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study proposes that Trb3 governs left-right (LR) axis patterning as a component of TGF-signaling in embryonic development
Study shows that Trib3 binds to SNRK, and downregulates UCP3 through PPARalpha. SNRK is increased in cardiomyopathy patients, and SNRK reduces infarct size after ischaemia/reperfusion. SNRK also decreases cardiac cell death in a UCP3-dependent manner.
A link between TRIB3 and the stereotypical pattern of gray matter loss in Alzheimer's disease.
the R141 site of TRIB3 dictates the strength of Akt binding but does not affect other Trbl-dependent developmental processes, suggesting a specificity that could serve as a drug target for metabolic diseases.
TRB3 is overexpressed in lesions of patients with psoriasis.
tribbles pseudokinase 3 (TRB3) and sestrin 2 may contribute to the development of obesity and its complications and can be considered interesting therapeutic target for the treatment of obesity
TRIB3, a single-domain protein with impaired kinase catalytic activity, has been described to perform a complex of roles, many of which are likely to be cell type-specific. (Review)
High TRB3 expression is associated with basal-like breast cancer.
TRIB3 promotes acute promyelocytic leukemia progression through stabilization of the oncoprotein PML-RARalpha and inhibition of p53-mediated senescence.
Downregulation of TRIB3 is associated with lung cancer.
This study aims to investigate whether the Tribbles 3 Q84R polymorphism has profound effects on serum semaphorin 3E and what effect semaphorin 3E exerts on carotid atherosclerosis.
overexpression of TRIB3 is associated with tumor angiogenesis and a poor prognosis in patients with gastric cancer (GC) . Our findings indicate that TRIB3 is a promising target for antiangiogenic therapy in GC.
Our findings suggest that good glucose and blood pressure control exhibited greater benefits on vascular outcomes in patients with TRIB3 (rs2295490) G allele.
In this exploratory analysis, IRS1, ENNP1 and TRIB3, known to be associated with type 2 diabetes and harboring genes playing a prominent role in mediating insulin signaling, may modulate a number of cardiometabolic phenotypes in patients of Italian ancestry with newly-diagnosed type 2 diabetes.
TRIB3 acts as a crucial 'stress adjusting switch' that links homeostasis, metabolic disease and cancer; and is being actively investigated as a disease biomarker and therapeutic target
TRB3 is upregulated in macrophages upon treatment with ox-LDL. TRB3 promotes lipid accumulation and suppresses cytokine expression, suggesting inflammation and foam cell formation can be reciprocally regulated.
Studies suggest that pseudo-kinase family of tribbles (TRIB) proteins TRIB1, TRIB2 and TRIB3 play roles in pathogenesis of rheumatoid arthritis (RA) and osteoarthritis.
Studies suggest that pseudo-kinase family of tribbles (TRIB) proteins TRIB1, TRIB2 and TRIB3 were involved in the pathogenesis of inflammation.
Studies indicate that small molecules can reveal rate-limiting signalling outputs and functions of pseudo-kinase family of tribbles (TRIB) proteins TRIB1, TRIB2 and TRIB3 in cells and intact organisms, serving as guides for the development of new drugs.
Studies suggest that the tribbles homolog 3 (Drosophila) protein (TRIB3) Q84R missense polymorphis contributes to atherosclerosis.
Studies show a remarkable reduction in tribbles 2 protein (Trib2) expression during oocyte maturation whereas tribbles 1 protein (Trib1) and tribbles 3 protein (Trib3) expression was significantly increased during this process.
Using SNRK transgenic and KO mouse models, study found that SNRK decreases cardiac metabolic substrate usage and mitochondrial coupling, while protecting against ischaemia/reperfusion injury. Effects on substrate usage and cell death are dependent on UCP3, which is downregulated through suppression of PPARalpha by Trib3, a novel binding partner of SNRK.
Overexpressed Trib3, specifically in skeletal muscle tissues, displayed impaired glucose homeostasis by suppressing insulin-stimulated glucose uptake.
under nutrient-limiting conditions that stimulate ATF4 activity, TRIB3 is implicated in the regulation of metabolic adaptation by restraining the transcription of Fgf21.
