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FOXO1, 3, and 4 as well as their upstream regulator, AKT/p-AKT, was examined in rhesus macaque ovaries of three developmental stages: fetal, prepubertal, and adult
Low FOXO4 expression is associated with recurrence and metastasis of nasopharyngeal carcinoma.
Hsa_circRNA_103809 participates in the regulation of biological functions through the miR-532-3P/FOXO4 axis in the colorectal cancer
FOXO4 is involved in prostate cancer progression, and it can inhibit prostate cancer cell invasion by regulating EMT of prostate cancer cells
Study reports that CK1alpha similarly destabilizes FOXO4 in RAS-mutant cells by phosphorylation at serines 265/268.
In this review, we introduce the regulation of FOXO4 in physiological and pathological conditions. Particularly, the pathophysiological processes and molecular pathways regulated by FOXO4 in the development and progression of cancer are also summarized
The results of this genomic analysis suggest that low FOXO4 expression is a significant risk factor for epileptic seizures in patients with LGGs and is associated with the seizure outcome.
NF-kappaB/snail/YY1/RKIP circuitry regulated by FOXO4 were likely involved in miR-150-induced EMT event.
Negative expression of FoxO3/FoxO4 and lymph node metastasis were the risk factors for the poor prognosis of bladder cancer.
Knockdown of FOXO4 but not FOXO1 expression decreased proteasome activity. Following neural differentiation, the HD-iPSC-derived neural progenitor cells (NPCs) demonstrated lower levels of proteasome activity and FOXO expressions than their WT counterparts. More importantly, overexpression of FOXO4 but not FOXO1 in HD NPCs dramatically enhanced proteasome activity.
Results show that a small subset of lymphoma cells surviving treatment with doxorubicin or phenylbutyrate showed stem cell-like properties and resistance to chemotherapeuty. The overexpression of FOXO4 was found in these surviving cells, and DLBCL patients with FOXO4-positive tumor cells had poor prognosis.
FOXO4 and FOXD3 were shown independently predictive of overall survival in gastric cancer
FoxO1 and FoxO4 antagonize Tat-mediated transactivation of HIV-1 promoter through the repression of Tat protein expression.
FOXO4 has an inhibitory effect in clearcell renal carcinoma cells, at least in part through inducing apoptosis via upregulation of Bim in the mitochondria-dependent pathway.
knockdown of Ku70 inhibited cell proliferation accompanying an increase in p27(kip1) levels through interacting with FOXO4
miR-664 functions as an oncogene miRNA and has an important role in promoting human osteosarcoma cell proliferation by suppressing FOXO4 expression.
The data demonstrated that elevated miR-150 targets FOXO4 expression and therefore regulates multiple genes expression, resulting in cervical cancer cell growth and survival.
Porphyromonas gingivalis-induced reactive oxygen species activate FOXO transcription factors through JNK signalling, and that FOXO1 controls oxidative stress responses, inflammatory cytokine production and cell survival.
Cox regression analysis indicated FoxO4 to be an independent prognostic factor in non-small cell lung cancers and suggested that FoxO4 might inhibit the process of EMT in non-small cell lung cancers, and might therefore be a target for therapy.
FOXOs support the metabolic requirements of normal and tumor cells by promoting IDH1 expression.
data strongly suggest that increased PI3K/AKT-mediated metastatic invasiveness in CaP is associated with FOXO4 loss, and that mechanisms to induce FOXO4 re-expression might suppress CaP metastatic aggressiveness.
These findings suggest that WNK1 is involved in the physiological regulation of mammalian skeletal muscle hypertrophy and atrophy via interactions with FOXO4.
FOXO transcription factors play a salutary role in the protection against the diet-induced fatty liver disease.
FoxOs exacerbate the loss of cancellous bone mass associated with type 1 diabetes.
Foxo1, Foxo3a, and Foxo4 in chondrocytes regulate endochondral bone formation.
The effect of Sirt1 stimulators on osteoclastogenesis was abrogated in cells lacking FoxO1, FoxO3, and FoxO4.
FoxO4 is collectively required to maintain MODYrelated gene networks, which in turn are required to enable a gene expression program that permits proper substrate selection (glucose versus fatty acids) for mitochondrial oxidative phosphorylation.
FoxO4 transcription factor is present during both oocyte and embryo in vivo maturation and FoxOs may regulate in vitro embryo development under stress conditions.
FoxO4 activates Arg1 transcription in endothelial cells in response to MI, leading to downregulation of nitric oxide and upregulation of neutrophil infiltration to the infarct area.
Foxo1, Foxo3, and Foxo4 transcriptional network regulates autophagy and the ubiquitin-proteasome system during muscle atrophy.
Liver-specific ablation of FoxO1,FoxO3 and FoxO4 prevents the induction of glucose-6-phosphatase and the repression of glucokinase during fasting, thus increasing lipogenesis.
FOXO1, FOXO3a and FOXO4, are indispensable for SIRT1-dependent cell survival against oxidative stress.
FoxO1/3/4 transcription factors play important roles in hepatic glucose homeostasis.
Mice lacking Foxo1, -3, and -4 in bipotential progenitors of osteoblast and adipocytes exhibit increased osteoblast number and high bone mass.
Foxk1 promotes muscle progenitor cell proliferation by repressing Foxo4 transcriptional activity and inhibits myogenic differentiation by repressing Mef2 activity.
Genetic ablation of the 3 genes encoding FoxO isoforms 1, 3a, and 4, in myeloid cells resulted in an expansion of the granulocyte/monocyte progenitor compartment and was associated with increased atherosclerotic lesion formation.
FoxO4 inhibits atherosclerosis through bone marrow derived cells, possibly by inhibition of reactive oxygen species and inflammatory cytokines that promote monocyte recruitment and/or retention.
In NIH3T3 cells, tetrahydrocurcumin induced nuclear accumulation of FOXO4
Data show that glomeruli isolated from diabetic db/db mice have increased acetylation of Foxo4, suppressed expression of Sirt1, and increased expression of Bcl2l11 compared to non-diabetic littermates.
Foxo4 may be a useful target for suppression in the treatment of HBV-associated hepatocellular carcinoma cells.
Data indicate that FoxOs work in concert to regulate multiple aspects of hepatic glucose metabolism.
This gene encodes a member of the O class of winged helix/forkhead transcription factor family. Proteins encoded by this class are regulated by factors involved in growth and differentiation indicating they play a role in these processes. A translocation involving this gene on chromosome X and the homolog of the Drosophila trithorax gene, encoding a DNA binding protein, located on chromosome 11 is associated with leukemia. Multiple transcript variants encoding different isoforms have been found for this gene.
similar to Putative fork head domain transcription factor AFX1 (Forkhead box protein O4)
, forkhead box O4
, forkhead box protein O4-like
, fork head domain transcription factor AFX1
, forkhead box protein O4
, myeloid/lymphoid or mixed-lineage leukemia (trithorax homolog, Drosophila); translocated to, 7
, forkhead protein
, myeloid/lymphoid or mixed lineage-leukemia translocation to 7 homolog
, forkhead box O1A