Zobrazeno 1 - 10
of 12
pro vyhledávání: '"Kim D. Allen"'
Autor:
Kim D Allen, Matthew J Regier, Changchi Hsieh, Panayiotis Tsokas, Maya Barnard, Shwetha Phatarpekar, Jason Wolk, Todd C Sacktor, André A Fenton, A Iván Hernández
Publikováno v:
PLoS ONE, Vol 13, Iss 10, p e0203374 (2018)
The transition from short-term to long-term forms of synaptic plasticity requires protein synthesis and new gene expression. Most efforts to understand experience-induced changes in neuronal gene expression have focused on the transcription products
Externí odkaz:
https://doaj.org/article/3107d3cc03814cc89e1c93bd4807af16
Autor:
Kim D Allen, Andrei V Gourov, Christopher Harte, Peng Gao, Clarice Lee, Darlene Sylvain, Joshua M Splett, William C Oxberry, Paula S van de Nes, Matthew J Troy-Regier, Jason Wolk, Juan M Alarcon, A Iván Hernández
Publikováno v:
PLoS ONE, Vol 9, Iss 8, p e104364 (2014)
Long-term memory (LTM) formation requires new protein synthesis and new gene expression. Based on our work in Aplysia, we hypothesized that the rRNA genes, stimulation-dependent targets of the enzyme Poly(ADP-ribose) polymerase-1 (PARP-1), are primar
Externí odkaz:
https://doaj.org/article/25063816b40f43d28fe0314baf7f13c0
Autor:
He Gong, Nina V Romanova, Kim D Allen, Pavithra Chandramowlishwaran, Kavita Gokhale, Gary P Newnam, Piotr Mieczkowski, Michael Y Sherman, Yury O Chernoff
Publikováno v:
PLoS Genetics, Vol 8, Iss 4, p e1002634 (2012)
Polyglutamine expansion causes diseases in humans and other mammals. One example is Huntington's disease. Fragments of human huntingtin protein having an expanded polyglutamine stretch form aggregates and cause cytotoxicity in yeast cells bearing end
Externí odkaz:
https://doaj.org/article/6c8122be073a44bba6c5f45d4da6a25e
Autor:
André A. Fenton, Matthew J. Regier, Panayiotis Tsokas, Shwetha Phatarpekar, A. Iván Hernández, Maya Barnard, Changchi Hsieh, Todd Charlton Sacktor, Jason Wolk, Kim D. Allen
Publikováno v:
PLoS ONE, Vol 13, Iss 10, p e0203374 (2018)
PLoS ONE
PLoS ONE
The transition from short-term to long-term forms of synaptic plasticity requires protein synthesis and new gene expression. Most efforts to understand experience-induced changes in neuronal gene expression have focused on the transcription products
Autor:
Keith D. Wilkinson, Susanne Müller, Peggy A. Winslett, Gary P. Newnam, Yury O. Chernoff, Tatiana A. Chernova, Kristin B. Wittich, Kim D. Allen, Renee D. Wegrzyn
Publikováno v:
Genetics. 169:1227-1242
[PSI+] is a prion isoform of the yeast release factor Sup35. In some assays, the cytosolic chaperones Ssa1 and Ssb1/2 of the Hsp70 family were previously shown to exhibit “pro-[PSI+]” and “anti-[PSI+]” effects, respectively. Here, it is demon
Publikováno v:
Molecular and Cellular Biology. 19:8103-8112
Propagation of the yeast protein-based non-Mendelian element [PSI], a prion-like form of the release factor Sup35, was shown to be regulated by the interplay between chaperone proteins Hsp104 and Hsp70. While overproduction of Hsp104 protein cures ce
Autor:
Kavita C. Gokhale, Yury O. Chernoff, He Gong, Kim D. Allen, Michael Y. Sherman, Gary P. Newnam, Nina V. Romanova, Pavithra Chandramowlishwaran, Piotr A. Mieczkowski
Publikováno v:
PLoS Genetics, Vol 8, Iss 4, p e1002634 (2012)
PLoS Genetics
PLoS Genetics
Polyglutamine expansion causes diseases in humans and other mammals. One example is Huntington's disease. Fragments of human huntingtin protein having an expanded polyglutamine stretch form aggregates and cause cytotoxicity in yeast cells bearing end
Publikováno v:
The FASEB Journal. 22
Publikováno v:
Communicative & Integrative Biology
Widely thought to be a housekeeping process, the regulation and synthesis of rRNA emerges as a potentially central mechanism for the maintenance of synaptic plasticity and memory. We have recently shown that an essential component of late-phase synap
Publikováno v:
The Journal of biological chemistry. 282(5)
The yeast prion [PSI+] is a self-propagating amyloidogenic isoform of the translation termination factor Sup35. Overproduction of the chaperone protein Hsp104 results in loss of [PSI+]. Here we demonstrate that this effect is decreased by deletion of