Kinetics of histone hyperacetylation and deacetylation in human diploid fibroblasts

Duncan, Michael R.; Robinson, Margaret J.; Dell’Orco, Robert T.

doi:10.1016/0167-4889(83)90074-5

Cited by 14 publications

(2 citation statements)

References 20 publications

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“…A correlation between the onset of hyperacetylation and radiosensitization has been established for a variety of HDAC inhibitors across a series of tumor cell lines. However, histone acetylation and deacetylation is a dynamic process with some species of acetylated histones having a half-life on the order of minutes . The standard protocol testing an HDAC inhibitor in combination with radiation involves exposing cells to the inhibitor for 24 to 48 h irradiation, followed by trypsinization and seeding cells into HDAC inhibitor-free media for analysis of clonogenic survival.…”

Section: Targets For Intrinsic Tumor Cell Radiosensitizationmentioning

confidence: 99%

“…However, histone acetylation and deacetylation is a dynamic process with some species of acetylated histones having a half-life on the order of minutes. 105 The standard protocol testing an HDAC inhibitor in combination with radiation involves exposing cells to the inhibitor for 24 to 48 h irradiation, followed by trypsinization and seeding cells into HDAC inhibitor-free media for analysis of clonogenic survival. Following this treatment protocol often resulted in minor to no increase in radiosensitivity.…”

Section: Histone Deacetylasementioning

confidence: 99%

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Molecular Targets for Tumor Radiosensitization

Tofilon

Camphausen

2009

Chem. Rev.

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Francisco (UCSF), in the pharmacology department and then moved with his thesis advisor to the University of Nebraska Medical Center in Omaha where he received his Ph.D. in 1981. In the fall of 1981 he returned to UCSF accepting a postdoctoral fellowship with Dr. Dennis Deen in the Brain Tumor Research Center where he was introduced to radiobiology, which has continued to be his primary area of research. In 1984, he joined the faculty of the Department of Experimental Radiation Oncology at the University of Texas M.D. Anderson Cancer Center in Houston as an assistant professor. His research at M.D. Anderson focused on drug-radiation interactions. He was eventually promoted to professor in 1996 with a joint appointment as professor in the Department of Neurosurgery. In June of 2001, he joined the National Cancer Institute as Chief of the newly created Molecular Radiation Therapeutics Branch. He relocated to the H. Lee Moffitt Cancer Center in 2006 as Professor/Member in the Drug Discovery Department. His current research is focused on the identification of the molecular determinants of radiosensitivity and the development of molecularly targeted radiosensitizers. Kevin Camphausen received his undergraduate degree from Purdue University in 1988. He then completed his MD (1996) and medical internship (1997) at Georgetown University Medical Center. He next completed his residency in radiation oncology at the Joint Center of Radiation Therapy at Harvard Medical School (2001). While there, he worked in the laboratory of Dr. Judah Folkman studying the interactions of antiangiogenic therapy and radiotherapy. He joined the Radiation Oncology Branch in 2001 as a tenure track investigator. He has recently received tenure at the NIH (2007) and was promoted to be the Chief of the Radiation Oncology Branch (ROB), Center for Cancer Research (CCR), NCI (2007). He is a physician/scientist who has a laboratory program focusing on the development and characterization of agents that alter the tumoral response to radiation. He has been successful in translating his work from the laboratory to the clinic. Dr. Camphausen is an internationally recognized leader in his field and an expert in the field of drug-induced tumor radiosensitization including the use of antiangiogenic agents in combination with radiotherapy.

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Section: Targets For Intrinsic Tumor Cell Radiosensitizationmentioning

confidence: 99%

Section: Histone Deacetylasementioning

confidence: 99%

Molecular Targets for Tumor Radiosensitization

Tofilon

Camphausen

2009

Chem. Rev.

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Epigenetic Histone Changes in the Toxicologic Mode of Action of Arsenic

Reichard

Puga

2012

Toxicology and Epigenetics

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KAT(ching) Metabolism by the Tail: Insight into the Links between Lysine Acetyltransferases and Metabolism

Albaugh¹,

Arnold²,

Denu³

2010

ChemBioChem

102

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Post-translational modifications of histones elicit structural and functional changes within chromatin that regulate various epigenetic processes. Epigenetic mechanisms rely on enzymes whose activities are driven by co-enzymes and metabolites from intermediary metabolism. Lysine acetyltransferases (KATs) catalyze the transfer of acetyl groups from acetyl-CoA to epsilon amine groups. Utilization of this critical metabolite suggests these enzymes are modulated by the metabolic status of the cell. This review highlights studies linking KATs to metabolism. We cover newly identified acyl-modifications (propionylation and butyrylation), discuss the control of KAT activity by cellular acetyl-CoA levels, and provide insights into how acetylation regulates metabolic proteins. Lastly, we conclude with a discussion of the current approaches for identifying novel KATs and their metabolic substrates.

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Kinetics of histone hyperacetylation and deacetylation in human diploid fibroblasts

Cited by 14 publications

References 20 publications

Molecular Targets for Tumor Radiosensitization

Molecular Targets for Tumor Radiosensitization

Epigenetic Histone Changes in the Toxicologic Mode of Action of Arsenic

KAT(ching) Metabolism by the Tail: Insight into the Links between Lysine Acetyltransferases and Metabolism

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