Characterizing the multiple roles of FGF-2 in SOD1
Amyotrophic Lateral Sclerosis
/ enzymology
Animals
Astrocytes
/ enzymology
Cell Death
Cells, Cultured
Disease Models, Animal
Enzyme Activation
Extracellular Signal-Regulated MAP Kinases
/ metabolism
Fibroblast Growth Factor 2
/ deficiency
Gene Expression Regulation, Developmental
Mice, Inbred C57BL
Mice, Knockout
Motor Neurons
/ enzymology
Muscle, Skeletal
/ enzymology
Mutation
Proto-Oncogene Proteins c-akt
/ metabolism
Signal Transduction
Superoxide Dismutase-1
/ genetics
AKT
amyotrophic lateral sclerosis (ALS)
astrocytes
extracellular-signal-regulated kinase (ERK)
fibroblast growth factor-2 (FGF-2)
glial-cell-line-derived neurotrophic factor (GDNF)
motor neurons
superoxide dismutase 1 (SOD1)
Journal
Journal of cellular physiology
ISSN: 1097-4652
Titre abrégé: J Cell Physiol
Pays: United States
ID NLM: 0050222
Informations de publication
Date de publication:
05 2019
05 2019
Historique:
received:
29
05
2018
accepted:
07
09
2018
pubmed:
30
10
2018
medline:
31
3
2020
entrez:
30
10
2018
Statut:
ppublish
Résumé
We have previously shown that knockout of fibroblast growth factor-2 (FGF-2) and potential compensatory effects of other growth factors result in amelioration of disease symptoms in a transgenic mouse model of amyotrophic lateral sclerosis (ALS). ALS is a rapidly progressive neurological disorder leading to degeneration of cortical, brain stem, and spinal motor neurons followed by subsequent denervation and muscle wasting. Mutations in the superoxide dismutase 1 (SOD1) gene are responsible for approximately 20% of familial ALS cases and SOD1 mutant mice still are among the models best mimicking clinical and neuropathological characteristics of ALS. The aim of the present study was a thorough characterization of FGF-2 and other growth factors and signaling effectors in vivo in the SOD1
Substances chimiques
SOD1 protein, human
0
Fibroblast Growth Factor 2
103107-01-3
Superoxide Dismutase-1
EC 1.15.1.1
Proto-Oncogene Proteins c-akt
EC 2.7.11.1
Extracellular Signal-Regulated MAP Kinases
EC 2.7.11.24
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
7395-7410Informations de copyright
© 2018 Wiley Periodicals, Inc.