Phosphohexose isomerase/autocrine motility factor/neuroleukin/maturation factor is a multifunctional phosphoprotein

Haga, Akihiro; Niinaka, Yasufumi; Raz, Avraham

doi:10.1016/s0167-4838(00)00075-3

Cited by 85 publications

(74 citation statements)

References 33 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…It is possible that the GPI that is presented to the B cells in the draining LN is at a higher local concentration or in a more immunogenic form. GPI, a crucial component of the glycolytic pathway is expressed in every cell throughout the body as an intracellular protein, but has also been detected as a secreted protein (autocrine motility factor, neuroleukin) (28,29). In humans, higher levels of GPI protein have been measured in the synovial fluid around inflamed joints (30).…”

Section: Discussionmentioning

confidence: 99%

Despite ubiquitous autoantigen expression, arthritogenic autoantibody response initiates in the local lymph node

Mandik-Nayak

Wipke

Shih

et al. 2002

Proc. Natl. Acad. Sci. U.S.A.

View full text Add to dashboard Cite

K͞BxN mice develop an inflammatory joint disease with many features characteristic of rheumatoid arthritis. In this model, the KRN transgenic T cells and nontransgenic B cells both recognize the glycolytic enzyme glucose-6-phosphate-isomerase (GPI) as an autoantigen. Here, we followed the anti-GPI B cell response that naturally arises in K͞BxN mice. The anti-GPI B cell response was robust and arose at the same time as the development of serum anti-GPI autoantibody and joint inflammation. Surprisingly, although GPI was expressed systemically, the anti-GPI B cell response was focused to the lymph nodes (LN) draining the distal joints where arthritis was evident. In lymphotoxin-␤ receptor-Ig-treated mice, which lack LNs, the development of arthritis was completely inhibited up to 5-6 weeks. At later times, some arthritis did develop, but at a significantly reduced level. Thus, in this spontaneous model of autoimmunity, the LNs draining the distal joints are essential for both the inhibition and amplification of the arthritogenic B cell response. These findings imply that the immune physiology of a joint is unique, resulting in a local immune response to a systemic autoantigen.

show abstract

Section: Discussionmentioning

confidence: 99%

Despite ubiquitous autoantigen expression, arthritogenic autoantibody response initiates in the local lymph node

Mandik-Nayak

Wipke

Shih

et al. 2002

Proc. Natl. Acad. Sci. U.S.A.

View full text Add to dashboard Cite

show abstract

“…The functions of FHF-4 are not fully understood but are expected to include aspects of cell activation (12). Neuroleukin, a neurotropic growth factor that promotes motor neuron regeneration in vivo and the survival of peripheral and central neurons in vitro (13,14), is strongly up-regulated late in the infection (days 6 and 7).…”

Section: Discussionmentioning

confidence: 99%

Effect of rabies virus infection on gene expression in mouse brain

Prosniak

Hooper

Dietzschold

et al. 2001

Proc. Natl. Acad. Sci. U.S.A.

103

View full text Add to dashboard Cite

A variety of molecular genetic approaches were used to study the effect of rabies virus (RV) infection on host gene expression in mouse brain. The down-regulation of gene expression was found to be a major effect of RV infection by using subtraction hybridization. However, a combination of techniques identified approximately 39 genes activated by infection. These included genes involved in regulation of cell metabolism, protein synthesis, synaptic activity, and cell growth and differentiation. Northern blot analysis to monitor temporal activation of several of these genes following infection revealed essentially two patterns of activation: (i) an early response with up-regulation beginning within 3 days after infection and correlating with transcription of RV nuclear protein; and (ii) a late response with enhanced expression occurring at days 6 -7 after infection and associated with peak RV replication. The gene activation patterns and the known functions of their products suggest that a number of host genes may be involved in the replication and spread of RV in the brain.T he outcome of rabies virus (RV) infection is determined by the convergence of several different virus-host interactions, including those that contribute to virus replication and spread, pathogenic effects on cells, and antiviral responses. RV is particularly suitable for the study of virus-host interactions because of the small size of its genome and its high specificity for infection of neurons. Nevertheless, the mechanisms involved in the disease process are undoubtedly complex. For example, the virus, which uses the neuronal network to spread within the host, must initially replicate in neurons without causing significant functional impairment that would compromise the infection cycle (1). While there is some understanding of the roles of viral proteins in rabies pathogenesis, the contribution of host factors to RV transcription͞replication and axonal͞trans-synaptic spread remain unknown. Various technologies are now available to identify host genes that might be essential for the life cycle of RV, important in antiviral defense, or activated nonspecifically in RV infection (2-4). Because each technology is suited for the detection of different classes of genes and different levels of gene expression, we used a variety of assays, including differential display (DD), cDNA array hybridization, subtraction hybridization (SH), and restriction fragment differential display (RFDD), to assess gene expression in rabies-infected mouse brain. With these approaches, we have revealed the effects of rabies infection on select gene expression patterns in the brain. Based on known functional properties of several gene products as well as the timing of their up-regulation after infection, we discuss possible contributions of host genes to the pathogenesis of rabies. Materials and MethodsVirus Infection of Mice. Female, 6-to 8-week-old Swiss Webster mice were purchased from Taconic Farms. Mice were maintained under pathogen-free conditions and used to 10 w...

show abstract

“…AMF Protein Purification-Recombinant AMF (rAMF) fusion protein was kindly provided from Dr. Avraham Raz (28). AMF protein was isolated as a glutathione S-transferase fusion protein.…”

Section: Methodsmentioning

confidence: 99%

Phosphoglucose Isomerase/Autocrine Motility Factor Promotes Melanoma Cell Migration through ERK Activation Dependent on Autocrine Production of Interleukin-8

Araki

Shimura

Yajima

et al. 2009

Journal of Biological Chemistry

Self Cite

View full text Add to dashboard Cite

It is well known that phosphoglucose isomerase/autocrine motility factor (AMF) promotes cell migration in an autocrine manner in various tumor cells. However, it remains unclear whether certain cytokines modulate the effects of AMF on tumor cell migration. Because interleukin (IL)-8, a proinflammatory cytokine, is produced by melanoma cells and has been correlated with melanoma migration, the migratory ability of melanoma cells induced by AMF may also involve induction of IL-8 expression. In the present study, we assessed whether AMF promotes melanoma cell migration through autocrine production of IL-8. We found that AMF stimulation increased IL-8 production through up-regulation of IL-8 mRNA transcription, especially in biologically early stage melanoma cells. AMF-induced migration of these cells was inhibited by a specific neutralizing antibody against IL-8. The IL-8 production induced by AMF was mediated by the ERK1/2 pathways. These findings suggest that melanoma migration induced by AMF is mediated by autocrine production of IL-8 as a novel downstream modulator of the AMF signaling pathway.

show abstract

Phosphohexose isomerase/autocrine motility factor/neuroleukin/maturation factor is a multifunctional phosphoprotein

Cited by 85 publications

References 33 publications

Despite ubiquitous autoantigen expression, arthritogenic autoantibody response initiates in the local lymph node

Despite ubiquitous autoantigen expression, arthritogenic autoantibody response initiates in the local lymph node

Effect of rabies virus infection on gene expression in mouse brain

Phosphoglucose Isomerase/Autocrine Motility Factor Promotes Melanoma Cell Migration through ERK Activation Dependent on Autocrine Production of Interleukin-8

Contact Info

Product

Resources

About