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TNFAIP1 was identified as a gene whose expression can be induced by the tumor necrosis factor alpha (TNF) in umbilical vein endothelial cells. Zusätzlich bieten wir Ihnen TNFAIP1 Proteine (8) und viele weitere Produktgruppen zu diesem Protein an.
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Human Polyclonal TNFAIP1 Primary Antibody für IHC (f), ICC - ABIN967193
Wolf, Marks, Sarma, Byers, Katz, Shows, Dixit: Characterization of a novel tumor necrosis factor-alpha-induced endothelial primary response gene. in The Journal of biological chemistry 1992
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TNFAIP1 silence significantly increased the migrated and invaded cells compared to that in control, while these increases were abolished by miR (zeige MLXIP Antikörper)-424 suppression.
CREB (zeige CREB1 Antikörper) is a negative regulator of the TNFAIP1 gene.
TNFAIP1 plays an important role in mediating miR (zeige MLXIP Antikörper)-15a dependent biological functions in osteosarcoma.
MiR (zeige MLXIP Antikörper)-181a played a critical role in regulating pancreatic cancer growth and migration, likely interacting with TNFAIP1.
Results showed that the expression of TNFAIP1 protein was significantly increased in osteosarcoma tissues and associated with distant metastasis.
Expression of TNFAIP1 is regulated by the transcriptional factor Sp1 (zeige PSG1 Antikörper).
TNFAIP1 inhibited the transcriptional activities of nuclear factor kappa B (NF-kappaB (zeige NFKB1 Antikörper)) and activating protein-1 reporters
CK2 (zeige CSNK2A1 Antikörper) could phosphorylate TNFAIP1 in vitro and in vivo, which facilitated the distribution of TNFAIP1 in nucleus and enhanced its interaction with PCNA (zeige PCNA Antikörper).
The promoter region of human TNFAIP1 gene was functionally characterized.
suggest that the TNFAIP1/POLDIP2 (zeige POLDIP2 Antikörper) complex sense-antisense architecture represents a clinically significant transcriptional structural-functional gene module associated with amplification of the genomic region on 17q11.2 in breast cancer.
Results demonstrated that TNFAIP1 was significantly upregulated by Abeta25-35 in mouse primary cortical neurons and N2a cells, and TNFAIP1 may be a key player that mediated Abeta25-35-induced neurotoxicity by inactivating the Akt (zeige AKT1 Antikörper)/CREB (zeige CREB1 Antikörper) signaling pathway, and in turn downregulating anti-apoptotic protein Bcl-2 (zeige BCL2 Antikörper).
ABETA (zeige APP Antikörper) 25-35 downregulated miR (zeige MLXIP Antikörper)-137 and upregulated TNFAIP1 in cortical neurons and N2a cells.
Study identifies Bacurd1/Kctd13 and Bacurd2/Tnfaip1 as interacting partners to RhoA GTPase proteins which influence the development of cortical neurons.
Bacurd2 influences the multipolar-to-bipolar transition of radially migrating neurons in a cell autonomous fashion. Bacurd2 and Rnd2 (zeige RND2 Antikörper) interact to promote radial migration within the embryonic cortex.
Estrogen and ERbeta (zeige ESR2 Antikörper) regulate Tnfaip1 expression in mouse hippocampus.
This gene was identified as a gene whose expression can be induced by the tumor necrosis factor alpha (TNF) in umbilical vein endothelial cells. Studies of a similar gene in mouse suggest that the expression of this gene is developmentally regulated in a tissue-specific manner.
BTB/POZ domain-containing protein TNFAIP1
, tumor necrosis factor, alpha-induced protein 1 (endothelial)
, BTB/POZ domain-containing adapter for CUL3-mediated RhoA degradation protein 2
, tumor necrosis factor, alpha-induced protein 1-like
, BTB/POZ domain-containing protein TNFAIP1-like
, tumor necrosis factor induced protein 1
, tumor necrosis factor-induced protein 1