Evidence map›Paper›PMID 30923091›Full record

ArticleHaematologica2019

A Tie2-Notch1 signaling axis regulates regeneration of the endothelial bone marrow niche.

Lijian Shao, Kilian Sottoriva, Karol Palasiewicz, Jizhou Zhang, James Hyun, Sweta S Soni, Na Yoon Paik, Xiaopei Gao, Henar Cuervo, Asrar B Malik and 3 more

Open access · goldAbstract read
In one paragraph

Article in Haematologica, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

18 citing papers in PubMed, 24 citations in OpenAlex.

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  15. Article
  16. Vascular Notch Signaling in Stress Hematopoiesis.Frontiers in cell and developmental biology · 2020
    Review
  17. Review
  18. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

13 authors at 3 institutions in 1 country.

Lijian ShaoDepartment of Pharmacology, The University of Illinois College of Medicine, Chicago, IL.
Kilian SottorivaDepartment of Pharmacology, The University of Illinois College of Medicine, Chicago, IL.
Karol PalasiewiczDepartment of Pharmacology, The University of Illinois College of Medicine, Chicago, IL.
Jizhou ZhangDivision of Experimental Hematology and Cancer Biology, Cincinnati Children's Medical Center, Cincinnati, OH.
James HyunDepartment of Pharmacology, The University of Illinois College of Medicine, Chicago, IL.
Sweta S SoniDepartment of Pharmacology, The University of Illinois College of Medicine, Chicago, IL.
Na Yoon PaikDepartment of Pharmacology, The University of Illinois College of Medicine, Chicago, IL.
Xiaopei GaoDepartment of Pharmacology, The University of Illinois College of Medicine, Chicago, IL.
Henar CuervoDepartment of Physiology and Biophysics, The University of Illinois College of Medicine, Chicago, IL.
Asrar B MalikDepartment of Pharmacology, The University of Illinois College of Medicine, Chicago, IL.
Jalees RehmanDepartment of Pharmacology, The University of Illinois College of Medicine, Chicago, IL.
Daniel LucasDivision of Experimental Hematology and Cancer Biology, Cincinnati Children's Medical Center, Cincinnati, OH.
Kostandin V PajciniDepartment of Pharmacology, The University of Illinois College of Medicine, Chicago, IL kvp@uic.edu.
Illinois College · USUniversity of Illinois Chicago · USChildren's Medical Center · US

Funding

TRAINING PROGRAM IN LUNG BIOLOGY AND PATHOBIOLOGYT32HL007829 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI DOLLY MEHTA · 1995 to 2026
$15.6M
The role of Notch signaling in fetal hematopoietic stem cellsR01HL134971 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI PAJCINI, KOSTANDIN · 2017 to 2021
$2.2M
Cellular crosstalk in the hematopoietic microenvironmentR01HL136529 · NHLBI · CINCINNATI CHILDRENS HOSP MED CTR · PI LUCAS, DANIEL · 2018 to 2021
$1.6M
NHLBI NIH HHS R01 HL134971NHLBI NIH HHS R01 HL136529NHLBI NIH HHS T32 HL007829
6 · The paper itself

Abstract

Loss-of-function studies have determined that Notch signaling is essential for hematopoietic and endothelial development. By deleting a single allele of the Notch1 transcriptional activation domain we generated viable, post-natal mice exhibiting hypomorphic Notch signaling. These heterozygous mice, which lack only one copy of the transcriptional activation domain, appear normal and have no endothelial or hematopoietic phenotype, apart from an inherent, cell-autonomous defect in T-cell lineage development. Following chemotherapy, these hypomorphs exhibited severe pancytopenia, weight loss and morbidity. This phenotype was confirmed in an endothelial-specific, loss-of-function Notch1 model system. Ang1, secreted by hematopoietic progenitors after damage, activated endothelial Tie2 signaling, which in turn enhanced expression of Notch ligands and potentiated Notch1 receptor activation. In our heterozygous, hypomorphic model system, the mutant protein that lacks the Notch1 transcriptional activation domain accumulated in endothelial cells and interfered with optimal activity of the wildtype Notch1 transcriptional complex. Failure of the hypomorphic mutant to efficiently drive transcription of key gene targets such as

Indexed as

Cellular MicroenvironmentRegenerationSignal TransductionAnimalsBone MarrowEndothelial CellsFluorouracilGamma RaysGene Expression ProfilingGene Expression RegulationHematopoietic Stem CellsHumansMiceMice, KnockoutPancytopeniaReceptor, Notch1FluorouracilReceptor, Notch1Receptor, TIE-2

Identifiers

PMID30923091
PMCPMC6821596
OpenAlexW2935411939

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.