anti-Tumor Necrosis Factor-Inducible Protein 6 (TNFAIP6) Antikörper

Mouse (Murine) Tumor Necrosis Factor-Inducible Protein 6 (TNFAIP6) Interaktionspartner

1. TSG-6 deficiency protects against airway hyperresponsiveness after ozone (in vivo) or short-fragment hyaluronan (sHA) (in vitro and in vivo) exposure. Moreover, TSG-6(-/-) tracheal ring non-responsiveness to sHA was reversed by exogenous TSG-6 addition.

2. Loss of TSG6 expression is associated with Embryos failing to Initiate Midgut Rotation.

3. TSG-6 up-regulation counteracts the progression of atherosclerosis. (Review)

4. our results showed that the increase of oxidative stress, activation of the NLRP3 inflammasome and NF-kappaB signaling in SAP was substantially inhibited following administration of hMSCs or TSG-6, which was dependent on the presence of CD-44 receptors in acinar cells.

5. TSG-6 protects hepatocytes from damage by enhancing autophagy influx and contributes to liver regeneration

6. TSG6 functions by converting macrophages from a proinflammatory to an anti-inflammatory phenotype secondary to suppression of TLR4/NF-kappaB signaling and STAT1 and STAT3 activation.

7. This study provided the first evidence of TSG-6 secreted by mesenchymal stem cells promoting corneal epithelial wound healing in diabetic mice through activating corneal epithelial stem/progenitor cells and accelerating M2 macrophage polarization

8. This study shows that TSG-6 is expressed in the CNS, suggesting a role for TSG-6 in astrocyte activation and tissue repair.

9. Data (including data from studies in knockout mice) suggest that TSG-6 is needed for release of hyaluronan rafts (leukocyte-adhesive rafts) from apical surface of tracheal mucosa into bronchoalveolar lavage fluid as heavy chain hyaluronan complexes.

10. the well characterized hyaluronan-binding site in the TSG-6 Link module is not used for recognition during transfer of HCs onto HA.

11. Thus, TSG6, HA, and IalphaI were crucial factors for the settlement and probably the subsequent differentiation of MSCs.

12. BM-MSCs injected into mice with colitis do not localize to the intestine but instead form aggregates in the peritoneum where they produce immunoregulatory molecules, including TSG6, that reduce intestinal inflammation.

13. This study demonstrated that following stimulation with TNF-alpha, MSCs modulate microglia activity through TSG-6.

14. suggest that TSG-6 plays an important role in MSCs-mediated immunosuppressive effect on DC

15. This study provides insight into what we believe to be a previously undescribed multifaceted role of mesenchymal stem cell-released TSG-6 in wound healing.

16. TSG-6 is implicated in the experimental murine model of allergic pulmonary inflammation and is likely to contribute to the pathogenesis of asthma

17. TSG-6 increases the accumulation of HA in the cell-associated matrix, partially by preventing its dissolution from the cell-associated matrix into the conditioned medium, but primarily by inducing HA synthesis

18. analysis of irreversible heavy chain transfer to hyaluronan oligosaccharides by tumor necrosis factor-stimulated gene-6

19. cells expressing CD44/TSG-6 failed to roll on hyaluronan, instead, they stuck and remained "tethered" to the substrate under fluid flow

20. observations identify tumor necrosis factor-alpha-stimulated gene 6 as a target of prostaglandin action and show that its production in ovulatory follicles is associated with proper formation of the cumulus-derived extracellular matrix

Human Tumor Necrosis Factor-Inducible Protein 6 (TNFAIP6) Interaktionspartner

1. TSG-6 is constitutively expressed in some tissues, which are either highly active or subject to challenges. The diversity of its functions depend on its binding to ligands such as glycosaminoglycans, immune regulators and growth factors that themselves interact with these linear polysaccharides. TSG-6 can directly affect matrix structure and modulate its interaction with the extracellular signaling molecules. [review]

2. The expression levels of Fas, FasL, FADD, caspase-3 and caspase- 8 were significantly raised in the TSG-6 overexpressing hypertrophic scar fibroblasts.

3. Findings indicate that TSG6 is a novel regulator of keloid fibrogenesis.

4. TSG-6 secreted by human adipose tissue-derived mesenchymal stem cells (hAT-MSCs) protects pancreatic acinar cells in severe acute pancreatitis model mice via the inhibition of endoplasmic reticulum stress, as well as inflammatory responses. This study has revealed a new area for ER stress-targeted therapy in SAP patients

5. the results suggest that MSCs inhibit inflammatory neovascularization in the cornea by suppressing pro-angiogenic monocyte/macrophage recruitment in a TSG-6-dependent manner.

6. We demonstrated that hAT-MSC-secreted TSG-6 induced macrophages that infiltrated into the colon to switch to the M2 phenotype, thus regulating the expression of inflammatory cytokines and the alleviation of DSS-induced colitis symptoms in mice.

7. TSG-6 up-regulation counteracts the progression of atherosclerosis. (Review)

8. TSG-6 from MSCs attenuated severe burn-induced excessive inflammation via inhibiting activation of P38 and JNK signaling.

9. TSG-6 secreted by human mesenchymal stem cells suppresses inflammatory reactions through p38 and ERK in the mitogen-activated protein kinase pathway

10. This review will focus on the potential of mesenchymal stem/stromal cells for treatment of fibrotic diseases, with emphasis on the role of TSG-6 as a mediator of anti-inflammatory effects

11. abnormally elevated in both the plasma and aortic wall of patients with abdominal aortic aneurysms

12. Single nucleotide polymorphism in TNFAIP6 gene is associated with Systemic lupus erythematosus.

13. TNFAIP6 expression is significantly upregulated in human masticatory mucosa during wound healing

14. Data show that TNF-stimulated gene-6 (TSG-6) interacts with chemokines through their glycosaminoglycans (GAGs)-binding sites and inhibits their binding to GAGs and endothelial cell surfaces.

15. The current study describes a novel mechanism linking the TSG-6 transfer of the newly described HC5 to the HA-dependent control of cell phenotype. The interaction of HC5 with cell surface HA was essential for TGFbeta1-dependent differentiation of fibroblasts to myofibroblasts, highlighting its importance as a novel potential therapeutic target.

16. Data postulate that the molecular cross-linking enhanced by the multiple binding modes of the Link module might be critical for remodeling the ECM during inflammation/ovulation and might contribute to other functions of TSG-6.

17. the well characterized hyaluronan-binding site in the TSG-6 Link module is not used for recognition during transfer of HCs onto HA.

18. TSG-6 exhibited anti-inflammatory effects during the wound healing process and cicatrization and significantly diminished hypertrophic scar formation in a rabbit ear model

19. results suggest that systemic administration of hASC or TSG-6 may be novel approaches to reverse CS-induced myelosuppression.

20. TSG-6 activity in tissues, was examined.