ArticleBlood2013
PKR regulates proliferation, differentiation, and survival of murine hematopoietic stem/progenitor cells.
Article in Blood, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
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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.
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.
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Who cites it
20 citing papers in PubMed.
- Emerging roles for integrated stress response signaling in homeostasis.The FEBS journal · 2025Review
- Nucleic acid-induced inflammation on hematopoietic stem cells.Experimental hematology · 2024Article
- The causes of pulmonary hypertension and the benefits of aerobic exercise for pulmonary hypertension from an integrated perspective.Frontiers in physiology · 2024Review
- Luteolin protects DYT-Frontiers in pharmacology · 2023Article
- Targeting the integrated stress response in hematologic malignancies.Experimental hematology & oncology · 2022Review
- A tale of two proteins: PACT and PKR and their roles in inflammation.The FEBS journal · 2021Review
- Cell fate determined by the activation balance between PKR and SPHK1.Cell death and differentiation · 2021Article
- Glycogen synthase kinase (GSK)-3 and the double-strand RNA-dependent kinase, PKR: When two kinases for the common good turn bad.Biochimica et biophysica acta. Molecular cell research · 2020Review
- Overexpression of HOXA10 is associated with unfavorable prognosis of acute myeloid leukemia.BMC cancer · 2020Article
- Article
- eIF2α promotes vascular remodeling via autophagy in monocrotaline-induced pulmonary arterial hypertension rats.Drug design, development and therapy · 2019Article
- Article
- Human noncoding RNA 886 (nc886) adopts two structurally distinct conformers that are functionally opposing regulators of PKR.RNA (New York, N.Y.) · 2017Article
- Inhibition of PKR protects against HScientific reports · 2016Article
- EZH2 promotes colorectal cancer stem-like cell expansion by activating p21cip1-Wnt/β-catenin signaling.Oncotarget · 2016Article
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- Article
- PKR negatively regulates leukemia progression in association with PP2A activation, Bcl-2 inhibition and increased apoptosis.Blood cancer journal · 2013Article
- PIG3 functions in DNA damage response through regulating DNA-PKcs homeostasis.International journal of biological sciences · 2013Article
- Endoplasmic reticulum stress and pulmonary hypertension.Pulmonary circulationReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
Abstract
Protein kinase R (PKR) is an interferon (IFN)-inducible, double-stranded RNA-activated kinase that initiates apoptosis in response to cellular stress. To determine the role of PKR in hematopoiesis, we developed transgenic mouse models that express either human PKR (TgPKR) or a dominant-negative PKR (TgDNPKR) mutant specifically in hematopoietic tissues. Significantly, peripheral blood counts from TgPKR mice decrease with age in association with dysplastic marrow changes. TgPKR mice have reduced colony-forming capacity and the colonies also are more sensitive to hematopoietic stresses. Furthermore, TgPKR mice have fewer hematopoietic stem/progenitor cells (HSPCs), and the percentage of quiescent (G0) HSPCs is increased. Importantly, treatment of TgPKR bone marrow (BM) with a PKR inhibitor specifically rescues sensitivity to growth factor deprivation. In contrast, marrow from PKR knockout (PKRKO) mice has increased potential for colony formation and HSPCs are more actively proliferating and resistant to stress. Significantly, TgPKR HSPCs have increased expression of p21 and IFN regulatory factor, whereas cells from PKRKO mice display mechanisms indicative of proliferation such as reduced eukaryotic initiation factor 2α phosphorylation, increased extracellular signal-regulated protein kinases 1 and 2 phosphorylation, and increased CDK2 expression. Collectively, data reveal that PKR is an unrecognized but important regulator of HSPC cell fate and may play a role in the pathogenesis of BM failure.
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Registered trials
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.