| 27114850 | Hypoxia stabilizes the expression of hypoxia-inducible transcription factor-1alpha (HIF-1alpha), which controls the expression of hundreds of survival genes related to e |
| 27114850 | Moreover, many stress-related signaling mechanisms, such as oxidative stress and energy metabolic disturbances, as well as the signaling cascades via ceramide, mTOR, NF-kappaB, and TGF-beta pathways, can also induce the expression of HIF-1alpha protein to facilitate cell survival in normoxia |
| 27114850 | Screening studies have indicated that the stabilization of HIF-1alpha increases the expression of distinct histone lysine demethylases (KDM) |
| 27114850 | HIF-1alpha stimulates the expression of KDM3A, KDM4B, KDM4C, and KDM6B, which enhance gene transcription by demethylating H3K9 and H3K27 sites (repressive epigenetic marks) |
| 27114850 | In addition, HIF-1alpha induces the expression of KDM2B and KDM5B, which repress transcription by demethylating H3K4me2,3 sites (activating marks) |
| 27114850 | Hypoxia-inducible KDMs support locally the gene transcription induced by HIF-1alpha, although they can also control genome-wide chromatin landscape, especially KDMs which demethylate H3K9 and H3K27 sites |
| 27114850 | A chronic stimulation of HIF-1alpha can provoke tissue fibrosis and cellular senescence, which both are increasingly present with aging and age-related diseases |
| 26923269 | Over the last decade, extensive studies have demonstrated that SIRT1 can activate several transcriptional factors, such as peroxisome proliferator activated receptor gamma co-activator 1alpha (PGC-1alpha) and hypoxia-inducible factor 1alpha (HIF-1alpha) resulting in ameliorated mitochondria biogenesis and extended life span |
| 26873092 | We found that circ-Foxo3 was mainly distributed in the cytoplasm, where it interacted with the anti-senescent protein ID-1 and the transcription factor E2F1, as well as the anti-stress proteins FAK and HIF1alpha |
| 26873092 | CONCLUSION: We conclude that ID-1, E2F1, FAK, and HIF1alpha interact with circ-Foxo3 and are retained in the cytoplasm and could no longer exert their anti-senescent and anti-stress roles, resulting in increased cellular senescence |
| 26827661 | Thus, we hypothesized that overexpression of Hif-1alpha may improve the vasculogenesis-related phenotype of pbEPCs |
| 26827661 | In the present study, we overexpressed Hif-1alpha in pbEPCs and cbEPCs by using recombinant adenoviruses and investigated effects on stem cell- and vasculogenesis-related cell parameters |
| 26827661 | Overexpression of Hif-1alpha enhanced proliferation, invasion, cell survival and in vitro capillary sprout formation of both EPC populations |
| 26827661 | Migration was increased in cbEPCs upon Hif-1alpha overexpression, but not in pbEPCs |
| 26827661 | Similarly, the colony-formation capacity was much higher in cbEPCs in comparison to pbEPCs and was further increased by Hif-1alpha overexpression, whereas Hif-1alpha transduction exerted no significant influence on colony formation of pbEPCs |
| 26827661 | In summary, our experiments illustrated multifarious effects of Hif-1alpha overexpression on stem cell and vasculogenic parameters |
| 26827661 | Therefore, Hif-1alpha overexpression may represent a therapeutic option to improve cellular functions of adult as well as postnatal EPCs |
| 26826302 | Loss of function study using SENP1 siRNA was performed to investigate the regulatory role of sumoylation on the function of hypoxia inducible factor 1alpha (HIF-1alpha) and the hypoxic tolerance of IVD cells |
| 26826302 | Although downregulation of SENP1 decreased the transcriptional activity of HIF-1alpha, the viability of disc cells showed no significant loss under hypoxia |
| 26057707 | Expression of the hypoxia inducible factors HIF1-alpha (HIF1A gene) and HIF2-alpha (EPAS1 gene) and/or hypoxia-regulated pathways has been shown to promote the undifferentiated phenotype of NBL cells |
