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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 Antibodies (82) and and many more products for this protein.
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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-424 suppression.
CREB is a negative regulator of the TNFAIP1 gene.
TNFAIP1 plays an important role in mediating miR-15a dependent biological functions in osteosarcoma.
MiR-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.
TNFAIP1 inhibited the transcriptional activities of nuclear factor kappa B (NF-kappaB) and activating protein-1 reporters
CK2 could phosphorylate TNFAIP1 in vitro and in vivo, which facilitated the distribution of TNFAIP1 in nucleus and enhanced its interaction with PCNA.
The promoter region of human TNFAIP1 gene was functionally characterized.
suggest that the TNFAIP1/POLDIP2 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.
TNFAIP1 shows increased transcript levels in Alzheimer's disease brains
Expression levels of TNFAIP1 are high in COS7 and NIH3T3 cell lines but low in the cancer cell lines.
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/CREB signaling pathway, and in turn downregulating anti-apoptotic protein Bcl-2.
ABETA 25-35 downregulated miR-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 interact to promote radial migration within the embryonic cortex.
Estrogen and ERbeta 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