Relevant bibliographies by topics / SOD1G85R mouse

Contents

  1. Journal articles
  2. Dissertations / Theses

Academic literature on the topic 'SOD1G85R mouse'

Author: Grafiati
Published: 4 June 2021
Last updated: 7 February 2022

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources on the topic 'SOD1G85R mouse.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Journal articles on the topic "SOD1G85R mouse"

1

Leyton-Jaimes, Marcel F., Clara Benaim, Salah Abu-Hamad, et al. "Endogenous macrophage migration inhibitory factor reduces the accumulation and toxicity of misfolded SOD1 in a mouse model of ALS." Proceedings of the National Academy of Sciences 113, no. 36 (2016): 10198–203. http://dx.doi.org/10.1073/pnas.1604600113.

Full text
Abstract:
Mutations in superoxide dismutase (SOD1) cause amyotrophic lateral sclerosis (ALS), a fatal neurodegenerative disease characterized by the loss of upper and lower motor neurons in the brain and spinal cord. It has been suggested that the toxicity of mutant SOD1 results from its misfolding and accumulation on the cytoplasmic faces of intracellular organelles, including the mitochondria and endoplasmic reticulum (ER) of ALS-affected tissues. Recently, macrophage migration inhibitory factor (MIF) was shown to directly inhibit the accumulation of misfolded SOD1 and its binding to intracellular mem
APA, Harvard, Vancouver, ISO, and other styles
2

Pambo-Pambo, Arnaud, Jacques Durand, and Jean-Patrick Gueritaud. "Early Excitability Changes in Lumbar Motoneurons of Transgenic SOD1G85R and SOD1G93A-Low Mice." Journal of Neurophysiology 102, no. 6 (2009): 3627–42. http://dx.doi.org/10.1152/jn.00482.2009.

Full text
Abstract:
This work characterizes the properties of wild-type (WT) mouse motoneurons in the second postnatal week and compares these at the same age and in the same conditions to those of two different SOD1 mutant lines used as models of human amyotrophic lateral sclerosis (ALS), the SOD1G93A low expressor line and SOD1G85R line, to describe any changes in the functional properties of mutant motoneurons (Mns) that may be related to the pathogenesis of human ALS. We show that very early changes in excitability occur in SOD1 mutant Mns that have different properties from those of WT animals. The SOD1G93A-
APA, Harvard, Vancouver, ISO, and other styles
3

BK, Binukumar, Susan Skuntz, Michaela Prochazkova, et al. "Overexpression of the Cdk5 inhibitory peptide in motor neurons rescue of amyotrophic lateral sclerosis phenotype in a mouse model." Human Molecular Genetics 28, no. 19 (2019): 3175–87. http://dx.doi.org/10.1093/hmg/ddz118.

Full text
Abstract:
Abstract Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disease that affects motor nerve cells in the brain and the spinal cord. Etiological mechanisms underlying the disease remain poorly understood; recent studies suggest that deregulation of p25/Cyclin-dependent kinase 5 (Cdk5) activity leads to the hyperphosphorylation of Tau and neurofilament (NF) proteins in ALS transgenic mouse model (SOD1G37R). A Cdk5 involvement in motor neuron degeneration is supported by analysis of three SOD1G37R mouse lines exhibiting perikaryal inclusions of NF proteins and hyperphosphoryl
APA, Harvard, Vancouver, ISO, and other styles
4

Robertson, Janice, Mohammad M. Doroudchi, Minh Dang Nguyen, et al. "A neurotoxic peripherin splice variant in a mouse model of ALS." Journal of Cell Biology 160, no. 6 (2003): 939–49. http://dx.doi.org/10.1083/jcb.200205027.

Full text
Abstract:
Peripherin, a neuronal intermediate filament (nIF) protein found associated with pathological aggregates in motor neurons of patients with amyotrophic lateral sclerosis (ALS) and of transgenic mice overexpressing mutant superoxide dismutase-1 (SOD1G37R), induces the selective degeneration of motor neurons when overexpressed in transgenic mice. Mouse peripherin is unique compared with other nIF proteins in that three peripherin isoforms are generated by alternative splicing. Here, the properties of the peripherin splice variants Per 58, Per 56, and Per 61 have been investigated in transfected c
APA, Harvard, Vancouver, ISO, and other styles
5

Marques, Christine, Thibaut Burg, Jelena Scekic-Zahirovic, Mathieu Fischer, and Caroline Rouaux. "Upper and Lower Motor Neuron Degenerations Are Somatotopically Related and Temporally Ordered in the Sod1 Mouse Model of Amyotrophic Lateral Sclerosis." Brain Sciences 11, no. 3 (2021): 369. http://dx.doi.org/10.3390/brainsci11030369.

