Zobrazeno 1 - 7
of 7
pro vyhledávání: '"Mannie M Y Fan"'
Autor:
Malcolm A. Smith, Mannie M. Y. Fan, Lawrence D. Mayer, Richard B. Lock, Peter J. Houghton, Hernan Carol, Troy Harasym, Ingrid Boehm
Publikováno v:
Pediatric Blood & Cancer. 62:65-71
Background CPX-351, a liposomal formulation of cytarabine and daunorubicin co-encapsulated at an optimized synergistic 5:1 molar ratio, has demonstrated improved clinical outcomes over conventional cytarabine/daunorubicin treatment in a randomized ph
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::d47f727894f658adf16eeb3e23a81751
https://doi.org/10.1002/pbc.25133
https://doi.org/10.1002/pbc.25133
Autor:
Mannie M Y Fan, Lily Y. J. Zhang, Lynn A. Raymond, Catherine M. Cowan, Michael R. Hayden, Jacqueline Shehadeh, Rona K. Graham, Jing Fan
Publikováno v:
The Journal of neuroscience : the official journal of the Society for Neuroscience. 28(48)
Huntington disease (HD), caused by CAG expansion in the ubiquitously expressed huntingtin gene, is characterized by early dysfunction and death of striatal medium-sized spiny neurons (MSNs). Previous work has shown MSN-specific alterations in NMDA re
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::a564cc43a8fc94c3e2a6d3680497a3e3
https://pubmed.ncbi.nlm.nih.gov/19036965
https://pubmed.ncbi.nlm.nih.gov/19036965
Publikováno v:
Journal of neurochemistry. 104(3)
Huntington's disease is caused by a polyglutamine expansion in the huntingtin (htt) protein, and previous data indicate that over-activation of NMDA receptors (NMDARs) may be involved in the selective degeneration of cells expressing NR1/NR2B NMDARs.
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::e07fb5b661ac21d705800accad684f32
https://pubmed.ncbi.nlm.nih.gov/17971125
https://pubmed.ncbi.nlm.nih.gov/17971125
Overactivation of NMDA receptors (NMDARs) is believed to play a role in degeneration of striatal medium-sized spiny neurons (MSNs) in Huntington's disease (HD). This hereditary disorder is caused by an expansion >35 in the polyglutamine (polyQ) regio
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::812229cbc927a9e055578bc54b128d8b
https://europepmc.org/articles/PMC6672397/
https://europepmc.org/articles/PMC6672397/
Proliferating neural precursor cells as first step toward neuroregeneration in Huntington's disease?
Autor:
Mannie M Y, Fan, Jing, Fan
Publikováno v:
The Journal of neuroscience : the official journal of the Society for Neuroscience. 26(52)
Neural stem and progenitor cells are located in the subependyma of the adult forebrain. An increase in adult subependymal cell proliferation is reported after various kinds of brain injury. We demonstrate an expansion of neural precursor cells in the
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=pmid________::d8b14a2a6d652634e748b0f3d9092e6a
https://pubmed.ncbi.nlm.nih.gov/17035529
https://pubmed.ncbi.nlm.nih.gov/17035529
Autor:
Mannie M Y Fan, Lynn A. Raymond
Publikováno v:
Progress in neurobiology. 81(5-6)
Many lines of evidence support a role for neuronal damage arising as a result of excessive activation of glutamate receptors by excitatory amino acids in the pathogenesis of Huntington disease. The N-methyl-d-aspartate subclass of ionotropic glutamat
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::0dc103c41bedd2edd17daccb714fa1cb
https://pubmed.ncbi.nlm.nih.gov/17188796
https://pubmed.ncbi.nlm.nih.gov/17188796
Autor:
Mannie M Y Fan, Jing Fan
Publikováno v:
The Journal of Neuroscience. 26:13411-13412
Endogenous neural stem cells (NSCs) within the adult mammalian forebrain have been demonstrated to undergo enhanced cell proliferation and differentiation in response to neurodegenerative disease. Increased proliferation of cells in the subependyma (
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::6ddb0729a34564000c2569e468cf4616
https://doi.org/10.1523/jneurosci.4832-06.2006
https://doi.org/10.1523/jneurosci.4832-06.2006