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Tumor necrosis factor, alpha-induced protein 6

The protein encoded by this gene is a secretory protein that contains a hyaluronan-binding domain, and thus is a member of the hyaluronan-binding protein family. The hyaluronan-binding domain is known to be involved in extracellular matrix stability and cell migration. This protein has been shown to form a stable complex with inter-alpha-inhibitor (I alpha I), and thus enhance the serine protease inhibitory activity of I alpha I, which is important in the protease network associated with inflammation. This gene can be induced by proinflammatory cytokines such as tumor necrosis factor alpha and interleukin-1. Enhanced levels of this protein are found in the synovial fluid of patients with osteoarthritis and rheumatoid arthritis.[provided by RefSeq, Dec 2010] (from NCBI)
Top mentioned proteins: TSG, CAN, V1a, CD44, HAD
Papers on TSG-6
Nuclear Magnetic Resonance Insight into the Multiple Glycosaminoglycan Binding Modes of the Link Module from Human TSG-6.
Prestegard et al., Athens, United States. In Biochemistry, Feb 2016
Tumor necrosis factor-stimulated gene-6 (TSG-6) is a hyaluronan (HA)-binding protein that is essential for stabilizing and remodeling the extracellular matrix (ECM) during ovulation and inflammatory disease processes such as arthritis.
Hyaluronan Rafts on Airway Epithelial Cells.
Hascall et al., Cleveland, United States. In J Biol Chem, Feb 2016
The transesterification transfer of HCs from chondroitin sulfate to HA is mediated by tumor necrosis factor-induced gene 6 (TSG-6), which is up-regulated in inflammatory reactions.
Niche Regulation of Limbal Epithelial Stem Cells: Relationship between Inflammation and Regeneration.
Chen et al., Miami, United States. In Ocul Surf, Feb 2016
HC-HA complex is covalently formed by hyaluronan (HA) and heavy chain 1 (HC1) of inter-α-trypsin inhibitor by the catalytic action of tumor necrosis factor-stimulated gene-6 (TSG-6) and are tightly associated with pentraxin 3 (PTX3) to form HC-HA/PTX3.
Mesenchymal stem/stromal cells precondition lung monocytes/macrophages to produce tolerance against allo- and autoimmunity in the eye.
Oh et al., Seoul, South Korea. In Proc Natl Acad Sci U S A, Feb 2016
However, MSCs with TSG-6 knockdown did not induce MHC II(+)B220(+)CD11b(+) cells, and failed to attenuate EAU.
Ephrin-A5 is required for optimal fertility and a complete ovulatory response to gonadotropins in the female mouse.
Deroo et al., Saint-Hyacinthe, Canada. In Endocrinology, Jan 2016
These results corresponded with a reduction in ovarian mRNA levels of several LH-responsive genes, including Pgr, Ptgs2, Tnfaip6, Ereg, Btc, and Adamts4, suggesting that Efna5(-/-) ovaries exhibit a partially attenuated response to luteinizing hormone.
JNK2 controls aggrecan degradation in murine articular cartilage and the development of experimental osteoarthritis.
Saklatvala et al., Oxford, United Kingdom. In Arthritis Rheumatol, Jan 2016
These included Has1, ADAMTS4, Tnf, IL6, IL18, Inhba, Cd68, Ngf, Ccr2, Wnt16, Tnfaip6 and Il1r, but not ADAMTS-5.
An RNA interference screen identifies new avenues for nephroprotection.
Kandel et al., Buffalo, United States. In Cell Death Differ, Dec 2015
We used an RNA interference screen to identify genes (BCL2L14, BLOC1S2, C2ORF42, CPT1A, FBP1, GCNT3, RHOB, SCIN, TACR1, and TNFAIP6) whose suppression improves survival of kidney epithelial cells in in vitro models of oxygen and glucose deprivation.
The Rise and Fall of Hyaluronan in Respiratory Diseases.
Aronica et al., Cleveland, United States. In Int J Cell Biol, 2014
During inflammation in the airways, HA is often covalently modified with heavy chains from inter-alpha-inhibitor via the enzyme tumor-necrosis-factor-stimulated-gene-6 (TSG-6) and this modification promotes the interaction of leukocytes with HA matrices at sites of inflammation.
