Evidence map›Paper›PMID 27481995›Full record

ArticleMolecular and cellular biology2016

OLA1, a Translational Regulator of p21, Maintains Optimal Cell Proliferation Necessary for Developmental Progression.

Zonghui Ding, Yue Liu, Valentina Rubio, Jinjie He, Laurie J Minze, Zheng-Zheng Shi

Open access · bronzeAbstract read
In one paragraph

Article in Molecular and cellular biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 1 pooled it
1.4field-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

26 citing papers in PubMed, 1 synthesis or guideline pooled it, 35 citations in OpenAlex.

  1. Pooled it
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  10. OLA1 Phosphorylation Governs the Mitochondrial Bioenergetic Function of Pulmonary Vascular Cells.American journal of respiratory cell and molecular biology · 2023
    Article
  11. Article
  12. Association of Common Variants inInternational journal of molecular sciences · 2022
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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

6 authors at 2 institutions in 2 countries.

Zonghui DingDepartment of Cardiovascular Sciences, Houston Methodist Research Institute, Weill Cornell Medical College, Houston, Texas, USA.
Yue LiuDepartment of Cardiovascular Sciences, Houston Methodist Research Institute, Weill Cornell Medical College, Houston, Texas, USA Department of Surgical Oncology, The Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang, China.
Valentina RubioDepartment of Cardiovascular Sciences, Houston Methodist Research Institute, Weill Cornell Medical College, Houston, Texas, USA.
Jinjie HeDepartment of Cardiovascular Sciences, Houston Methodist Research Institute, Weill Cornell Medical College, Houston, Texas, USA Department of Surgical Oncology, The Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang, China.
Laurie J MinzeImmunobiology Research Center, Houston Methodist Research Institute, Weill Cornell Medical College, Houston, Texas, USA.
Zheng-Zheng ShiDepartment of Cardiovascular Sciences, Houston Methodist Research Institute, Weill Cornell Medical College, Houston, Texas, USA zshi@houstonmethodist.org.
Cornell University · USHouston Methodist · US

Funding

Inhibition of OLA1: A Novel Strategy for Anti-Metastasis TherapyR01CA155069 · NCI · METHODIST HOSPITAL RESEARCH INSTITUTE · PI SHI, ZHENG-ZHENG · 2011 to 2015
$1.6M
NCI NIH HHS R01 CA155069
6 · The paper itself

Abstract

OLA1, an Obg-family GTPase, has been implicated in eukaryotic initiation factor 2 (eIF2)-mediated translational control, but its physiological functions remain obscure. Here we report that mouse embryos lacking OLA1 have stunted growth, delayed development leading to immature organs-especially lungs-at birth, and frequent perinatal lethality. Proliferation of primary Ola1(-/-) mouse embryonic fibroblasts (MEFs) is impaired due to defective cell cycle progression, associated with reduced cyclins D1 and E1, attenuated Rb phosphorylation, and increased p21(Cip1/Waf1) Accumulation of p21 in Ola1(-/-) MEFs is due to enhanced mRNA translation and can be prevented by either reconstitution of OLA1 expression or treatment with an eIF2α dephosphorylation inhibitor, suggesting that OLA1 regulates p21 through a translational mechanism involving eIF2. With immunohistochemistry, overexpression of p21 protein was detected in Ola1-null embryos with reduced cell proliferation. Moreover, we have generated p21(-/-) Ola1(-/-) mice and found that knockout of p21 can partially rescue the growth retardation defect of Ola1(-/-) embryos but fails to rescue them from developmental delay and the lethality. These data demonstrate, for the first time, that OLA1 is required for normal progression of mammalian development. OLA1 plays an important role in promoting cell proliferation at least in part through suppression of p21 and organogenesis via factors yet to be discovered.

Indexed as

Embryonic DevelopmentAdenosine TriphosphatasesAnimalsCell ProliferationCyclin-Dependent Kinase Inhibitor p21Embryo, MammalianFibroblastsGene Knockout TechniquesMiceMutationOrganogenesisProtein BiosynthesisUp-RegulationAdenosine TriphosphatasesCdkn1a protein, mouseCyclin-Dependent Kinase Inhibitor p21

Identifiers

PMID27481995
PMCPMC5038148
OpenAlexW2500121575

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.