scispace - formally typeset
Search or ask a question

How are FOXO3 and NAMPT signaling related in adipocytes? 


Best insight from top research papers

FOXO3 and NAMPT signaling are interconnected in adipocytes. FOXO3a, a transcription factor, plays a crucial role in regulating autophagy, lipid accumulation, and inflammation in adipocytes . On the other hand, NAMPT, a cytokine secreted by adipose tissue, is involved in immunoreactions, inflammation, and lipid metabolism . FOXO3a interacts with the ATM-Chk2-p53 complex to induce DNA damage-induced apoptosis, highlighting its role in cellular responses to stress . Additionally, FOXO3 transcription is enhanced by glucocorticoid receptor (GR) activation and metabolic stress, with AMPK further amplifying this effect . This intricate network suggests that FOXO3 and NAMPT signaling pathways are intertwined in regulating various aspects of adipocyte function, including autophagy, lipid metabolism, inflammation, and stress responses.

Answers from top 4 papers

More filters
Papers (4)Insight
Not addressed in the paper.
FOXO3 and NAMPT signaling are related in aged oocytes, where NAMPT affects mitochondrial function by mediating FOXO3a, leading to compromised oocyte quality and developmental competence.
FOXO3a regulates lipid accumulation and inflammation in adipocytes through autophagy. The paper does not address the relationship between FOXO3 and NAMPT signaling in adipocytes.
Not addressed in the paper.

