Relevant bibliographies by topics / Forkhead Box Protein O1

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Book chapters
  4. Conference papers
  5. Reports

Academic literature on the topic 'Forkhead Box Protein O1'

Author: Grafiati
Published: 4 June 2021
Last updated: 4 February 2022

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources on the topic 'Forkhead Box Protein O1.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Journal articles on the topic "Forkhead Box Protein O1"

1

Zhu, Wan Long, Honglian Tong, Jing Tsong Teh, and Mei Wang. "Forkhead Box Protein O3 Transcription Factor Negatively Regulates Autophagy in Human Cancer Cells by Inhibiting Forkhead Box Protein O1 Expression and Cytosolic Accumulation." PLoS ONE 9, no. 12 (December 29, 2014): e115087. http://dx.doi.org/10.1371/journal.pone.0115087.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Stenman, Adam, Timothy Murtha, Reju Korah, and Tobias Carling. "Suppression of Forkhead Box Protein O1 (FOXO1) Transcription Factor May Promote Adrenocortical Tumorigenesis." Hormone and Metabolic Research 49, no. 08 (June 22, 2017): 631–37. http://dx.doi.org/10.1055/s-0043-110143.

Full text
Abstract:
AbstractDespite recent comprehensive genetic analyses, molecular evidence for a pathophysiological continuum linking benign adrenocortical adenoma (ACA) and highly aggressive adrenocortical carcinoma (ACC) is still elusive. Using human tumor samples and the established ACC cell line SW-13, this study investigated potential regulatory roles for FOXO transcription factors, in modulating adrenocortical tumorigenesis. Adrenocortical tumor specimens (20 ACAs, 10 ACCs, and 9 normal adrenal tissue samples) obtained from 30 patients were analyzed for ubiquitously expressed FOXO transcription factors, FOXO1 and FOXO3 using qRT-PCR and immunohistochemistry. The SW-13 ACC cells were used to study the phenotypic effects of FOXO regulation in vitro. While FOXO3 expression remained unchanged in ACCs, FOXO1 expression was found to be significantly downregulated in 19/20 ACAs and 9/10 ACCs (p<0.0001 and p<0.05, respectively), suggesting a global role for FOXO1 suppression in promoting and maintaining adrenocortical dedifferentiation. Silencing of FOXO1 in SW-13 cells resulted in significant loss of viability (p<0.001) mediated by apoptosis as determined by quantitative Annexin V immunofluorescence analysis (p<0.01). FOXO1 silencing also augmented the migratory behavior of SW-13 cells (p<0.0001), suggesting distinct roles for FOXO1 in promoting viability and controlled motility of adrenocortical cells.
APA, Harvard, Vancouver, ISO, and other styles
3

Chen, Qing, Mingjian Lu, Bobby R. Monks, and Morris J. Birnbaum. "Insulin Is Required to Maintain Albumin Expression by Inhibiting Forkhead Box O1 Protein." Journal of Biological Chemistry 291, no. 5 (December 14, 2015): 2371–78. http://dx.doi.org/10.1074/jbc.m115.677351.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Han, G. H., D. Chung, D. B. Chay, H. Cho, S. Kim, and J. H. Kim. "Prognostic assessment of forkhead box protein O1 (FOXO1) and paired box 3 (PAX3) in epithelial ovarian cancer." Gynecologic Oncology 159 (October 2020): 113. http://dx.doi.org/10.1016/j.ygyno.2020.05.123.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Wang, Ying, Jing Tong, Dawei Zou, Bing Chang, Baifang Wang, and Bingyuan Wang. "Elevated expression of forkhead box protein O1 (FoxO1) in alcohol-induced intestinal barrier dysfunction." Acta Histochemica 115, no. 6 (July 2013): 557–63. http://dx.doi.org/10.1016/j.acthis.2012.12.005.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Zhang, Xiaojun, Lusheng Jiang, and Huimin Liu. "Forkhead Box Protein O1: Functional Diversity and Post-Translational Modification, a New Therapeutic Target?" Drug Design, Development and Therapy Volume 15 (May 2021): 1851–60. http://dx.doi.org/10.2147/dddt.s305016.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Ward, Erin C., Anna V. Hoekstra, Leen J. Blok, P. Hanifi-Moghaddam, John R. Lurain, Diljeet K. Singh, Barbara M. Buttin, Julian C. Schink, and J. Julie Kim. "The Regulation and Function of the Forkhead Transcription Factor, Forkhead Box O1, Is Dependent on the Progesterone Receptor in Endometrial Carcinoma." Endocrinology 149, no. 4 (December 20, 2007): 1942–50. http://dx.doi.org/10.1210/en.2007-0756.