Data (including data from studies in transgenic and mutant mice) suggest that Akt2 plays critical role in type 1 diabetes in metallothionein-mediated preservation of cardiac insulin-stimulated metabolic signaling (insulin resistance) and preservation of cardiac function; this mechanism appear to involve inhibition of cardiac Trb3. (Akt2 = protein kinase Akt-2; Trb3 = tribbles pseudokinase 3)
restoration of TRB3 expression markedly abolished the effect of miR-124 on hepatic TG metabolism.
TRB3 regulates protein synthesis and breakdown via the Akt/mTOR/FoxO pathways in skeletal muscle.
Chac1 expression is detrimental to arsenite-treated cell survival and TRIB3 is critical for restraining the pro-death potential of Chac1 during arsenite stress.
Under physiological conditions, muscle TRIB3 also influences energy expenditure and substrate metabolism, indicating that the decrease and increase in muscle TRIB3 under fasting and nutrient excess, respectively, are critical for metabolic homeostasis.
In a knockout mouse model, Trib3 disruption modestly increased steady-state erythrocyte numbers and decreased mean corpuscular volume.
Palmitate increased TRB3 expression, activated IRE1alpha signaling, and reduced the insulin-dependent Akt phosphorylation. Knocking down TRB3 or IRE1alpha did not prevent the inhibitory effect of palmitate on Akt phosphorylation. Results support the idea that ER stress is not responsible for lipid-induced IR in C2C12 myotubes.
These data demonstrate that TRB3 inhibits insulin signaling in BAT, resulting in impaired differentiation and function.
TRB3 is a novel profibrotic mediator in SSc. TGF-beta induces TRB3, which in turn activates canonical TGF-beta/Smad signaling and stimulates the release of collagen, creating a positive feedback loop that may contribute to aberrant TGF-beta signalling in SSc.
study presents the finding that activation of the NF-kappaB pathway by Porphyromonas endodontalis LPS is important for Wnt5a expression in osteoblasts, and that TRIB3 may modulate the sustained expression of Wnt5a in osteoblasts stimulated by P. endodontalis
TRIB1 and TRIB3 are more strongly expressed than TRIB2 in cumulus cells (CC) surrounding oocytes from preovulatory follicles than in CC of immature ones.
Trib3 interferes with the Parkinson's disease-associated prosurvival protein Parkin to mediate death
These observations support the notion that loss of TRIB3 is associated with a more aggressive phenotype in various types of tumors by enhancing the activity of the mTORC2/AKT/FOXO axis.
This study showed that hepatic PSAT1 expression and liver serine levels are reduced in 2 mouse strains, and that PSAT1 inhibited the expression of hepatic TRB3 in vitro and in vivo.
Tribbles 3 regulates the fibrosis cytokine TGF- beta 1 through ERK1/2-MAPK signaling pathway in diabetic nephropathy.
Fibroblasts from two long-lived mice mutants (Snell dwarf and PAPP-A knockout) expressed higher levels of TRB3 (a ATF4 target gene) during stress, suggesting a connection to longevity.
This work aimed to study the porcine tribbles homolog 3 (TRIB3) gene and to evaluate its association with meat quality and carcass traits in pigs.
The protein encoded by this gene is a putative protein kinase that is induced by the transcription factor NF-kappaB. The encoded protein is a negative regulator of NF-kappaB and can also sensitize cells to TNF- and TRAIL-induced apoptosis. In addition, this protein can negatively regulate the cell survival serine-threonine kinase AKT1.
tribbles homolog 3
, tribbles homolog 3 (Drosophila)
, tribbles homolog 3-like
, neuronal cell death inducible putative kinase
, neuronal cell death-inducible putative kinase
, p65-interacting inhibitor of NF-kappa-B
, p65-interacting inhibitor of NF-kappaB
, induced in fatty liver dystrophy 2
, Neuronal cell death Inducible Putative Kinase
, tribbles 3