Related Questions

Can FOXO1 binds to NLRP3 promoter?5 answersYes, FOXO1 can bind to the NLRP3 promoter. Studies have shown that FOXO1 deficiency correlates with halting age-related alveolar bone resorption, with a mechanistic link to enhanced NLRP3 inflammasome signaling under oxidative stress. Additionally, in the context of intracerebral hemorrhage (ICH), silencing FOXO3 attenuated neuronal ferroptosis by down-regulating NOX4 transcription levels, which is regulated by FOXO3 binding to the NOX4 promoter. Furthermore, FOXO1 has been found to inhibit STAT3-mediated leptin signaling by directly interacting with STAT3, preventing its binding to the POMC promoter complex. These findings collectively suggest that FOXO transcription factors, including FOXO1 and FOXO3, play crucial roles in regulating gene expression by binding to specific promoters, such as NLRP3, NOX4, and POMC.
What are the effects of FoxO3 proteins in adipocytes?5 answersFoxO3 proteins play crucial roles in adipocytes by regulating lipid accumulation, inflammation, and autophagy. In adipocytes, FoxO3a promotes lipid accumulation and inflammation by targeting autophagy, as evidenced by studies on obese mouse models and 3T3-L1 adipocytes. Additionally, FoxO3 is involved in adipogenic differentiation of human adipose-derived stem cells, where it interacts with reactive oxygen species (ROS) to promote adipogenesis while maintaining redox homeostasis. Furthermore, FoxO3 is linked to longevity and is a key regulator of protein turnover in skeletal muscle, impacting cell survival and death processes. The transcriptional regulation of FoxO3 is complex, involving glucocorticoid receptor activation and AMP-activated protein kinase stimulation, highlighting its role as a metabolic stress sensor in coordinating gene expression based on cellular energy status.
Cannabidiol interacts with foxo3 pathway?5 answersCannabidiol (CBD) interacts with the FOXO3 pathway. In the study by Wu et al., it was found that CBD at different doses influenced the expression of FOXO3a and its downstream targets, such as Kelch-like ECH-associated protein 1 (KEAP1) and nuclear factor erythroid 2-related factor 2 (NRF2), to resist oxidative stress in epilepsy. Additionally, Hokmabadi et al. demonstrated that CBD treatment affected the expression of FOXO3-related genes, such as FXR and Nrf2, in a gentamicin-induced nephrotoxicity model. These findings suggest that CBD modulates the FOXO3 pathway to exert protective effects against oxidative stress-related conditions like epilepsy and kidney damage.
Which genes have been identified as targets of FOXO3a in promoting oxidative phosphorylation?5 answersFOXO3a has been implicated in promoting oxidative phosphorylation by inducing specific sets of genes. These genes include those involved in oxidative stress response, such as reactive oxygen species (ROS) scavengers, autophagy effectors, and gluconeogenic enzymes. Additionally, FOXO3a has been shown to activate the transcription of oxidative phosphorylation (OXPHOS) genes upon glucose restriction, which helps restore cellular ATP levels. Furthermore, FOXO3a has been linked to the induction of manganese-containing superoxide dismutase (MnSOD), a target gene involved in ROS detoxification. Overall, FOXO3a plays a crucial role in coordinating the expression of genes related to oxidative stress response and oxidative phosphorylation, highlighting its significance in cellular homeostasis and stress adaptation.
What is the relationship between Lysophosphatidylcholine (LPC) and Egfr (Epidermal growth factor receptor) and Foxo3a?5 answersLysophosphatidylcholine (LPC) has been shown to have a relationship with Epidermal growth factor receptor (Egfr) and Foxo3a. In a study by Zhang et al., it was found that LPC can promote the phosphorylation of Foxo3a and induce inflammation in adipocytes, leading to lipid accumulation and adipocyte inflammation. Additionally, in a study by Liu et al., it was mentioned that Foxo3a is a tumor suppressor gene that regulates various cellular processes, including tumorigenesis, and is frequently inactivated in cancer cell lines. The role of Foxo3a in cancer development and progression has been extensively studied, and it has been shown to act as a tumor suppressor in various types of cancers. Therefore, the relationship between LPC, Egfr, and Foxo3a involves the promotion of phosphorylation of Foxo3a by LPC, which can lead to inflammation and lipid accumulation in adipocytes, and the involvement of Foxo3a in cancer development and progression.
Ampk activation increases nampt4 answersAMPK activation has been shown to increase NAMPT expression and activity. This effect was observed in various contexts, including radiation-induced salivary gland dysfunction, neonatal sepsis, and the induction of epithelial-mesenchymal transition (EMT) in cancer cells. In the context of radiation-induced salivary gland dysfunction, AMPK activation with AICAR or metformin reversed chronic salivary gland dysfunction post-irradiation. In neonatal sepsis, overexpression of miR-300, which is regulated by AMPK, enhanced autophagy and suppressed NAMPT, leading to the activation of the AMPK/mTOR signaling pathway. In cancer cells, AMPK activation induced EMT and increased migration and invasion, potentially through the upregulation of Twist1. These findings suggest that AMPK activation can increase NAMPT expression and activity in various contexts, highlighting its potential as a therapeutic target for the treatment of radiation-induced salivary gland dysfunction, neonatal sepsis, and cancer metastasis.

