Evidence map›Paper›PMID 15899865›Full record

ArticleMolecular and cellular biology2005

YB-1 is important for late-stage embryonic development, optimal cellular stress responses, and the prevention of premature senescence.

Zhi Hong Lu, Jason T Books, Timothy J Ley

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 82 papers.

0numbers the graph read from it
0cells of the map it votes in
82citing papers in PubMed
3.4field-weighted citation impact, top 7% 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

82 citing papers in PubMed, 182 citations in OpenAlex.

  1. YBX1 as a developmental regulator of ventricular morphogenesis and a potential target in cardiac pathology.American journal of physiology. Heart and circulatory physiology · 2026
    Article
  2. Deletion of Ybx1 results in germ cell hypoplasia in mouse embryos.The Journal of reproduction and development · 2026
    Article
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  4. Review
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  11. Y-Box-Binding Proteins Have a Dual Impact on Cellular Translation.International journal of molecular sciences · 2024
    Article
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  15. Review
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  20. High salt diet-induced proximal tubular phenotypic changes and sodium-glucose cotransporter-2 expression are coordinated by cold shock Y-box binding protein-1.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021
    Article

22 more citing papers are in PubMed but not listed here.

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 1 institution in 1 country.

Zhi Hong LuDivision of Oncology, Department of Medicine, Siteman Cancer Center, Washington University School of Medicine, St. Louis, Missouri 63110, USA.
Jason T Books
Timothy J Ley
Washington University in St. Louis · US

Funding

REGULATION OF HEMOGLOBINR37DK038682 · NIDDK · WASHINGTON UNIVERSITY · PI LEY, TIMOTHY J. · 1996 to 2008
$2.4M
Correction of globin gene mutations by gene targetingF32HL077048 · NHLBI · WASHINGTON UNIVERSITY · PI LU, ZHI HONG · 2004 to 2005
$104k
REGULATION OF FETAL AND ADULT HUMAN HEMOGLOBIN PRODUCTIONR56DK038682 · NIDDK · WASHINGTON UNIVERSITY · PI LEY, TIMOTHY J. · 2010 to 2010
$100k
REGULATION OF HEMOGLOBIN PRODUCTIONR01DK038682 · NIDDK · WASHINGTON UNIVERSITY · PI LEY, TIMOTHY J · 1987 to 1998
–
NHLBI NIH HHS F32 HL077048NIDDK NIH HHS DK38682NIDDK NIH HHS R37 DK038682NIDDK NIH HHS R56 DK038682
6 · The paper itself

Abstract

Proteins containing "cold shock" domains belong to the most evolutionarily conserved family of nucleic acid-binding proteins known among bacteria, plants, and animals. One of these proteins, YB-1, is widely expressed throughout development and has been implicated as a cell survival factor that regulates the transcription and/or translation of many cellular growth and death-related genes. For these reasons, YB-1 deficiency has been predicted to be incompatible with cell survival. However, the majority of YB-1(-/-) embryos develop normally up to embryonic day 13.5 (E13.5). After E13.5, YB-1(-/-) embryos exhibit severe growth retardation and progressive mortality, revealing a nonredundant role of YB-1 in late embryonic development. Fibroblasts derived from YB-1(-/-) embryos displayed a normal rate of protein synthesis and minimal alterations in the transcriptome and proteome but demonstrated reduced abilities to respond to oxidative, genotoxic, and oncogene-induced stresses. YB-1(-/-) cells under oxidative stress expressed high levels of the G(1)-specific CDK inhibitors p16Ink4a and p21Cip1 and senesced prematurely; this defect was corrected by knocking down CDK inhibitor levels with specific small interfering RNAs. These data suggest that YB-1 normally represses the transcription of CDK inhibitors, making it an important component of the cellular stress response signaling pathway.

Indexed as

Embryonic DevelopmentAnimalsCell Cycle ProteinsCellular SenescenceCyclin-Dependent Kinase Inhibitor p16Cyclin-Dependent Kinase Inhibitor p21DNA-Binding ProteinsDown-RegulationEmbryo, MammalianFetal Growth RetardationFibroblastsGenes, LethalGene TargetingMiceOxidative StressProtein BiosynthesisCdkn1a protein, mouseCell Cycle ProteinsCyclin-Dependent Kinase Inhibitor p16Cyclin-Dependent Kinase Inhibitor p21DNA-Binding ProteinsProtein Kinase InhibitorsRepressor ProteinsTranscription FactorsYbx1 protein, mouse

Identifiers

PMID15899865
PMCPMC1140647
OpenAlexW2155331947

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.