| 26057707 | Our hypothesis is that HIF1A and EPAS1 expression represent one of the mechanisms responsible for the lack of responsiveness of NBL to differentiation therapy |
| 26057707 | Clinically, high levels of HIF1A and EPAS1 expression were associated with inferior survival in two NBL microarray datasets, and patient subgroups with lower expression of HIF1A and EPAS1 showed significant enrichment of pathways related to neuronal differentiation |
| 26057707 | In NBL cell lines, the combination of all-trans retinoic acid (ATRA) with HIF1A or EPAS1 silencing led to an acquired glial-cell phenotype and enhanced expression of glial-cell differentiation markers |
| 26057707 | Furthermore, HIF1A or EPAS1 silencing might promote cell senescence independent of ATRA treatment |
| 25699017 | These gene products include mTOR, IKK-beta/NF-kappaB complex, and HIF-1alpha, an important cellular survival signal |
| 25699017 | One of the actions of succinate is to stabilize the hypoxia and cellular stress conditions by inducing the transcriptional regulator HIF-1alpha |
| 25077541 | We demonstrate that miR-17 targets both ADCY5 and IRS1, upregulating the downstream signals MKP7, FoxO3, LC3B, and HIF1alpha, and downregulating mTOR, c-myc, cyclin D1, and JNK |
| 25077541 | Repression of ADCY5 by miR-17 translocated membrane-bound RGS2 into the nucleus, promoting interactions of RGS2 with HIF1alpha and the MKP7 promoter, enhancing MKP7 transcription |
| 24729935 | Studies have identified alterations in the level or activity of factors such as SIRT1, PGC-1alpha, HIF-1alpha and c-MYC involved in key regulatory processes in the maintenance of mitochondrial structural integrity, biogenesis and function |
| 23764844 | Gamma rays induce a p53-independent mitochondrial biogenesis that is counter-regulated by HIF1alpha |
| 23764844 | Although the main effector of the response to gamma-rays is the p53-p21 axis, we demonstrated that mitochondrial biogenesis is only indirectly regulated by p53, whose activation triggers a murine double minute 2 (MDM2)-mediated hypoxia-inducible factor 1alpha (HIF1alpha) degradation, leading to the release of peroxisome-proliferator activated receptor gamma co-activator 1beta inhibition by HIF1alpha, thus promoting mitochondrial biogenesis |
| 23764844 | Mimicking hypoxia by HIF1alpha stabilization, in fact, blunts the mitochondrial response to gamma-rays as well as the induction of p21-mediated cell senescence, indicating prevalence of the hypoxic over the genotoxic response |
| 23764844 | Finally, we also show in vivo that post-radiotherapy mitochondrial DNA copy number increase well correlates with lack of HIF1alpha increase in the tissue, concluding this may be a useful molecular tool to infer the trigger of a hypoxic response during radiotherapy, which may lead to failure of activation of cell senescence |
| 23119050 | We have also assessed HIF-1alpha, p38-MAPK and CD36 immunostaining in the mucosa of patients with inflammatory bowel disease |
| 23119050 | Addition of a p38-MAPK inhibitor significantly reduced the increase in CD36 and TSP-1 expression provoked by hypoxia and decreased HIF-1alpha stabilization in macrophages |
| 23119050 | Immunohistochemical studies revealed CD36, HIF-1alpha and p38-MAPK expression in the mucosa of patients with inflammatory bowel disease |
| 23119050 | A positive and significant correlation between HIF-1alpha and CD36 expression and CD36 and p38-MAPK expression was observed in cells of the lamina propria of the damaged mucosa |
| 22847439 | Suppression of geroconversion was p53- and HIF-1-independent, as hypoxia also suppressed geroconversion in cells lacking functional p53 and HIF-1alpha |
| 22130126 | BACKGROUND: Tumor hypoxia is a common feature of prostate tumors associated with the stabilization of hypoxia-inducible-factor 1alpha (HIF-1alpha) and poor prognosis following radiation therapy |
| 22130126 | These modified cellular responses appeared mediated by HIF-1alpha |
