<?xml version="1.0" encoding="UTF-8"?>
<rdf:RDF xmlns:rdf="http://www.w3.org/1999/02/22-rdf-syntax-ns#" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns="http://purl.org/rss/1.0/"><channel rdf:about="http://www.cgfr.co.uk/?rss=yes"><title>Cytokine &amp; Growth Factor Reviews</title><description>Cytokine &amp; Growth Factor Reviews RSS feed: Current Issue.    
 
 
 
 Cytokine &amp; Growth Factor Reviews   publishes thought-provoking articles (critical reviews, 
state-of-the-art reviews, letters to the editor, meeting reviews) devoted to important advances in the rapidly changing fields of growth 
factor and cytokine research. Major emphasis is placed on the multidisciplinary significance of cytokines and growth factors in areas 
as diverse as signal transduction, cell growth and differentiation, embryonic development, immunology, tumorigenesis and clinical medicine.   </description><link>http://www.cgfr.co.uk/?rss=yes</link><dc:publisher>Elsevier Inc.</dc:publisher><dc:language>en</dc:language><dc:rights> © 2012 Published by Elsevier Inc. All rights reserved. </dc:rights><prism:publicationName>Cytokine &amp; Growth Factor Reviews</prism:publicationName><prism:issn>1359-6101</prism:issn><prism:volume>23</prism:volume><prism:number>1-2</prism:number><prism:publicationDate>February 2012</prism:publicationDate><prism:copyright> © 2012 Published by Elsevier Inc. All rights reserved. </prism:copyright><prism:rightsAgent>healthpermissions@elsevier.com</prism:rightsAgent><items><rdf:Seq><rdf:li rdf:resource="http://www.cgfr.co.uk/article/PIIS1359610112000093/abstract?rss=yes"/><rdf:li rdf:resource="http://www.cgfr.co.uk/article/PIIS1359610111000712/abstract?rss=yes"/><rdf:li rdf:resource="http://www.cgfr.co.uk/article/PIIS1359610112000020/abstract?rss=yes"/><rdf:li rdf:resource="http://www.cgfr.co.uk/article/PIIS1359610112000032/abstract?rss=yes"/><rdf:li rdf:resource="http://www.cgfr.co.uk/article/PIIS1359610112000044/abstract?rss=yes"/><rdf:li rdf:resource="http://www.cgfr.co.uk/article/PIIS1359610112000056/abstract?rss=yes"/><rdf:li rdf:resource="http://www.cgfr.co.uk/article/PIIS1359610112000068/abstract?rss=yes"/><rdf:li rdf:resource="http://www.cgfr.co.uk/article/PIIS135961011200007X/abstract?rss=yes"/></rdf:Seq></items></channel><item rdf:about="http://www.cgfr.co.uk/article/PIIS1359610112000093/abstract?rss=yes"><title>Editorial Board</title><link>http://www.cgfr.co.uk/article/PIIS1359610112000093/abstract?rss=yes</link><description></description><dc:title>Editorial Board</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S1359-6101(12)00009-3</dc:identifier><dc:source>Cytokine &amp; Growth Factor Reviews 23, 1 (2012)</dc:source><dc:date>2012-02-01</dc:date><prism:publicationName>Cytokine &amp; Growth Factor Reviews</prism:publicationName><prism:publicationDate>2012-02-01</prism:publicationDate><prism:volume>23</prism:volume><prism:number>1-2</prism:number><prism:issueIdentifier>S1359-6101(12)X0002-9</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>CO2</prism:startingPage><prism:endingPage>CO2</prism:endingPage></item><item rdf:about="http://www.cgfr.co.uk/article/PIIS1359610111000712/abstract?rss=yes"><title>Anti-cytokine auto-vaccinations as tools for the analysis of cytokine function in vivo</title><link>http://www.cgfr.co.uk/article/PIIS1359610111000712/abstract?rss=yes</link><description>Abstract: Braking B cell tolerance to generate antibodies against autologous cytokines or chemokines offers an alternative to gene inactivation for functional analysis of these factors in vivo. It is clearly less potent than the genetic approach but offers the advantage of extreme flexibility. The basic principle is to enable a self-reactive B cell to attract T cell help by presenting foreign peptides, a process we called “deceptive” antigen presentation. We here review the different auto-vaccine procedures that are currently used and provide several examples of functional information acquired by this procedure or by mAbs derived from auto-vaccinated mice.