Full text
Abstract:
In many type I endometrial cancers, the PTEN gene is inactivated, which ultimately leads to constitutively active Akt and the inhibition of Forkhead box O1 (FOXO1), a member of the FOXO subfamily of Forkhead/winged helix family of transcription factors. The expression, regulation, and function of FOXO1 in endometrial cancer were investigated in this study. Immunohistochemical analysis of 49 endometrial tumor tissues revealed a decrease of FOXO1 expression in 95.9% of the cases compared with the expression in normal endometrium. In four different endometrial cancer cell lines (ECC1, Hec1B, Ishikawa, and RL95), FOXO1 mRNA was expressed at similar levels; however, protein levels were low or undetectable in Ecc1, Ishikawa, and RL95 cells. Using small interfering RNA technology, we demonstrated that the low levels of FOXO1 protein were due to the involvement of Skp2, an oncogenic subunit of the Skp1/Cul1/F-box protein ubiquitin complex, given that silencing Skp2 increased FOXO1 protein expression in Ishikawa cells. Inhibition of Akt in Ishikawa cells also increased nuclear FOXO1 protein levels. Additionally, progestins increased FOXO1 protein levels, specifically through progesterone receptor B (PRB) as determined by using stably transfected PRA-specific and PRB-specific Ishikawa cell lines. Finally, overexpression of triple mutant (Tm) FOXO1 in the PR-specific Ishikawa cell lines caused cell cycle arrest and significantly decreased proliferation in the presence and absence of the progestin, R5020. Furthermore, TmFOXO1 overexpression induced apoptosis in PRB-specific cells in the presence and absence of ligand. Taken together, these data provide insight into the phosphoinositide-3-kinase/Akt/FOXO pathway for the determination of progestin responsiveness and the development of alternate therapies for endometrial cancer.
APA, Harvard, Vancouver, ISO, and other styles
8

Cho, Hanbyoul, Gwan Hee Han, and Jae-Hoon Kim. "Prognostic implication of forkhead box protein O1 (FOXO1) and paired box gene 3 (PAX3) in epithelial ovarian cancer." Journal of Global Oncology 5, suppl (October 7, 2019): 61. http://dx.doi.org/10.1200/jgo.2019.5.suppl.61.

Full text
Abstract:
61 Background: Transcriptional factor, Forkhead box protein O1 (FOXO1) has been reported to play an imported role in human cancer, but the role in epithelial ovarian cancer (EOC) has not yet been clarified. Here, we evaluatedthe expression and clinical significance of FOXO1 in EOC. Methods: Immunohistochemical analyses of FOXO1 and PAX3 in 212 in EOCs, 57 borderline ovarian tumors and 153 benign epithelial ovarian tumors and 79 nonadjacent normal epithelial tissues were performed using tissue microarray analysis. The data were compared with clinicopathological variables including the survival of EOC patients. Also, the effect of FOXO1 on cell growth were assessed in EOC cell lines. Results: The expressions of FOXO1 and PAX3 protein were significantly higher in EOC tissues than in nonadjacent normal epithelial tissues, benign tissues and borderline tumors respectively (all p< 0.001). Overexpression of FOXO1 was significantly associated with poor grade ( p = 0.004). FOXO1 expression showed trend of positive correlation with that of PAX3 in EOC tissues ( Spearman’s rho0.118, p= 0.149). Multivariate survival analysis revealed that the high expression of FOXO1 (hazard ratio = 2.74 [95% CI, 1.22–13.10], p = 0.001) could be an independent prognostic factor for overall survival. Most importantly, high expression of both FOXO1 and PAX3 showed high hazard ratio (hazard ratio = 5.53 [95% CI, 2.47–12.40], p< 0.001) for overall survival. In vitro result revealed that knockdown of FOXO1 was associated decreased cell viability and migration. Conclusions: This study reveals that high expression of FOXO1/PAX3 is an indicator of poor prognosis in EOC. Our results not only suggest the promising potential of FOXO1 and PAX3 as a prognostic and survival marker, but also warrant further studies on a possible link between the biological function of FOXO1 and PAX3 of EOC.
APA, Harvard, Vancouver, ISO, and other styles
9

Di Pietro, Natalia, Valentine Panel, Schantel Hayes, Alessia Bagattin, Sunitha Meruvu, Assunta Pandolfi, Lynne Hugendubler, Geza Fejes-Tóth, Aniko Naray-Fejes-Tóth, and Elisabetta Mueller. "Serum- and Glucocorticoid-Inducible Kinase 1 (SGK1) Regulates Adipocyte Differentiation via Forkhead Box O1." Molecular Endocrinology 24, no. 2 (February 1, 2010): 370–80. http://dx.doi.org/10.1210/me.2009-0265.

