Zobrazeno 1 - 10
of 20
pro vyhledávání: '"Jannic Boehm"'
Publikováno v:
Neurobiology of Disease, Vol 91, Iss , Pp 94-104 (2016)
Alzheimer disease (AD) is initially characterized as a disease of the synapse that affects synaptic transmission and synaptic plasticity. While amyloid-beta and tau have been traditionally implicated in causing AD, recent studies suggest that other f
Externí odkaz:
https://doaj.org/article/e5e5f2d6cc144c498eb77d67308fa681
Publikováno v:
PLoS ONE, Vol 8, Iss 6, p e65350 (2013)
Alzheimer disease is characterized by a gradual decrease of synaptic function and, ultimately, by neuronal loss. There is considerable evidence supporting the involvement of oligomeric amyloid-beta (Aβ) in the etiology of Alzheimer's disease. Histor
Externí odkaz:
https://doaj.org/article/583b3404b9b34a6b950187dddadf9771
Publikováno v:
International Journal of Alzheimer's Disease, Vol 2012 (2012)
Alzheimer’s disease (AD) is defined by the concurrence of accumulation of abnormal aggregates composed of two proteins: Amyloid beta (Aβ) and tau, and of cellular changes including neurite degeneration and loss of neurons and cognitive functions.
Externí odkaz:
https://doaj.org/article/638414c97a7e4465aeba84a4da2054f2
Autor:
Jannic Boehm, Nicolas Paradis-Isler
Publikováno v:
Journal of Biological Chemistry. 293:9311-9325
Argonaute (AGO) proteins are essential components of the microRNA (miRNA) pathway. AGO proteins are loaded with miRNAs to target mRNAs and thereby regulate mRNA stability and protein translation. As such, AGO proteins are important actors in controll
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::47eec527401022632035be069f8289e0
https://doi.org/10.1074/jbc.ra117.001007
https://doi.org/10.1074/jbc.ra117.001007
Autor:
Emilie Trillaud-Doppia, Jannic Boehm
Publikováno v:
Biological Psychiatry. 83:406-415
Background Human studies and mouse models of Alzheimer's disease suggest that the amyloid precursor protein (APP) can cause changes in synaptic plasticity and is contributing to the memory deficits seen in Alzheimer's disease. While most of these stu
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::098b7e20306615e6fa837923ada26db8
https://doi.org/10.1016/j.biopsych.2016.12.015
https://doi.org/10.1016/j.biopsych.2016.12.015
Publikováno v:
Neurobiology of Disease, Vol 91, Iss, Pp 94-104 (2016)
Alzheimer disease (AD) is initially characterized as a disease of the synapse that affects synaptic transmission and synaptic plasticity. While amyloid-beta and tau have been traditionally implicated in causing AD, recent studies suggest that other f
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::c82120616604f65aa912a20ca9c2eed1
http://www.sciencedirect.com/science/article/pii/S0969996116300377
http://www.sciencedirect.com/science/article/pii/S0969996116300377
Publikováno v:
Current biology : CB. 30(7)
Synaptic plasticity, with its two most studied forms, long-term potentiation (LTP) and long-term depression (LTD), is the cellular mechanism underlying learning and memory. Although it has been known for two decades that bidirectional synaptic plasti
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::0a2e5c30c5cc457c8a988bdfe9823c9d
https://pubmed.ncbi.nlm.nih.gov/32084406
https://pubmed.ncbi.nlm.nih.gov/32084406
Autor:
Roberto Malinow, Taisuke Tomita, Takeshi Iwatsubo, Jannic Boehm, Helen Hsieh, Chihiro Sato, Sangram S. Sisodia
Publikováno v:
Neuron. 52(5):831-843
Beta amyloid (Abeta), a peptide generated from the amyloid precursor protein (APP) by neurons, is widely believed to underlie the pathophysiology of Alzheimer's disease. Recent studies indicate that this peptide can drive loss of surface AMPA and NMD
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::e29511b910be584f58df183848949955
Publikováno v:
The EMBO Journal. 20:4153-4162
The BOB.1/OBF.1 coactivator is critically involved in mediating octamer-dependent transcriptional activity in B lymphocytes. Mice lacking this coactivator show various defects in B-cell development, most notably they completely lack germinal centers.
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::9580d653b91a73bd9db2295d89337b72
https://doi.org/10.1093/emboj/20.15.4153
https://doi.org/10.1093/emboj/20.15.4153
Publikováno v:
The European journal of neuroscience. 37(12)
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::fb022415f2d21228e8c7c8a64d9b0e4b
https://pubmed.ncbi.nlm.nih.gov/23773056
https://pubmed.ncbi.nlm.nih.gov/23773056