Evidence map›Paper›PMID 19608464›Full record

ArticleDNA repair2009

Characterization of DNA damage-dependent cell cycle checkpoints in a menin-deficient model.

Molly C Kottemann, Allen E Bale

Abstract read
In one paragraph

Article in DNA repair, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

16 citing papers in PubMed, 23 citations in OpenAlex.

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  12. Trithorax group proteins: switching genes on and keeping them active.Nature reviews. Molecular cell biology · 2011
    Review
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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

2 authors at 1 institution in 1 country.

Molly C KottemannDepartment of Genetics, Yale University School of Medicine, 333 Cedar St., SHM-I 321, New Haven, CT 06510, USA.
Allen E Bale
Yale University · US

Funding

GENETICS AND GENOMICS OF HUMAN DISEASET32HD007149 · NICHD · YALE UNIVERSITY · PI James P Noonan · 1985 to 2026
$8.2M
Functional analysis of MEN1 in Drosophila modelR01GM066079 · NIGMS · YALE UNIVERSITY · PI BALE, ALLEN EVERETT · 2002 to 2004
$838k
NICHD NIH HHS T32 HD007149NICHD NIH HHS T32-HD07149-29NIGMS NIH HHS R01 GM066079NIGMS NIH HHS R01-GM66079
6 · The paper itself

Abstract

MEN1, the gene responsible for the cancer predisposition syndrome multiple endocrine neoplasia type I, has been implicated in DNA repair, cell cycle control, and transcriptional regulation. It is unclear to what degree these processes are integrated into a single encompassing function in normal cellular physiology and how deficiency of the MEN1-encoded protein, "menin", contributes to cancer pathogenesis. In this study, we found that loss of Men1 in mouse embryonic fibroblasts caused abrogation of the G1/S and intra-S checkpoints following ionizing radiation. The cyclin-dependent kinase inhibitor, p21, failed to be upregulated in the mutant although upstream checkpoint signaling remained intact. Menin localized to the p21 promoter in a DNA damage-dependent manner. The MLL histone methyltransferase, a positive transcriptional regulator, bound to the same region in the presence of menin but not in Men1(-/-) cells. Finally, p53 retained damage-responsive binding to the p21 promoter in the Men1 mutant. These data indicate that menin participates in the checkpoint response in a transcriptional capacity, upregulating the DNA damage-responsive target p21.

Indexed as

Cell CycleDNA DamageModels, BiologicalAnimalsAtaxia Telangiectasia Mutated ProteinsCell Cycle ProteinsCyclin-Dependent Kinase Inhibitor p21Embryo, MammalianFibroblastsG1 PhaseHistone-Lysine N-MethyltransferaseMiceMutagensMutationMyeloid-Lymphoid Leukemia ProteinPhenotypeAtaxia Telangiectasia Mutated ProteinsAtr protein, mouseCell Cycle ProteinsCyclin-Dependent Kinase Inhibitor p21Histone-Lysine N-MethyltransferaseKmt2a protein, mouseMen1 protein, mouseMutagensMyeloid-Lymphoid Leukemia ProteinProtein Serine-Threonine KinasesProto-Oncogene ProteinsTumor Suppressor Protein p53

Identifiers

PMID19608464
PMCPMC2745199
OpenAlexW1998633850

What OpenQuestion holds

Textmetadata
LicenceTDM
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.