Small GTPase RAS in multiple sclerosis - exploring the role of RAS GTPase in the etiology of multiple sclerosis.


Journal

Small GTPases
ISSN: 2154-1256
Titre abrégé: Small GTPases
Pays: United States
ID NLM: 101530974

Informations de publication

Date de publication:
09 2020
Historique:
pubmed: 26 7 2018
medline: 17 7 2021
entrez: 26 7 2018
Statut: ppublish

Résumé

signaling is involved in the development of autoimmunity in general. Multiple sclerosis (MS) is a T cell-mediated autoimmune disease of the central nervous system. It is widely recognized that a reduction of Foxp3+ regulatory T (Treg) cells is an immunological hallmark of MS, but the underlying mechanisms are unclear. In experimental autoimmune models, N-Ras and K-Ras inhibition triggers an anti-inflammatory effect up-regulating, FTIs: Farnesyl Transferase Inhibitors; MS: Multiple Sclerosis; RRMS: Relapsing Remitting Multiple Sclerosis; PPMS: Primary Progressive Multiple Sclerosis; Tregs: regulatory T-cells; Foxp3: Forkhead box P3; EAE: Experimental Autoimmune Encephalomyelitis; T1D: Type 1 Diabete; SLE: Systemic Lupus Erythematosus; RA: Rheumatoid Arthritis; CNS: Central Nervous System; TMEV: Theiler's murine encephalomyelitis virus; FTS: farnesyl thiosalicylic acid; TCR: T-Cell Receptor; AIA: Adjuvant-induced Arthritis; EAN: experimental autoimmune neuritis; HVR: hypervariable region; HMG-CoA: 3-hydroxy-3-methylglutaryl coenzyme A reductase; PBMC: Peripheral Blood Mononuclear Cells.

Identifiants

pubmed: 30043672
doi: 10.1080/21541248.2018.1502591
pmc: PMC7549689
doi:

Substances chimiques

Monomeric GTP-Binding Proteins EC 3.6.5.2
ras Proteins EC 3.6.5.2

Types de publication

Journal Article Review

Langues

eng

Sous-ensembles de citation

IM

Pagination

312-319

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Auteurs

Samantha Messina (S)

Department of Human Sciences, Society and Health, University of Cassino and Southern Lazio, Cassino , Italy.

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Classifications MeSH