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Acts as a negative regulator of innate and adaptive immunity by maintaining immune homeostasis. Zusätzlich bieten wir Ihnen Tumor Necrosis Factor, alpha-Induced Protein 8-Like 2 Antikörper (55) und viele weitere Produktgruppen zu diesem Protein an.
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TIPE2 suppressed tumor invasiveness and angiogenesis in non-small cell lung cancer via inhibiting the activation of Rac1 and subsequently weakening its downstream effects, including F-actin polymerization and VEGF expression.
the expression of TIPE2 protein could be a predictor of better prognosis for DLBCL.
Insufficient expression of TIPE2 might be involved in the hyperreactivity of monocyte to Toll (zeige TLR4 Proteine)-like receptor ligands in primary biliary cirrhosis.
data provided the first evidence that TIPE2 inhibits gastric cancer cell migration, invasion and metastasis very probably via reversal of EMT (zeige ITK Proteine), revealing that TIPE2 may be a novel therapeutic target for human gastric cancer EMT (zeige ITK Proteine) and metastasis.
Authors demonstrated that TIPE2 overexpression may suppress proliferation, migration, and invasion in prostate cancer cells by inhibiting the PI3K (zeige PIK3CA Proteine)/Akt (zeige AKT1 Proteine) signaling pathway.
TIPE2 suppressed breast cancer tumorigenesis, growth and metastasis possibly via regulation of the AKT (zeige AKT1 Proteine) and p38 (zeige CRK Proteine) signaling pathways.
these data suggest that TIPE2 overexpression inhibited hypoxia-induced Wnt (zeige WNT2 Proteine)/beta-catenin (zeige CTNNB1 Proteine) pathway activation and EMT (zeige ITK Proteine) in glioma cells.
this study shows that TIPE2 contributes to the pathogenesis of ankylosing spondylitis
TIPE2 expression was significantly decreased in human breast cancer tissue and cell lines. Overexpression of TIPE2 inhibited the proliferation in vitro and tumor xenograft growth in vivo. TIPE2 also inhibited the migration/invasion of breast cancer cells through preventing the epithelial-to-mesenchymal transition (EMT (zeige ITK Proteine)) phenotype.
Low expression of TIPE2 is associated with hepatocellular carcinogenesis.
Results suggest that tumor necrosis factor alpha-induced protein 8-like 2 (TIPE2) appeared to be a critical immunoregulatory molecule which affected dendritic cells (DCs) maturation and subsequent T-cell mediated immunity.
The results reported here indicated a crucial role for TIPE2 in the infiltration of leukocytes into neural tissue in Experimental Autoimmune Encephalomyelitis.
TIPE2 inhibited breast cancer development and metastasis possibly via promoting CD8 (zeige CD8A Proteine)(+) T and NK cell-mediated antitumor immune responses
Our current study shows that TIPE2-deficient bone-marrow cells are defective in IL-4 (zeige IL4 Proteine) induced M2 macrophage differentiation in vitro. TIPE2 promotes phosphoinositide metabolism and the activation of the down-stream AKT (zeige AKT1 Proteine) signaling pathway, which in turn leads to the expression of markers specific for M2 macrophages.
The present study demonstrates that TIPE2 acts as a novel negative regulator of inflammatory and immune responses through TAK1 (zeige NR2C2 Proteine) signaling.
Data show that after tumor necrosis factor alpha-induced protein 8 like-2 (TIPE2) gene was down-regulated, the expression of the CD69 antigen (zeige CD69 Proteine) was increased, and the proliferation of T lymphocytes and the secretion of cytokines IL-2 (zeige IL2 Proteine) and IFN-gamma (zeige IFNG Proteine) were enhanced.
TIPE2 alleviates experimental SLE through induction of macrophage polarization to a M2 phenotype, which may be used as a promising therapeutic strategy for treating SLE.
TIPE2 acts as a negative regulator linking NOD2 and inflammatory responses.
TIPE2 plays a suppressive role in injury-induced restenosis and may serve as a new therapeutic target for treating the disease.
Tipe2 provides a molecular bridge between miR (zeige MLXIP Proteine)-21 and cell apoptosis; miR (zeige MLXIP Proteine)-21 suppresses apoptosis in activated T cells at least in part through directly targeting tumor suppressor gene Tipe2.
Acts as a negative regulator of innate and adaptive immunity by maintaining immune homeostasis. Negative regulator of Toll-like receptor and T-cell receptor function. Prevents hyperresponsiveness of the immune system and maintains immune homeostasis. Inhibits jun/ap1 and NF-kappa-B activation. Promotes Fas-induced apoptosis (By similarity).
TNF alpha-induced protein 8-like protein 2
, TNFAIP8-like protein 2
, inflammation factor 20
, inflammation factor protein 20
, tumor necrosis factor alpha-induced protein 8-like protein 2
, tumor necrosis factor, alpha-induced protein 8-like protein 2
, Tumor necrosis factor, alpha-induced protein 8-like protein 2
, tumor necrosis factor, alpha-induced protein 8-like protein 2 a