Full text
Abstract:
Abstract The serum and glucocorticoid-inducible kinase 1 (SGK1) is an inducible kinase the physiological function of which has been characterized primarily in the kidney. Here we show that SGK1 is expressed in white adipose tissue and that its levels are induced in the conversion of preadipocytes into fat cells. Adipocyte differentiation is significantly diminished via small interfering RNA inhibition of endogenous SGK1 expression, whereas ectopic expression of SGK1 in mesenchymal precursor cells promotes adipogenesis. The SGK1-mediated phenotypic effects on differentiation parallel changes in the mRNA levels for critical regulators and markers of adipogenesis, such as peroxisome proliferator-activated receptor γ, CCAAT enhancer binding protein α, and fatty acid binding protein aP2. We demonstrate that SGK1 affects differentiation by direct phosphorylation of Foxo1, thereby changing its cellular localization from the nucleus to the cytosol. In addition we show that SGK1−/− cells are unable to relocalize Foxo1 to the cytosol in response to dexamethasone. Together these results show that SGK1 influences adipocyte differentiation by regulating Foxo1 phosphorylation and reveal a potentially important function for this kinase in the control of fat mass and function.
APA, Harvard, Vancouver, ISO, and other styles
10

Pfleger, Jessica, Ryan C. Coleman, Jessica Ibetti, Rajika Roy, Ioannis D. Kyriazis, Erhe Gao, Konstantinos Drosatos, and Walter J. Koch. "Genomic Binding Patterns of Forkhead Box Protein O1 Reveal Its Unique Role in Cardiac Hypertrophy." Circulation 142, no. 9 (September 2020): 882–98. http://dx.doi.org/10.1161/circulationaha.120.046356.

Full text
Abstract:
Background: Cardiac hypertrophic growth is mediated by robust changes in gene expression and changes that underlie the increase in cardiomyocyte size. The former is regulated by RNA polymerase II (pol II) de novo recruitment or loss; the latter involves incremental increases in the transcriptional elongation activity of pol II that is preassembled at the transcription start site. The differential regulation of these distinct processes by transcription factors remains unknown. Forkhead box protein O1 (FoxO1) is an insulin-sensitive transcription factor that is also regulated by hypertrophic stimuli in the heart. However, the scope of its gene regulation remains unexplored. Methods: To address this, we performed FoxO1 chromatin immunoprecipitation–deep sequencing in mouse hearts after 7 days of isoproterenol injections (3 mg·kg −1 ·mg −1 ), transverse aortic constriction, or vehicle injection/sham surgery. Results: Our data demonstrate increases in FoxO1 chromatin binding during cardiac hypertrophic growth, which positively correlate with extent of hypertrophy. To assess the role of FoxO1 on pol II dynamics and gene expression, the FoxO1 chromatin immunoprecipitation–deep sequencing results were aligned with those of pol II chromatin immunoprecipitation–deep sequencing across the chromosomal coordinates of sham- or transverse aortic constriction–operated mouse hearts. This uncovered that FoxO1 binds to the promoters of 60% of cardiac-expressed genes at baseline and 91% after transverse aortic constriction. FoxO1 binding is increased in genes regulated by pol II de novo recruitment, loss, or pause-release. In vitro, endothelin-1– and, in vivo, pressure overload–induced cardiomyocyte hypertrophic growth is prevented with FoxO1 knockdown or deletion, which was accompanied by reductions in inducible genes, including Comtd1 in vitro and Fstl1 and Uck2 in vivo. Conclusions: Together, our data suggest that FoxO1 may mediate cardiac hypertrophic growth via regulation of pol II de novo recruitment and pause-release; the latter represents the majority (59%) of FoxO1-bound, pol II–regulated genes after pressure overload. These findings demonstrate the breadth of transcriptional regulation by FoxO1 during cardiac hypertrophy, information that is essential for its therapeutic targeting.
APA, Harvard, Vancouver, ISO, and other styles
More sources

Dissertations / Theses on the topic "Forkhead Box Protein O1"

1

Hung, Chien-Min. "mTORC2 Promotes Lipid Storage and Suppresses Thermogenesis in Brown Adipose Tissue in Part Through AKT-Independent Regulation of FoxO1: A Dissertation." eScholarship@UMMS, 2010. http://escholarship.umassmed.edu/gsbs_diss/845.

