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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. Additionally we are shipping TNFAIP1 Proteins (8) and and many more products for this protein.
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Human Polyclonal TNFAIP1 Primary Antibody for 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
Show all 2 Pubmed References
TNFAIP1 silence significantly increased the migrated and invaded cells compared to that in control, while these increases were abolished by miR (show MLXIP Antibodies)-424 suppression.
CREB (show CREB1 Antibodies) is a negative regulator of the TNFAIP1 gene.
TNFAIP1 plays an important role in mediating miR (show MLXIP Antibodies)-15a dependent biological functions in osteosarcoma.
MiR (show MLXIP Antibodies)-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 (show PSG1 Antibodies).
TNFAIP1 inhibited the transcriptional activities of nuclear factor kappa B (NF-kappaB (show NFKB1 Antibodies)) and activating protein-1 reporters
CK2 (show CSNK2A1 Antibodies) could phosphorylate TNFAIP1 in vitro and in vivo, which facilitated the distribution of TNFAIP1 in nucleus and enhanced its interaction with PCNA (show PCNA Antibodies).
The promoter region of human TNFAIP1 gene was functionally characterized.
suggest that the TNFAIP1/POLDIP2 (show POLDIP2 Antibodies) 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 (show AKT1 Antibodies)/CREB (show CREB1 Antibodies) signaling pathway, and in turn downregulating anti-apoptotic protein Bcl-2 (show BCL2 Antibodies).
ABETA (show APP Antibodies) 25-35 downregulated miR (show MLXIP Antibodies)-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 (show RND2 Antibodies) interact to promote radial migration within the embryonic cortex.
Estrogen and ERbeta (show ESR2 Antibodies) 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