</description><dc:title>Anti-cytokine auto-vaccinations as tools for the analysis of cytokine function in vivo</dc:title><dc:creator>Catherine Uyttenhove, Jacques Van Snick</dc:creator><dc:identifier>10.1016/j.cytogfr.2011.12.001</dc:identifier><dc:source>Cytokine &amp; Growth Factor Reviews 23, 1 (2012)</dc:source><dc:date>2012-01-11</dc:date><prism:publicationName>Cytokine &amp; Growth Factor Reviews</prism:publicationName><prism:publicationDate>2012-01-11</prism:publicationDate><prism:volume>23</prism:volume><prism:number>1-2</prism:number><prism:issueIdentifier>S1359-6101(12)X0002-9</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>1</prism:startingPage><prism:endingPage>6</prism:endingPage></item><item rdf:about="http://www.cgfr.co.uk/article/PIIS1359610112000020/abstract?rss=yes"><title>Interferon-α (IFNα) neurotoxicity</title><link>http://www.cgfr.co.uk/article/PIIS1359610112000020/abstract?rss=yes</link><description>Abstract: Clinical studies indicate that increased central nervous system (CNS) interferon-alpha (IFNα) is associated with cognitive dysfunction in a wide variety of conditions. This has perhaps been best studied in HIV-associated neurocognitive disorders (HAND). These findings on IFNα neurotoxicity have been corroborated in animal studies. Probably the best demonstration of the neurotoxicity of IFNα was through the use of a mouse model of HAND, where it was shown that blocking IFNα with neutralizing antibodies prevented behavioral deficits and associated histopathological effects. In vitro studies have demonstrated a dose dependent, detrimental effect of IFNα on neuronal dendrites. Development of therapeutics that block IFNα may prove to be an effective treatment of HAND and other inflammatory conditions where there is increased CNS IFNα.</description><dc:title>Interferon-α (IFNα) neurotoxicity</dc:title><dc:creator>Cari Fritz-French, William Tyor</dc:creator><dc:identifier>10.1016/j.cytogfr.2012.01.001</dc:identifier><dc:source>Cytokine &amp; Growth Factor Reviews 23, 1 (2012)</dc:source><dc:date>2012-02-20</dc:date><prism:publicationName>Cytokine &amp; Growth Factor Reviews</prism:publicationName><prism:publicationDate>2012-02-20</prism:publicationDate><prism:volume>23</prism:volume><prism:number>1-2</prism:number><prism:issueIdentifier>S1359-6101(12)X0002-9</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>7</prism:startingPage><prism:endingPage>14</prism:endingPage></item><item rdf:about="http://www.cgfr.co.uk/article/PIIS1359610112000032/abstract?rss=yes"><title>Truncated TrkB: Beyond a dominant negative receptor</title><link>http://www.cgfr.co.uk/article/PIIS1359610112000032/abstract?rss=yes</link><description>Abstract: BDNF activates trkB receptors to regulate neuronal survival, differentiation, and proliferation. Mutations in the BDNF gene, altered BDNF expression, and altered trkB expression are associated with degenerative and psychiatric disorders. The full-length trkB receptor (trkB.tk+) undergoes autophosphorylation to activate intracellular signaling pathways. The truncated trkB receptor (trkB.t1) is abundantly expressed in the brain but lacks the catalytic tyrosine kinase domain. TrkB.t1 is a dominant-negative receptor that inhibits trkB.tk+ signaling. While this is an important function of trkB.t1, it is only one of its many functions. TrkB.t1 sequesters and translocate BDNF, induces filopodia and neurite outgrowth, stimulates intracellular signaling cascades, regulates Rho GTPase signaling, and modifies cytoskeletal structures. TrkB.t1 is an active signaling molecule with regulatory effects on neurons and astrocytes.</description><dc:title>Truncated TrkB: Beyond a dominant negative receptor</dc:title><dc:creator>Barbara M. Fenner</dc:creator><dc:identifier>10.1016/j.cytogfr.2012.01.002</dc:identifier><dc:source>Cytokine &amp; Growth Factor Reviews 23, 1 (2012)</dc:source><dc:date>2012-02-17</dc:date><prism:publicationName>Cytokine &amp; Growth Factor Reviews</prism:publicationName><prism:publicationDate>2012-02-17</prism:publicationDate><prism:volume>23</prism:volume><prism:number>1-2</prism:number><prism:issueIdentifier>S1359-6101(12)X0002-9</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>15</prism:startingPage><prism:endingPage>24</prism:endingPage></item><item