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  • Cell Research
    Medical Center Dallas TX 75390 9148 USA Correspondence Zhijian J Chen E mail Zhijian Chen UTSouthwestern edu Best known for its role in targeting protein degradation by the proteasome ubiquitin modification has also emerged as an important mechanism that regulates cell signaling through proteasome independent mechanisms The role of ubiquitin as a versatile signaling tag is characteristically illustrated in the NF κB pathways which regulate a variety of physiological and

    Original URL path: http://www.cell-research.com/arts.asp?id=418 (2016-02-14)
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  • Cell Research
    ISSUE 1 1 2011 22 39 Deubiquitinases in the regulation of NF κB signaling Edward W Harhaj 1 and Vishva M Dixit 2 1 Department of Microbiology and Immunology Sylvester Comprehensive Cancer Center The University of Miami Miller School of Medicine 1550 NW 10 Avenue Miami FL 33136 USA 2 Department of Physiological Chemistry Genentech Inc 1 DNA Way South San Francisco CA 94080 USA Correspondence Edward W Harhaj Vishva M Dixit Tel 1 305 243 7893 1 650 225 1312 E mail eharhaj med miami edu dixit gene com Nuclear factor kappa B NF κB is a critical regulator of multiple biological functions including innate and adaptive immunity and cell survival Activation of NF κB is tightly regulated to preclude chronic signaling that may lead to persistent inflammation and cancer Ubiquitination of key signaling molecules by E3 ubiquitin ligases has emerged as an important regulatory mechanism for NF κB signaling Deubiquitinases DUBs counteract E3 ligases and therefore play a prominent role in the downregulation of NF κB signaling and homeostasis Understanding the mechanisms of NF κB downregulation by specific DUBs such as A20 and CYLD may provide therapeutic opportunities for the treatment of chronic inflammatory diseases and cancer Cell

    Original URL path: http://www.cell-research.com/arts.asp?id=419 (2016-02-14)
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  • Cell Research
    Biology Ghent University Technologiepark 927 Ghent B 9052 Belgium Correspondence Rudi Beyaert Tel 32 9 3313770 E mail rudi beyaert dmbr ugent be Caspases are intracellular proteases that are best known for their function in apoptosis signaling It has become evident that many caspases also function in other signaling pathways that propagate cell proliferation and inflammation but studies on the inflammatory function of caspases have mainly been limited to caspase 1 mediated cytokine processing Emerging evidence however indicates an important contribution of caspases as mediators or regulators of nuclear factor κB NF κB signaling which plays a key role in inflammation and immunity Much still needs to be learned about the mechanisms that govern the activation and regulation of NF κB by caspases and this review provides an update of this area Whereas apoptosis signaling is dependent on the catalytic activity of caspases they mainly act as scaffolding platforms for other signaling proteins in the case of NF κB signaling Caspase proteolytic activity however counteracts the pro survival function of NF κB by cleaving specific signaling molecules A striking exception is the paracaspase mucosa associated lymphoid tissue 1 MALT1 whose adaptor and proteolytic activity are both needed to initiate a

    Original URL path: http://www.cell-research.com/arts.asp?id=420 (2016-02-14)
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  • Cell Research
    regulated by CARMA family of scaffold proteins Marzenna Blonska and Xin Lin Department of Molecular and Cellular Oncology University of Texas M D Anderson Cancer Center 1515 Holcombe Blvd Unit 108 Houston TX 77030 Correspondence Xin Lin Tel 713 792 8969 E mail xllin mdanderson org The NF κB family of transcription factors plays a crucial role in cell activation survival and proliferation Its aberrant activity results in cancer immunodeficiency or autoimmune disorders Over the past two decades tremendous progress has been made in our understanding of the signals that regulate NF κB activation especially how scaffold proteins link different receptors to the NF κB activating complex the IκB kinase complex The growing number of these scaffolds underscores the complexity of the signaling networks in different cell types In this review we discuss the role of scaffold molecules in signaling cascades induced by stimulation of antigen receptors G protein coupled receptors and C type Lectin receptors resulting in NF κB activation Especially we focus on the family of Caspase recruitment domain CARD containing proteins known as CARMA and their function in activation of NF κB as well as the link of these scaffolds to the development of various neoplastic diseases

