ArticleMolecular and cellular biology2000
The HAND1 basic helix-loop-helix transcription factor regulates trophoblast differentiation via multiple mechanisms.
Article in Molecular and cellular biology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 92 papers.
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Who cites it
92 citing papers in PubMed, 229 citations in OpenAlex.
- OVOL2 reinforces epithelial identity and promotes SynT-I differentiation in the mouse placenta†.Biology of reproduction · 2026Article
- Maternal obesity disrupts trophoblast differentiation and causes female-specific labyrinth defects in the mouse placenta.American journal of physiology. Cell physiology · 2026Article
- Select Histochemical and Immunohistochemical Methods to Investigate the Cell and Tissue Composition of the Mouse Placenta and Metrial Gland.Toxicologic pathology · 2026Review
- FNDC5 deficiency alters placental development, maternal body weight, and fetal-placental growth in mice.Scientific reports · 2026Article
- Chronic replication stress-mediated genomic instability disrupts placenta development in mice.PLoS genetics · 2026Article
- Eomesodermin in conjunction with the BAF complex promotes expansion and invasion of the trophectoderm lineage.Nature communications · 2025Article
- Exploring the differentiation potential of EomesDevelopmental biology · 2025Article
- METTL7A improves bovine IVF embryo competence by attenuating oxidative stress†.Biology of reproduction · 2025Article
- METTL7A improves bovine IVF embryo competence by attenuating oxidative stress.bioRxiv : the preprint server for biology · 2024Article
- PDGFRA is a conserved HAND2 effector during early cardiac development.Nature cardiovascular research · 2024Article
- Computational Identification of Milk Trait Regulation Through Transcription Factor Cooperation in Murciano-Granadina Goats.Biology · 2024Article
- Vitamin C inactivates c-Jun N-terminal kinase to stabilize heart and neural crest derivatives expressed 1 (Hand1) in regulating placentation and maintenance of pregnancy.Cellular and molecular life sciences : CMLS · 2024Article
- Review
- Solutions to the fertility equation in beef embryo recipients.Animal reproduction · 2024Review
- Transcription Factor 23 is an Essential Determinant of Murine Term Parturition.Molecular and cellular biology · 2024Article
- Acquisition of neural fate by combination of BMP blockade and chromatin modification.iScience · 2023Article
- Hypoplastic Left Heart Syndrome: Signaling & Molecular Perspectives, and the Road Ahead.International journal of molecular sciences · 2023Review
- Article
- In Vitro Embryogenesis and Gastrulation Using Stem Cells in Mice and Humans.International journal of molecular sciences · 2023Review
- Trophoblast Differentiation: Mechanisms and Implications for Pregnancy Complications.Nutrients · 2023Review
32 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
The basic helix-loop-helix (bHLH) transcription factor genes Hand1 and Mash2 are essential for placental development in mice. Hand1 promotes differentiation of trophoblast giant cells, whereas Mash2 is required for the maintenance of giant cell precursors, and its overexpression prevents giant cell differentiation. We found that Hand1 expression and Mash2 expression overlap in the ectoplacental cone and spongiotrophoblast, layers of the placenta that contain the giant cell precursors, indicating that the antagonistic activities of Hand1 and Mash2 must be coordinated. MASH2 and HAND1 both heterodimerize with E factors, bHLH proteins that are the DNA-binding partners for most class B bHLH factors and which are also expressed in the ectoplacental cone and spongiotrophoblast. In vitro, HAND1 could antagonize MASH2 function by competing for E-factor binding. However, the Hand1 mutant phenotype cannot be solely explained by ectopic activity of MASH2, as the Hand1 mutant phenotype was not altered by further mutation of Mash2. Interestingly, expression of E-factor genes (ITF2 and ALF1) was down-regulated in the trophoblast lineage prior to giant cell differentiation. Therefore, suppression of MASH2 function, required to allow giant cell differentiation, may occur in vivo by loss of its E-factor partner due to loss of its expression and/or competition from HAND1. In giant cells, where E-factor expression was not detected, HAND1 presumably associates with a different bHLH partner. This may account for the distinct functions of HAND1 in giant cells and their precursors. We conclude that development of the trophoblast lineage is regulated by the interacting functions of HAND1, MASH2, and their cofactors.
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