Evidence map›Paper›PMID 33297302›Full record

ReviewInternational journal of molecular sciences2020

The Role of β-Arrestins in Regulating Stem Cell Phenotypes in Normal and Tumorigenic Cells.

Georgios Kallifatidis, Kenza Mamouni, Bal L Lokeshwar

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.6field-weighted citation impact, top 34% 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

7 citing papers in PubMed, 15 citations in OpenAlex.

  1. Cardiomyocyte β-arrestins mediate inflammation and cGAS-STING activation in CVB3 viral myocarditis.American journal of physiology. Heart and circulatory physiology · 2026
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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

3 authors at 2 institutions in 1 country.

Georgios KallifatidisDepartment of Biological Sciences, Augusta University, Augusta, GA 30912, USA.ORCID 0000-0003-3602-9537
Kenza MamouniGeorgia Cancer Center, Augusta University, Augusta, GA 30912, USA.ORCID 0000-0002-3178-8094
Bal L LokeshwarGeorgia Cancer Center, Augusta University, Augusta, GA 30912, USA.ORCID 0000-0002-1763-4718
Charlie Norwood VA Medical Center · USAugusta University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

β-Arrestins (ARRBs) are ubiquitously expressed scaffold proteins that mediate inactivation of G-protein-coupled receptor signaling, and in certain circumstances, G-protein independent pathways. Intriguingly, the two known ARRBs, β-arrestin1 (ARRB1) and β-Arrestin2 (ARRB2), seem to have opposing functions in regulating signaling cascades in several models in health and disease. Recent evidence suggests that ARRBs are implicated in regulating stem cell maintenance; however, their role, although crucial, is complex, and there is no universal model for ARRB-mediated regulation of stem cell characteristics. For the first time, this review compiles information on the function of ARRBs in stem cell biology and will discuss the role of ARRBs in regulating cell signaling pathways implicated in stem cell maintenance in normal and malignant stem cell populations. Although promising targets for cancer therapy, the ubiquitous nature of ARRBs and the plethora of functions in normal cell biology brings challenges for treatment selectivity. However, recent studies show promising evidence for specifically targeting ARRBs in myeloproliferative neoplasms.

Indexed as

Animalsbeta-ArrestinsCarcinogenesisCell Self RenewalHumansNeoplastic Stem CellsPhenotypePluripotent Stem Cellsbeta-Arrestinscancer stem cellsself-renewalstem cell phenotypeβ-arrestin1 (ARRB1)β-arrestin2 (ARRB2)

Identifiers

PMID33297302
PMCPMC7729818
OpenAlexW3112910140

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.