rdf:about="http://www.cgfr.co.uk/article/PIIS1359610112000044/abstract?rss=yes"><title>Crosstalk of Sp1 and Stat3 signaling in pancreatic cancer pathogenesis</title><link>http://www.cgfr.co.uk/article/PIIS1359610112000044/abstract?rss=yes</link><description>Abstract: Pancreatic cancer progression is attributed to genetic and epigenetic alterations and a chaotic tumor microenvironment. Those diverse “upstream signal” factors appear to converge on specific sets of central nuclear regulators, namely, transcription factors. Specificity Protein 1 (Sp1) and signal transducer and activator of transcription 3 (Stat3) are central transcription factors that regulate a number of pathways important to tumorigenesis, including tumor cell-cycle progression, apoptosis, angiogenesis, metastasis, and evasion of the immune system. Recently, researchers demonstrated many types of crosstalk of Sp1 and Stat3 in tumor signal transduction and that these factors function cooperatively to activate targeted genes and promote tumorigenesis in pancreatic cancer. Therefore, targeting both Sp1 and Stat3 is a potential preventive and therapeutic strategy for pancreatic cancer.</description><dc:title>Crosstalk of Sp1 and Stat3 signaling in pancreatic cancer pathogenesis</dc:title><dc:creator>Chen Huang, Keping Xie</dc:creator><dc:identifier>10.1016/j.cytogfr.2012.01.003</dc:identifier><dc:source>Cytokine &amp; Growth Factor Reviews 23, 1 (2012)</dc:source><dc:date>2012-02-17</dc:date><prism:publicationName>Cytokine &amp; Growth Factor Reviews</prism:publicationName><prism:publicationDate>2012-02-17</prism:publicationDate><prism:volume>23</prism:volume><prism:number>1-2</prism:number><prism:issueIdentifier>S1359-6101(12)X0002-9</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>25</prism:startingPage><prism:endingPage>35</prism:endingPage></item><item rdf:about="http://www.cgfr.co.uk/article/PIIS1359610112000056/abstract?rss=yes"><title>FGF23/Klotho axis: Phosphorus, mineral metabolism and beyond</title><link>http://www.cgfr.co.uk/article/PIIS1359610112000056/abstract?rss=yes</link><description>Abstract: In this work we summarizes the steps that allowed the identification of the fibroblast growth factor (FGF) 23/Klotho axis as the principal regulator of phosphate homeostasis, exerting actions on intestine, bone, parathyroid glands, and kidney. We review the not fully understood mechanisms of action of this axis on the regulation of mineral homeostasis and, in addition, we discuss its potential role in the pathophysiology of chronic kidney disease and the associated complications. We also reflect the actual tendency to consider the components of this system as better predictors of the pathological conditions frequently associated to mineral disorders, and review some recent studies linking these components to cardiovascular disease even in population without mineral disorders. Finally, we consider the numerous processes in which Klotho is involved, including anti-ageing and mineral control processes, independently of its functions as obligated-coreceptor for FGF23.</description><dc:title>FGF23/Klotho axis: Phosphorus, mineral metabolism and beyond</dc:title><dc:creator>Javier Donate-Correa, Mercedes Muros-de-Fuentes, Carmen Mora-Fernández, Juan F. Navarro-González</dc:creator><dc:identifier>10.1016/j.cytogfr.2012.01.004</dc:identifier><dc:source>Cytokine &amp; Growth Factor Reviews 23, 1 (2012)</dc:source><dc:date>2012-02-23</dc:date><prism:publicationName>Cytokine &amp; Growth Factor Reviews</prism:publicationName><prism:publicationDate>2012-02-23</prism:publicationDate><prism:volume>23</prism:volume><prism:number>1-2</prism:number><prism:issueIdentifier>S1359-6101(12)X0002-9</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>37</prism:startingPage><prism:endingPage>46</prism:endingPage></item><item rdf:about="http://www.cgfr.co.uk/article/PIIS1359610112000068/abstract?rss=yes"><title>Is interleukin-10 gene polymorphism a predictive marker in HCV infection?