Evidence map›Paper›PMID 37259315›Full record

ReviewPharmaceuticals (Basel, Switzerland)2023

EPHB4-RASA1-Mediated Negative Regulation of Ras-MAPK Signaling in the Vasculature: Implications for the Treatment of EPHB4- and RASA1-Related Vascular Anomalies in Humans.

Di Chen, Martijn A Van der Ent, Nathaniel L Lartey, Philip D King

Abstract readReview
In one paragraph

Review in Pharmaceuticals (Basel, Switzerland), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing 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

13 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. The C2 domain augments Ras GTPase-activating protein catalytic activity.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  7. Article
  8. Novel postzygoticClinical case reports · 2024
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. 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

4 authors.

Di ChenDepartment of Microbiology and Immunology, University of Michigan Medical School, Ann Arbor, MI 48109, USA.
Martijn A Van der EntDepartment of Microbiology and Immunology, University of Michigan Medical School, Ann Arbor, MI 48109, USA.
Nathaniel L LarteyDepartment of Microbiology and Immunology, University of Michigan Medical School, Ann Arbor, MI 48109, USA.ORCID 0000-0002-9810-2720
Philip D KingDepartment of Microbiology and Immunology, University of Michigan Medical School, Ann Arbor, MI 48109, USA.

Funding

Ras-MAPK Regulation of Lymphatic Vessel Valve DevelopmentR01HL120888 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI PHILIP D KING · 2015 to 2026
$4.6M
Molecular pathogenetic mechanisms in CM-AVMR01HL146352 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI KING, PHILIP D · 2020 to 2023
$2.2M
NHLBI NIH HHS R01 HL120888NHLBI NIH HHS R01 HL146352NIH HHS HL120888NIH HHS HL146352
6 · The paper itself

Abstract

Ephrin receptors constitute a large family of receptor tyrosine kinases in mammals that through interaction with cell surface-anchored ephrin ligands regulate multiple different cellular responses in numerous cell types and tissues. In the cardiovascular system, studies performed in vitro and in vivo have pointed to a critical role for Ephrin receptor B4 (EPHB4) as a regulator of blood and lymphatic vascular development and function. However, in this role, EPHB4 appears to act not as a classical growth factor receptor but instead functions to dampen the activation of the Ras-mitogen activated protein signaling (MAPK) pathway induced by other growth factor receptors in endothelial cells (EC). To inhibit the Ras-MAPK pathway, EPHB4 interacts functionally with Ras p21 protein activator 1 (RASA1) also known as p120 Ras GTPase-activating protein. Here, we review the evidence for an inhibitory role for an EPHB4-RASA1 interface in EC. We further discuss the mechanisms by which loss of EPHB4-RASA1 signaling in EC leads to blood and lymphatic vascular abnormalities in mice and the implications of these findings for an understanding of the pathogenesis of vascular anomalies in humans caused by mutations in

Indexed as

angiogenesiscapillary malformation arteriovenous malformationEphrin receptor B4lymphatic malformationRASA1Ras-MAPK pathwayvascular valves

Identifiers

PMID37259315
PMCPMC9959185

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Registered trials

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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.