Evidence map›Paper›PMID 22174156›Full record

ArticleBlood2012

R-Ras is required for murine dendritic cell maturation and CD4+ T-cell priming.

Gobind Singh, Daigo Hashimoto, Xiaocai Yan, Julie Helft, Patricia J-Y Park, Ge Ma, Rui F Qiao, Colin R Kennedy, Shu-Hsia Chen, Miriam Merad and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Blood, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
0.9field-weighted citation impact, top 28% of its field
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

17 citing papers in PubMed, 26 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Phosphoinositide Conversion Inactivates R-RAS and Drives Metastases in Breast Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022
    Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. FOXO1 regulates dendritic cell activity through ICAM-1 and CCR7.Journal of immunology (Baltimore, Md. : 1950) · 2015
    Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. 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

11 authors at 2 institutions in 1 country.

Gobind SinghDepartment of Oncological Sciences, Mount Sinai School of Medicine, New York, NY, USA.
Daigo Hashimoto
Xiaocai Yan
Julie Helft
Patricia J-Y Park
Ge Ma
Rui F Qiao
Colin R Kennedy
Shu-Hsia Chen
Miriam Merad
Andrew M Chan
Icahn School of Medicine at Mount Sinai · USMedical College of Wisconsin · US

Funding

TRAINING PROGRAM IN CANCER THERAPYT32CA078207 · NCI · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI James J Manfredi · 1999 to 2026
$11.6M
ERK control of Dendritic Cell Differentiation, Homeostasis and DiseaseR01CA154947 · NCI · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI CARL E ALLEN, MIRIAM MERAD · 2011 to 2026
$7.0M
Myeloid Suppressor Cell-Mediated Immune Suppression of Tumor Specific T CellsR01CA109322 · NCI · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI CHEN, SHU-HSIA · 2006 to 2015
$3.2M
R-Ras3 and Cell Survival in the CNSR01MH059771 · NIMH · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI CHAN, ANDREW M · 2000 to 2007
$2.2M
MECHANISMS OF R RAS CELL ADHESION SIGNALINGR29CA078509 · NCI · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI CHAN, ANDREW M · 1998 to 2002
$344k
NCI NIH HHS CA78509NCI NIH HHS R01 CA109322NCI NIH HHS R01 CA154947NCI NIH HHS T32 CA078207NCI NIH HHS T32CA078207NIMH NIH HHS MH59771NIMH NIH HHS R01 MH059771
6 · The paper itself

Abstract

R-Ras is a member of the RAS superfamily of small GTP-binding proteins. The physiologic function of R-Ras has not been fully elucidated. We found that R-Ras is expressed by lymphoid and nonlymphoid tissues and drastically up-regulated when bone marrow progenitors are induced to differentiate into dendritic cells (DCs). To address the role of R-Ras in DC functions, we generated a R-Ras-deficient mouse strain. We found that tumors induced in Rras(-/-) mice formed with shorter latency and attained greater tumor volumes. This finding has prompted the investigation of a role for R-Ras in the immune system. Indeed, Rras(-/-) mice were impaired in their ability to prime allogeneic and antigen-specific T-cell responses. Rras(-/-) DCs expressed lower levels of surface MHC class II and CD86 in response to lipopolysaccharide compared with wild-type DCs. This was correlated with a reduced phosphorylation of p38 and Akt. Consistently, R-Ras-GTP level was increased within 10 minutes of lipopolysaccharide stimulation. Furthermore, Rras(-/-) DCs have attenuated capacity to spread on fibronectin and form stable immunologic synapses with T cells. Altogether, these findings provide the first demonstration of a role for R-Ras in cell-mediated immunity and further expand on the complexity of small G-protein signaling in DCs.

Indexed as

AnimalsAntigen PresentationCD4-Positive T-LymphocytesCell DifferentiationCells, CulturedDendritic CellsFemaleImmunity, CellularLymphocyte ActivationMaleMiceMice, Inbred BALB CMice, Inbred C57BLMice, Knockoutras Proteinsras ProteinsRras protein, mouse

Identifiers

PMID22174156
PMCPMC3286347
OpenAlexW2043895576

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.