    Original URL path: http://www.cell-research.com/arts.asp?id=421 (2016-02-14)
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  • Cell Research
    Non canonical NF κB signaling pathway Shao Cong Sun Department of Immunology The University of Texas MD Anderson Cancer Center The University of Texas Graduate School of Biomedical Sciences at Houston 7455 Fannin Street Box 902 Houston TX 77030 USA Correspondence Shao Cong Sun Tel 1 713 563 3218 E mail 1 713 563 3218 The non canonical NF κB pathway is an important arm of NF κB signaling that predominantly targets activation of the p52 RelB NF κB complex This pathway depends on the inducible processing of p100 a molecule functioning as both the precursor of p52 and a RelB specific inhibitor A central signaling component of the non canonical pathway is NF κB inducing kinase NIK which integrates signals from a subset of TNF receptor family members and activates a downstream kinase IκB kinase α IKKα for triggering p100 phosphorylation and processing A unique mechanism of NIK regulation is through its fate control the basal level of NIK is kept low by a TRAF cIAP destruction complex and signal induced non canonical NF κB signaling involves NIK stabilization Tight control of the fate of NIK is important since deregulated NIK accumulation is associated with lymphoid malignancies Cell Research

    Original URL path: http://www.cell-research.com/arts.asp?id=422 (2016-02-14)
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  • Cell Research
    Tsui Andrew Caldwell and Alexander Hoffmann Signaling Systems Laboratory and San Diego Center for Systems Biology Department of Chemistry and Biochemistry University of California San Diego 9500 Gillman Dr La Jolla CA 92093 USA Correspondence Alexander Hoffmann E mail ahoffmann ucsd edu Two distinct nuclear factor κB NFκB signaling pathways have been described the canonical pathway that mediates inflammatory responses and the non canonical pathway that is involved in immune cell differentiation and maturation and secondary lymphoid organogenesis The former is dependent on the I B kinase adaptor molecule NEMO the latter is independent of it Here we review the molecular mechanisms of regulation in each signaling axis and attempt to relate the apparent regulatory logic to the physiological function Further we review the recent evidence for extensive cross regulation between these two signaling axes and summarize them in a wiring diagram These observations suggest that NEMO dependent and independent signaling should be viewed within the context of a single NFκB signaling system which mediates signaling from both inflammatory and organogenic stimuli in an integrated manner As in other regulatory biological systems a systems approach including mathematical models that include quantitative and kinetic information will be necessary to characterize the

    Original URL path: http://www.cell-research.com/arts.asp?id=423 (2016-02-14)
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  • Cell Research
    Free Sample Issue Submission Advanced Online Publication Current Issue Top 10 VOLUME 21 ISSUE 1 1 2011 103 115 Crosstalk of reactive oxygen species and NF κB signaling Michael J Morgan and Zheng gang Liu Cell and Cancer Biology Branch Center for Cancer Research National Cancer Institute NIH 37 Convent Drive RM1130 Bethesda MD 20892 Correspondence Zheng gang Liu E mail zgliu helix nih gov NF κB proteins are a family of transcription factors that are of central importance in inflammation and immunity NF κB also plays important roles in other processes including development cell growth and survival and proliferation and is involved in many pathological conditions Reactive Oxygen Species ROS are created by a variety of cellular processes as part of cellular signaling events While certain NF κB regulated genes play a major role in regulating the amount of ROS in the cell ROS have various inhibitory or stimulatory roles in NF κB signaling Here we review the regulation of ROS levels by NF κB targets and various ways in which ROS have been proposed to impact NF κB signaling pathways Cell Research 2011 21 103 115 doi 10 1038 cr 2010 178 published online 28 December 2010 keywords

    Original URL path: http://www.cell-research.com/arts.asp?id=424 (2016-02-14)
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  • Cell Research
    Wisconsin Institute for Medical Research 1111 Highland Avenue Madison WI 53705 USA Correspondence Shigeki Miyamoto E mail smiyamot wisc edu A large body of literature describes elaborate NF κB signaling networks induced by inflammatory and immune signals Decades of research has revealed that transcriptionally functional NF κB dimers are activated by two major pathways canonical and non canonical Both pathways involve the release of NF κB dimers from inactive cytoplasmic complexes to cause their nuclear translocation to modulate gene expression programs and biological responses NF κB is also responsive to genotoxic agents however signal communication networks that are initiated in the nucleus following DNA damage induction are less defined Evidence in the literature supports the presence of such signaling pathways induced by multiple distinct genotoxic agents resulting in the activation of cytoplasmic IKK complex An example is a pathway that involves the DNA damage responsive kinase ataxia telangiectasia mutated ATM and a series of post translational modifications of NF κB essential modulator NEMO in the nucleus of a genotoxin exposed cell Recent evidence also suggests that this nuclear initiated NF κB signaling pathway plays significant physiological and pathological roles particularly in lymphocyte development and human cancer progression This review will

    Original URL path: http://www.cell-research.com/arts.asp?id=425 (2016-02-14)
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