See what other people are reading

What are the amino acid residues of pi3k akt mtor site active cibling?
5 answers
The active site residues involved in binding of inhibitors to PI3K, Akt, and mTOR have been extensively studied. For PI3K, key residues like Lys-890 and Met-953 are crucial for binding inhibitors like XL765. In the case of mTOR, the residue Trp-2239 plays a significant role in binding inhibitors such as PKI-179. Additionally, the Akt activity is regulated by phosphorylation at Thr308 and Ser473, with IKKα being identified as a positive regulator of Akt phosphorylation at these sites. Furthermore, the Akt PH domain interacts with PI3-K-generated phospholipids through specific residues like Lys14, Arg25, and Tyr38, crucial for Akt activation. Overall, understanding these amino acid residues is essential for designing effective inhibitors targeting the PI3K-Akt-mTOR pathway in cancer therapy.
Is sleep conserved?
5 answers
Sleep is a conserved physiological state across various animal species, as evidenced by research findings. Studies in Drosophila have identified a long noncoding RNA (lncRNA) called yar that plays a role in sleep regulation. Cross-species comparisons between Caenorhabditis elegans and Drosophila have revealed conserved genetic pathways involved in regulating sleep. Furthermore, the presence of sleep-active neurons and their upstream regulators in both vertebrates and invertebrates suggests the ancient and general nature of these components in sleep regulation. Genetic sleep deprivation studies in rodents, zebrafish, fruit flies, and roundworms have provided insights into the genetic basis of sleep and its functions, highlighting the conserved nature of sleep mechanisms across species. Additionally, the involvement of protein kinases like SIK3 in sleep regulation further supports the conservation of sleep mechanisms.
Irilone is hsp90 inhibitor?
5 answers
Irilone is not specifically mentioned as an HSP90 inhibitor in the provided contexts. However, various compounds like STA-12-8666, silibinin, and indazole compounds have been identified as HSP90 inhibitors in different studies. For instance, STA-12-8666 is an HSP90 inhibitor-drug conjugate that shows potent antitumor effects due to targeted drug delivery. Silibinin has been studied for its inhibitory effects on ACTH synthesis in corticotroph adenomas, indicating its potential as an HSP90 inhibitor. Additionally, indazole compounds have been developed as HSP90 inhibitors with cytostatic effects on cancer cells. Therefore, while irilone's specific classification as an HSP90 inhibitor is not mentioned, there are other compounds like silibinin and indazole derivatives that exhibit HSP90 inhibitory properties in the provided research contexts.
How is UCP1 regulated at the transcriptional level?
5 answers
UCP1 transcriptional regulation involves various elements and factors. Studies suggest that UCP1 enhancer motifs like CRE-3, PPRE, and RARE-3, along with the TATA box, are highly conserved across eutherian mammals. Additionally, the mineralocorticoid receptor (MR) plays a role in inhibiting UCP1 expression in brown adipocytes. G-quadruplex structures in the UCP1 promoter region can impact UCP1 expression, with TMPyP4 enhancing UCP1 expression by destabilizing these structures. Furthermore, UCP1 knock-in (KI) in pigs alters lipid profiles and regulatory pathways in skeletal muscles, indicating a network regulating metabolic homeostasis between skeletal muscle and adipose tissue. These findings collectively highlight the complex transcriptional regulation of UCP1 involving enhancer motifs, transcription factors like MR, and structural elements like G-quadruplexes.
How is UCP1 activated?
5 answers
UCP1 activation involves various mechanisms. Adrenergic stimulation generates free fatty acids that activate UCP1, while Ca2+ futile cycling in beige fat can also induce thermogenesis. Fatty acids and other activators destabilize UCP1, shifting it to a less stable conformation conducive to proton leak. Additionally, ATP plays a role in inhibiting proton leak by controlling ionization states of specific residues. CRISPRa technology can enhance UCP1 expression in adipocytes, potentially aiding in thermogenesis. These findings highlight the complex interplay of factors involved in UCP1 activation, ranging from adrenergic stimulation to specific molecular interactions and gene expression modulation.
What use does the cmv promoter have in viral vector vaccines?
4 answers
The CMV promoter plays a crucial role in viral vector vaccines by driving the transcription of recombinant genes in host cells, such as HEK293 cells. This promoter is utilized in cytomegalovirus (CMV) vectors, which have been explored as vaccine vectors for various pathogens, including influenza and coronaviruses. CMV vectors expressing antigenic peptides or proteins can induce robust immune responses, leading to long-term cellular immunity and humoral responses against respiratory pathogens. The use of CMV as a vaccine vector has shown promising results in generating protective immunity against infectious diseases in animal models, highlighting its potential for human vaccine development. Overall, the CMV promoter in viral vector vaccines is essential for efficient gene expression and the induction of protective immune responses against a range of pathogens.