Full text
Abstract:
Amyotrophic lateral sclerosis (ALS) is a devastating and fatal neurodegenerative disease arising from the combined degeneration of upper motor neurons (UMN) in the motor cortex, and lower motor neurons (LMN) in the brainstem and spinal cord. This dual impairment raises two major questions: (i) are the degenerations of these two neuronal populations somatotopically related? and if yes (ii), where does neurodegeneration start? If studies carried out on ALS patients clearly demonstrated the somatotopic relationship between UMN and LMN degenerations, their temporal relationship remained an unanswe
APA, Harvard, Vancouver, ISO, and other styles
6

Kang, Jihong, and Serge Rivest. "MyD88-deficient bone marrow cells accelerate onset and reduce survival in a mouse model of amyotrophic lateral sclerosis." Journal of Cell Biology 179, no. 6 (2007): 1219–30. http://dx.doi.org/10.1083/jcb.200705046.

Full text
Abstract:
Increasing evidence suggests that neurotoxicity of secreted superoxide dismutase 1 (SOD1) mutants is associated with amyotrophic lateral sclerosis (ALS). We show here that mutant SOD1 protein activates microglia via a myeloid differentiation factor 88 (MyD88)–dependent pathway. This inflammatory response is also associated with a marked recruitment of bone marrow–derived microglia (BMDM) in the central nervous system. We then generated chimeric SOD1G37R and SOD1G93A mice by transplantation of bone marrow (BM) cells from MyD88-deficient or green fluorescent protein (GFP)–expressing mice. SOD1G3
APA, Harvard, Vancouver, ISO, and other styles
7

Filali, Mohammed, Robert Lalonde, and Serge Rivest. "Sensorimotor and cognitive functions in a SOD1G37R transgenic mouse model of amyotrophic lateral sclerosis." Behavioural Brain Research 225, no. 1 (2011): 215–21. http://dx.doi.org/10.1016/j.bbr.2011.07.034.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Martineau, Éric, Danielle Arbour, Joanne Vallée, and Richard Robitaille. "Properties of Glial Cell at the Neuromuscular Junction Are Incompatible with Synaptic Repair in the SOD1G37R ALS Mouse Model." Journal of Neuroscience 40, no. 40 (2020): 7759–77. http://dx.doi.org/10.1523/jneurosci.1748-18.2020.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Maier, Marcel, Tobias Welt, Fabian Wirth, et al. "A human-derived antibody targets misfolded SOD1 and ameliorates motor symptoms in mouse models of amyotrophic lateral sclerosis." Science Translational Medicine 10, no. 470 (2018): eaah3924. http://dx.doi.org/10.1126/scitranslmed.aah3924.

Full text
Abstract:
Mutations in the gene encoding superoxide dismutase 1 (SOD1) lead to misfolding and aggregation of SOD1 and cause familial amyotrophic lateral sclerosis (FALS). However, the implications of wild-type SOD1 misfolding in sporadic forms of ALS (SALS) remain unclear. By screening human memory B cells from a large cohort of healthy elderly subjects, we generated a recombinant human monoclonal antibody (α-miSOD1) that selectively bound to misfolded SOD1, but not to physiological SOD1 dimers. On postmortem spinal cord sections from 121 patients with ALS, α-miSOD1 antibody identified misfolded SOD1 in
APA, Harvard, Vancouver, ISO, and other styles
10

Hilton, James B., Kai Kysenius, Anthony R. White, and Peter J. Crouch. "The accumulation of enzymatically inactive cuproenzymes is a CNS-specific phenomenon of the SOD1G37R mouse model of ALS and can be restored by overexpressing the human copper transporter hCTR1." Experimental Neurology 307 (September 2018): 118–28. http://dx.doi.org/10.1016/j.expneurol.2018.06.006.

Full text
APA, Harvard, Vancouver, ISO, and other styles

Dissertations / Theses on the topic "SOD1G85R mouse"

1

Pambo-Pambo, Arnaud Brice. "Etude du développement postnatal des motoneurones lombaires de deux souches de souris transgéniques, modèles de la sclérose latérale amyotrophique." Thesis, Aix-Marseille 2, 2010. http://www.theses.fr/2010AIX20716.

Full text
Abstract:
Les modèles murins de la Sclérose Latérale Amyotrophique (SLA) ont permis des avancées dans la compréhension des mécanismes pouvant conduire à la mort sélective et progressive des motoneurones (Mns) mais ils présentent des disparités dans la sévérité et le décours temporel de la maladie. Parmi les hypothèses avancées figurent des modifications des propriétés intrinsèques des motoneurones conduisant à des modifications de l’excitabilité et de l’homéostasie du calcium intracellulaire et à la mort du motoneurone.Nous avons donc étudié les propriétés électrophysiologiques des Mns lombaires de sour
APA, Harvard, Vancouver, ISO, and other styles
We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!

To the bibliography