The Suv39H1 methyltransferase inhibitor chaetocin causes induction of integrated HIV-1 without producing a T cell response

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The Suv39H1 methyltransferase inhibitor chaetocin causes induction of integrated HIV-1 without producing a T cell response. / Bernhard, Wendy; Barreto, Kris; Saunders, Amy et al.
In: FEBS Letters, Vol. 585, No. 22, 16.11.2011, p. 3549-54.

Research output: Contribution to Journal/Magazine › Journal article › peer-review

Harvard

Bernhard, W, Barreto, K, Saunders, A, Dahabieh, MS, Johnson, P & Sadowski, I 2011, 'The Suv39H1 methyltransferase inhibitor chaetocin causes induction of integrated HIV-1 without producing a T cell response', FEBS Letters, vol. 585, no. 22, pp. 3549-54. https://doi.org/10.1016/j.febslet.2011.10.018

APA

Bernhard, W., Barreto, K., Saunders, A., Dahabieh, M. S., Johnson, P., & Sadowski, I. (2011). The Suv39H1 methyltransferase inhibitor chaetocin causes induction of integrated HIV-1 without producing a T cell response. FEBS Letters, 585(22), 3549-54. https://doi.org/10.1016/j.febslet.2011.10.018

Vancouver

Bernhard W, Barreto K, Saunders A, Dahabieh MS, Johnson P, Sadowski I. The Suv39H1 methyltransferase inhibitor chaetocin causes induction of integrated HIV-1 without producing a T cell response. FEBS Letters. 2011 Nov 16;585(22):3549-54. doi: 10.1016/j.febslet.2011.10.018

Author

Bernhard, Wendy ; Barreto, Kris ; Saunders, Amy et al. / The Suv39H1 methyltransferase inhibitor chaetocin causes induction of integrated HIV-1 without producing a T cell response. In: FEBS Letters. 2011 ; Vol. 585, No. 22. pp. 3549-54.

Bibtex

@article{33d9cbbea47e452fa7bc461d2a6f3503,

title = "The Suv39H1 methyltransferase inhibitor chaetocin causes induction of integrated HIV-1 without producing a T cell response",

abstract = "Latent HIV-1 (human immunodeficiency virus-1) provirus is unaffected by current AIDS (acquired immunodeficiency syndrome) therapies. We show here that chaetocin, an SUV39H1 histone methyltransferase inhibitor, causes 25-fold induction of latent HIV-1 expression, while producing minimal toxicity and without causing T cell activation. Induction is associated with loss of histone H3 lysine 9 (H3K9) trimethylation at the long terminal repeat (LTR) promoter, and a corresponding increase in H3K9 acetylation. The effect of chaetocin is amplified synergistically in combination with histone deacetylase (HDAC) inhibitors. These results indicate that chaetocin may provide a therapy to purge cells of latent HIV-1, possibly in combination with other chromatin remodeling drugs.",

keywords = "Acetylation, Chromatin Assembly and Disassembly, Drug Synergism, HIV Long Terminal Repeat, HIV-1/drug effects, Histone Deacetylase Inhibitors/pharmacology, Histones/metabolism, Humans, Jurkat Cells, Methylation, Methyltransferases/antagonists & inhibitors, Piperazines/pharmacology, Repressor Proteins/antagonists & inhibitors, T-Lymphocytes/immunology, Virus Activation, Virus Latency/drug effects",

author = "Wendy Bernhard and Kris Barreto and Amy Saunders and Dahabieh, {Matthew S} and Pauline Johnson and Ivan Sadowski",

year = "2011",

month = nov,

day = "16",

doi = "10.1016/j.febslet.2011.10.018",

language = "English",

volume = "585",

pages = "3549--54",

journal = "FEBS Letters",

issn = "0014-5793",

publisher = "Elsevier",

number = "22",

}

RIS

TY - JOUR

T1 - The Suv39H1 methyltransferase inhibitor chaetocin causes induction of integrated HIV-1 without producing a T cell response

AU - Bernhard, Wendy

AU - Barreto, Kris

AU - Saunders, Amy

AU - Dahabieh, Matthew S

AU - Johnson, Pauline

AU - Sadowski, Ivan

PY - 2011/11/16

Y1 - 2011/11/16

N2 - Latent HIV-1 (human immunodeficiency virus-1) provirus is unaffected by current AIDS (acquired immunodeficiency syndrome) therapies. We show here that chaetocin, an SUV39H1 histone methyltransferase inhibitor, causes 25-fold induction of latent HIV-1 expression, while producing minimal toxicity and without causing T cell activation. Induction is associated with loss of histone H3 lysine 9 (H3K9) trimethylation at the long terminal repeat (LTR) promoter, and a corresponding increase in H3K9 acetylation. The effect of chaetocin is amplified synergistically in combination with histone deacetylase (HDAC) inhibitors. These results indicate that chaetocin may provide a therapy to purge cells of latent HIV-1, possibly in combination with other chromatin remodeling drugs.

AB - Latent HIV-1 (human immunodeficiency virus-1) provirus is unaffected by current AIDS (acquired immunodeficiency syndrome) therapies. We show here that chaetocin, an SUV39H1 histone methyltransferase inhibitor, causes 25-fold induction of latent HIV-1 expression, while producing minimal toxicity and without causing T cell activation. Induction is associated with loss of histone H3 lysine 9 (H3K9) trimethylation at the long terminal repeat (LTR) promoter, and a corresponding increase in H3K9 acetylation. The effect of chaetocin is amplified synergistically in combination with histone deacetylase (HDAC) inhibitors. These results indicate that chaetocin may provide a therapy to purge cells of latent HIV-1, possibly in combination with other chromatin remodeling drugs.

KW - Acetylation

KW - Chromatin Assembly and Disassembly

KW - Drug Synergism

KW - HIV Long Terminal Repeat

KW - HIV-1/drug effects

KW - Histone Deacetylase Inhibitors/pharmacology

KW - Histones/metabolism

KW - Humans

KW - Jurkat Cells

KW - Methylation

KW - Methyltransferases/antagonists & inhibitors

KW - Piperazines/pharmacology

KW - Repressor Proteins/antagonists & inhibitors

KW - T-Lymphocytes/immunology

KW - Virus Activation

KW - Virus Latency/drug effects

U2 - 10.1016/j.febslet.2011.10.018

DO - 10.1016/j.febslet.2011.10.018

M3 - Journal article

C2 - 22020221

VL - 585

SP - 3549

EP - 3554

JO - FEBS Letters

JF - FEBS Letters

SN - 0014-5793

IS - 22

ER -

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