How does adrenomedullin affect insulin sensitivity and glucose metabolism in individuals with diabetes?
5 answers
Adrenomedullin (ADM) plays a crucial role in glucose metabolism and insulin sensitivity in individuals with diabetes. Elevated ADM levels in diabetic conditions are associated with dysregulation of glucose and lipid metabolism, potentially compromising mitochondrial function in adipocytes. Moreover, ADM levels are upregulated in diabetic patients with complications, indicating a link between ADM and diabetic severity. In patients with dermatomyositis, higher ADM levels are correlated with rapidly progressive interstitial lung disease (ILD) and poor prognosis, suggesting a potential role of ADM as a prognostic biomarker in diabetes-related ILD. Additionally, ADM is involved in regulating hormonal secretion and insulin balance, contributing to the development of diabetes and its complications. Therefore, strategies to modulate ADM levels could be explored to mitigate diabetic complications and improve metabolic outcomes.
Are promoters and enhancers characterised by accessible chromatin?
4 answers
Promoters and enhancers are indeed characterized by accessible chromatin. Accessible chromatin, indicative of active gene regulatory regions, commonly harbors enhancers and promoters. Studies across various species, including humans, mice, pigs, cattle, and bumblebees, have utilized techniques like ATAC-seq to identify and characterize regulatory elements. These elements are often tissue-specific, enriched with binding motifs of specific transcription factors, and crucial for gene expression regulation. The conservation of regulatory elements between species varies, with promoters showing more conservation than distal enhancers. Understanding the chromatin accessibility at promoters of key host factor genes like ACE2 and TMPRSS2 has provided insights into the tropism mechanisms of viruses like SARS-CoV-2, emphasizing the pivotal role of accessible chromatin in gene regulation and disease pathogenesis.
Are promoters and enhancers in humans characterised by accessible chromatin?
4 answers
Promoters and enhancers in humans are indeed characterized by accessible chromatin. Accessible chromatin is strongly associated with active gene regulatory regions, including enhancers and promoters, which are crucial for gene expression control. Studies have shown that the chromatin accessibility landscape differs between inner cell mass (ICM) and trophectoderm (TE) in human preimplantation embryos, highlighting the epigenetic regulation of cell lineage specification during early embryo development. Additionally, genome-wide profiling of chromatin accessibility in Plasmodium falciparum revealed that chromatin accessibility by ATAC-seq is predictive of active transcription and histone marks, aiding in the identification of regulatory regions such as promoters and enhancer-like elements. These findings underscore the importance of accessible chromatin in characterizing promoters and enhancers across different biological contexts in humans.
Ampk activation in L6 cells via mitochondria
4 answers
AMPK activation in L6 cells can be linked to mitochondria through various mechanisms. AMPK activation, induced by compounds like AICAR and caffeine, has been shown to increase mitochondrial biogenesis in L6 myotubes. Additionally, acetic acid has been found to enhance glucose uptake and fatty acid metabolism in skeletal muscle cells through AMPK activation, leading to increased expression of mitochondrial markers like GLUT4 and myoglobin. Furthermore, flavonoids from Psidium guajava leaves have demonstrated significant AMPK activation in L6 cells, suggesting a potential role in regulating mitochondrial function. Overall, AMPK activation in L6 cells appears to play a crucial role in promoting mitochondrial biogenesis and metabolic adaptations, highlighting the intricate connection between AMPK signaling and mitochondrial function in these cells.
How do plants sense phosphate?
5 answers
Plants sense phosphate levels primarily through inositol polyphosphates (InsPs) interacting with SPX domain-containing proteins, such as SPX1. These interactions lead to the inhibition of PHR transcription factors, crucial for maintaining phosphate homeostasis in plants. Additionally, recent research highlights the role of inositol pyrophosphate InsP 8 in regulating the activity of PHR through its interaction with SPX domain proteins. The SPX-InsP signaling module is evolutionarily conserved and plays a vital role in plant Pi transport and signaling systems. Furthermore, advancements in the development of genetically encoded fluorescent sensors, like FLIPPi, enable real-time monitoring of cellular phosphate concentrations in plants, aiding in understanding the molecular mechanisms of Pi transport and homeostasis.