A5087005928- Nerve injury and regeneration
- Neurogenetic and Muscular Disorders Research
- RNA modifications and cancer
- Autophagy in Disease and Therapy
- Signaling Pathways in Disease
- Neurogenesis and neuroplasticity mechanisms
- Neuroscience and Neuropharmacology Research
- Amyotrophic Lateral Sclerosis Research
- RNA Research and Splicing
- Computational Drug Discovery Methods
- Muscle Physiology and Disorders
- RNA Interference and Gene Delivery
- Neuroinflammation and Neurodegeneration Mechanisms
- Parkinson's Disease Mechanisms and Treatments
- Fuel Cells and Related Materials
- Calpain Protease Function and Regulation
- NF-κB Signaling Pathways
- Nuclear Receptors and Signaling
- Natural product bioactivities and synthesis
- Genetic Neurodegenerative Diseases
- Prion Diseases and Protein Misfolding
- Mitochondrial Function and Pathology
- Chemical Synthesis and Analysis
- Stress and Burnout Research
- Pharmacological Effects of Natural Compounds
Universitat de Lleida
2014-2024
Biomedical Research Institute of Lleida
2007-2024
University of St Andrews
1998
Universitat de València
1996
ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXTCharge Indexes. New Topological DescriptorsJ. Galvez, R. Garcia, M. T. Salabert, and SolerCite this: J. Chem. Inf. Comput. Sci. 1994, 34, 3, 520–525Publication Date (Print):May 1, 1994Publication History Published online1 May 2002Published inissue 1 1994https://doi.org/10.1021/ci00019a008RIGHTS & PERMISSIONSArticle Views569Altmetric-Citations225LEARN ABOUT THESE METRICSArticle Views are the COUNTER-compliant sum of full text article downloads since...
In this paper we demonstrated that by an adequate combination of different topological indices it is possible to select and design new active compounds in therapeutical scopes, with a very high efficiency level. Particularly successful the search "lead drugs", results show surprising ability methods describe molecular structures.
The members of the glial cell line-derived neurotrophic factor (GDNF) family factors (GDNF, neurturin, persephin, and artemin) are able to promote in vivo vitro survival different neuronal populations, including spinal cord motoneurons. These signal via multicomponent receptors that consist Ret receptor tyrosine kinase plus a member GDNF alpha (GRFalpha) glycosylphosphatidylinositol-linked coreceptors. Activation induces phosphorylation leads survival-promoting effects. causes activation...
Abstract : Chick embryo spinal cord motoneurons develop a trophic response to some neurotrophins when they are maintained in culture the presence of muscle extract. Thus, after 2 days culture, brain‐derived neurotrophic factor (BDNF) promotes motoneuron survival. In present study we have analyzed intracellular pathways that may be involved BDNF‐induced We observed BDNF activated extracellular‐regulated kinase (ERK) mitogen‐activated protein (MAP) and phosphatidylinositol (Pl) 3‐kinase...
Moderate increases of intracellular Ca2+ concentration ([Ca2+]i), induced by either the activation tropomyosin receptor kinase (Trk) receptors for neurotrophins or neuronal activity, regulate different pathways and survival. In present report we demonstrate that glial cell line-derived neurotrophic factor (GDNF) treatment also induces [Ca2+]i elevation mobilizing this cation from internal stores. The effects increase after membrane depolarization are mainly mediated calmodulin (CaM)....
Abstract Spinal muscular atrophy (SMA) is a recessive autosomal neuromuscular disease, due to homozygous mutations or deletions in the telomeric survival motoneuron gene 1 ( SMN1 ). SMA characterized by motor impairment, muscle atrophy, and premature death following neuron (MN) degeneration. Emerging evidence suggests that dysregulation of autophagy contributes MN We here investigated role SMNdelta7 mouse model II (intermediate form disease) which leads impairment postnatal day 5 (P5) P13....
The dysfunction of TAR DNA-binding protein 43 (TDP-43) is implicated in various neurodegenerative diseases, though the specific contributions its toxic gain-of-function versus loss-of-function effects remain unclear. This study investigates impact TARDBP loss on cellular metabolism and viability using human-induced pluripotent stem cell-derived motor neurons HeLa cells. silencing led to reduced metabolic activity cell growth, accompanied by neurite degeneration decreased oxygen consumption...
ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXTTopological Approach to AnalgesiaJ. Galvez, R. Garcia-Domenech, V. De Julian-Ortiz, and SolerCite this: J. Chem. Inf. Comput. Sci. 1994, 34, 5, 1198–1203Publication Date (Print):September 1, 1994Publication History Published online1 May 2002Published inissue 1 September 1994https://pubs.acs.org/doi/10.1021/ci00021a030https://doi.org/10.1021/ci00021a030research-articleACS PublicationsRequest reuse permissionsArticle...
In the present work, we find that elevation of extracellular K+ concentration promotes survival chick spinal cord motoneurons in vitro deprived any neurotrophic support. This treatment induces chronic depolarization neuronal plasma membrane, which activates L-type voltage-dependent Ca2+ channels, resulting influx and cytosolic free concentration. Pharmacological reduction intracellular or withdrawal reversed effects on survival. The response to membrane developed as an initial peak followed...
During embryonic development, most neuronal populations undergo a process usually referred to as naturally occurring death. For motoneurons (MTNs) of the lumbar spinal cord chick embryos, this takes place in well defined period time, between days 6 and 10 (E6–E10). Neurotrophins (NTs) are best characterized family neurotrophic factors exert their effects through activation specific Trk receptors. In vitro vivo studies have demonstrated that rodent survive response BDNF, NT3, NT4/5. contrast,...
Spinal muscular atrophy (SMA) is a genetic disorder characterized by degeneration of spinal cord motoneurons (MNs), resulting in and weakness. SMA caused mutations the Survival Motor Neuron 1 (SMN1) gene decreased SMN protein. ubiquitously expressed has general role assembly small nuclear ribonucleoproteins pre-mRNA splicing requirements. reduction causes neurite cell death without classical apoptotic features, but direct events leading to are still unknown. Autophagy conserved lysosomal...
Disruption in membrane excitability contributes to malfunction and differential vulnerability of specific neuronal subpopulations a number neurological diseases. The adaptor protein p11, background potassium channel TASK1, have overlapping distributions the CNS. Here, we report that transcription factor Sp1 controls p11 expression, which impacts on by hampering functional expression TASK1. In SOD1-G93A mouse model ALS, Sp1-p11-TASK1 dysregulation increased motor neurons. Interference with...
Spinal Muscular Atrophy (SMA) is a severe genetic neuromuscular disorder that occurs in childhood and caused by misexpression of the survival motor neuron (SMN) protein. SMN reduction induces spinal cord motoneuron (MN) degeneration, which leads to progressive muscular atrophy weakness. The link between deficiency molecular mechanisms altered SMA cells remains unclear. Autophagy, deregulation intracellular pathways ERK hyperphosphorylation may contribute SMN-reduced MNs collapse, offering...
It has been reported that phosphoinositide 3-kinase (PI 3-kinase) and its downstream target, protein kinase B (PKB), play a central role in the signaling of cell survival triggered by neurotrophins (NTs). In this report, we have analyzed involvement Ca2+ calmodulin (CaM) activation PKB induced NTs. We found reduction intracellular concentration or functional blockade CaM abolished NGF-induced PC12 cells. Similar results were obtained cultures chicken spinal cord motoneurons treated with...
Nerve growth factor is a member of the neurotrophin family trophic factors that have been reported to be essential for survival and development sympathetic neurons subset sensory neurons. exerts its effects mainly by interaction with specific receptor TrkA, which leads activation several intracellular signaling pathways. Once activated, TrkA also allows rapid moderate increase in calcium levels, would contribute triggered nerve In this report, we analyzed relationship Ras/extracellular...
Abstract Spinal muscular atrophy (SMA) is a neuromuscular genetic disease caused by reduced survival motor neuron (SMN) protein. SMN ubiquitous and deficient levels cause spinal cord motoneurons (MNs) degeneration muscle atrophy. Nevertheless, the mechanism which reduction in contributes to SMA not fully understood. Therefore, studies evaluating mechanisms muscles will contribute strengthening current knowledge of pathology. Here we propose evaluate autophagy muscle, pathway altered myotube...
In vivo and in vitro motoneuron survival depends on the support of neurotrophic factors. These factors activate signaling pathways related to cell or inactivate proteins involved neuronal death. present work, we analyzed involvement nuclear factor-κB (NF-κB) pathway mediating mouse spinal cord promoted by This comprises ubiquitously expressed transcription that could be activated two different routes: canonical pathway, associated with IKKα/IKKβ kinase phosphorylation translocation RelA...