Nerve Tissue Proteins

Publication Title: 
Genes & Development

The Spt-Ada-Gcn5-acetyltransferase (SAGA) chromatin-modifying complex possesses acetyltransferase and deubiquitinase activities. Within this modular complex, Ataxin-7 anchors the deubiquitinase activity to the larger complex. Here we identified and characterized Drosophila Ataxin-7 and found that reduction of Ataxin-7 protein results in loss of components from the SAGA complex.

Author(s): 
Mohan, Ryan D.
Dialynas, George
Weake, Vikki M.
Liu, Jianqi
Martin-Brown, Skylar
Florens, Laurence
Washburn, Michael P.
Workman, Jerry L.
Abmayr, Susan M.
Publication Title: 
Biochemical and Biophysical Research Communications

Calcium acts as a second messenger and plays a crucial role in signaling pathways involved in cell proliferation. Recently, calcium channels related to calcium influx into the cytosol of epithelial cells have attracted attention as a cancer therapy target. Of these calcium channels, TRPV6 is overexpressed in prostate cancer and is considered an important molecule in the process of metastasis. However, its exact role and mechanism is unclear. NUMB, well-known tumor suppressor gene, is a novel interacting partner of TRPV6.

Author(s): 
Kim, Sung-Young
Hong, Chansik
Wie, Jinhong
Kim, Euiyong
Kim, Byung Joo
Ha, Kotdaji
Cho, Nam-Hyuk
Kim, In-Gyu
Jeon, Ju-Hong
So, Insuk
Publication Title: 
Biogerontology

Insulin-induced PI3K/Akt activation is known to inhibit a family of Forkhead transcription factors (FOXO), which can lead to increased oxidative stress in several model organisms. One of major transcription factors activated by oxidative stress and responsible for the production of many proinflammatory cytokines is NF-kappaB. In the present study, We were carried out to determine the relationship between FOXO1 and NF-kappaB activation using HEK293T cells and aged kidney isolated from ad libitum fed (AL) and 40% calorie restriction (CR) rats.

Author(s): 
Kim, Dae Hyun
Kim, Ji Young
Yu, Byung Pal
Chung, Hae Young
Publication Title: 
Neurobiology of Disease

Huntington's disease (HD) is a lethal, neurodegenerative disorder caused by expansion of the polyglutamine repeat in the Huntingtin gene (HTT), leading to mutant protein misfolding, aggregation, and neuronal death. Feeding a Drosophila HD model cystamine, or expressing a transgene encoding the anti-htt intracellular antibody (intrabody) C4-scFv in the nervous system, demonstrated therapeutic potential, but suppression of pathology was incomplete.

Author(s): 
Bortvedt, S. F.
McLear, J. A.
Messer, A.
Ahern-Rindell, A. J.
Wolfgang, W. J.
Publication Title: 
Physiology & Behavior

Ketogenic diets are high in fat and low in carbohydrates, and have long been used as an anticonvulsant therapy for drug-intractable and pediatric epilepsy. Additionally, ketogenic diets have been shown to provide neuroprotective effects against acute and chronic brain injury, including beneficial effects in various rodent models of neurodegeneration. Huntington's disease is a progressive neurodegenerative disease characterized by neurological, behavioral and metabolic dysfunction, and ketogenic diets have been shown to increase energy molecules and mitochondrial function.

Author(s): 
Ruskin, David N.
Ross, Jessica L.
Kawamura, Masahito
Ruiz, Tiffany L.
Geiger, Jonathan D.
Masino, Susan A.
Publication Title: 
Nucleic Acids Research

Reln mRNA and protein levels are reduced by approximately 50% in various cortical structures of post-mortem brain from patients diagnosed with schizophrenia or bipolar illness with psychosis. To study mechanisms responsible for this down-regulation, we have analyzed the promoter of the human reelin gene. We show that the reelin promoter directs expression of a reporter construct in multiple human cell types: neuroblastoma cells (SHSY5Y), neuronal precursor cells (NT2), differentiated neurons (hNT) and hepatoma cells (HepG2).

Author(s): 
Chen, Ying
Sharma, Rajiv P.
Costa, Robert H.
Costa, Erminio
Grayson, Dennis R.
Publication Title: 
Pharmacopsychiatry

The molecular-genetic basis of non-mendelian, genetically influenced disorders (complex disorders) is beginning to be uncovered. Recently, major progress in localization and detection of disposition genes of schizophrenia and bipolar disorder was achieved. We provide a comprehensive overview of recent results of linkage and association studies in schizophrenia and bipolar disorder. Several disposition genes for schizophrenia (DTNBP1, NRG1, G72) were identified, whereas evidence for specific disposition genes in bipolar disorder is more limited.

Author(s): 
Maier, W.
Zobel, A.
Rietschel, M.
Publication Title: 
Schizophrenia Research

Covalent modifications of DNA and its surrounding chromatin constitute an essential and powerful regulatory mechanism for gene transcription. Epigenetics is the study of this regulatory system. There is now strong albeit indirect evidence that epigenetic mechanisms contribute to the pathophysiology of schizophrenia. Furthermore, the discovery that valproic acid, a widely used psychotropic, has powerful epigenetic effects in clinically relevant concentrations suggests new therapeutic possibilities, i.e., drugs that act on chromatin structure.

Author(s): 
Sharma, Rajiv P.
Publication Title: 
Proceedings of the National Academy of Sciences of the United States of America

The polygenic nature of complex psychiatric disorders suggests a common pathway that may be involved in the down-regulation of multiple genes through an epigenetic mechanism. To investigate the role of methylation in down-regulating the expression of mRNAs that may be associated with the schizophrenia phenotype, we have adopted a cell-culture model amenable to this line of investigation.

Author(s): 
Noh, Jai Sung
Sharma, Rajiv P.
Veldic, Marin
Salvacion, Alain A.
Jia, Xiaomei
Chen, Ying
Costa, Erminio
Guidotti, Alessandro
Grayson, Dennis R.
Publication Title: 
Neuroreport

The aim of this study was to investigate whether the DNA methylation pattern within the alpha synuclein promoter region is altered in intoxicated and early abstinence patients with alcoholism undergoing alcohol withdrawal. We observed a significant increase of the alpha synuclein promoter DNA methylation in patients with alcoholism which was significantly associated with their elevated homocysteine levels. No significant differences of the promoter DNA methylation within a control gene (presenilin-1) in alcoholics and controls were found.

Author(s): 
Bˆnsch, Dominikus
Lenz, Bernd
Kornhuber, Johannes
Bleich, Stefan

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