ArticleMolecular and cellular biology2002
Mice lacking paternally expressed Pref-1/Dlk1 display growth retardation and accelerated adiposity.
Article in Molecular and cellular biology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 196 papers, 1 of them a synthesis that pooled it.
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Who cites it
196 citing papers in PubMed, 1 synthesis or guideline pooled it, 455 citations in OpenAlex.
- Pooled it
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- Efficacy and tolerability of a novel herbal formulation for weight management in obese subjects: a randomized double blind placebo controlled clinical study.Lipids in health and disease · 2012Trial
- Regulatory mechanisms of maternal imprinting at the murine Dlk1-Dio3 domain.Nature communications · 2026Article
- Dlk1-deficient mice achieve puberty despite low body weight and low levels of leptin and kisspeptin.Journal of neuroendocrinology · 2026Article
- Polar Overdominance Inheritance ofInternational journal of molecular sciences · 2026Article
- Article
- DLK1: a novel therapeutic target in cancer.Endocrine-related cancer · 2026Review
- The Role of DLK1 Deficiency in Central Precocious Puberty and Association with Metabolic Dysregulation.Hormone research in paediatrics · 2026Article
- Gene expression analysis for feed efficiency trait in liver tissue of lactating Girolando cows.Genetics and molecular biology · 2026Article
- Adipose immune microenvironment: catalyst of age-related adipose tissue dysfunction.Immunity & ageing : I & A · 2025Review
- Association of DLK1 SNPs with body mass index and plasma lipid levels in children.Pediatric research · 2025Article
- Molecular mechanism of Activin receptor inhibition by DLK1.Nature communications · 2025Article
- Shared Pathophysiological Mechanisms and Genetic Factors in Early Menarche and Polycystic Ovary Syndrome.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Review
- A Male Japanese Patient with Temple Syndrome Complicated by Type 2 Diabetes Mellitus.Internal medicine (Tokyo, Japan) · 2025Article
- Genetics and Epigenetics of Human Pubertal Timing: The Contribution of Genes Associated With Central Precocious Puberty.Journal of the Endocrine Society · 2025Review
- Identification of maternal allele sequences of IG-DMR that are essential for neonatal viability.PloS one · 2025Article
- Genome-wide DNA methylation and gene expression in human placentas derived from assisted reproductive technology.Communications medicine · 2024Article
- DLK1 promoted ischemic angiogenesis through notch1 signaling in endothelial progenitor cells.Acta pharmacologica Sinica · 2024Article
136 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Preadipocyte factor 1 (Pref-1/Dlk1) inhibits in vitro adipocyte differentiation and has been recently reported to be a paternally expressed imprinted gene at human chromosome 14q32. Studies on human chromosome 14 deletions and maternal uniparental disomy (mUPD) 14 suggest that misexpression of a yet-to-be-identified imprinted gene or genes present on chromosome 14 causes congenital disorders. We generated Pref-1 knockout mice to assess the role of Pref-1 in growth and in vivo adipogenesis and to determine the contribution of Pref-1 in mUPD. Pref-1-null mice display growth retardation, obesity, blepharophimosis, skeletal malformation, and increased serum lipid metabolites. Furthermore, the phenotypes observed in Pref-1-null mice are present in heterozygotes that harbor a paternally inherited, but not in those with a maternally inherited pref-1-null allele. Our results demonstrate that Pref-1 is indeed paternally expressed and is important for normal development and for homeostasis of adipose tissue mass. We also suggest that Pref-1 is responsible for most of the symptoms observed in mouse mUPD12 and human mUPD14. Pref-1-null mice may be a model for obesity and other pathologies of human mUPD14.
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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.