Full text
Abstract:
Recent studies suggest adipose tissue plays a critical role in regulating whole body energy homeostasis in both animals and humans. In particular, activating brown adipose tissue (BAT) activity is now appreciated as a potential therapeutic strategy against obesity and metabolic disease. However, the signaling circuits that coordinate nutrient uptake and BAT function are poorly understood. Here, I investigated the role of the nutrient-sensing mTOR signaling pathway in BAT by conditionally deleting Rictor, which encodes an essential component of mTOR Complex 2 (mTORC2) either in brown adipocyte precursors or mature brown adipocytes. In general, inhibiting BAT mTORC2 reduces glucose uptake and de novo lipogenesis pathways while increases lipid uptake and oxidation pathways indicating a switch in fuel utilization. Moreover, several key thermogenic factors (Ucp1, Pgc1α, and Irf4) are elevated in Rictor-deficient BAT, resulting in enhanced thermogenesis. Accordingly, mice with mTORC2 loss in BAT are protected from HFD-induced obesity and metabolic disease at thermoneutrality. In vitro culture experiments further suggest that mTORC2 cell-autonomously regulates the BAT thermogenic program, especially Ucp1 expression, which depends on FoxO1 activity. Mechanistically, mTORC2 appears to inhibit FoxO1 by facilitating its lysine-acetylation but not through the canonical AKT-mediated phosphorylation pathway. Finally, I also provide evidence that β-adrenergic signaling which normally triggers thermogenesis also induces FoxO1 deacetylation in BAT. Based on these data, I propose a model in which mTORC2 functions in BAT as a critical signaling hub for coordinating nutrient uptake, fuel utilization, and thermogenic gene expression. These data provide a foundation for future studies into the mTORC2-FoxO1 signaling axis in different metabolic tissues and physiological conditions.
APA, Harvard, Vancouver, ISO, and other styles
2

Hung, Chien-Min. "mTORC2 Promotes Lipid Storage and Suppresses Thermogenesis in Brown Adipose Tissue in Part Through AKT-Independent Regulation of FoxO1: A Dissertation." eScholarship@UMMS, 2016. https://escholarship.umassmed.edu/gsbs_diss/845.

Full text
Abstract:
Recent studies suggest adipose tissue plays a critical role in regulating whole body energy homeostasis in both animals and humans. In particular, activating brown adipose tissue (BAT) activity is now appreciated as a potential therapeutic strategy against obesity and metabolic disease. However, the signaling circuits that coordinate nutrient uptake and BAT function are poorly understood. Here, I investigated the role of the nutrient-sensing mTOR signaling pathway in BAT by conditionally deleting Rictor, which encodes an essential component of mTOR Complex 2 (mTORC2) either in brown adipocyte precursors or mature brown adipocytes. In general, inhibiting BAT mTORC2 reduces glucose uptake and de novo lipogenesis pathways while increases lipid uptake and oxidation pathways indicating a switch in fuel utilization. Moreover, several key thermogenic factors (Ucp1, Pgc1α, and Irf4) are elevated in Rictor-deficient BAT, resulting in enhanced thermogenesis. Accordingly, mice with mTORC2 loss in BAT are protected from HFD-induced obesity and metabolic disease at thermoneutrality. In vitro culture experiments further suggest that mTORC2 cell-autonomously regulates the BAT thermogenic program, especially Ucp1 expression, which depends on FoxO1 activity. Mechanistically, mTORC2 appears to inhibit FoxO1 by facilitating its lysine-acetylation but not through the canonical AKT-mediated phosphorylation pathway. Finally, I also provide evidence that β-adrenergic signaling which normally triggers thermogenesis also induces FoxO1 deacetylation in BAT. Based on these data, I propose a model in which mTORC2 functions in BAT as a critical signaling hub for coordinating nutrient uptake, fuel utilization, and thermogenic gene expression. These data provide a foundation for future studies into the mTORC2-FoxO1 signaling axis in different metabolic tissues and physiological conditions.
APA, Harvard, Vancouver, ISO, and other styles
3

Tong, Ho-kwan. "Functional regulation of the forkhead box M1 transcription factor by Raf/MEK/MAPK signaling." Click to view the E-thesis via HKUTO, 2006. http://sunzi.lib.hku.hk/hkuto/record/B37654597.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Tong, Ho-kwan, and 湯皓鈞. "Functional regulation of the forkhead box M1 transcription factor by Raf/MEK/MAPK signaling." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2006. http://hub.hku.hk/bib/B37654597.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Ricci, Anamaria Ritti. "FOXO3a em leiomioma e leiomiossarcoma uterinos: avaliação de seu potencial para terapia alvo in vitro." Universidade de São Paulo, 2018. http://www.teses.usp.br/teses/disponiveis/5/5139/tde-27022019-123144/.