| 21746877 | Cyclin E-induced morphogenesis arrest is dependent upon hypoxia-inducible factor 1alpha (HIF-1alpha), which itself is induced by high cyclin E both in cultured mammary acini and in mammary epithelial tissues in a mouse model of deregulated cyclin E expression |
| 21746877 | We next determined that E2F activity directly regulates and is required for induction of HIF1A by cyclin E |
| 21746877 | Additionally, we found that cyclin E deregulation in mammary acini decreases, in an E2F-independent manner, expression of the EGLN1 prolyl hydroxylase that regulates HIF-1alpha degradation within the VHL ubiquitin ligase pathway |
| 21286718 | The combination could also inhibit the expression of Cyclin D1 and phosphorylated mTOR while had no impact on p53, p16, PTEN, and HIF-1alpha |
| 21239881 | We have recently shown that the oxygen dependent transcription factor hypoxia inducible factor 1alpha (Hif1alpha) is essential for maintenance of functional levels of telomerase in murine embryonic stem cells (mES) |
| 21239881 | Importantly, long-term proliferation of mES cells with reduced Hif1alpha levels led to telomere shortening and ultimately cell senescence |
| 19584087 | In association with these phenotypic changes and the absence of HIF-1 alpha protein expression, we have demonstrated significant increases in global levels of DNA methylation and H3K9 histone acetylation in these cells, concomitant with the increased expression of DNA methyltransferase DMNT3b and gene-specific changes in DNA methylation at key imprinting loci |
| 17998063 | Increasingly clear is an important regulatory role for hypoxia-inducible factor 1alpha (HIF-1alpha) in the expression of the cytokine/growth factor macrophage migration inhibitory factor (MIF) |
| 17998063 | The functional significance of hypoxia-induced MIF expression is revealed by findings demonstrating that HIF-1alpha-dependent MIF expression is necessary for hypoxia-induced evasion from cell senescence and that MIF is necessary for HIF-1alpha stabilization induced by hypoxia and prolyl hydroxylase (PHD) inhibitors |
| 17142669 | HIF1alpha delays premature senescence through the activation of MIF |
| 17142669 | We have investigated the role of the hypoxia-inducible factor 1alpha (HIF1alpha) transcription factor in preventing senescence in aerobic and hypoxic conditions |
| 17142669 | Using embryonic fibroblasts from a conditional HIF1alpha knockout mouse, we found that loss of HIF1alpha under aerobic conditions significantly accelerated the onset of cellular senescence, and decreased proliferation under hypoxia |
| 17142669 | Furthermore, we identify the macrophage migration inhibitory factor (MIF) as a crucial effector of HIF1alpha that delays senescence |
| 17142669 | Inhibition of MIF phenocopies loss of HIF1alpha |
| 17142669 | Our findings highlight a novel role for HIF1alpha under aerobic conditions, and identify MIF as a target responsible for this function |
| 16915281 | PML inhibits HIF-1alpha translation and neoangiogenesis through repression of mTOR |
| 16915281 | We demonstrate that in hypoxic conditions PML acts as a negative regulator of the synthesis rate of hypoxia-inducible factor 1alpha (HIF-1alpha) by repressing mammalian target of rapamycin (mTOR) |
| 16827160 | The data demonstrated that, in all cell types assayed, either hypoxia or CoCl2 induced the main regulator of transcriptional responses to reduced oxygen tension, namely the hypoxia inducible factor-1alpha (HIF-1alpha), in a dose- and time-dependent manner |
| 16827160 | In the immortalized HDFs, the transcriptional activity of HIF-1alpha was also evident by the accumulation of its main downstream gene targets, namely erythropoietin (EPO) and the vascular endothelial growth factor (VEGF) |
| 16827160 | Interestingly, the immortalized HDFs were found to exhibit higher HIF-1alpha endogenous levels and induction, following cell exposure to hypoxic conditions, as compared to either young or senescent cells |
| 16161047 | Induction of human endometrial cancer cell senescence through modulation of HIF-1alpha activity by EGLN1 |
