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recruitment of specific sets of coregulators. To follow-up on this hypothesis, in the present study, we aimed to identify possible ligand-specific recruitment of coregulators to TRB1 isoforms. Here, we identified Jab1 as a TRB1 partner and showed that this
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Macrophage migration inhibitory factor (MIF) is an essential regulator of the macrophage responses to endotoxin. MIF also has the ability to override the anti-inflammatory actions of glucocorticoids during an immune response, and is thus an important pro-inflammatory factor. The presence of MIF in cells of the anterior pituitary has been described, and high levels of MIF in other rapidly proliferating tIssues have also been demonstrated. It has been hypothesised that MIF release from these cells is influenced by the hypothalamo-pituitary-adrenal axis, and that ACTH and MIF are released simultaneously to exert counter-regulatory effects on cortisol. However, another intracellular role for MIF has also been suggested as it has been shown that MIF exerts an effect on the inhibitory cell cycle control protein p27 through an interaction with Jab1, a protein implicated in p27 degradation. We studied MIF expression in different normal and adenomatous human pituitary samples using immunohistochemistry and RT-PCR. There was evidence of co-immunoprecipitation of MIF with Jab1, suggesting an interaction of the two proteins. Our results showed that there is increased expression of MIF protein in the nuclei of all pituitary adenomas compared with normal tIssue (P=0.0067), but there was no statistically significant difference in nuclear MIF expression between the different adenoma types. Nuclear MIF expression correlated positively with p27 and its phosphorylated form in normal tIssue (P=0.0028 and P<0.0001); however, this relationship was not seen in the adenoma samples. Cytoplasmic expression of MIF was found to be variable both in normal and adenomatous samples, with no consistent pattern. MIF mRNA was demonstrated to be present in all tumour and normal samples studied. Somatotroph tumours showed higher MIF mRNA expression compared with normal pituitary or other types of adenomas. In conclusion, MIF is expressed in cell nuclei in pituitary adenomas to a greater extent than in normal pituitary tIssue. We speculate that it may play a role in the control of the cell cycle, but whether its higher level in adenomas is a cause or a consequence of the tumorigenic process remains to be clarified.
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The immunological and neuroendocrine properties of macrophage migration inhibitory factor (MIF) are diverse. In this article we review the known cellular, molecular and genetic properties of MIF that place it as a key regulatory cytokine, acting within both the innate and adaptive immune responses.The unexpected and paradoxical induction of MIF secretion by low concentrations of glucocorticoids is explored. The role of MIF as a locally acting modulator of glucocorticoid sensitivity within foci of inflammation is also discussed. MIF has no homology with any other pro-inflammatory cytokine and until recently lacked a recognised transmembrane receptor. MIF has also been shown to be directly taken up into target cells and to interact with intracellular signalling molecules, including the Jun activation domain-binding protein Jab-1.Comprehensive analysis of the MIF gene has identified important functional polymorphisms and a series of genetic studies has revealed both association and linkage of MIF with inflammatory diseases. Altered MIF regulation may therefore be pivotal to acquiring chronic inflammation following an innate immune response.
