Evidence map›Paper›PMID 20592034›Full record

ArticleThe Journal of biological chemistry2010

Chromatin protein L3MBTL1 is dispensable for development and tumor suppression in mice.

Jinzhong Qin, Denille Van Buren, Hsien-Sung Huang, Lei Zhong, Raul Mostoslavsky, Schahram Akbarian, Hanno Hock

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

19 citing papers in PubMed, 27 citations in OpenAlex.

  1. Article
  2. Sticky, Adaptable, and Many-sided: SAM protein versatility in normal and pathological hematopoietic states.BioEssays : news and reviews in molecular, cellular and developmental biology · 2023
    Review
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  19. L3MBTL1 polycomb protein, a candidate tumor suppressor in del(20q12) myeloid disorders, is essential for genome stability.Proceedings of the National Academy of Sciences of the United States of America · 2010
    Article
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

7 authors at 3 institutions in 1 country.

Jinzhong QinCancer Center, Massachusetts General Hospital, Boston, Massachusetts 02114, USA.
Denille Van Buren
Hsien-Sung Huang
Lei Zhong
Raul Mostoslavsky
Schahram Akbarian
Hanno Hock
Massachusetts General Hospital · USNeuropsychiatric Research Institute · USHarvard Stem Cell Institute · US

Funding

Mammalian SIRT6 Is A Master Regulator Of Glucose HomeostasisR01DK088190 · NIDDK · MASSACHUSETTS GENERAL HOSPITAL · PI MOSTOSLAVSKY, RAUL · 2010 to 2014
$1.9M
The histone deacetylase SIRT6 functions as a co-repressor of Hif1 alpha in glucosR01GM093072 · NIGMS · MASSACHUSETTS GENERAL HOSPITAL · PI MOSTOSLAVSKY, RAUL · 2010 to 2014
$1.7M
Chromatin Alterations in Rett SyndromeR01HD048489 · NICHD · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI AKBARIAN, SCHAHRAM · 2005 to 2009
$1.4M
NICHD NIH HHS HD 048489NICHD NIH HHS R01 HD048489NIDDK NIH HHS R01 DK088190NIGMS NIH HHS R01 GM093072
6 · The paper itself

Abstract

L3MBTL1, a paralogue of Drosophila tumor suppressor lethal(3)malignant brain tumor (l(3)mbt), binds histones in a methylation state-dependent manner and contributes to higher order chromatin structure and transcriptional repression. It is the founding member of a family of MBT domain-containing proteins that has three members in Drosophila and nine in mice and humans. Knockdown experiments in cell lines suggested that L3MBTL1 has non-redundant roles in the suppression of oncogene expression. We generated a mutant mouse strain that lacks exons 13-20 of L3mbtl1. Markedly reduced levels of a mutant mRNA with an out-of-frame fusion of exons 12 and 21 were expressed, but a mutant protein was undetectable by Western blot analysis. L3MBTL1(-/-) mice developed and reproduced normally. The highest expression of L3MBTL1 was detected in the brain, but its disruption did not affect brain development, spontaneous movement, and motor coordination. Despite previous implications of L3mbtl1 in the biology of hematopoietic transcriptional regulators, lack of L3MBTL1 did not result in deficiencies in lymphopoiesis or hematopoiesis. In contrast with its demonstrated biochemical activities, embryonic stem (ES) cells lacking L3MBTL1 displayed no abnormalities in H4 lysine 20 (H4K20) mono-, di-, or trimethylation; had normal global chromatin density as assessed by micrococcal nuclease digests; and expressed normal levels of c-myc. Embryonic fibroblasts lacking L3MBTL1 displayed unaltered cell cycle arrest and down-regulation of cyclin E expression after irradiation. In cohorts of mice followed for more than 2 years, lack of L3MBTL1 did not alter normal lifespan or survival with or without sublethal irradiation.

Indexed as

Amino Acid SequenceAnimalsBase SequenceBrainCell CycleChromatinCyclin EGene Expression RegulationGene Knockout TechniquesGrowth and DevelopmentHeLa CellsHistonesHumansLongevityLymphopoiesisLysineChromatinCyclin EHistonesL3MBTL1 protein, mouseLysineNuclear ProteinsRepressor ProteinsTumor Suppressor Proteins

Identifiers

PMID20592034
PMCPMC2934644
OpenAlexW1967038041

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.