ArticleMechanisms of development2013
Conditional deletions refine the embryonic requirement for Dlk1.
Article in Mechanisms of development, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.
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Who cites it
27 citing papers in PubMed, 1 synthesis or guideline pooled it, 66 citations in OpenAlex.
- Roles of Epigenetic Modifications in the Differentiation and Function of Pancreatic β-Cells.Frontiers in cell and developmental biology · 2020Pooled it
- Dlk1-deficient mice achieve puberty despite low body weight and low levels of leptin and kisspeptin.Journal of neuroendocrinology · 2026Article
- The Role of DLK1 Deficiency in Central Precocious Puberty and Association with Metabolic Dysregulation.Hormone research in paediatrics · 2026Article
- Untangling the genetics of beta cell dysfunction and death in type 1 diabetes.Molecular metabolism · 2024Review
- ImprintedeLife · 2023Article
- Dlk1 maintains adult mice long-term HSCs by activating Notch signaling to restrict mitochondrial metabolism.Experimental hematology & oncology · 2023Article
- Balanced gene dosage control rather than parental origin underpins genomic imprinting.Nature communications · 2022Article
- Case Report: Hypoglycemia Due to a Novel Activating Glucokinase Variant in an Adult - a Molecular Approach.Frontiers in endocrinology · 2022Article
- Article
- Partners in Crime: Beta-Cells and Autoimmune Responses Complicit in Type 1 Diabetes Pathogenesis.Frontiers in immunology · 2021Review
- DLK1 Expressed in Mouse Orexin Neurons Modulates Anxio-Depressive Behavior but Not Energy Balance.Brain sciences · 2020Article
- Article
- Expression and Functional Analyses of Dlk1 in Muscle Stem Cells and Mesenchymal Progenitors during Muscle Regeneration.International journal of molecular sciences · 2019Article
- Similarities and differences in tissue distribution of DLK1 and DLK2 during E16.5 mouse embryogenesis.Histochemistry and cell biology · 2019Article
- Dlk1-Mediated Temporal Regulation of Notch Signaling Is Required for Differentiation of Alveolar Type II to Type I Cells during Repair.Cell reports · 2019Article
- Intrauterine hyperglycemia induces intergenerational Dlk1-Gtl2 methylation changes in mouse placenta.Oncotarget · 2018Article
- Fetus-derived DLK1 is required for maternal metabolic adaptations to pregnancy and is associated with fetal growth restriction.Nature genetics · 2016Article
- Preadipocyte factor 1 induces pancreatic ductal cell differentiation into insulin-producing cells.Scientific reports · 2016Article
- Maternal and zygotic Zfp57 modulate NOTCH signaling in cardiac development.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- What does genetics tell us about imprinting and the placenta connection?Cellular and molecular life sciences : CMLS · 2015Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Numerous studies have implicated Delta-like 1 (DLK1), a transmembrane protein that shares homology with Notch ligands, in embryonic growth and differentiation. Dlk1 expression is widespread, though not ubiquitous, during early development, but is confined to a few specific cell types in adults. Adult Dlk1-expressing tissues include the Insulin-producing β-cells of the pancreas and the Growth hormone-producing somatotrophs of the pituitary gland. Previously generated Dlk1 null mice (Dlk1(Sul-pat)), display a partially penetrant neonatal lethality and a complex pattern of developmental and adult phenotypes. Here we describe the generation of a conditional Dlk1 mouse line (Dlk1(flox)) to facilitate cell type-specific deletion of the Dlk1 gene, providing a powerful system to explore each aspect of the Dlk1 null phenotype. Four tissue-specific Cre mouse lines were used to produce individual Dlk1 deletions in pancreatic β-cells, pituitary somatotrophs and the endothelial cells of the embryo and placenta, key candidates for the Dlk1 phenotype. Contrary to expectations, all of these conditional mice were fully viable, and none recapitulated any aspect of the Dlk1(Sul-pat) null mice. Dlk1 expression is therefore not essential for the normal development of β-cells, somatotrophs and endothelial cells, and the tissues responsible for the Dlk1 null phenotype remain to be identified. Dlk1(flox) mice will continue to provide an important tool for further research into the function of Dlk1.
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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.