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Study found that TR4 might be able to function through activation of the AKT3 (show AKT3 Proteins) expression to drive the EMT (show ITK Proteins) phenotype and enhance the seminoma cell proliferation and invasion.
Altering TR4-ATF3 (show ATF3 Proteins) signaling increases the efficacy of cisplatin to suppress hepatocellular carcinoma growth/progression.
High TAK1 (show MAP3K7 Proteins) expression is associated with the progression of hepatocellular carcinoma.
Here, we report that Pseudomonas aeruginosa ExoY inhibits proinflammatory cytokine production through suppressing the activation of TAK1 (show MAP3K7 Proteins) as well as downstream NF-kappaB (show NFKB1 Proteins) and mitogen-activated protein (MAP) kinases.
SIRT7 inhibits TR4 degradation by deacetylation of DDB1.
TR4 binds GR to play an important role in glucocorticoid-directed corticotroph tumor POMC (show POMC Proteins) regulation in addition to modulating glucocorticoid actions on other GR targets.
this study shows that TAP1 (show TAP1 Proteins) plays a novel role in the negative regulation of virus-triggered NF-kappaB (show NFKB1 Proteins) signaling and the innate immune response by targeting the TAK1 (show MAP3K7 Proteins) complex
TAK1 (show MAP3K7 Proteins)/TAB1 (show TAB1 Proteins) expression in non-small cell lung carcinoma tissue is significantly increased and closely associated with patient clinical prognosis.
miR (show MLXIP Proteins)-203 represses NF-kappaB (show NFKB1 Proteins) signaling via targeting TAK1 (show MAP3K7 Proteins) and PI3KCA and miR (show MLXIP Proteins)-203 overexpression may contribute to the COPD (show ARCN1 Proteins) initiation.
DK1 inhibits the formation of the TAK1 (show MAP3K7 Proteins)-TAB2 (show TAB2 Proteins)-TRAF6 (show TRAF6 Proteins) complex and leads to the inhibition of TRAF6 (show TRAF6 Proteins) ubiquitination.
TNFalpha (show TNF Proteins)-induced phosphorylation of RIPK1 (show RIPK1 Proteins) in the intermediate domain by TAK1 plays a key role in regulating the decision between three distinct mechanisms of cell death: necroptosis, RIPK1 (show RIPK1 Proteins)-independent and dependent apoptosis.
The results suggest that an intron-free Renilla luciferase reporter may provide a satisfactory internal control for TR4 at certain dose range. Findings advocate caution on the use of Renilla luciferase as an internal control in TR4-directed studies to avoid misleading data interpretation.
We conclude that TR4 is required for the normal differentiation and proliferation of erythroid cells, in addition to its previously characterized roles in embryonic and fetal globin gene repression
CNS-specific Tak1 deletion prevented ER-stress-induced hypothalamic leptin (show LEP Proteins) resistance and hyperphagic obesity under a high-fat diet (HFD). Thus, TAK1 is a crucial regulator of ER stress in vivo, which could be a target for alleviation of ER stress and its associated disease conditions.
this study shows that TAK1 negatively regulates lipopolysaccharide-induced cytokine secretion in myeloid cells by inhibiting MEKK3 (show MAP3K3 Proteins) activities
The present study demonstrates that TIPE2 (show TNFAIP8L2 Proteins) acts as a novel negative regulator of inflammatory and immune responses through TAK1 signaling.
this study shows that increased activity of TAK1 contributes to diabetic nephropathy
Salidroside (SDS (show SDS Proteins)) downregulated protein expression of toll-like receptor 4 (TLR4 (show TLR4 Proteins)) and CD14 (show CD14 Proteins). SDS (show SDS Proteins) inhibited LPS (show TLR4 Proteins)-triggered phosphorylation of LPS (show TLR4 Proteins)-activated kinase 1 (TAK1), p38 (show CRK Proteins), c-Jun (show JUN Proteins) terminal kinase (JNK (show MAPK8 Proteins)), and extracellular signal-regulated kinase (ERK (show EPHB2 Proteins)).
Members of the nuclear hormone receptor family, such as NR2C2, act as ligand-activated transcription factors. The proteins have an N-terminal transactivation domain, a central DNA-binding domain with 2 zinc fingers, and a ligand-binding domain at the C terminus. The activated receptor/ligand complex is translocated to the nucleus where it binds to hormone response elements of target genes (Yoshikawa et al., 1996
Nuclear hormone receptor TR4
, TR4 nuclear hormone receptor
, nuclear receptor subfamily 2 group C member 2
, orphan nuclear receptor TAK1
, orphan nuclear receptor TR4
, testicular nuclear receptor 4
, testicular receptor 4
, TR4 orphan receptor
, TR4-NS orphan receptor
, orphan receptor TR4
, TGF-beta activated kinase 1
, mitogen-activated protein kinase kinase kinase 7
, nuclear receptor subfamily 2, group H, member 2
, orphan receptor, TR4