ArticleDevelopment (Cambridge, England)2007
SHP-2 is required for the maintenance of cardiac progenitors.
Article in Development (Cambridge, England), 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
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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.
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.
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Who cites it
23 citing papers in PubMed, 32 citations in OpenAlex.
- DDIT3 is associated with breast cancer prognosis and immune microenvironment: an integrative bioinformatic and immunohistochemical analysis.Journal of Cancer · 2024Article
- From Stem to Sternum: The Role of Shp2 in the Skeleton.Calcified tissue international · 2023Review
- Use of Frogs as a Model to Study the Etiology of HLHS.Journal of cardiovascular development and disease · 2023Article
- Case report: Clinical manifestations and genotype analysis of a child withFrontiers in pediatrics · 2022Article
- PTPN11 Gene Mutations and Its Association with the Risk of Congenital Heart Disease.Disease markers · 2022Article
- Swimming toward solutions: Using fish and frogs as models for understanding RASopathies.Birth defects research · 2020Review
- Proteomic Analysis of Myocardia Containing the Obscurin R4344Q Mutation Linked to Hypertrophic Cardiomyopathy.Frontiers in physiology · 2020Article
- Protein tyrosine phosphatases in cardiac physiology and pathophysiology.Heart failure reviews · 2018Review
- Vascular mechanotransduction data in a rodent model of diabetes: Pressure-induced regulation of SHP2 and associated signaling in the rat inferior vena cava.Data in brief · 2017Article
- Expanding the genetic toolkit in Xenopus: Approaches and opportunities for human disease modeling.Developmental biology · 2017Review
- The role of the protein tyrosine phosphatase SHP2 in cardiac development and disease.Seminars in cell & developmental biology · 2015Review
- Congenital heart disease protein 5 associates with CASZ1 to maintain myocardial tissue integrity.Development (Cambridge, England) · 2014Article
- Differential regulation of CASZ1 protein expression during cardiac and skeletal muscle development.Developmental dynamics : an official publication of the American Association of Anatomists · 2014Article
- Proteomic profiling of cardiac tissue by isolation of nuclei tagged in specific cell types (INTACT).Development (Cambridge, England) · 2014Article
- Tcf21 regulates the specification and maturation of proepicardial cells.Development (Cambridge, England) · 2013Article
- SHP-2 acts via ROCK to regulate the cardiac actin cytoskeleton.Development (Cambridge, England) · 2012Article
- Xenopus: An emerging model for studying congenital heart disease.Birth defects research. Part A, Clinical and molecular teratology · 2011Review
- Myocardial lineage development.Circulation research · 2010Review
- Focal adhesion kinase is essential for cardiac looping and multichamber heart formation.Genesis (New York, N.Y. : 2000) · 2010Article
- The BMP pathway acts to directly regulate Tbx20 in the developing heart.Development (Cambridge, England) · 2010Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
The isolation and culturing of cardiac progenitor cells has demonstrated that growth factor signaling is required to maintain cardiac cell survival and proliferation. In this study, we demonstrate in Xenopus that SHP-2 activity is required for the maintenance of cardiac precursors in vivo. In the absence of SHP-2 signaling, cardiac progenitor cells downregulate genes associated with early heart development and fail to initiate cardiac differentiation. We further show that this requirement for SHP-2 is restricted to cardiac precursor cells undergoing active proliferation. By demonstrating that SHP-2 is phosphorylated on Y542/Y580 and that it binds to FRS-2, we place SHP-2 in the FGF pathway during early embryonic heart development. Furthermore, we demonstrate that inhibition of FGF signaling mimics the cellular and biochemical effects of SHP-2 inhibition and that these effects can be rescued by constitutively active/Noonan-syndrome-associated forms of SHP-2. Collectively, these results show that SHP-2 functions within the FGF/MAPK pathway to maintain survival of proliferating populations of cardiac progenitor cells.
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Registered trials
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.