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10.2353/ajpath.2009.080583 http://scihub22266oqcxt.onion/10.2353/ajpath.2009.080583 19164506/?report=reader!2665749!19164506     free     free     free Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 267.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Am+J+Pathol 2009 ; 174 (3): 891-7 Nephropedia Template TP {{tp|p=19164506|t=2009. The neuronal expression of MYC causes a neurodegenerative phenotype in a novel transgenic mouse |pdf=|usr=}}{{19164506}} gab.com Text The neuronal expression of MYC causes a neurodegenerative phenotype in a novel transgenic mouse JO: Am J Pathol http://www.kidney.de/pget.php?&tw=1&pmid=19164506 #FOAvip Many different proteins associated with the cell cycle, including cyclins, cyclin-dependent kinases, and proto-oncogenes such as c-MYC (MYC), are increased in degenerating neurons. Consequently, an ectopic activation of the cell cycle machinery in neurons has emerged as a potential pathogenic mechanism of neuronal dysfunction and death in many neurodegenerative diseases, including Alzheimer's disease. However, the exact role of cell cycle re-entry during disease pathogenesis is unclear, primarily because of the lack of relevant research models to study the effects of cell cycle re-entry on mature neurons in vivo. To address this issue, we developed a new transgenic mouse model in which forebrain neurons (CaMKII-MYC) can be induced to enter the cell cycle using the physiologically relevant proto-oncogene MYC to drive cell cycle re-entry. We show that such cell cycle re-entry results in neuronal cell death, gliosis, and cognitive deficits. These findings provide compelling evidence that dysregulation of cell cycle re-entry results in neurodegeneration in vivo. Our current findings, coupled with those of previous reports, strengthen the hypothesis that neurodegeneration in Alzheimer's disease, similar to cellular proliferation in cancer, is a disease that results from inappropriate cell cycle control. Twit Text FOAVip The neuronal expression of MYC causes a neurodegenerative phenotype in a novel transgenic mouse ????Am J Pathol http://www.kidney.de/pget.php?&tw=1&pmid=19164506 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=19164506 #FOAvip English Wikipedia <ref>{{Cite pmid|19164506}}</ref> The neuronal expression of MYC causes a neurodegenerative phenotype in a novel transgenic mouse #MMPMID19164506 Lee HG; Casadesus G; Nunomura A; Zhu X; Castellani RJ; Richardson SL; Perry G; Felsher DW; Petersen RB; Smith MA Am J Pathol 2009[Mar]; 174 (3): 891-7 PMID19164506show ga Many different proteins associated with the cell cycle, including cyclins, cyclin-dependent kinases, and proto-oncogenes such as c-MYC (MYC), are increased in degenerating neurons. Consequently, an ectopic activation of the cell cycle machinery in neurons has emerged as a potential pathogenic mechanism of neuronal dysfunction and death in many neurodegenerative diseases, including Alzheimer's disease. However, the exact role of cell cycle re-entry during disease pathogenesis is unclear, primarily because of the lack of relevant research models to study the effects of cell cycle re-entry on mature neurons in vivo. To address this issue, we developed a new transgenic mouse model in which forebrain neurons (CaMKII-MYC) can be induced to enter the cell cycle using the physiologically relevant proto-oncogene MYC to drive cell cycle re-entry. We show that such cell cycle re-entry results in neuronal cell death, gliosis, and cognitive deficits. These findings provide compelling evidence that dysregulation of cell cycle re-entry results in neurodegeneration in vivo. Our current findings, coupled with those of previous reports, strengthen the hypothesis that neurodegeneration in Alzheimer's disease, similar to cellular proliferation in cancer, is a disease that results from inappropriate cell cycle control. |*Genes, myc[MESH] |Animals[MESH] |Cell Cycle[MESH] |Gene Expression Regulation[MESH] |Heredodegenerative Disorders, Nervous System/*genetics/pathology[MESH] |Hippocampus/physiology[MESH] |Humans[MESH] |Maze Learning[MESH] |Mice[MESH] |Mice, Transgenic[MESH] |Nerve Degeneration/genetics/pathology[MESH] |Neurons/*physiology[MESH] |Phenotype[MESH] |Proto-Oncogene Mas[MESH]The neuronal expression of MYC causes a neurodegenerative phenotype in(epmc).pdf DeepDyve Pubget Overpricing