Evidence map›Paper›PMID 23979845›Full record

ArticleMolecular endocrinology (Baltimore, Md.)2013

Research resource: progesterone receptor targetome underlying mammary gland branching morphogenesis.

Ashlee R Lain, Chad J Creighton, Orla M Conneely

Abstract read
In one paragraph

Article in Molecular endocrinology (Baltimore, Md.), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
–field-weighted citation impact
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

25 citing papers in PubMed.

  1. Article
  2. Review
  3. A molecular toolbox to study progesterone receptor signaling.Journal of mammary gland biology and neoplasia · 2023
    Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. In-silico QTL mapping of postpubertal mammary ductal development in the mouse uncovers potential human breast cancer risk loci.Mammalian genome : official journal of the International Mammalian Genome Society · 2015
    Article
  19. Article
  20. 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

3 authors.

Ashlee R LainDepartment of Molecular and Cellular Biology, Baylor College of Medicine, One Baylor Plaza, Houston, Texas 77030. orlac@bcm.edu.
Chad J Creighton
Orla M Conneely

Funding

Tumor BiologyP30CA125123 · NCI · BAYLOR COLLEGE OF MEDICINE · PI DAVID R ROWLEY · 2007 to 2026
$73.9M
TRANSGENIC MOUSE MODELS TO STUDY OVARIAN FUNCTIONU54HD007495 · NICHD · BAYLOR COLLEGE OF MEDICINE · PI RICHARDS, JOANNE STEWART · 1998 to 2013
$19.9M
Initiative for Maximizing Student Development (IMSD) ProgramR25GM056929 · NIGMS · BAYLOR COLLEGE OF MEDICINE · PI PEREIRA, FRED A · 1998 to 2023
$12.4M
PROGESTERONE RECEPTORS IN DEVELOPMENT AND TUMORIGENESISR01HD032007 · NICHD · BAYLOR COLLEGE OF MEDICINE · PI CONNEELY, ORLA M. · 1994 to 2008
$2.5M
NCI NIH HHS P30 CA125123NICHD NIH HHS R01 HD032007NICHD NIH HHS R01 HD32007NICHD NIH HHS U54 HD007495NIGMS NIH HHS GM056929NIGMS NIH HHS R25 GM056929
6 · The paper itself

Abstract

Progesterone (P4)-activated progesterone receptors (PRs) play an essential role in driving pregnancy-associated mammary ductal side-branching morphogenesis and alveologenesis. However, the global cistromic and transcriptome responses that are required to elicit P4-dependent branching morphogenesis have not been elucidated. By combining chromatin immunoprecipitation followed by deep sequencing to identify genome-wide PR-binding sites in PR-positive luminal epithelial cells with global gene expression signatures acutely regulated by PRs in the mammary gland, we have identified a mammary epithelial PR targetome associated with active P4-dependent branching morphogenesis in vivo. We demonstrate that P4-induced side-branching is initiated by epithelial cell rearrangement into a multilayered epithelium that sprouts laterally from quiescent ducts via a mechanism requiring P4-dependent activation of Rac-GTPase signaling. We identify effectors of Rac-GTPases as direct transcriptional targets of PRs, and we demonstrate that disruption of the P4-activated Rac-GTPase signaling axis is sufficient to eliminate P4-dependent side-branching. Our data reveal that the molecular mediators of P4-dependent ductal side-branching overlap with those implicated in breast cancer.

Indexed as

MorphogenesisAnimalsEpitheliumEstradiolFemaleGene Expression RegulationMammary Glands, AnimalMice, 129 StrainMice, Inbred BALB CMice, Inbred C57BLMice, KnockoutProgesteronerac GTP-Binding ProteinsReceptors, ProgesteroneSignal TransductionTranscriptomeEstradiolProgesteronerac GTP-Binding ProteinsReceptors, Progesterone

Identifiers

PMID23979845
PMCPMC3787126

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.