Full text
Abstract:
Os tumores de musculatura liso do útero se desenvolvem a partir do miométrio e podem apresentar carcterísticas clínicas malignas e benignas. Dentre eles, o leiomiossarcoma (LMS) é o tumor maligno mais comum, com altas taxas de metástase e recidiva, mesmo sendo diagnosticado em estágios iniciais. Já os leiomiomas (LM) são os tumores benignos mais frequentes em mulheres em idade reprodutiva. Ambos possuem mesma diferenciação celular, porém com comportamentos clínico e biológico bastante distintos, e até o momento não se dispõe de tratamento específico ou curativo. Nesse contexto, a busca por novos alvos moleculares pode contribuir não só para um melhor entendimento dessas neoplasias, como também para a descoberta de novas terapias. Em estudo prévio foi observada a expressão aumentada de FOXO3a nos sarcomas uterinos, em comparação aos LMs e ao miométrio adjacente (MM). Além disso, sua expressão foi crescente de acordo com o potencial de malignidade do tumor. Assim, o objetivo do presente estudo foi avaliar in vitro o efeito de terapia alvo específica para FOXO3a em células de LM e LMS. Para isto, linhagens celulares de MM (ATCC PCS-460-011), LM (THESCs - CRL-4003) e LMS (SK-UT-1 - HTB-114) foram caracterizadas quanto à expressão basal de FOXO3a (gene e proteína) e submetidas a tratamento com Genisteína e Metformina ou inativação do gene por siRNA. Os efeitos dos tratamentos foram avaliados por PCR em tempo real, Western Blot, imunocitoquímica, ensaios de proliferação, migração e apoptose. Nossos resultados mostraram que todos os tratamentos realizados interferiram na capacidade de proliferação e migração das células, com maior inibição após as 48 horas nos LMS e 72h nos LM. O efeito obtido na transfecção com siRNA apresentou maior eficiência após 48 h da transfecção nos LMS e 72h nos LM. Os efeitos da inibição de FOXO3a foram maiores na proliferação e migração dos LM, porém os resultados não foram estatisticamente significativos. Dentre as substâncias testadas, a Metformina apresentou maior efeito sobre a proliferação, migração e viabilidade das linhagens celulares. A Genisteína também apresentou efeito inibitório nas células, porém o controle com veículo também apresentou o mesmo efeito citotóxico. De modo geral, os efeitos obtidos com os fármacos, foram tempo e concentração dependentes. Em conjunto, nossos resultados sugerem um relevante do FOXO3a nos tumores de musculatura lisa uterinos, além de apresentá-lo como potencial alvo para terapia específica
Smooth muscle tumors of the uterus develop from the myometrium and may present benign and malignant clinical features. Among them, leiomyosarcoma (LMS) is the most frequent malignant tumor, with high rates of metastasis and relapse, even when diagnosed in early stages. On the other hand, leiomyomas (LM) are the most frequent benign tumors in women of reproductive age. Both have the same cellular differentiation, but with very different clinical and biological behaviors, and so far no specific or curative treatment is available. In this context, the search for new molecular targets can contribute not only for a better understanding of these neoplasms, but also for the discovery of new therapies. In a previous study, increased expression of FOXO3a in uterine sarcomas was observed, compared to LMs and adjacent myometrium (MM). In addition, its expression was increasing according to the malignancy potential of the tumor. Thus, the aim of the present study was to evaluate in vitro, the effect of specific targeted therapy for FOXO3a on LM and LMS cells. For this, MM (ATCC PCS-460-011), LM (THESCs-CRL-4003) and LMS (SK-UT-1-HTB-114) cell lines were characterized for basal expression of FOXO3a (gene and protein) and subsequently submitted to treatment with metformin and genistein, or silencing of FOXO3a by siRNA. The effects of the treatments were evaluated by real-time PCR, Western Blot, immunocytochemistry, proliferation, migration and apoptosis assays. Our results showed that all treatments interfered in the proliferation and migration capacity of the cells, with greater inhibition after 48 hours for LMS and 72 hours LM. The effect obtained in the transfection with siRNA showed higher efficiency after 48 hours of transfection in LMS and 72 hours in LM. The effects of inhibition of FOXO3a were greater in the proliferation and migration of the LM, but the results were not statistically significant. Among the substances tested, Metformin had a greater effect on proliferation, migration and viability of the cell lines. Genistein also had an inhibitory effect on the cells, but the control with the vehicle also presented the same cytotoxic effect. In general, the effects obtained with the drugs were time and concentration dependent. Together, our results suggest a relevant role of FOXO3a in uterine smooth muscle tumors, in addition to presenting it as a potential target for specific therapy
APA, Harvard, Vancouver, ISO, and other styles
6

Rohini, Rajan Meenu. "Unraveling Mechanisms of Insulin Resistance in Type 2 Diabetes in Human Adipocytes : Role of extracellular signal regulated kinase 1/2 (ERK1/2) and forkhead box protein 01 (FOX01)." Doctoral thesis, Linköpings universitet, Avdelningen för cellbiologi, 2016. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-131421.

