Evidence map›Paper›PMID 38536963›Full record

ArticleeLife2024

Affinity-tagged SMAD1 and SMAD5 mouse lines reveal transcriptional reprogramming mechanisms during early pregnancy.

Zian Liao, Suni Tang, Kaori Nozawa, Keisuke Shimada, Masahito Ikawa, Diana Monsivais, Martin Matzuk

Open access · goldAbstract read
In one paragraph

Article in eLife, 2024. 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
0.8field-weighted citation impact, top 24% 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, 5 citations in OpenAlex.

  1. Review
  2. Versatile SMAD2 and SMAD3 epitope-tagged mouse models for genomic profiling of TGFβ signaling: Uncovering GDF9-SMAD2/3 targets.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  3. Article
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  6. Review
  7. Article
  8. Review
  9. Article
  10. SMAD5 as a novel gene for familial pulmonary arterial hypertension.Clinical science (London, England : 1979) · 2025
    Article
  11. Article
  12. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 2 countries.

Zian LiaoDepartment of Pathology & Immunology, Baylor College of Medicine, Houston, United States.ORCID https://orcid.org/0000-0002-7198-2182
Suni TangDepartment of Pathology & Immunology, Baylor College of Medicine, Houston, United States.
Kaori NozawaDepartment of Pathology & Immunology, Baylor College of Medicine, Houston, United States.
Keisuke ShimadaResearch Institute for Microbial Diseases, Osaka University, Osaka, Japan.ORCID https://orcid.org/0000-0003-3739-7163
Masahito IkawaResearch Institute for Microbial Diseases, Osaka University, Osaka, Japan.ORCID https://orcid.org/0000-0001-9859-6217
Diana MonsivaisDepartment of Pathology & Immunology, Baylor College of Medicine, Houston, United States.ORCID https://orcid.org/0000-0001-5660-6392
Martin MatzukDepartment of Pathology & Immunology, Baylor College of Medicine, Houston, United States.ORCID https://orcid.org/0000-0002-1445-8632
Baylor College of Medicine · USThe University of Osaka · JP

Funding

Transforming growth factor β family signaling pathways in ovarian and uterine biologyR01HD032067 · NICHD · BAYLOR COLLEGE OF MEDICINE · PI MARTIN M. MATZUK · 1994 to 2026
$9.9M
Kinases as Therapeutic Targets for EndometriosisR01HD110038 · NICHD · BAYLOR COLLEGE OF MEDICINE · PI MARTIN M. MATZUK · 2022 to 2026
$3.4M
Targeting the endometrial stem cell niche inendometriosisR01HD105800 · NICHD · BAYLOR COLLEGE OF MEDICINE · PI Diana Monsivais · 2022 to 2026
$2.5M
The role of SMAD1 and SMAD5 in hormonal response, endometrial receptivity and glandular functionR00HD096057 · NICHD · BAYLOR COLLEGE OF MEDICINE · PI MONSIVAIS, DIANA · 2020 to 2022
$728k
The role of SMAD1 and SMAD5 in hormonal response, endometrial receptivity and glandular functionK99HD096057 · NICHD · BAYLOR COLLEGE OF MEDICINE · PI MONSIVAIS, DIANA · 2018 to 2019
$260k
NICHD NIH HHS K99 HD096057NICHD NIH HHS R00 HD096057NICHD NIH HHS R01 HD032067NICHD NIH HHS R01 HD105800NICHD NIH HHS R01 HD110038
6 · The paper itself

Abstract

Endometrial decidualization, a prerequisite for successful pregnancies, relies on transcriptional reprogramming driven by progesterone receptor (PR) and bone morphogenetic protein (BMP)-SMAD1/SMAD5 signaling pathways. Despite their critical roles in early pregnancy, how these pathways intersect in reprogramming the endometrium into a receptive state remains unclear. To define how SMAD1 and/or SMAD5 integrate BMP signaling in the uterus during early pregnancy, we generated two novel transgenic mouse lines with affinity tags inserted into the endogenous SMAD1 and SMAD5 loci (

Indexed as

EndometriumUterusAnimalsEmbryo ImplantationFemaleHumansMicePregnancySignal TransductionSmad5 ProteinSmad5 ProteinSMAD5 protein, humanbone morphogenetic proteinsdecidualizationdevelopmental biologyendometriumgeneticsgenomicshumanmouseprogesteroneSMAD proteinsuterus

Identifiers

PMID38536963
PMCPMC10972565
OpenAlexW4388904629

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.