Evidence map›Paper›PMID 30043672›Full record

ReviewSmall GTPases2020

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

Samantha Messina

Abstract readReview
In one paragraph

Review in Small GTPases, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

5 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. CD40 induces selective routing of Ras isoforms to subcellular compartments.Journal of cell communication and signaling · 2023
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

1 author.

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

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

rassignaling 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, ABBREVIATIONS: 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.

Indexed as

AnimalsHumansMonomeric GTP-Binding ProteinsMultiple Sclerosisras ProteinsMonomeric GTP-Binding Proteinsras ProteinsEAEFTIsHRASKRASmultiple sclerosisNRASRegulatory T-cellstatins

Identifiers

PMID30043672
PMCPMC7549689

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.