ArticleThe Journal of biological chemistry2011
Arginine deficiency causes runting in the suckling period by selectively activating the stress kinase GCN2.
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 14 citations in OpenAlex.
- Effects of Individual Essential Amino Acids on Growth Rates of Young Rats Fed a Low-Protein Diet.Animals : an open access journal from MDPI · 2024Article
- Roles of chicken growth hormone receptor antisense transcript in chicken muscle development and myoblast differentiation.Poultry science · 2019Article
- Hypoargininemia exacerbates airway hyperresponsiveness in a mouse model of asthma.Respiratory research · 2018Article
- Molecular evolution and functional divergence of eukaryotic translation initiation factor 2-alpha kinases.PloS one · 2018Article
- Arginase 1 deletion in myeloid cells affects the inflammatory response in allergic asthma, but not lung mechanics, in female mice.BMC pulmonary medicine · 2017Article
- Immunohistochemical detection of arginase-I expression in formalin-fixed lung and other tissues.Journal of histotechnology · 2013Article
- General control nonderepressible 2 (GCN2) kinase protects oligodendrocytes and white matter during branched-chain amino acid deficiency in mice.The Journal of biological chemistry · 2013Article
- Eukaryotic initiation factor 2 phosphorylation and translational control in metabolism.Advances in nutrition (Bethesda, Md.) · 2012Review
- Arginases and arginine deficiency syndromes.Current opinion in clinical nutrition and metabolic care · 2012Review
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 3 countries.
Funding
Abstract
Suckling "F/A2" mice, which overexpress arginase-I in their enterocytes, develop a syndrome (hypoargininemia, reduced hair and muscle growth, impaired B-cell maturation) that resembles IGF1 deficiency. The syndrome may result from an impaired function of the GH-IGF1 axis, activation of the stress-kinase GCN2, and/or blocking of the mTORC1-signaling pathway. Arginine deficiency inhibited GH secretion and decreased liver Igf1 mRNA and plasma IGF1 concentration, but did not change muscle IGF1 concentration. GH supplementation induced Igf1 mRNA synthesis, but did not restore growth, ruling out direct involvement of the GH-IGF1 axis. In C2C12 muscle cells, arginine withdrawal activated GCN2 signaling, without impacting mTORC1 signaling. In F/A2 mice, the reduction of plasma and tissue arginine concentrations to ∼25% of wild-type values activated GCN2 signaling, but mTORC1-mediated signaling remained unaffected. Gcn2-deficient F/A2 mice suffered from hypoglycemia and died shortly after birth. Because common targets of all stress kinases (eIF2α phosphorylation, Chop mRNA expression) were not increased in these mice, the effects of arginine deficiency were solely mediated by GCN2.
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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.