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      Expression profiling of the ubiquitin conjugating enzyme UbcM2 in murine brain reveals modest age-dependent decreases in specific neurons.

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          Abstract

          UbcM2 is a ubiquitin-conjugating enzyme with roles in the turnover of damaged and misfolded proteins, cell cycle progression, development, and regulation of the antioxidant transcription factor, Nrf2. Recent screens have identified binding partners of the enzyme that are associated with various neurodegenerative diseases, and our previous studies have shown that UbcM2 is enriched in retina and brain.

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          Nonlinear mixed effects models for repeated measures data.

          M Lindstrom, D M Bates (1990)
          We propose a general, nonlinear mixed effects model for repeated measures data and define estimators for its parameters. The proposed estimators are a natural combination of least squares estimators for nonlinear fixed effects models and maximum likelihood (or restricted maximum likelihood) estimators for linear mixed effects models. We implement Newton-Raphson estimation using previously developed computational methods for nonlinear fixed effects models and for linear mixed effects models. Two examples are presented and the connections between this work and recent work on generalized linear mixed effects models are discussed.
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            A protein-protein interaction network for human inherited ataxias and disorders of Purkinje cell degeneration.

            Janghoo Lim, Tong Hao, Chad Shaw … (2006)
            Many human inherited neurodegenerative disorders are characterized by loss of balance due to cerebellar Purkinje cell (PC) degeneration. Although the disease-causing mutations have been identified for a number of these disorders, the normal functions of the proteins involved remain, in many cases, unknown. To gain insight into the function of proteins involved in PC degeneration, we developed an interaction network for 54 proteins involved in 23 inherited ataxias and expanded the network by incorporating literature-curated and evolutionarily conserved interactions. We identified 770 mostly novel protein-protein interactions using a stringent yeast two-hybrid screen; of 75 pairs tested, 83% of the interactions were verified in mammalian cells. Many ataxia-causing proteins share interacting partners, a subset of which have been found to modify neurodegeneration in animal models. This interactome thus provides a tool for understanding pathogenic mechanisms common for this class of neurodegenerative disorders and for identifying candidate genes for inherited ataxias.
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              NRF2, a member of the NFE2 family of transcription factors, is not essential for murine erythropoiesis, growth, and development.

              Peter Chan, Anita S. Y. Kan, Jui-fen R Lu … (1996)
              The locus control region of the beta-globin gene is composed of four erythroid-specific hypersensitive sites. Hypersensitive site 2 has been shown to be a powerful enhancer and contains a tandem repeat sequence for the transcription factors AP1 and NFE2 (activating protein 1 and nuclear factor erythroid 2, respectively). The human NRF2 (NFE2 related factor 2) has been isolated by bacterial expression screening using this core sequence as a probe. p45-NFE2, NRF1, and NRF2 belong to the CNC ("cap 'n' collar") subfamily of the basic region-leucine zipper transcription factors, which exhibits strong homology at specific regions such as the "CNC" and the DNA binding and leucine zipper domains. Although the erythroid-specific p45-NFE2 has been implicated in globin gene regulation, p45-NFE2 null mice succumb to bleedings due to lack of platelets and those that survive exhibit only a mild anemia. To determine the function of NRF2, which we found to be widely expressed in vivo, we have characterized the genomic structure of the mouse NRF2 gene, disrupted the Nrf2 gene by homologous recombination in mouse embryonic stem cells (ES cells), and generated NRF2-/- mice. Homozygous mutant mice developed normally, were not anemic, reached adulthood, and reproduced. Our studies indicate that NRF2 is dispensable for mouse development.
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                Author and article information

                Journal
                Journal ID (iso-abbrev): BMC Neurosci
                Title: BMC neuroscience
                Publisher: Springer Science and Business Media LLC
                ISSN (Electronic): 1471-2202
                ISSN (Print): 1471-2202
                Publication date (Electronic): Nov 13 2015
                Volume: 16
                Affiliations
                [1 ] Aging and Metabolism Research Program, Oklahoma Medical Research Foundation, 825 Northeast 13th Street, Oklahoma City, OK, USA. larabeec@omrf.org.
                [2 ] Oklahoma Center for Neuroscience, University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA. larabeec@omrf.org.
                [3 ] Arthritis and Clinical Immunology Research Program, Oklahoma Medical Research Foundation, 825 Northeast 13th Street, Oklahoma City, OK, USA. georgescuc@omrf.org.
                [4 ] Arthritis and Clinical Immunology Research Program, Oklahoma Medical Research Foundation, 825 Northeast 13th Street, Oklahoma City, OK, USA. wrenj@omrf.org.
                [5 ] Aging and Metabolism Research Program, Oklahoma Medical Research Foundation, 825 Northeast 13th Street, Oklahoma City, OK, USA. plafkers@omrf.org.
                [6 ] Oklahoma Center for Neuroscience, University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA. plafkers@omrf.org.
                Article
                Publisher Item ID: 10.1186/s12868-015-0194-y
                DOI: 10.1186/s12868-015-0194-y
                PMC ID: 4644300
                PubMed ID: 26566974
                SO-VID: e778e663-ea89-4a0f-9ef6-b28db2c2e3bc
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