A distinct inflammatory gene expression profile in patients with psoriatic arthritis

Stoeckman, Angela K.; Baechler, E. C.; Ortmann, Ward; Behrens, Timothy W.; Michet, Clement J.; Peterson, Erik

doi:10.1038/sj.gene.6364334

Cited by 36 publications

(29 citation statements)

References 38 publications

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“…Glut4EF ½also called the Huntington's disease gene regulatory regionbinding protein (HDBP) 1 (Tanaka et al 2004) and SLC2A4RG was originally characterized and named for its ability to bind to the enhancer of the Glucose Transporter 4 gene (Oshel et al 2000). Glut4EF proteins are also highly similar to papillomavirus binding factor (PBF) (Boeckle et al 2002), also called HDBP2 (Tanaka et al 2004), osteosarcoma antigen (Tsukahara et al 2004), and ZNF395 (Stoeckman et al 2006) (Figure 4A), and in our search of the database we found a previously uncharacterized human EST ZNF704 ½similar to the mouse EST Zfp704 (Blackshaw et al 2004), also called mouse glucocorticoid-induced gene 1 (Gig1) that was highly related to Glut4EF proteins and represents a third mammalian family member ( Figure 4A). Therefore, the gene disrupted in stretch mutants represents the Drosophila member of a new family of transcription factors conserved from Drosophila to mammals.…”

Section: Resultsmentioning

confidence: 99%

The Glucose Transporter (GLUT4) Enhancer Factor Is Required for Normal Wing Positioning in Drosophila

Yazdani

Huang

Terman³

2008

Genetics

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Many of the transcription factors and target genes that pattern the developing adult remain unknown. In the present study, we find that an ortholog of the poorly understood transcription factor, glucose transporter (GLUT4) enhancer factor (Glut4EF, GEF) ½also known as the Huntington's disease gene regulatory region-binding protein (HDBP) 1, plays a critical role in specifying normal wing positioning in adult Drosophila. Glut4EF proteins are zinc-finger transcription factors named for their ability to regulate expression of GLUT4 but nothing is known of Glut4EF's in vivo physiological functions. Here, we identify a family of Glut4EF proteins that are well conserved from Drosophila to humans and find that mutations in Drosophila Glut4EF underlie the wing-positioning defects seen in stretch mutants. In addition, our results indicate that previously uncharacterized mutations in Glut4EF are present in at least 11 publicly available fly lines and on the widely used TM3 balancer chromosome. These results indicate that previous observations utilizing these common stocks may be complicated by the presence of Glut4EF mutations. For example, our results indicate that Glut4EF mutations are also present on the same chromosome as two gain-of-function mutations of the homeobox transcription factor Antennapedia (Antp) and underlie defects previously attributed to Antp. In fact, our results support a role for Glut4EF in the modulation of morphogenetic processes mediated by Antp, further highlighting the importance of Glut4EF transcription factors in patterning and morphogenesis.

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Section: Resultsmentioning

confidence: 99%

The Glucose Transporter (GLUT4) Enhancer Factor Is Required for Normal Wing Positioning in Drosophila

Yazdani

Huang

Terman³

2008

Genetics

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“…This geneexpression profile differentiated PsA patients from RA patients and controls. Stoeckman et al [32 ] performed microarray analysis on whole blood and showed downregulation of a number of genes involved in T-cell function such as IL-2 receptor, RUNX3 and fyn. These genes are mainly involved in negative regulatory function and their downregulation agrees with the model of PsA as a T-cell dependent inflammatory disease.…”

Section: Potential Mechanisms Of Cardiovascular Complications In Sponmentioning

confidence: 99%

Cardiovascular risks in spondyloarthritides

Heeneman

Daemen

2007

Current Opinion in Rheumatology

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“…DNA microarray approaches examining the global gene expression in PBMCs have been proven to be a powerful tool in identifying proinflammatory pathways involved in the pathogenesis of a variety of autoimmune disorders, including systemic lupus erythematosus [141,[154][155][156][157], rheumatoid arthritis [158][159][160], multiple sclerosis [161,162], Crohn's disease and ulcerative colitis [163], psoriasis [164], and Juvenile Idiopathic Arthritis (SoJIA) [154]. Using this technology, 282 genes were observed to be increased in PBMCs from diabetic patients with the highest level observed for IL-1 and myc genes [165].…”

Section: Innate Immunity In Human Diabetesmentioning

confidence: 99%

The Role of Toll-Like Receptor Pathways in the Mechanism of Type 1 Diabetes

Lien¹,

Zipris²

2009

CMM

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Toll-like receptors (TLRs) and the innate immune system play a key role in sensing and eliminating microbial infections. Interactions between TLRs and their ligands expressed by microbial pathogens induce a cascade of intracellular signaling events, culminating in the upregulation of proinflammatory pathways. Over the past two decades, numerous studies have established the role of the acquired immune system in the mechanism triggering type 1 diabetes (T1D). The recent discovery of TLRs has led to the recognition that the innate immune system may act, under some circumstances, as a double-edged sword. In addition to its beneficial role in host defense, it may lead to upregulation of proinflammatory autoimmune responses, islet destruction and diabetes. Indeed, recent observations are consistent with the hypothesis that altered innate functions exist in patients with T1D and could be part of the mechanism leading to disease onset, but the underlying mechanisms and the relevance of these alterations to early events triggering disease remain to be identified. Data obtained from mouse and rat models of T1D implicated TLR pathways in both disease induction and prevention. In both the NOD mouse and diabetes-prone BB (BBDP) rat, TLR upregulation can suppress disease. In the BioBreeding Diabetes Resistant (BBDR) rat, however, diabetes induced by virus infection involves the upregulation of TLR9 pathways, and generic TLR upregulation synergizes with virus infection on diabetes induction. Studies performed in mouse models of T1D with spontaneous or induced T1D implicate TLR1, TLR2, TLR3, and TLR7 in disease mechanisms. The finding that TLR pathways are involved in mediating islet inflammation holds great promise for identifying new molecules that could potentially be targeted to specifically suppress the autoimmune process in individuals at high risk for disease development. The potential link between TLR upregulation and autoimmunity emphasizes the need for caution in using new therapies involving TLR agonists as vaccine adjuvants.

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A distinct inflammatory gene expression profile in patients with psoriatic arthritis

Cited by 36 publications

References 38 publications

The Glucose Transporter (GLUT4) Enhancer Factor Is Required for Normal Wing Positioning in Drosophila

The Glucose Transporter (GLUT4) Enhancer Factor Is Required for Normal Wing Positioning in Drosophila

Cardiovascular risks in spondyloarthritides

The Role of Toll-Like Receptor Pathways in the Mechanism of Type 1 Diabetes

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