Evidence map›Paper›PMID 29875320›Full record

ArticleJCI insight2018

Wild-type Kras expands and exhausts hematopoietic stem cells.

Joshua P Sasine, Heather A Himburg, Christina M Termini, Martina Roos, Evelyn Tran, Liman Zhao, Jenny Kan, Michelle Li, Yurun Zhang, Stéphanie C de Barros and 3 more

Open access · goldAbstract read
In one paragraph

Article in JCI insight, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed, 1 pooled it
1.5field-weighted citation impact, top 18% 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

13 citing papers in PubMed, 1 synthesis or guideline pooled it, 19 citations in OpenAlex.

  1. Pooled it
  2. SystemicProceedings of the National Academy of Sciences of the United States of America · 2025
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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

13 authors at 4 institutions in 2 countries.

Joshua P SasineDivision of Hematology/Oncology, Department of Medicine.
Heather A HimburgDivision of Hematology/Oncology, Department of Medicine.
Christina M TerminiDivision of Hematology/Oncology, Department of Medicine.
Martina RoosDivision of Hematology/Oncology, Department of Medicine.
Evelyn TranDivision of Hematology/Oncology, Department of Medicine.
Liman ZhaoDivision of Hematology/Oncology, Department of Medicine.
Jenny KanDivision of Hematology/Oncology, Department of Medicine.
Michelle LiDivision of Hematology/Oncology, Department of Medicine.
Yurun ZhangDivision of Hematology/Oncology, Department of Medicine.
Stéphanie C de BarrosDepartment of Pathology and Laboratory Medicine, UCLA, Los Angeles, California, USA.
Dinesh S RaoDivision of Hematology/Oncology, Department of Medicine.
Christopher M CounterDepartment of Pharmacology and Cancer Biology, Duke University, Durham, North California, USA.
John P ChuteDivision of Hematology/Oncology, Department of Medicine.
University of California, Los Angeles · USUniversity of Colorado Cancer Center · USDuke University · USLaboratoire d’immunologie intégrative du cancer · FR

Funding

UCLA Center for Biological RadioprotectorsU19AI067769 · NIAID · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI CHUTE, JOHN P, MCBRIDE, WILLIAM H. · 2005 to 2019
$44.6M
Project 4: The role of codon bias in RAS tumorigenesisP01CA203657 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI DER, CHANNING J. · 2016 to 2020
$7.9M
Semaphorin signaling regulates vascular and hematopoietic regenerationR01HL086998 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI CHUTE, JOHN P · 2008 to 2022
$4.6M
RalA signal transductionR01CA094184 · NCI · DUKE UNIVERSITY · PI COUNTER, CHRISTOPHER M · 2002 to 2018
$4.1M
Dynamic requirements of Ras signaling during cancerR01CA123031 · NCI · DUKE UNIVERSITY · PI COUNTER, CHRISTOPHER M · 2007 to 2018
$3.5M
Epidermal growth factor mitigates radiation-induced hematopoietic failureU01AI107333 · NIAID · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI CHUTE, JOHN P · 2013 to 2017
$2.6M
NCI NIH HHS P01 CA203657NCI NIH HHS R01 CA094184NCI NIH HHS R01 CA123031NHLBI NIH HHS R01 HL086998NIAID NIH HHS U01 AI107333NIAID NIH HHS U19 AI067769
6 · The paper itself

Abstract

Oncogenic Kras expression specifically in hematopoietic stem cells (HSCs) induces a rapidly fatal myeloproliferative neoplasm in mice, suggesting that Kras signaling plays a dominant role in normal hematopoiesis. However, such a conclusion is based on expression of an oncogenic version of Kras. Hence, we sought to determine the effect of simply increasing the amount of endogenous wild-type Kras on HSC fate. To this end, we utilized a codon-optimized version of the murine Kras gene (Krasex3op) that we developed, in which silent mutations in exon 3 render the encoded mRNA more efficiently translated, leading to increased protein expression without disruption to the normal gene architecture. We found that Kras protein levels were significantly increased in bone marrow (BM) HSCs in Krasex3op/ex3op mice, demonstrating that the translation of Kras in HSCs is normally constrained by rare codons. Krasex3op/ex3op mice displayed expansion of BM HSCs, progenitor cells, and B lymphocytes, but no evidence of myeloproliferative disease or leukemia in mice followed for 12 months. BM HSCs from Krasex3op/ex3op mice demonstrated increased multilineage repopulating capacity in primary competitive transplantation assays, but secondary competitive transplants revealed exhaustion of long-term HSCs. Following total body irradiation, Krasex3op/ex3op mice displayed accelerated hematologic recovery and increased survival. Mechanistically, HSCs from Krasex3op/ex3op mice demonstrated increased proliferation at baseline, with a corresponding increase in Erk1/2 phosphorylation and cyclin-dependent kinase 4 and 6 (Cdk4/6) activation. Furthermore, both the enhanced colony-forming capacity and in vivo repopulating capacity of HSCs from Krasex3op/ex3op mice were dependent on Cdk4/6 activation. Finally, BM transplantation studies revealed that augmented Kras expression produced expansion of HSCs, progenitor cells, and B cells in a hematopoietic cell-autonomous manner, independent from effects on the BM microenvironment. This study provides fundamental demonstration of codon usage in a mammal having a biological consequence, which may speak to the importance of codon usage in mammalian biology.

Indexed as

AnimalsBone Marrow TransplantationCells, CulturedCodonExonsFemaleHematopoiesisHematopoietic Stem CellsMaleMiceMice, TransgenicModels, AnimalMutationPrimary Cell CultureProto-Oncogene Proteins p21(ras)Transplantation ChimeraCodonHras protein, mouseProto-Oncogene Proteins p21(ras)HematologyHematopoietic stem cellsStem cells

Identifiers

PMID29875320
PMCPMC6124423
OpenAlexW2805295706

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.