Evidence map›Paper›PMID 8643513›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America1996

An AML-1 consensus sequence binds an osteoblast-specific complex and transcriptionally activates the osteocalcin gene.

C Banerjee, S W Hiebert, J L Stein, J B Lian, G S Stein

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
12.6field-weighted citation impact, top 1% 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

30 citing papers in PubMed, 169 citations in OpenAlex.

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  18. Nuclear microenvironments support physiological control of gene expression.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2003
    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

5 authors at 1 institution in 1 country.

C BanerjeeDepartment of Cell Biology and Cancer Center, University of Massachusetts Medical Center, Worcester, 01655, USA.
S W Hiebert
J L Stein
J B Lian
G S Stein
St. Jude Children's Research Hospital · US

Funding

CONTROL OF OSTEOBLAST PROLIFERATION AND DIFFERENTIATIONR01AR039588 · NIAMS · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI LIAN, JANE B., STEIN, GARY S. · 1990 to 2019
$8.0M
NUCLEAR MATRIX MEDIATED TRANSCRIPTIONAL CONTROL OF OSTEOBLAST GENE EXPRESSIONP01AR042262 · NIAMS · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI STEIN, JANET L · 1994 to 1997
–
SYNTHESIS OF OSTEOCALCIN IN BONER01AR033920 · NIAMS · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI LIAN, JANE B · 1986 to 1995
–
NIAMS NIH HHS AR33920NIAMS NIH HHS AR39588NIAMS NIH HHS AR42262
6 · The paper itself

Abstract

Tissue and cell-type specific expression of the rat osteocalcin (rOC) gene involves the interplay of multiple transcriptional regulatory factors. In this report we demonstrate that AML-1 (acute myeloid leukemia-1), a DNA-binding protein whose genes are disrupted by chromosomal translocations in several human leukemias, interacts with a sequence essential for enhancing tissue-restricted expression of the rOC gene. Deletion analysis of rOC promoter-chloramphenicol acetyltransferase constructs demonstrates that an AML-1-binding sequence within the proximal promoter (-138 to -130 nt) contributes to 75% of the level of osteocalcin gene expression. The activation potential of the AML-1-binding sequence has been established by overexpressing AML-1 in osteoblastic as well as in nonosseous cell lines. Overexpression not only enhances rOC promoter activity in osteoblasts but also mediates OC promoter activity in a nonosseous human fibroblastic cell line. A probe containing this site forms a sequence specific protein-DNA complex with nuclear extracts from osteoblastic cells but not from nonosseous cells. Antisera supershift experiments indicate the presence of AML-1 and its partner protein core-binding factor beta in this osteoblast-restricted complex. Mutations of the critical AML-1-binding nucleotides abrogate formation of the complex and strongly diminish promoter activity. These results indicate that an AML-1 related protein is functional in cells of the osteoblastic lineage and that the AML-1-binding site is a regulatory element important for osteoblast-specific transcriptional activation of the rOC gene.

Indexed as

DNA-Binding ProteinsProto-Oncogene ProteinsAnimalsBase SequenceBinding SitesCell LineConsensus SequenceCore Binding Factor Alpha 2 SubunitDNADNA, ComplementaryHumansMolecular Sequence DataNeoplasm ProteinsOsteoblastsOsteocalcinPromoter Regions, GeneticCore Binding Factor Alpha 2 SubunitDNADNA-Binding ProteinsDNA, ComplementaryNeoplasm ProteinsOsteocalcinProto-Oncogene ProteinsRecombinant ProteinsRUNX1 protein, humanRunx1 protein, ratTranscription Factors

Identifiers

PMID8643513
PMCPMC39389
OpenAlexW2084937656

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.