clear vs WBGene00000912

Most specifically we show that nuclear localization and thus activation of the DAF-16/forkhead box transcription factor occurs in response to selenium exposure although this was not observed in motor neurons of the ventral cord.

Furthermore, the lignans can induce the nuclear translocation of the transcription factor DAF-16 and up-regulate its expression, suggesting that a possible underlying mechanism of the observed longevity-promoting activity of lignans depends on DAF-16 mediated signaling pathway.

AKT/PKB signaling antagonizes nuclear translocation of the DAF-16/FOXO transcription factor.

HSE and HCA increased the nuclear localisation of the pivotal transcription factors DAF-16 and SKN-1 indicating an activation of these factors.

Mechanistically, administration of Carbamazepine or Calmagite induced nuclear translocation of the transcription factor DAF-16 and thus up-regulated its downstream genes numr-1/-2, which are known to promote resistance to metal-induced stresses and longevity.

In a previous study we have shown in Caenorhabditis elegans expressing human Aβ in muscle cells, that inhibition of steroid-signaling, by RNAi of respective members of the signaling pathway or by reducing cellular cholesterol uptake, both increases the nuclear translocation of the foxo transcription factor DAF-16 and concomitantly reduces Aβ-induced paralysis.

Using transgenic nematode models, the peptides were shown to promote nuclear translocation of the DAF-16/FOXO transcription factor, a pivotal regulator of stress response and lifespan, and induce the expression of superoxide dismutase 3 (SOD-3), an antioxidant enzyme.

The nuclear export of DAF-16 requires heat shock transcription factor HSF-1 and Hsp70/HSP-1.

Consistent with the aforementioned results, lentinan enhanced the nuclear translocation of DAF-16 and SKN-1.

In Caenorhabditis elegans, nuclear translocation of DAF-16 and SKN-1 was inhibited by Cu, which in turn suppressed antioxidant-related enzymes activities.

Forced locomotion during lethargus results in nuclear translocation of DAF-16.

We also found that HLEA-P1 activates nuclear localization of DAF-16 transcription factor of insulin/IGF-1 signaling (IIS) pathway.

Starvation conditioning induces nuclear translocation of DAF-16 in ASER and degradation of DAF-16 before starvation conditioning causes defects in taste avoidance learning.

Forced nuclear localization of DAF-16 in ASER biased chemotaxis towards lower salt concentrtions and this effect required the Gq/PKC pathway and neuropeptide processing enzymes.

Remarkably, we found that cholesterol plays an important role in the fasting-induced nuclear accumulation of DAF-16.

Steroid hormone and insulin/insulin-like growth factor signaling (IIS) pathways control development and lifespan in the nematode Caenorhabditis elegans by regulating the activity of the nuclear receptor DAF-12 and the FoxO transcription factor DAF-16, respectively.

Moreover, the survival of C. elegans to oxidative stimuli (juglone and H2O2), and the nuclear translocation of DAF-16 and SKN-1 were evaluated.

Moreover, the mechanism study revealed that NPRG was able to promote the nuclear localization of DAF-16 resulting in the activation of antioxidant enzymatic systems under oxidative stress.

Reducing IIS function leads to the nuclear accumulation of the DAF-16/FOXO transcription factor, which extends lifespan by regulating downstream longevity genes.

Elimination of RLE-1 expression in C. elegans causes increased transcriptional activation and sustained nuclear localization of DAF-16.

Supplementation of the antioxidant coenzyme Q(10) reversed this nuclear translocation of DAF-16.

In the case of ZnO-NPs exposure, inhibition of nuclear translocation of DAF-16 and SKN-1 was restored by GABA.

Mechanistically, corylin promoted nuclear translocation of DAF-16 and upregulated the expression of DAF-16/SKN-1 target genes.

Also, in an in vivo model, the extract increased the survival rate of Caenorhabditis elegans worms pretreated with the pro-oxidant juglone from 43 to 64%, decreased intracellular ROS inside the wild-type nematodes by 47.90%, and induced nuclear translocation of the transcription factor DAF-16 in the transgenic strain TJ356.

Mechanistically, lmwptp RNAi promoted adipogenesis by modulating the insulin-like growth factor 1 signaling pathway, facilitating the nuclear translocation of DAF-16, which in turn upregulated fat-7 expression.

Furthermore, treatment with the derivatives induced a much stronger nuclear localization of the DAF-16 transcription factor (FoxO homologue).

Worms exposed to parabens show significant down-regulation of vitellogenin genes, high levels of reactive oxygen species and anti-oxidant transcripts, the latter being concordant with nuclear localization of DAF-16 and up-regulation of HSF-1 and SKN-1/Nrf.

Gene expression analysis indicated that phlorizin reversed the downregulation of IIS, mTOR and lipid metabolism pathways and promoted the nuclear translocation of DAF-16.

