Evidence map›Paper›PMID 18224409›Full record

ArticleInternational journal of hematology2008

Chromatin regulation by AML1 complex.

Hitoshi Yoshida, Issay Kitabayashi

Abstract read
PubMed Publisher
In one paragraph

Article in International journal of hematology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

12 citing papers in PubMed, 26 citations in OpenAlex.

  1. Review
  2. RUNX1-ETO: Attacking the Epigenome for Genomic Instable Leukemia.International journal of molecular sciences · 2019
    Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Fadd and Skp2 are possible downstream targets of RUNX1-EVI1.International journal of hematology · 2013
    Article
  9. Article
  10. Article
  11. Review
  12. Review
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.

Hitoshi YoshidaMolecular Oncology Division, National Cancer Center Research Institute, Chuo-Ku, Tokyo 104-0045, Japan.
Issay Kitabayashi
National Cancer Research Institute · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The AML1 gene is the most frequent target of chromosomal translocations in acute leukemias. AML1 is essential for definitive hematopoiesis and regulates transcription of its target genes by binding to the specific DNA sequence. AML1 forms large multiprotein complexes including CBFbeta as a "core component" as well as several classes of chromatin modulators such as p300/CBP, MOZ, PML and HIPK2 as "regulatory complex". In this review, we describe the mechanisms by which AML1 complex regulates gene transcription and hematopoiesis, and its disruption by the leukemia-associated chromosomal translocations that affect genes for components of AML1 complex in view of deregulation of chromatin structure.

Indexed as

ChromatinCarrier ProteinsCore Binding Factor Alpha 2 SubunitHematopoiesisHistone AcetyltransferasesHumansLeukemiaProtein Serine-Threonine KinasesTranscription, GeneticTranslocation, GeneticCarrier ProteinsChromatinCore Binding Factor Alpha 2 SubunitHIPK2 protein, humanHistone AcetyltransferasesKAT6A protein, humanProtein Serine-Threonine KinasesRUNX1 protein, human

Identifiers

PMID18224409
OpenAlexW2007840858

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.