</title><link>http://www.cgfr.co.uk/article/PIIS1359610112000068/abstract?rss=yes</link><description>Abstract: The clinical outcome of hepatitis C virus (HCV) infection varies between individuals – from spontaneous viral clearance and persistence without complication, to chronic hepatitis, cirrhosis and hepatocellular carcinoma. Also patterns of response to interferon-based anti-HCV therapy are different from person to person. This diversity may be affected by host genetic factors, including alterations in genes encoding cytokines. Interleukin-10, as an anti-inflammatory cytokine and immune response modulator, may influence on HCV infection susceptibility as well as spontaneous and treatment-induced HCV eradication. Moreover, it is stated that IL-10 has antifibrotic properties and play a role in progression of liver disease. This review summarized studies on interleukin-10 gene polymorphisms (mainly promoter SNPs at positions −1082(G/A), −819(C/T) and −592(C/A)), which may determine IL-10 production, regarding susceptibility to HCV infection, course of HCV-related liver disease (fibrosis, cirrhosis, hepatocellular carcinoma, ALT abnormalities), spontaneous viral elimination as well as hepatitis C treatment outcomes. Analysis of hereby summarized studies shows that it is difficult to unambiguously determine the importance of IL-10 polymorphism as a predictor of clinical outcome of hepatitis C and response to anti-HCV therapy before its beginning. Thus, future larger studies need to address these issues. Continuation of studies on interleukin-10 polymorphisms as well as identification of other candidate predictive markers in HCV infection has important practical implications and there is a chance that may contribute to reduce the scale of hepatitis C problem.</description><dc:title>Is interleukin-10 gene polymorphism a predictive marker in HCV infection?</dc:title><dc:creator>Bogna J. Świątek</dc:creator><dc:identifier>10.1016/j.cytogfr.2012.01.005</dc:identifier><dc:source>Cytokine &amp; Growth Factor Reviews 23, 1 (2012)</dc:source><dc:date>2012-03-05</dc:date><prism:publicationName>Cytokine &amp; Growth Factor Reviews</prism:publicationName><prism:publicationDate>2012-03-05</prism:publicationDate><prism:volume>23</prism:volume><prism:number>1-2</prism:number><prism:issueIdentifier>S1359-6101(12)X0002-9</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>47</prism:startingPage><prism:endingPage>59</prism:endingPage></item><item rdf:about="http://www.cgfr.co.uk/article/PIIS135961011200007X/abstract?rss=yes"><title>The signaling and functions of heterodimeric bone morphogenetic proteins</title><link>http://www.cgfr.co.uk/article/PIIS135961011200007X/abstract?rss=yes</link><description>Abstract: Heterodimeric bone morphogenetic proteins (BMPs) consist of disulfide-linked dimeric monomers derived from different BMP members. Owing to this specific constitution pattern, they bear high affinity to both type I and type II BMP receptors simultaneously. Meanwhile, the antagonism efficiency of extracellular antagonists to heterodimeric BMPs is also significantly lower than that to homodimeric ones. All these specific properties confer heterodimeric BMPs with distinct signaling and bio-functions that are characterized by more speediness, lower concentration/dose threshold and higher efficiency than homodimeric BMPs. Consequently, heterodimeric BMPs bear promising application potential in inducing osteogenesis. In addition, they may play indispensible roles in organogenesis. In this review, we summarize the current knowledge of heterodimeric BMPs in their signaling pathways and bio-functions.</description><dc:title>The signaling and functions of heterodimeric bone morphogenetic proteins</dc:title><dc:creator>Jing Guo, Gang Wu</dc:creator><dc:identifier>10.1016/j.cytogfr.2012.02.001</dc:identifier><dc:source>Cytokine &amp; Growth Factor Reviews 23, 1 (2012)</dc:source><dc:date>2012-03-15</dc:date><prism:publicationName>Cytokine &amp; Growth Factor Reviews</prism:publicationName><prism:publicationDate>2012-03-15</prism:publicationDate><prism:volume>23</prism:volume><prism:number>1-2</prism:number><prism:issueIdentifier>S1359-6101(12)X0002-9</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>61</prism:startingPage><prism:endingPage>67</prism:endingPage></item></rdf:RDF>
