ArticleMolecular and cellular biology2004
Null mutation of the Lmo4 gene or a combined null mutation of the Lmo1/Lmo3 genes causes perinatal lethality, and Lmo4 controls neural tube development in mice.
Article in Molecular and cellular biology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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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.
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Who cites it
48 citing papers in PubMed, 78 citations in OpenAlex.
- Article
- Cerebellum Lecture: the Cerebellar Nuclei-Core of the Cerebellum.Cerebellum (London, England) · 2024Review
- The transcription regulator Lmo3 is required for the development of medial ganglionic eminence derived neurons in the external globus pallidus.Developmental biology · 2023Article
- Genetic predisposition to neuroblastoma results from a regulatory polymorphism that promotes the adrenergic cell state.The Journal of clinical investigation · 2023Article
- Gene expression atlas of energy balance brain regions.JCI insight · 2021Article
- Activation of tyrosine phosphatase PTP1B in pyramidal neurons impairs endocannabinoid signaling by tyrosine receptor kinase trkB and causes schizophrenia-like behaviors in mice.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2020Article
- Mapping developmental trajectories and subtype diversity of normal and glaucomatous human retinal ganglion cells by single-cell transcriptome analysis.Stem cells (Dayton, Ohio) · 2020Article
- Regulation of anxiety-like behavior and Crhr1 expression in the basolateral amygdala by LMO3.Psychoneuroendocrinology · 2018Article
- GATA4-dependent organ-specific endothelial differentiation controls liver development and embryonic hematopoiesis.The Journal of clinical investigation · 2017Article
- Compensatory Actions of Ldb Adaptor Proteins During Corticospinal Motor Neuron Differentiation.Cerebral cortex (New York, N.Y. : 1991) · 2017Article
- LMO4 is a prognostic marker involved in cell migration and invasion in non-small-cell lung cancer.Journal of thoracic disease · 2016Article
- LMO1 gene polymorphisms contribute to decreased neuroblastoma susceptibility in a Southern Chinese population.Oncotarget · 2016Article
- LMO2 at 25 years: a paradigm of chromosomal translocation proteins.Open biology · 2015Review
- Candidate Gene Association Analysis of Neuroblastoma in Chinese Children Strengthens the Role of LMO1.PloS one · 2015Article
- Increased behavioral responses to ethanol in Lmo3 knockout mice.Genes, brain, and behavior · 2014Article
- LIM-domain-only proteins: multifunctional nuclear transcription coregulators that interacts with diverse proteins.Molecular biology reports · 2014Review
- Article
- LMO4 is essential for paraventricular hypothalamic neuronal activity and calcium channel expression to prevent hyperphagia.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
- A modular gain-of-function approach to generate cortical interneuron subtypes from ES cells.Neuron · 2013Article
- Bivalent promoter marks and a latent enhancer may prime the leukaemia oncogene LMO1 for ectopic expression in T-cell leukaemia.Leukemia · 2013Article
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The LIM-only family of proteins comprises four members; two of these (LMO1 and LMO2) are involved in human T-cell leukemia via chromosomal translocations, and LMO2 is a master regulator of hematopoiesis. We have carried out gene targeting of the other members of the LIM-only family, viz., genes Lmo1, Lmo3 and Lmo4, to investigate their role in mouse development. None of these genes has an obligatory role in lymphopoiesis. In addition, while null mutations of Lmo1 or Lmo3 have no discernible phenotype, null mutation of Lmo4 alone causes perinatal lethality due to a severe neural tube defect which occurs in the form of anencephaly or exencephaly. Since the Lmo1 and Lmo3 gene sequences are highly related and have partly overlapping expression domains, we assessed the effect of compound Lmo1/Lmo3 null mutations. Although no anatomical defects were apparent in compound null pups, these animals also die within 24 h of birth, suggesting that a compensation between the related Lmo1 and 3 proteins can occur during embryogenesis to negate the individual loss of these genes. Our results complete the gene targeting of the LIM-only family in mice and suggest that all four members of this family are important in regulators of distinct developmental pathways.
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