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Promotes clear cell renal carcinoma vasculogenic mimicry (VM) formation and its associated metastasis by modulating the miR490-3p-vimentin signals
The senescence-associated secretory phenotype is potentiated by feedforward regulatory mechanisms involving Zscan4 and TAK1.
Targeting the Cripto-1/TAK-1/NF-kappaB/Survivin pathway may be an effective approach to combat apoptosis resistance in cancer.
blockage of RhoA/ROCK repressed the TAK1/NOD2-mediated NF-kappaB pathway in HaCaT cells exposed to UVB.
Study found that TR4 might be able to function through activation of the AKT3 expression to drive the EMT phenotype and enhance the seminoma cell proliferation and invasion.
Altering TR4-ATF3 signaling increases the efficacy of cisplatin to suppress hepatocellular carcinoma growth/progression.
High TAK1 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 as well as downstream NF-kappaB 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 regulation in addition to modulating glucocorticoid actions on other GR targets.
this study shows that TAP1 plays a novel role in the negative regulation of virus-triggered NF-kappaB signaling and the innate immune response by targeting the TAK1 complex
TAK1/TAB1 expression in non-small cell lung carcinoma tissue is significantly increased and closely associated with patient clinical prognosis.
miR-203 represses NF-kappaB signaling via targeting TAK1 and PI3KCA and miR-203 overexpression may contribute to the COPD initiation.
DK1 inhibits the formation of the TAK1-TAB2-TRAF6 complex and leads to the inhibition of TRAF6 ubiquitination.
IFIT5 promotes SeV-induced IKK phosphorylation and NF-kappaB activation by regulating the recruitment of IKK to TAK1.
USP18 negatively regulates NF-kappaB signaling by targeting TAK1 and NEMO for deubiquitination through distinct mechanisms.
Helicobacter pylori induces internalization of EGFR via novel TAK1-p38-serine activation pathway which is independent of HB-EGF.
Together, these results demonstrate that LYTAK1 inhibits LPS-induced production of several pro-inflammatory cytokines and endotoxin shock probably through blocking TAK1-regulated signalings.
TR4 expression in NSCLC samples is significantly associated with poor clinicopathological features, and TR4 plays an important role in the metastatic capacity of NSCLC cells by EMT regulation.
TR4 may increase prostate cancer metastasis and invasion via decreasing the miR-373-3p expression that resulted in the activation of the TGFbetaR2/p-Smad3 signals.
TNFalpha-induced phosphorylation of RIPK1 in the intermediate domain by TAK1 plays a key role in regulating the decision between three distinct mechanisms of cell death: necroptosis, RIPK1-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 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 activities
The present study demonstrates that TIPE2 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) downregulated protein expression of toll-like receptor 4 (TLR4) and CD14. SDS inhibited LPS-triggered phosphorylation of LPS-activated kinase 1 (TAK1), p38, c-Jun terminal kinase (JNK), and extracellular signal-regulated kinase (ERK).
miR-133a regulates TR4 expression in ox-LDL-induced mouse RAW 264.7 macrophages
TAK1 participates in intestinal integrity through separately modulating bacteria-derived reactive oxygen species and receptor-interacting protein kinase 3-dependent Paneth cell loss.
We confirmed that PGC-1b inhibited downstream inflammatory signals via binding with TAB1 and thus preventing TAB1/TAK1 binding and TAK1 activation.
Hepatocyte TRAF3 promotes liver steatosis and insulin resistance through targeting TAK1-dependent signaling.
Bacterial polysaccharide-responsive miR-150 and miR-143 RIPK2 and TAK1 to suppress NOD2-induced immunomodulators.
TR4-mediated enhancement of fatty acid synthesis in adipocytes requires increased expression of PC gene
TR4 nuclear receptor functions as a tumor suppressor for prostate tumorigenesis via modulation of DNA damage/repair system.
These data provide new insights into our understanding of globin gene regulation and raise the interesting possibility that the PGC-1 coactivators can interact with TR4 to elicit differential stage-specific effects on globin gene transcription.
TR4 transcriptionally activates proopiomelanocortin through binding of a direct repeat 1 response element in the promoter, and that this is enhanced by MAPK-mediated TR4 phosphorylation.
The very profound pain and itch processing defects after TR4 deletion reflects loss of functionally distinct, and possibly independent, excitatory interneuronal circuits in the dorsal horn.
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
, nuclear receptor subfamily 2, group H, member 2
, orphan receptor, TR4