Mice, Inbred C57BL

Publication Title: 
The Journal of Biological Chemistry

Elevated LDL-cholesterol is a risk factor for the development of cardiovascular disease. Thus, proper control of LDL-cholesterol homeostasis is critical for organismal health. Genetic analysis has identified PCSK9 (proprotein convertase subtilisin/kexin type 9) as a crucial gene in the regulation of LDL-cholesterol via control of LDL receptor degradation. Although biochemical characteristics and clinical implications of PCSK9 have been extensively investigated, epigenetic regulation of this gene is largely unknown.

Tao, Rongya
Xiong, Xiwen
DePinho, Ronald A.
Deng, Chu-Xia
Dong, X. Charlie
Publication Title: 
Methods in Molecular Biology (Clifton, N.J.)

Calorie restriction is the most powerful method currently known to delay aging-associated disease and extend lifespan. Use of this technique in combination with genetic models has led to identification of key metabolic regulators of lifespan. Limiting energy availability by restricting caloric intake leads to redistribution of energy expenditure and storage.

Curtis, Jessica
de Cabo, Rafael
Publication Title: 
Clinical Cancer Research: An Official Journal of the American Association for Cancer Research

PURPOSE: To test ribozymes targeting mouse telomerase RNA (mTER) for suppression of the progression of B16-F10 murine melanoma metastases in vivo. EXPERIMENTAL DESIGN: Hammerhead ribozymes were designed to target mTER. The ribozyme sequences were cloned into a plasmid expression vector containing EBV genomic elements that substantially prolong expression of genes delivered in vivo. The activity of various antitelomerase ribozymes or control constructs was examined after i.v. injection of cationic liposome:DNA complexes containing control or ribozyme constructs.

Nosrati, Mehdi
Li, Shang
Bagheri, Sepideh
Ginzinger, David
Blackburn, Elizabeth H.
Debs, Robert J.
Kashani-Sabet, Mohammed
Publication Title: 
Proceedings of the National Academy of Sciences of the United States of America

Recent studies have demonstrated a role for telomerase in driving tumor progression, but its mechanism of action remains unclear. Here we show that stable, ribozyme-mediated suppression of mouse telomerase RNA reduced telomerase RNA expression, telomerase activity, and telomere length, which significantly reduced tumor invasion and metastatic potential. Our studies reveal that previously unidentified effects of telomerase may mediate its tumor-promoting effects.

Bagheri, Sepideh
Nosrati, Mehdi
Li, Shang
Fong, Sylvia
Torabian, Sima
Rangel, Javier
Moore, Dan H.
Federman, Scot
Laposa, Rebecca R.
Baehner, Frederick L.
Sagebiel, Richard W.
Cleaver, James E.
Haqq, Christopher
Debs, Robert J.
Blackburn, Elizabeth H.
Kashani-Sabet, Mohammed
Publication Title: 
Mammalian Genome: Official Journal of the International Mammalian Genome Society

Prader-Willi syndrome (PWS) results from loss of function of a 1.0- to 1.5-Mb domain of imprinted, paternally expressed genes in human Chromosome (Chr) 15q11-q13. The loss of imprinted gene expression in the homologous region in mouse Chr 7C leads to a similar neonatal PWS phenotype. Several protein-coding genes in the human PWS region are intronless, possibly arising by retrotransposition. Here we present evidence for continued acquisition of genes by the mouse PWS region during evolution.

Chai, J. H.
Locke, D. P.
Ohta, T.
Greally, J. M.
Nicholls, R. D.
Publication Title: 
Biological Psychiatry

BACKGROUND: There has been recent interest in the possibility that epigenetic mechanisms might contribute to the transgenerational transmission of stress-induced vulnerability. Here, we focused on possible paternal transmission with the social defeat stress paradigm. METHODS: Adult male mice exposed to chronic social defeat stress or control nondefeated mice were bred with normal female mice, and their offspring were assessed behaviorally for depressive- and anxiety-like measures. Plasma levels of corticosterone and vascular endothelial growth factor were also assayed.

Dietz, David M.
LaPlant, Quincey
Watts, Emily L.
Hodes, Georgia E.
Russo, Scott J.
Feng, Jian
Oosting, Ronald S.
Vialou, Vincent
Nestler, Eric J.
Publication Title: 
Science (New York, N.Y.)

Environmental stressors during childhood and adolescence influence postnatal brain maturation and human behavioral patterns in adulthood. Accordingly, excess stressors result in adult-onset neuropsychiatric disorders. We describe an underlying mechanism in which glucocorticoids link adolescent stressors to epigenetic controls in neurons.

Niwa, Minae
Jaaro-Peled, Hanna
Tankou, Stephanie
Seshadri, Saurav
Hikida, Takatoshi
Matsumoto, Yurie
Cascella, Nicola G.
Kano, Shin-ichi
Ozaki, Norio
Nabeshima, Toshitaka
Sawa, Akira
Publication Title: 
Molecular Psychiatry

Postpartum depression (PPD) affects ?10-18% of women in the general population and results in serious consequences to both the mother and offspring. We hypothesized that predisposition to PPD risk is due to an altered sensitivity to estrogen-mediated epigenetic changes that act in a cell autonomous manner detectable in the blood. We investigated estrogen-mediated epigenetic reprogramming events in the hippocampus and risk to PPD using a cross-species translational design.

Guintivano, J.
Arad, M.
Gould, T. D.
Payne, J. L.
Kaminsky, Z. A.
Publication Title: 
Proceedings of the National Academy of Sciences of the United States of America

Transcriptional dysregulation is an early feature of Huntington disease (HD). We observed gene-specific changes in histone H3 lysine 4 trimethylation (H3K4me3) at transcriptionally repressed promoters in R6/2 mouse and human HD brain. Genome-wide analysis showed a chromatin signature for this mark. Reducing the levels of the H3K4 demethylase SMCX/Jarid1c in primary neurons reversed down-regulation of key neuronal genes caused by mutant Huntingtin expression. Finally, reduction of SMCX/Jarid1c in primary neurons from BACHD mice or the single Jarid1 in a Drosophila HD model was protective.

Vashishtha, Malini
Ng, Christopher W.
Yildirim, Ferah
Gipson, Theresa A.
Kratter, Ian H.
Bodai, Laszlo
Song, Wan
Lau, Alice
Labadorf, Adam
Vogel-Ciernia, Annie
Troncosco, Juan
Ross, Christopher A.
Bates, Gillian P.
Krainc, Dimitri
Sadri-Vakili, Ghazaleh
Finkbeiner, Steven
Marsh, J. Lawrence
Housman, David E.
Fraenkel, Ernest
Thompson, Leslie M.
Publication Title: 
Nature Neuroscience

Chronic exposure to drugs of abuse or stress regulates transcription factors, chromatin-modifying enzymes and histone post-translational modifications in discrete brain regions. Given the promiscuity of the enzymes involved, it has not yet been possible to obtain direct causal evidence to implicate the regulation of transcription and consequent behavioral plasticity by chromatin remodeling that occurs at a single gene.

Heller, Elizabeth A.
Cates, Hannah M.
PeÒa, Catherine J.
Sun, HaoSheng
Shao, Ningyi
Feng, Jian
Golden, Sam A.
Herman, James P.
Walsh, Jessica J.
Mazei-Robison, Michelle
Ferguson, Deveroux
Knight, Scott
Gerber, Mark A.
Nievera, Christian
Han, Ming-Hu
Russo, Scott J.
Tamminga, Carol S.
Neve, Rachael L.
Shen, Li
Zhang, H. Steve
Zhang, Feng
Nestler, Eric J.


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