We also evaluated the lifespan of worms defective in genes involved in the insulin/IGF-1-mediated pathway and monitored the nuclear translocation of DAF-16.

Importantly, GSF promoted the nuclear translocation of DAF-16 and SKN-1 in C. elegans TG356 and LC333, respectively.

Moreover, quantitative fluorescence of polyglutamic acid and nuclear localization of DAF-16 were observed.

We show here that the energy-sensing adenosine monophosphate (AMP)-activated protein kinase (AMPK) signaling pathway plays a key role in mediating similar defects caused by different mtDNA mutations in Caenorhabditis elegans, including loss or reduction of osmotic, chemical and olfactory sensing, locomotion, and associative learning and memory, as well as increased embryonic lethality. mtDNA mutations cause reduced ATP (adenosine triphosphate) levels, activation of C. elegans AMPK AAK-2, and nuclear translocation of the FOXO transcription factor DAF-16.

The Caenorhabditis elegans nuclear hormone receptor, DAF-12, interacted with the C. elegans forkhead factor, DAF-16, paralleling the interaction between PPARgamma and Foxo1. daf-12 and daf-16 have been implicated in C. elegans insulin-like signaling pathways, and PPARgamma and Foxo1 likewise have been linked to mammalian insulin signaling pathways.

Mechanistic investigations revealed that PKP-1b exerts its anti-aging effects by inhibiting the insulin/IGF-1 signaling (IIS) pathway, which in turn promotes nuclear translocation of the transcription factor DAF-16/FOXO, upregulates expression of the antioxidant gene sod-3, thereby enhancing overall antioxidant capacity and reducing oxidative damage.

With the treatment of Exendin-4, the nuclear translocation of DAF-16 in the transgenic nematode TJ356 was enhanced.

HT115 diet promoted the nuclear translocation of DAF-16 (ortholog of the FOXO family of transcription factors), a phenomenon previously reported to underlie neuroprotection caused by down-regulation of the insulin receptor in this system.

In addition, enhanced nuclear translocation of DAF-16 was observed in the hispidol-fed DAF-16::GFP fused transgenic mutants, suggesting the requirement of DAF-16/FOXO activation for the longevity effect of hispidol.

Furthermore, we observed that the xylofuranosides induced nuclear translocation of the transcription factor DAF-16/FOXO, which in the worm is known to regulate stress responsiveness, aging and metabolism.

At an upstream signaling level, SCO prompts changes to C. elegans fat regulation by stimulating nuclear translocation of transcription factor DAF-16/FOXO, an event that requires AMP-activated protein kinase under this condition.

Since the insulin/IGF-like signaling (IIS) cascade is a key regulator of lifespan, all compounds were tested for the ability to cause nuclear translocation of the FOXO transcription factor DAF-16 and changes in target gene expression.

Furthermore, it promoted an increased life expectancy in wild-type nematodes and increased the expression of superoxide dismutase and the nuclear translocation of DAF-16.

We show that disulfide formation with transportin-1 is required for nuclear localization and the activation of FOXO4/DAF-16 induced by ROS, but not by the loss of insulin signaling.

HT115 diet promoted the nuclear translocation of DAF-16 (ortholog of the FOXO family of transcription factors), a phenomenon previously reported to underlie neuroprotection caused by down-regulation of the insulin receptor in this system.

And the nuclear localization of DAF-16 of strain TJ356 was significantly increased in PAO1-induced C. elegans by PGG.

Conclusions: Our results suggest, that cholecalciferol inhibits Aβ-induced paralysis in C. elegans through inhibition of steroid-signaling and the concomitant nuclear translocation of DAF-16.

Moreover, the mechanism study revealed that NPRG was able to promote the nuclear localization of DAF-16 resulting in the activation of antioxidant enzymatic systems under oxidative stress.

Furthermore, it promoted an increased life expectancy in wild-type nematodes and increased the expression of superoxide dismutase and the nuclear translocation of DAF-16.

Finally, MSE induced nuclear DAF-16::GFP localization.

Here, we report that lowbush cranberry (Vaccinium vitis-idaea) treatment causes marked nuclear localization of the central aging-related transcription factor DAF-16/FOXO in aged Caenorhabditis elegans.

In addition, G2019S inhibited ftt2 (a 14-3-3 gene homolog in C. elegans) knockdown-associated nuclear translocation of DAF-16.

We found that G2019S transgenic worms had increased sensitivity to stress (heat and juglone treatment) and impaired stress-induced nuclear translocation of DAF-16.

However, incubation with pinoresinol caused an enhanced nuclear accumulation of the transcription factor DAF-16 (insulin/IGF-like signalling pathway).

Furthermore, treatment with the derivatives induced a much stronger nuclear localization of the DAF-16 transcription factor (FoxO homologue).