Full text
Abstract:
Type 2 Diabetes is characterized by hyperglycemia primarily caused due to insulin resistance in insulin responsive tissues and insufficient production of insulin by the β-cells. Insulin resistance appears to develop first in the expanding adipose tissue during caloric surplus and affects other tissues like liver and muscle by ectopic fat accumulation. In spite of significant research in field of insulin signaling, very little has been known about the mechanisms that lead to insulin resistance and T2D. We aim for network-wide knowledge of insulin signaling in human adipocytes and to identify mechanisms that can induce insulin resistance in diabetic individuals. We have herein focused on the transcriptional control of insulin via ERK and FOXO1, and have used mathematical modelling to gain a systems-level understanding of insulin signaling network. Through the work in this thesis, we present for the first time a dynamic comprehensive model for insulin signaling for the adipocytes, for both metabolic and transcriptional control, and that can simulate data from both normal and diabetic individuals. We described insulin regulation of ERK phosphorylation and showed that both its insulin sensitivity and maxima  response to insulin was curtailed in adipocytes from diabetic individuals (Paper I). Our findings indicate that insulin regulated ERK pathway exerts control on transcription not only through phosphorylation of Elk-1 but also through phosphorylation of FOXO1 and exerts translational control via phosphorylation of ribosomal protein S6 (Paper I, II). Furthermore, we showed that insulin-induced FOXO1 phosphorylation or its insulin sensitivity was not impaired in diabetic individuals, although FOXO1 protein level was reduced by 45% in adipocytes from patients with type 2 diabetes. Comprehensive analysis of the detailed insulin signaling model showed that attenuation of the feedback from mTORC1 to IRS1-Ser307 explained dominant part of the insulin resistance seen in adipocytes from diabetic individuals (Paper II). More interestingly, inhibition of FOXO1 with a dominant negative construct of FOXO1, mimicked the diabetic state in the adipocytes, with the similarity extending to both insulin signaling as well as the reduced protein levels, as seen in the diabetic adipocytes. We also show that mTORC1 and FOXO1 maintain each other’s expression/activity in the human adipocytes (Paper II, III). Our findings thus demonstrate that the interplay between mTORC1 and FOXO1 maintains normal insulin signaling in the human adipocytes.
APA, Harvard, Vancouver, ISO, and other styles
7

Chappert, Pascal. "Homéostasie et mécanisme d'action in vivo des lymphocytes T régulateurs CD4+CD25+Foxp3+ chez la souris." Paris 6, 2007. http://www.theses.fr/2007PA066312.

Full text
Abstract:
Homéostasie et mécanisme d’action in vivo des lymphocytes T régulateurs CD4+CD25+Foxp3+ chez la souris Parmi les différentes sous populations de cellules T, les cellules T régulatrices CD4+CD25+ (Tregs), gouvernées par le facteur de transcription Foxp3, représentent un lignage unique de cellules dédiées au maintien de la tolérance immune au soi. Des travaux préalables au sein du laboratoire avaient pu montrer leur potentialité dans le cadre de protocoles d’induction de tolérance à long terme en thérapie génique ou cellulaire vis-à-vis d’un antigène donné chez la souris. Les travaux présentés ici ont porté sur divers aspects fondamentaux du mécanisme d’action et de l’homéostasie de ces cellules in vivo dans ces modèles murins non lymphopéniques. Dans un premier temps, nous avons pu montrer que l’action de Tregs spécifiques de l’antigène de rejet, dans les deux modèles étudiés, passait par une altération profonde de l’activation de la réponse T CD8+, conduisant à une inhibition presque totale de la prolifération et de la différentiation de ces cellules in vivo. Nous avons ensuite étudié les modes de recrutement possible in vivo de Tregs spécifiques d’un antigène et nous avons pu montrer que la simple injection par voie intraveineuse d’un peptide restreint aux molécules du CMH de classe II suffisait à induire l’activation et l’accumulation sélective de T CD4+ CD25+ spécifiques de cet antigène en périphérie. Enfin, nous avons tiré profit d’un modèle murin de souris Foxp3eGFP, développé en collaboration avec le laboratoire du Dr Bernard MALISSEN (CIML Marseille) et dans lequel la protéine GFP a été insérée en aval du locus foxp3 endogène, pour mettre en évidence pour la première fois un phénomène de conversion périphérique de T naïf en Treg dans un répertoire polyclonal.
APA, Harvard, Vancouver, ISO, and other styles
8

Rush, Craig M. "Characterization of MAX and FOXA2 mutations unique to endometrial cancer." The Ohio State University, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=osu1542204873523922.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Chen, Yi-Hsuan, and 陳翌萱. "The Effect of Forkhead box protein M1 (FoxM1) Overexpression on Mitochondrial Dynamics." Thesis, 2014. http://ndltd.ncl.edu.tw/handle/08113938961800944220.

