Evidence map›Paper›PMID 17485162›Full record

ArticleMolecular and cellular endocrinology2007

Regulation of growth hormone expression by Delta-like protein 1 (Dlk1).

Peter J Ansell, Yunli Zhou, Brit-Maren Schjeide, Alissa Kerner, Jing Zhao, Xun Zhang, Anne Klibanski

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular endocrinology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

24 citing papers in PubMed, 40 citations in OpenAlex.

  1. Trial
  2. Polar Overdominance Inheritance ofInternational journal of molecular sciences · 2026
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  8. ImprintedeLife · 2023
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  16. DLK1/PREF1 regulates nutrient metabolism and protects from steatosis.Proceedings of the National Academy of Sciences of the United States of America · 2014
    Article
  17. Article
  18. Article
  19. Article
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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

7 authors at 2 institutions in 1 country.

Peter J AnsellNeuroendocrine Unit, Massachusetts General Hospital and Harvard Medical School, Bulfinch 457B, 55 Fruit Street, Boston, MA 02114, United States.
Yunli Zhou
Brit-Maren Schjeide
Alissa Kerner
Jing Zhao
Xun Zhang
Anne Klibanski
Massachusetts General Hospital · USHarvard University · US

Funding

ROLE OF DIETARY CONSTITUENTS ON GENE EXPRESSION IN INTESTINAL EPITHELIUMP30DK040561 · NIDDK · MASSACHUSETTS GENERAL HOSPITAL · PI CHRISTOPHER P DUGGAN · 1994 to 2026
$31.6M
HORMONE REGULATION AND PATHOGENESIS OF PITUITARY TUMORSR01DK040947 · NIDDK · MASSACHUSETTS GENERAL HOSPITAL · PI KLIBANSKI, ANNE · 1989 to 2010
$2.7M
Role of post-transcriptional RNA methylation in the regulation of RNA activityR01GM110090 · NIGMS · SANFORD BURNHAM PREBYS MEDICAL DISCOVERY INSTITUTE · PI ZHAO, CRYSTAL · 2015 to 2019
$1.9M
NIDDK NIH HHS P30 DK040561NIDDK NIH HHS R01 DK040947NIDDK NIH HHS R01-DK-40947NIGMS NIH HHS R01 GM110090
6 · The paper itself

Abstract

Delta-like protein 1 (Dlk1) is a transmembrane protein characterized by epidermal growth factor (EGF)-like repeats. Dlk1, which is also known as preadipocyte factor 1 (pref-1) because of its ability to inhibit preadipocyte differentiation, regulates the differentiation of several other cell types through unknown mechanisms. To elucidate Dlk1 functions, identification of Dlk1-regulated target genes is critical. The observation that Dlk1 is expressed in many endocrine tissues suggests that Dlk1 may have endocrine-related functions. Because Dlk1 is expressed in GH producing cells, we hypothesize that one function of Dlk1 is to regulate GH expression. We found that GH mRNA, protein, and secretion were significantly decreased in GH3 pituitary cell clones that stably express Dlk1. In contrast, Dlk1 expression was unable to alter prolactin expression. Co-transfection of GH3 cells with a GH promoter-regulated reporter gene showed that Dlk1 repressed GH promoter activity. Deletion and mutation analysis of the GH promoter indicated that Pit-1 binding sites in the GH promoter are required for Dlk1-mediated repression. Furthermore, Dlk1 expression represses Pit-1-mediated transcription when both proteins are co-expressed in MCF-7 cells. Deletion analysis of Dlk1 revealed that the ability of Dlk1 to regulate GH promoter activity is independent of both its EGF-like repeats and its ability to modulate MAP kinase activity. The observation that Dlk1 regulates GH expression identifies the first endocrine function of Dlk1, establishes GH as a Dlk1-regulated target gene, and provides a model system to facilitate studies of Dlk1-mediated signaling.

Indexed as

Gene Expression RegulationAnimalsCalcium-Binding ProteinsCell LineGrowth HormoneHumansIntercellular Signaling Peptides and ProteinsMiceMitogen-Activated Protein KinasesMolecular Sequence DataPromoter Regions, GeneticRatsRNA, MessengerTranscription Factor Pit-1Calcium-Binding ProteinsDlk1 protein, mouseGrowth HormoneIntercellular Signaling Peptides and ProteinsMitogen-Activated Protein KinasesRNA, MessengerTranscription Factor Pit-1

Identifiers

PMID17485162
PMCPMC1974851
OpenAlexW2074305055

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.