Evidence map›Paper›PMID 22736770›Full record

ArticleThe Journal of biological chemistry2012

Mammalian alteration/deficiency in activation 3 (Ada3) is essential for embryonic development and cell cycle progression.

Shakur Mohibi, Channabasavaiah Basavaraju Gurumurthy, Alo Nag, Jun Wang, Sameer Mirza, Yousaf Mian, Meghan Quinn, Bryan Katafiasz, James Eudy, Sanjit Pandey and 4 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

22 citing papers in PubMed, 33 citations in OpenAlex.

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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

14 authors at 2 institutions in 1 country.

Shakur MohibiDepartment of Genetics, Cell Biology, and Anatomy, University of Nebraska Medical Center, Omaha, NE 68198-5805, USA.
Channabasavaiah Basavaraju Gurumurthy
Alo Nag
Jun Wang
Sameer Mirza
Yousaf Mian
Meghan Quinn
Bryan Katafiasz
James Eudy
Sanjit Pandey
Chittibabu Guda
Mayumi Naramura
Hamid Band
Vimla Band
University of Nebraska Medical Center · USNorthShore University HealthSystem · US

Funding

UNMC Structural Biology CoreP20GM103427 · NIGMS · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI Heather Colleen Jensen-Smith · 2012 to 2026
$59.2M
ZINC FINGER-INSPIRED FLUORESCENT CHEMOSENSORSP20RR016469 · NCRR · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI TURPEN, JAMES B · 2001 to 2011
$36.2M
TYROSINE KINASE REGULATION VIA PROTEIN DEGRADATIONR01CA087986 · NCI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI BAND, HAMID · 2000 to 2015
$4.2M
MOLECULAR CONTROL OF EGF RECEPTOR DOWN-REGULATIONR01CA099163 · NCI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI BAND, HAMID · 2003 to 2012
$3.7M
Targeting Endocytic Recycling of EGF Receptor in Cancer R01CA105489 · NCI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI BAND, HAMID · 2004 to 2014
$3.0M
A novel regulator of p53 functionR01CA096844 · NCI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI BAND, VIMLA · 2002 to 2011
$2.7M
High Capacity Nanocarriers for Cancer ChemotherapeuticsU01CA151806 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI KABANOV, ALEXANDER V · 2010 to 2014
$2.0M
Ecd as a regulator of cell cycle and breast oncogenesisR01CA144027 · NCI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI BAND, VIMLA · 2011 to 2015
$1.6M
ErbB2 Downregulation Through HSP90 InhibitionR01CA116552 · NCI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI BAND, HAMID · 2007 to 2011
$1.4M
NCI NIH HHS 5U01CA151806-02NCI NIH HHS CA105489NCI NIH HHS CA116552NCI NIH HHS CA144027NCI NIH HHS CA87986NCI NIH HHS CA96844NCI NIH HHS CA99163NCI NIH HHS R01 CA087986NCI NIH HHS R01 CA096844NCI NIH HHS R01 CA099163NCI NIH HHS R01 CA105489NCI NIH HHS R01 CA116552NCI NIH HHS R01 CA144027NCI NIH HHS U01 CA151806NCRR NIH HHS 5P20RR016469NCRR NIH HHS P20 RR016469NIGMS NIH HHS 8P20GM103427NIGMS NIH HHS P20 GM103427
6 · The paper itself

Abstract

Ada3 protein is an essential component of histone acetyl transferase containing coactivator complexes conserved from yeast to human. We show here that germline deletion of Ada3 in mouse is embryonic lethal, and adenovirus-Cre mediated conditional deletion of Ada3 in Ada3(FL/FL) mouse embryonic fibroblasts leads to a severe proliferation defect which was rescued by ectopic expression of human Ada3. A delay in G(1) to S phase of cell cycle was also seen that was due to accumulation of Cdk inhibitor p27 which was an indirect effect of c-myc gene transcription control by Ada3. We further showed that this defect could be partially reverted by knocking down p27. Additionally, drastic changes in global histone acetylation and changes in global gene expression were observed in microarray analyses upon loss of Ada3. Lastly, formation of abnormal nuclei, mitotic defects and delay in G(2)/M to G(1) transition was seen in Ada3 deleted cells. Taken together, we provide evidence for a critical role of Ada3 in embryogenesis and cell cycle progression as an essential component of HAT complex.

Indexed as

AcetylationAnimalsCell CycleCells, CulturedCyclin-Dependent Kinase Inhibitor p27Embryo, MammalianEmbryonic DevelopmentFibroblastsGene Expression Regulation, DevelopmentalHistonesHumansMiceMice, KnockoutTranscription FactorsCDKN1B protein, humanCdkn1b protein, mouseCyclin-Dependent Kinase Inhibitor p27HistonesTADA3 protein, humanTranscription Factors

Identifiers

PMID22736770
PMCPMC3436190
OpenAlexW2063639409

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.