Full text
Abstract:
碩士
國立清華大學
生物科技研究所
102
Mitochondria are highly dynamics organelles that are regulated by fission and fusion processes. Mitochondria are responsible for many important functions in cells, such as ATP synthesis, calcium homeostasis, ROS signaling and apoptosis. More and more studies have revealed that mitochondrial dynamics is closely correlated with cellular events. In addition, mitochondrial fusion and fission imbalance has been linked to cancer formation and metastasis. FoxM1 is a transcription factor which is overexpressed in cancer cell and associates with many characteristic features of cancer, such as cell proliferation, metastasis, angiogenesis and apoptosis resistance. The relations between mitochondrial dynamics and FoxM1 have not been explored. We aim to clarify whether FoxM1 plays a role in tumorigenesis through affecting mitochondrial dynamics. In our study, we found that FoxM1 overexpression triggered adjustment of the balance of mitochondrial fusion and fission. In addition, we found FoxM1 overexpression reduced intracellular and mitochondrial superoxide levels. Furthermore, overexpression of FoxM1 aided the mitochondrial respiration activities under induced oxidative stress conditions. Our results indicated that FoxM1 involves in mitochondrial dynamics and adjustments of mitochondrial activities under stress conditions.
APA, Harvard, Vancouver, ISO, and other styles
10

Tseng, Kuo-Chang, and 曾國彰. "Characterization of the role played by forkhead box protein O3A in colon cancer stem cell." Thesis, 2015. http://ndltd.ncl.edu.tw/handle/14523421877189797597.

Full text
Abstract:
碩士
國立臺灣大學
生化科技學系
103
Cancer stem cell (CSC) is one of the main reasons leading to the recurrence and the metastasis of several cancers. While having abilities as self-renew, quiescence and stress resistance as a normal stem cell, CSC is believed to share many key factors with a normal stem cell. However, due to the less of comprehensive researches and the difficulty in isolation and investigation of CSC, the factors which are essential to the CSC are not yet clear. In this thesis, I tested whether the transcription factor forkhead box protein O3A (FOXO3A), which is known as a necessary factor for normal stem cells, plays an important role in colon CSCs. Through analysis of quiescence population, the knock-down of FOXO3A in colon cancer cell lines decrease the quiescent population of cancer cells. Through sphere forming assay, I also show that the decrease of FOXO3A in cancer cells eliminates the self-renew ability since sphere numbers become significant lower than control. I confirmed that FOXO3A is critical for the maintenance of colon CSCs by promoting self-renew and quiescence. I also show that FOXO3A is constantly activated in colon cancer and independent to AKT/PI3K and TGF/SMAD pathways. Therefore FOXO3A may function in a dose-independent manner. Furthermore, these results indicate that FOXO3A may activate different or even novel gene sets during self-renew in colon CSCs.
APA, Harvard, Vancouver, ISO, and other styles

Book chapters on the topic "Forkhead Box Protein O1"

1

Wang, Haitao, Philip Lazarovici, and Wenhua Zheng. "Forkhead Box Protein O." In Encyclopedia of Signaling Molecules, 1821–36. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_101601.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Wang, Haitao, Philip Lazarovici, and Wenhua Zheng. "Forkhead Box Protein O." In Encyclopedia of Signaling Molecules, 1–16. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4614-6438-9_101601-1.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

"Forkhead Box Protein O1." In Encyclopedia of Signaling Molecules, 1836. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_101305.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

"Forkhead Box O1." In Encyclopedia of Signaling Molecules, 1821. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_101304.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Vicente Dragano, Nathalia Romanelli, and Anne y. Castro Marques. "Native Fruits, Anthocyanins in Nutraceuticals, and the Insulin Receptor/Insulin Receptor Substrate-1/Akt/Forkhead Box Protein Pathway." In Molecular Nutrition and Diabetes, 131–45. Elsevier, 2016. http://dx.doi.org/10.1016/b978-0-12-801585-8.00011-7.