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molecular characteristics to brown adipocytes including abundant mitochondrial content and high uncouple protein 1 (UCP-1) expression ( Ikeda et al . 2018 ). UCP-1 plays a role in mediating proton leak and induces uncoupled respiration. Through this process
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Kapurniotu A Fingerle-Rowson G Roger T Leng L Thiele M Calandra T Bucala R Bernhagen J 2006 Rapid and transient activation of the ERK MAPK signalling pathway by macrophage migration inhibitory factor (MIF) and dependence on JAB1/CSN5 and
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peripheral tissues, the genomic effects of TH occur after the intracellular transport of the predominate TH, thyroxine (T 4 ) and its deiodination to triiodothyronine (T 3 ), by either deiodinase type 1 (DI1) or type II (DI2). The activity of these enzymes
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cultures derived from individuals with SSc ( Sappino et al . 1990 , Kirk et al . 1995 ). The fibrotic response also involves increased production of several cytokines and growth factors, including transforming growth factor-β1 (TGFB1) and connective
College of Veterinary Medicine, Yangzhou University, Yangzhou, Jiangsu Province, China
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College of Veterinary Medicine, Yangzhou University, Yangzhou, Jiangsu Province, China
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College of Veterinary Medicine, Yangzhou University, Yangzhou, Jiangsu Province, China
Department of Cell and Molecular Medicine, Rush University Medical Center, Chicago, Illinois, USA
Jiangsu Co-innovation Center for Prevention and Control of Important Animal Infectious Diseases and Zoonosis, Yangzhou University, Yangzhou, China
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(IRS) ( Fig. 1B ) ( Guo 2013 , 2014 ). Tyrosine-phosphorylated IRS interact with the p85 subunit of the PI-3 kinase and activate its catalytic p110 subunit ( Fig. 1B ). PI-3 kinase activation leads to serine phosphorylation and activation of the
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phosphorylation of insulin receptor substrate 1 (IRS1) in serine residues and a decreased phosphorylation in tyrosine residues, which decrease insulin action ( Paz et al. 1997 , Fornes et al. 2010 , Diamanti-Kandarakis & Dunaif 2012 ). In the last decades, a
Instituto de Investigaciones en Ingeniería Genética y Biología Molecular, Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET) and University of Buenos Aires, V. Obligado 2490, 1428 Buenos Aires, Argentina
UVA Health System Charlottesville, Virginia, USA
Lawson Health Research Institute, London, Ontario, Canada
Center for the Study of Weight Regulation, Oregon Health & Science University, Portland, Oregon, USA
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Instituto de Investigaciones en Ingeniería Genética y Biología Molecular, Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET) and University of Buenos Aires, V. Obligado 2490, 1428 Buenos Aires, Argentina
UVA Health System Charlottesville, Virginia, USA
Lawson Health Research Institute, London, Ontario, Canada
Center for the Study of Weight Regulation, Oregon Health & Science University, Portland, Oregon, USA
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Instituto de Investigaciones en Ingeniería Genética y Biología Molecular, Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET) and University of Buenos Aires, V. Obligado 2490, 1428 Buenos Aires, Argentina
UVA Health System Charlottesville, Virginia, USA
Lawson Health Research Institute, London, Ontario, Canada
Center for the Study of Weight Regulation, Oregon Health & Science University, Portland, Oregon, USA
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Instituto de Investigaciones en Ingeniería Genética y Biología Molecular, Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET) and University of Buenos Aires, V. Obligado 2490, 1428 Buenos Aires, Argentina
UVA Health System Charlottesville, Virginia, USA
Lawson Health Research Institute, London, Ontario, Canada
Center for the Study of Weight Regulation, Oregon Health & Science University, Portland, Oregon, USA
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Instituto de Investigaciones en Ingeniería Genética y Biología Molecular, Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET) and University of Buenos Aires, V. Obligado 2490, 1428 Buenos Aires, Argentina
UVA Health System Charlottesville, Virginia, USA
Lawson Health Research Institute, London, Ontario, Canada
Center for the Study of Weight Regulation, Oregon Health & Science University, Portland, Oregon, USA
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Instituto de Investigaciones en Ingeniería Genética y Biología Molecular, Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET) and University of Buenos Aires, V. Obligado 2490, 1428 Buenos Aires, Argentina
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Instituto de Investigaciones en Ingeniería Genética y Biología Molecular, Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET) and University of Buenos Aires, V. Obligado 2490, 1428 Buenos Aires, Argentina
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Lawson Health Research Institute, London, Ontario, Canada
Center for the Study of Weight Regulation, Oregon Health & Science University, Portland, Oregon, USA
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Instituto de Investigaciones en Ingeniería Genética y Biología Molecular, Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET) and University of Buenos Aires, V. Obligado 2490, 1428 Buenos Aires, Argentina
UVA Health System Charlottesville, Virginia, USA
Lawson Health Research Institute, London, Ontario, Canada
Center for the Study of Weight Regulation, Oregon Health & Science University, Portland, Oregon, USA
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types of dwarf mouse, Snell ( dw , dw j , or Pit1; Eicher & Beamer 1980 ) and Ames ( df or Prop-1), with absent GH and prolactin (PRL) were used to elucidate physiological roles of GH and PRL long before the nature of the spontaneous mutations was