Current research on hyaluronic acid-drug bioconjugates.
Zhai et al., Jinan, China. In Eur J Med Chem, 2014
In addition, multifarious receptors of HA like CD44, RHAMM and TSG6 are over-expressed on the surface of malignant cells, which play important roles in targeting ability.
A review of therapeutic effects of mesenchymal stem cell secretions and induction of secretory modification by different culture methods.
Riordan et al., Guntūr, India. In J Transl Med, 2013
Finally we review in detail the most important factors present in conditioned medium of MSC that can be considered protagonists of MSC physiological effects including HGF, TGF-b, VEGF, TSG-6, PGE2 and galectins 1, and 9.
Concise review: two negative feedback loops place mesenchymal stem/stromal cells at the center of early regulators of inflammation.
Prockop, Temple, United States. In Stem Cells, 2013
In the second loop, the activated MSCs secrete TSG-6 that interacts with CD44 on resident macrophages to decrease TLR2/NFκ-B signaling and thereby decrease the secretion of proinflammatory mediators of inflammation.
Long pentraxin 3/tumor necrosis factor-stimulated gene-6 interaction: a biological rheostat for fibroblast growth factor 2-mediated angiogenesis.
Presta et al., Brescia, Italy. In Arterioscler Thromb Vasc Biol, 2012
TSG-6 reverts the inhibitory effects exerted by PTX3 on FGF2-mediated angiogenesis through competition of FGF2/PTX3 interaction.
Tumour necrosis factor-stimulated gene (TSG)-6 controls epithelial-mesenchymal transition of proximal tubular epithelial cells.
Steadman et al., Cardiff, United Kingdom. In Int J Biochem Cell Biol, 2011
TSG-6 was central to EMT through effects on HA macromolecular structure and through CD44-dependent triggering of cell responses.
The inflammation-associated protein TSG-6 cross-links hyaluronan via hyaluronan-induced TSG-6 oligomers.
Richter et al., San Sebastián, Spain. In J Biol Chem, 2011
TSG-6 is a potent HA cross-linking agent
TSG-6 protein, a negative regulator of inflammatory arthritis, forms a ternary complex with murine mast cell tryptases and heparin.
Mikecz et al., Chicago, United States. In J Biol Chem, 2011
TSG-6 protein, a negative regulator of inflammatory arthritis, forms a ternary complex with murine mast cell tryptases and heparin.
Hyaluronan, TSG-6, and inter-α-inhibitor in periprosthetic breast capsules: reduced levels of free hyaluronan and TSG-6 expression in contracted capsules.
Bayat et al., Manchester, United Kingdom. In Aesthet Surg J, 2011
negative correlation between TSG-6 expression levels and severity of capsular contracture (CC) suggests a possible protective role for TSG-6 in the context of CC formation, and this may have a clinically relevant role in prevention of breast CC
Intravenous hMSCs improve myocardial infarction in mice because cells embolized in lung are activated to secrete the anti-inflammatory protein TSG-6.
Prockop et al., New Orleans, United States. In Cell Stem Cell, 2009
The hMSCs in lung upregulated expression of multiple genes, with a large increase in the anti-inflammatory protein TSG-6.
Sleuthing the source of regeneration by MSCs.
Pittenger, Baltimore, United States. In Cell Stem Cell, 2009
In this issue of Cell Stem Cell, Lee et al. (2009) investigate the production of the soluble inflammation inhibitor TSG-6 by MSCs.
Using Molecular Dynamics Simulations To Provide New Insights into Protein Structure on the Nanosecond Timescale:  Comparison with Experimental Data and Biological Inferences for the Hyaluronan-Binding Link Module of TSG-6.
Day et al., Oxford, United Kingdom. In J Chem Theory Comput, 2007
A high-resolution NMR-structure of the Link module from the protein product of tumor necrosis factor-stimulated gene-6 (Link_TSG6) has been determined, but a fuller appreciation of protein dynamics may be necessary to understand its hyaluronan-binding.
Solution structure of the link module: a hyaluronan-binding domain involved in extracellular matrix stability and cell migration.
Day et al., Oxford, United Kingdom. In Cell, 1996
The solution structure of the Link module from human TSG-6 was determined and found to consist of two alpha helices and two antiparallel beta sheets arranged around a large hydrophobic core.
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