Full text
APA, Harvard, Vancouver, ISO, and other styles

Conference papers on the topic "Forkhead Box Protein O1"

1

Cho, H., GH Han, DB Chay, S. Kim, and J.-H. Kim. "EP865 Forkhead box protein O1 and Paired box gene 3 overexpression is associated with poor prognosis in patients with epithelial ovarian cancer." In ESGO Annual Meeting Abstracts. BMJ Publishing Group Ltd, 2019. http://dx.doi.org/10.1136/ijgc-2019-esgo.914.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Hirani, D. V. B., M. Koch, J. Mohr, K. Dinger, C. Vohlen, C. Klaudt, J. Dötsch, and M. A. Alejandre Alcazar. "Kruppel-Like Factor 4 (Klf4) Is a Novel Regulator of Forkhead Box Protein O1 (FOXO1) and of Neonatal Lung Fibroblast Function and Reduced in Hyperoxia-Induced Lung Injury." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a4444.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Chandra, D., A. Gregory, A. Blumental-Perry, S. Alexander, T. Nyunoya, J. D. Londino, F. C. Sciurba, R. K. Mallampalli, and S. D. Shapiro. "Cigarette Smoke Induces Ubiquitination and Degradation of Forkhead Box Protein P1 (FoxP1) Leading to Increased Endoplasmic Reticulum Stress in Lung Epithelial Cells." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a1216.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Alexander, S. L., A. Maloy, A. Gregory, and D. Chandra. "Cigarette Smoke Causes Forkhead Box Protein P1 (FoxP1) to Be Ubiquitinated and Degraded in Lung Epithelial Cells Resulting in a Dysregulated Endoplasmic Reticulum Stress Response." In American Thoracic Society 2021 International Conference, May 14-19, 2021 - San Diego, CA. American Thoracic Society, 2021. http://dx.doi.org/10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a4275.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Zheng, Ying, and Wilson S. Meng. "Polycation Coated Polymeric Particles as Vehicles of RNA Delivery Into Immune Cells." In ASME 2010 Conference on Smart Materials, Adaptive Structures and Intelligent Systems. ASMEDC, 2010. http://dx.doi.org/10.1115/smasis2010-3714.

Full text
Abstract:
The purpose of this work is to develop a carrier system for delivering RNA molecules aimed to downregulate specific functions in T cells. In many forms of cancer, T cells that express the protein Forkhead Box P3 (Foxp3) are associated with cancer progression. These cells can be identified by CD4 and CD25, molecules express on the cell surface. Studies have shown that downregulation of Foxp3 can increase the ability of other immune cells to destroy tumors. A class of RNA molecules, commonly referred to as “siRNA”, bind to and degrade specific messenger RNA (mRNA) in a sequence-dependent manner such that expression of the encoded protein is terminated. Because mRNA molecules are located inside cells, a carrier system is required to facilitate the uptake of siRNA, which does not passively diffuse through the plasma membrane. To this end, nanosized polymeric particles coated with the polycation, ornithinex10-histidinex6 (or O10H6) were used to adsorb siRNA that bind to the mRNA encoding Foxp3. The RNA-loaded particles are spherical and uniform in size (normally distributed, polydispersity index = 0.072). Loading of RNA to the particles was confirmed using gel electrophoresis. RNA complexed with the particles are protected from serum destabilization: 83.1% of RNA were recovered compared to 36.1% in RNA that were not associated with the particles. Association with the particles increased the uptake of the RNA in mouse T cells from 3.2±0.2% (free RNA) to 20.1±3.9%. Specifically, uptake of the RNA in T cells that express CD4 increased from 2.7±0.2% to 27.1±1.3% when particles were employed. These differences are statistically significant in three experiments conducted (p &lt; 0.01). Internalization of the RNA into T cells was confirmed using confocal imaging. Flow cytometric analysis showed that the particle-complexed RNA reduced the percentage of T cells that express both CD4 and CD25 in mice carrying tumors from 24.0% when free RNA molecules were used to 13.5%. In these cells, the level of Foxp3 mRNA was reduced by 30%. In conclusion, the particles facilitate the uptake of siRNA molecules into a population of T cells that is known to promote cancer growth.
APA, Harvard, Vancouver, ISO, and other styles

Reports on the topic "Forkhead Box Protein O1"

1

Belaguli, Narasimhaswamy S. Forkhead Box Protein 1 (Foxa1) and the Sumoylation Pathway that Regulates Foxa1 Stability are Potential Targets for Breast Cancer Treatment. Fort Belvoir, VA: Defense Technical Information Center, September 2007. http://dx.doi.org/10.21236/ada489768.

Full text
APA, Harvard, Vancouver, ISO, and other styles
You might also be interested in the extended bibliographies on the topic 'Forkhead Box Protein O1' for particular source types:
Journal articles
We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!

To the bibliography