 in independent complexes

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