Evidence map›Paper›PMID 19007851›Full record

ReviewMolecular and cellular endocrinology2009

Complex assembly on the human CYP17 promoter.

Marion B Sewer, Srinath Jagarlapudi

Open access · greenAbstract readReview
In one paragraph

Review in Molecular and cellular endocrinology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

7 citing papers in PubMed, 29 citations in OpenAlex.

  1. 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.

Marion B SewerSchool of Biology and the Parker H. Petit Institute for Bioengineering & Bioscience, Georgia Institute of Technology, Atlanta, GA 30332, United States. marion.sewer@biology.gatech.edu
Srinath Jagarlapudi
Georgia Institute of Technology · US

Funding

Regulation of Steroidogenic Genes by Trophic HormonesR01GM073241 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI SEWER, MARION B. · 2004 to 2013
$2.2M
Regulation of Steroidogenic Genes by Trophic HormonesR56GM073241 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI SEWER, MARION B. · 2009 to 2009
$281k
NIGMS NIH HHS GM073241NIGMS NIH HHS R01 GM073241NIGMS NIH HHS R56 GM073241
6 · The paper itself

Abstract

Optimal steroid hormone biosynthesis occurs via the integration of multiple regulatory processes, one of which entails a coordinate increase in the transcription of all genes required for steroidogenesis. In the human adrenal cortex adrenocorticotropin (ACTH) activates a signaling cascade that promotes the dynamic assembly of protein complexes on the promoters of steroidogenic genes. For CYP17, multiple transcription factors, including steroidogenic factor-1 (SF-1), GATA-6, and sterol regulatory binding protein 1 (SREBP1), are recruited to the promoter during activated transcription. The ability of these factors to increase CYP17 mRNA expression requires the formation of higher order coregulatory complexes, many of which contain enzymatic activities that post-translationally modify both the transcription factors and histones. We discuss the mechanisms by which transcription factors and coregulatory proteins regulate CYP17 transcription and summarize the role of kinases, phosphatases, acetyltransferases, and histone deacetylases in controlling CYP17 mRNA expression.

Indexed as

Gene Expression Regulation, EnzymologicPromoter Regions, GeneticAdrenal GlandsHumansSteroid 17-alpha-HydroxylaseTranscription FactorsSteroid 17-alpha-HydroxylaseTranscription Factors

Identifiers

PMID19007851
PMCPMC2754694
OpenAlexW2002260125

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.