Furthermore, DPTVP induced nuclear translocation of the transcriptional factor DAF-16/FOXO, which regulates stress responsiveness and aging in worms.

A pronounced antioxidant activity in vivo, which can be attributed to its ability to promote the nuclear translocation of DAF-16/FOXO, the main transcription factor regulating the expression of stress response genes.

Remarkably, we found that cholesterol plays an important role in the fasting-induced nuclear accumulation of DAF-16.

How ROS regulate the nuclear translocation of FOXO/DAF-16 is largely unknown.

We show that disulfide formation with transportin-1 is required for nuclear localization and the activation of FOXO4/DAF-16 induced by ROS, but not by the loss of insulin signaling.

Furthermore, we observed that the xylofuranosides induced nuclear translocation of the transcription factor DAF-16/FOXO, which in the worm is known to regulate stress responsiveness, aging and metabolism.

However, it remains unclear how DAF-16 achieves its specificity in regulating these various biological processes.

Furthermore, treatment of the fat-2-RNAi worm with PUFA--using the fatty acids from linoleic acid through eicosapentaenoic acid--suppressed nuclear localization of DAF-16.

Thus, EAK proteins regulate the activity of nuclear DAF-16/FoxO.

Since the insulin/IGF-like signaling (IIS) cascade is a key regulator of lifespan, all compounds were tested for the ability to cause nuclear translocation of the FOXO transcription factor DAF-16 and changes in target gene expression.

With Caenorhabditis elegans as a model system, this study demonstrates that clozapine is unique among antipsychotic drugs because it requires β-arrestin and serum and glucocorticoid-inducible kinase (SGK) in addition to Akt to suppress the nuclear localization of DAF-16 (Forkhead box O [FOXO]).

Lithium, a mood stabilizer often used to treat psychosis, also requires β-arrestin and SGK to suppress the nuclear localization of DAF-16.

JNK regulates lifespan in Caenorhabditis elegans by modulating nuclear translocation of forkhead transcription factor/DAF-16.

Reducing IIS function leads to the nuclear accumulation of the DAF-16/FOXO transcription factor, which extends lifespan by regulating downstream longevity genes.

Our findings implicate nuclear-pore modification in p53-dependent cell death, because inhibiting nuclear-pore genes that are upregulated by DAF-16 blocks p53-dependent cell death in the tumor, but not normal, p53-independent, germline cell death.

Both aspects converge on controlling the nuclear translocation and activation of the FOXO transcription factor DAF-16.

Environmental stresses, such as starvation, heat, and oxidative stress, cause rapid nuclear localization of DAF-16.

At an upstream signaling level, SCO prompts changes to C. elegans fat regulation by stimulating nuclear translocation of transcription factor DAF-16/FOXO, an event that requires AMP-activated protein kinase under this condition.

Moreover, nuclear accumulation of DAF-16 was promoted upon CLJP treatment.

We also found that HLEA-P1 activates nuclear localization of DAF-16 transcription factor of insulin/IGF-1 signaling (IIS) pathway.

Taken together, the results indicate that GS-Rd significantly reduces Aβ aggregation by targeting the MAPK signal pathway, induces nuclear translocation of DAF-16 to activate downstream signaling pathways and increases resistance to oxidative stress in C. elegans to protect against Aβ-induced toxicity.

Mechanistically, Asp promoted the expression and nuclear localization of the DAF-16 protein, an upstream regulator of the above two autophagy-related genes.

Gene expression analysis indicated that phlorizin reversed the downregulation of IIS, mTOR and lipid metabolism pathways and promoted the nuclear translocation of DAF-16.

Additionally, we demonstrated that swimming exercise induces nuclear localization of DAF-16 in an AMPK-dependent manner.

In addition, the flower extract and apigenin induced the nuclear localization of DAF-16, which is involved in lipogenesis in nematodes.

Moreover, ethanol could induce the nuclear translocation of DAF-16 in the nematodes.

NP and NP-9 induced the activation and nuclear translocation of DAF-16, suggesting that transcription of stress-response genes may be mediated by the insulin/IGF-1 signaling pathway.

Furthermore, reducing zinc levels led to greater nuclear localization of DAF-16 and enhanced dauer formation compared to controls, suggesting that the lifespan effects of zinc are mediated in part by the insulin/IGF-1 pathway.

Functional genomic analysis and molecular biology validation suggest that defective endocytosis, the decreased activity of the citrate cycle and the reduced nuclear translocation of DAF-16 transcription factor play key roles in inducing the observed a-SWCNT toxicity in worms.

RNAi of fat-2 induced nuclear translocation of DAF-16 and increased the level of TAG that could be detected by Oil Red-O, but suppressed the accumulation of lipid dyed by Nile red.

MI could also induce the nuclear localization of the DAF-16.