Smyd3 regulates cancer cell phenotypes and catalyzes histone H4 lysine 5 methylation

Glenn S. van Aller; Nicolas Reynoird; Olena Barbash; Michael Huddleston; Shichong Liu; Anne Flore Zmoos; Patrick McDevitt; Robert Sinnamon; Bao Chau Le; Gloria Mas; Roland Annan; Julien Sage; Benjamin A. Garcia; Peter J. Tummino; Or Gozani; Ryan G. Kruger

doi:10.4161/epi.19506

Smyd3 regulates cancer cell phenotypes and catalyzes histone H4 lysine 5 methylation

Glenn S. van Aller
, Nicolas Reynoird
, Olena Barbash
, Michael Huddleston
, Shichong Liu
, Anne Flore Zmoos
, Patrick McDevitt
, Robert Sinnamon
, Bao Chau Le
, Gloria Mas
, Roland Annan
, Julien Sage
, Benjamin A. Garcia
, Peter J. Tummino
, Or Gozani
, Ryan G. Kruger

Research output: Contribution to journal › Article › peer-review

157 Scopus citations

Abstract

Smyd3 is a lysine methyltransferase implicated in chromatin and cancer regulation. Here we show that Smyd3 catalyzes histone H4 methylation at lysine 5 (H4K5me). This novel histone methylation mark is detected in diverse cell types and its formation is attenuated by depletion of Smyd3 protein. Further, Smyd3-driven cancer cell phenotypes require its enzymatic activity. Thus, Smyd3, via H4K5 methylation, provides a potential new link between chromatin dynamics and neoplastic disease.

Original language	English
Pages (from-to)	340-343
Number of pages	4
Journal	Epigenetics
Volume	7
Issue number	4
DOIs	https://doi.org/10.4161/epi.19506
State	Published - Apr 2012

Keywords

Cancer Smyd3
Epigenetics
Lysine
Methylation
Oncogene
Oncology

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10.4161/epi.19506

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@article{27b2f64df1aa43efac74444665ac1c14,

title = "Smyd3 regulates cancer cell phenotypes and catalyzes histone H4 lysine 5 methylation",

abstract = "Smyd3 is a lysine methyltransferase implicated in chromatin and cancer regulation. Here we show that Smyd3 catalyzes histone H4 methylation at lysine 5 (H4K5me). This novel histone methylation mark is detected in diverse cell types and its formation is attenuated by depletion of Smyd3 protein. Further, Smyd3-driven cancer cell phenotypes require its enzymatic activity. Thus, Smyd3, via H4K5 methylation, provides a potential new link between chromatin dynamics and neoplastic disease.",

keywords = "Cancer Smyd3, Epigenetics, Lysine, Methylation, Oncogene, Oncology",

author = "\{van Aller\}, \{Glenn S.\} and Nicolas Reynoird and Olena Barbash and Michael Huddleston and Shichong Liu and Zmoos, \{Anne Flore\} and Patrick McDevitt and Robert Sinnamon and Le, \{Bao Chau\} and Gloria Mas and Roland Annan and Julien Sage and Garcia, \{Benjamin A.\} and Tummino, \{Peter J.\} and Or Gozani and Kruger, \{Ryan G.\}",

note = "Funding Information: and Linda Myers for technical support. This work was supported in part by grants to O.G. (NIH R01 GM079641 and GlaxoSmithKline), to B.A.G. (DP2OD007447 and NSF CAREER Award), and J.S. and O.G. (CIRM RB1-01385). N.R. was funded by a Fondation pour la Recherche Medicale Postdoctoral Fellowship. O.G. is a recipient of an Ellison Senior Scholar in Aging Award.",

year = "2012",

month = apr,

doi = "10.4161/epi.19506",

language = "English",

volume = "7",

pages = "340--343",

journal = "Epigenetics",

issn = "1559-2294",

number = "4",

}

TY - JOUR

T1 - Smyd3 regulates cancer cell phenotypes and catalyzes histone H4 lysine 5 methylation

AU - van Aller, Glenn S.

AU - Reynoird, Nicolas

AU - Barbash, Olena

AU - Huddleston, Michael

AU - Liu, Shichong

AU - Zmoos, Anne Flore

AU - McDevitt, Patrick

AU - Sinnamon, Robert

AU - Le, Bao Chau

AU - Mas, Gloria

AU - Annan, Roland

AU - Sage, Julien

AU - Garcia, Benjamin A.

AU - Tummino, Peter J.

AU - Gozani, Or

AU - Kruger, Ryan G.

N1 - Funding Information: and Linda Myers for technical support. This work was supported in part by grants to O.G. (NIH R01 GM079641 and GlaxoSmithKline), to B.A.G. (DP2OD007447 and NSF CAREER Award), and J.S. and O.G. (CIRM RB1-01385). N.R. was funded by a Fondation pour la Recherche Medicale Postdoctoral Fellowship. O.G. is a recipient of an Ellison Senior Scholar in Aging Award.

PY - 2012/4

Y1 - 2012/4

N2 - Smyd3 is a lysine methyltransferase implicated in chromatin and cancer regulation. Here we show that Smyd3 catalyzes histone H4 methylation at lysine 5 (H4K5me). This novel histone methylation mark is detected in diverse cell types and its formation is attenuated by depletion of Smyd3 protein. Further, Smyd3-driven cancer cell phenotypes require its enzymatic activity. Thus, Smyd3, via H4K5 methylation, provides a potential new link between chromatin dynamics and neoplastic disease.

AB - Smyd3 is a lysine methyltransferase implicated in chromatin and cancer regulation. Here we show that Smyd3 catalyzes histone H4 methylation at lysine 5 (H4K5me). This novel histone methylation mark is detected in diverse cell types and its formation is attenuated by depletion of Smyd3 protein. Further, Smyd3-driven cancer cell phenotypes require its enzymatic activity. Thus, Smyd3, via H4K5 methylation, provides a potential new link between chromatin dynamics and neoplastic disease.

KW - Cancer Smyd3

KW - Epigenetics

KW - Lysine

KW - Methylation

KW - Oncogene

KW - Oncology

UR - https://www.scopus.com/pages/publications/84860549203

U2 - 10.4161/epi.19506

DO - 10.4161/epi.19506

M3 - Article

C2 - 22419068

AN - SCOPUS:84860549203

SN - 1559-2294

VL - 7

SP - 340

EP - 343

JO - Epigenetics

JF - Epigenetics

IS - 4

ER -

Smyd3 regulates cancer cell phenotypes and catalyzes histone H4 lysine 5 methylation

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