ArticlePloS one2013
Deletion of Snai2 and Snai3 results in impaired physical development compounded by lymphocyte deficiency.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 24 citations in OpenAlex.
- Genetic factors underlying Mandibular prognathism: insights from recent human and animal studies.Mammalian genome : official journal of the International Mammalian Genome Society · 2025Review
- Dissecting the Complexity of Skeletal-Malocclusion-Associated Phenotypes: Mouse for the Rescue.International journal of molecular sciences · 2023Review
- An "unexpected" role for EMT transcription factors in hematological development and malignancy.Frontiers in immunology · 2023Review
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- Epithelial-mesenchymal transition-related genes in coronary artery disease.Open medicine (Warsaw, Poland) · 2022Article
- Stromal SNAI2 Is Required for ERBB2 Breast Cancer Progression.Cancer research · 2020Article
- Prognostic values of SNAI family members in breast cancer patients.Annals of translational medicine · 2020Article
- Article
- Snai2 and Snai3 transcriptionally regulate cellular fitness and functionality of T cell lineages through distinct gene programs.Immunobiology · 2016Article
- Candidate Gene Analyses of Skeletal Variation in Malocclusion.Journal of dental research · 2015Article
- Snai1 regulates cell lineage allocation and stem cell maintenance in the mouse intestinal epithelium.The EMBO journal · 2015Article
- Fatal autoimmunity results from the conditional deletion of Snai2 and Snai3.Cellular immunology · 2015Article
- Snail transcription factors in hematopoietic cell development: a model of functional redundancy.Experimental hematology · 2014Review
- An overlapping set of genes is regulated by both NFIB and the glucocorticoid receptor during lung maturation.BMC genomics · 2014Article
- Article
- Article
- Absence of a major role for the snai1 and snai3 genes in regulating skeletal muscle regeneration in mice.PLoS currents · 2013Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The Snail family of transcriptional regulators consists of three highly conserved members. These proteins regulate (repress) transcription via the recruitment of histone deacetylases to target gene promoters that possess the appropriate E-box binding sequences. Murine Snai1 is required for mouse development while Snai2 deficient animals survive with some anomalies. Less is known about the third member of the family, Snai3. To investigate the function of Snai3, we generated a conditional knockin mouse. Utilizing Cre-mediated deletion to facilitate the ablation of Snai3 in T cells or the entire animal, we found little to no effect of the loss of Snai3 in the entire animal or in T cell lineages. This finding provided the hypothesis that absence of Snai3 was mitigated, in part, by the presence of Snai2. To test this hypothesis we created Snai2/Snai3 double deficient mice. The developmental consequences of lacking both of these proteins was manifested in stunted growth, a paucity of offspring including a dramatic deficiency of female mice, and impaired immune cell development within the lymphoid lineages.
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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.