Zobrazeno 1 - 10
of 10
pro vyhledávání: '"Marianna D'Arco"'
Autor:
Shehrazade Dahimene, Karen M. Page, Manuela Nieto-Rostro, Wendy S. Pratt, Marianna D'Arco, Annette C. Dolphin
Publikováno v:
Neurobiology of Disease, Vol 93, Iss , Pp 243-256 (2016)
Episodic ataxia 2 (EA2) is an autosomal dominant disorder caused by mutations in the gene CACNA1A that encodes the pore-forming CaV2.1 calcium channel subunit. The majority of EA2 mutations reported so far are nonsense or deletion/insertion mutations
Externí odkaz:
https://doaj.org/article/7f9c96e2028b44edbadf8d67e0de0f2f
Publikováno v:
The Journal of Neuroscience. 35:5891-5903
As auxiliary subunits of voltage-gated Ca2+channels, the α2δ proteins modulate membrane trafficking of the channels and their localization to specific presynaptic sites. Following nerve injury, upregulation of the α2δ-1 subunit in sensory dorsal
Autor:
Shu Fun Josephine Ng, Wendy S. Pratt, Michael G. Fadel, Marianna D'Arco, Ryan Walker-Gray, Ivan Kadurin, Anita Alvarez-Laviada, Annette C. Dolphin
Publikováno v:
The Journal of Biological Chemistry
Background: We examined the role of membrane anchoring of voltage-gated calcium channel α2δ subunits. Results: We used a truncated α2δ-1 construct (α2δ-1ΔC-term), which still increases CaV2.1/β1b currents, despite being mainly secreted. Concl
Autor:
Vanessa Leone, Rashid Giniatullin, Nicol Birsa, Marianna D'Arco, Elsa Fabbretti, Paolo Carloni, Asha Nair, Andrea Nistri
Publikováno v:
Journal of Biological Chemistry. 284:21393-21401
On sensory neurons, sensitization of P2X(3) receptors gated by extracellular ATP contributes to chronic pain. We explored the possibility that receptor sensitization may arise from down-regulation of an intracellular signal negatively controlling rec
Autor:
Alessandra Fabbro, Andrea Nistri, Marianna D'Arco, Elsa Fabbretti, Manuela Simonetti, Rashid Giniatullin
Publikováno v:
Journal of Neuroscience. 26:6163-6171
Recent evidence indicates a key role for the neuropeptide calcitonin gene-related peptide (CGRP) in migraine pain, as demonstrated by the strong analgesic action of CGRP receptor antagonists, although the mechanisms of this effect remain unclear. Mos
Autor:
Elsa Fabbretti, Andrea Nistri, Marianna D'Arco, Alessandra Fabbro, Rashid Giniatullin, Lara Masten, Elena Sokolova
Publikováno v:
Journal of Biological Chemistry. 279:53109-53115
On nociceptive neurons, one important mechanism to generate pain signals is the activation of P2X(3) receptors, which are membrane proteins gated by extracellular ATP. In the presence of the agonist, P2X(3) receptors rapidly desensitize and then reco
Autor:
Marianna D'Arco, Annette C. Dolphin
Publikováno v:
Science Signaling. 5
Calcium signaling resulting from depolarization of neurons can trigger changes in transcription, and this response has been called excitation-transcription (E-T) coupling. In neurons, voltage-gated and ligand-gated calcium-permeable channels contribu
Autor:
Manuela Simonetti, Marianna D'Arco, Andrea Nistri, Elsa Fabbretti, Rashid Giniatullin, Alessandra Fabbro, Asha Nair
The molecular mechanisms of migraine pain are incompletely understood, although migraine mediators such as NGF and calcitonin gene-related peptide (CGRP) are believed to play an algogenic role. Although NGF block is proposed as a novel analgesic appr
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::29dc0c5ce8cc394f70626dbbc316d85f
http://hdl.handle.net/20.500.11767/12101
http://hdl.handle.net/20.500.11767/12101
Autor:
Alessandra Fabbro, Manuela Simonetti, Marina Zweyer, Elsa Fabbretti, Rashid Giniatullin, Andrea Nistri, Marianna D'Arco
Publikováno v:
Molecular Pain, Vol 2, Iss 1, p 11 (2006)
Molecular Pain
Molecular Pain
Background Cultured sensory neurons are a common experimental model to elucidate the molecular mechanisms of pain transduction typically involving activation of ATP-sensitive P2X or capsaicin-sensitive TRPV1 receptors. This applies also to trigeminal
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::fd7a19d6c942ea671df3477f4e0ab2c2
http://hdl.handle.net/11368/1745774
http://hdl.handle.net/11368/1745774
Autor:
Shehrazade Dahimene, Karen M. Page, Manuela Nieto-Rostro, Wendy S. Pratt, Marianna D'Arco, Annette C. Dolphin
Publikováno v:
Neurobiology of Disease
Neurobiology of Disease, Vol 93, Iss, Pp 243-256 (2016)
Neurobiology of Disease, Vol 93, Iss, Pp 243-256 (2016)
Episodic ataxia 2 (EA2) is an autosomal dominant disorder caused by mutations in the gene CACNA1A that encodes the pore-forming CaV2.1 calcium channel subunit. The majority of EA2 mutations reported so far are nonsense or deletion/insertion mutations