dc.creator | Danelon, Víctor | |
dc.creator | Cragnolini, Andrea Beatriz | |
dc.creator | Masco, Daniel Hugo | |
dc.date.accessioned | 2018-04-18T13:53:39Z | |
dc.date.accessioned | 2018-11-06T16:00:51Z | |
dc.date.available | 2018-04-18T13:53:39Z | |
dc.date.available | 2018-11-06T16:00:51Z | |
dc.date.created | 2018-04-18T13:53:39Z | |
dc.date.issued | 2016-12 | |
dc.identifier | Danelon, Víctor; Cragnolini, Andrea Beatriz; Masco, Daniel Hugo; TrkB and the calpain dependent-Tc TrkB receptor isoforms: possible neurological therapeutic targets; Sciaccess Publishers; Journal of Neurology and Neuromedicine; 1; 7; 12-2016; 31-36 | |
dc.identifier | 2572-942X | |
dc.identifier | http://hdl.handle.net/11336/42424 | |
dc.identifier | CONICET Digital | |
dc.identifier | CONICET | |
dc.identifier.uri | http://repositorioslatinoamericanos.uchile.cl/handle/2250/1903527 | |
dc.description.abstract | Several neurological conditions share a characteristic feature: an increase in intracellular calcium levels ([Ca2+]i). It has been demonstrated that calcium
influx induces changes ranging from an increase in the expression levels of several genes to the activation of proteases such as calpains. Calpains are a family of Ca2+-dependent non-lysosomal cysteine proteases, whose substrates include several proteins that play critical roles in several cellular functions including synaptic plasticity and neuronal apoptosis.
TrkB is a type of tyrosine related kinase receptor that can promote neuronal survival and differentiation upon ligand binding. It has been recently shown that in several neurological diseases, the level of full-length TrkB protein decreases before the onset of neuronal death due to one of two different processes: a) a reverse regulation of TrkB isoforms mRNA, or b) calpainmediated processing of TrkB full-length, which yields a truncated form of TrkB (Tc-TrkB). Because the most notorious feature of calpain proteolytic activity is that the products of calpain-mediated leavage may have biological activity, here we review the hypotheses by which calpain- generated isoform Tc-TrkB may perform biological functions. | |
dc.language | eng | |
dc.publisher | Sciaccess Publishers | |
dc.relation | info:eu-repo/semantics/altIdentifier/url/http://www.jneurology.com/articles/trkb-and-the-calpain-dependenttc-trkb-receptor-isoforms-possible-neurological-therapeutic-targets-neuromed-1-1076.php | |
dc.rights | https://creativecommons.org/licenses/by-nc-sa/2.5/ar/ | |
dc.rights | info:eu-repo/semantics/openAccess | |
dc.subject | TrkB | |
dc.subject | TrkB-Tk | |
dc.subject | Tc-TrkB | |
dc.subject | CALPAIN | |
dc.subject | NEUROLOGICAL CONDITIONS | |
dc.subject | INTERECELLULAR CALCIUM LEVELS | |
dc.title | TrkB and the calpain dependent-Tc TrkB receptor isoforms: possible neurological therapeutic targets | |
dc.type | Artículos de revistas | |
dc.type | Artículos de revistas | |
dc.type | Artículos de revistas | |