A5048704899- Cancer, Hypoxia, and Metabolism
- Cancer-related Molecular Pathways
- Angiogenesis and VEGF in Cancer
- Protein Kinase Regulation and GTPase Signaling
- Adipose Tissue and Metabolism
- Ubiquitin and proteasome pathways
- High Altitude and Hypoxia
- Mitochondrial Function and Pathology
- RNA modifications and cancer
- melanin and skin pigmentation
- Cell death mechanisms and regulation
- Neuroinflammation and Neurodegeneration Mechanisms
- Cancer-related molecular mechanisms research
- Nanoparticle-Based Drug Delivery
- Eicosanoids and Hypertension Pharmacology
- PARP inhibition in cancer therapy
- Reproductive Biology and Fertility
- Endoplasmic Reticulum Stress and Disease
- Cancer Research and Treatments
- Metabolism, Diabetes, and Cancer
- Cancer-related gene regulation
- Hemoglobin structure and function
- RNA Research and Splicing
- Adrenal and Paraganglionic Tumors
- Sphingolipid Metabolism and Signaling
CIC bioGUNE
2016-2025
Centro de Investigación Biomédica en Red de Cáncer
2020-2024
Instituto de Salud Carlos III
2024
Ikerbasque
2024
Centre National de la Recherche Scientifique
1999-2009
Inserm
2009
Hôpital Européen Georges-Pompidou
2009
Paris Cardiovascular Research Center
2009
Université Paris Cité
2009
Université Côte d'Azur
2007-2009
Hypoxia-inducible factor-1 (HIF-1) controls the expression of a number genes such as vascular endothelial growth factor and erythropoietin in low oxygen conditions. However, molecular mechanisms that underlie activation limiting subunit, HIF-1α, are still poorly resolved. Results showing endogenous HIF-1α migrated 12 kDa higher than vitrotranslated protein led us to evaluate possible role phosphorylation on this phenomenon. We report here is strongly phosphorylated vivo responsible for...
Hypoxia is a feature of the microenvironment growing tumor. The transcription factor NFkappaB activated in hypoxia, an event that has significant implications for tumor progression. Here, we demonstrate hypoxia activates through pathway involving activation IkappaB kinase-beta (IKKbeta) leading to phosphorylation-dependent degradation IkappaBalpha and liberation NFkappaB. Furthermore, increasing pool and/or potential IKKbeta, amplifies cellular sensitivity stimulation with TNFalpha. Within...
Recent evidence demonstrates that the protein kinase C & ( P K ) isoform is required for activation of nuclear factor KB (NF-KB) and mitogenic signaling in Xenopus oocytes mammalian cells.The mechanism whereby regulates NF-KB most probably involves a putative IKB molecular mass -50 kDa, which phosphorylates inactivates IKB.Tumor necrosis (TNFa) interleukin-1, besides activating phospholipase C-mediated breakdown phosphatidylcholine, also generate ceramide, produced by stimulation...
Hypoxia-inducible factor-1 (HIF-1) controls the expression of a number genes such as vascular endothelial growth factor (VEGF) and Erythropoietin in low oxygen conditions (hypoxia). VEGF is strongly induced at both mRNA protein level by hormones factors smooth muscle cells (VSMC) independently environment. However, role HIF-1α this induction has not been studied. We report here that levels are increased fetal calf serum quiescent VSMC. More interestingly, Angiotensin II (Ang II), thrombin,...
Considerable attention has recently been focused on the role played by different kinase cascades in control of apoptosis. The triggering stress-activated kinases concomitant with inhibition extracellular signal-regulated (ERK) pathway observed a number cell systems undergoing programmed death. In addition, activation phosphoinositide 3-kinase (PI 3-kinase)-Akt signaling cascade shown to protect from Here we have explored potential ERK stress as well possible cross-talk PI HeLa cells. We show...
Cell adaptation to changes in oxygen (O 2 ) availability is controlled by two subfamilies of O -dependent enzymes: the hypoxia inducible factor (HIF)–prolyl and asparaginyl hydroxylases [prolyl domain (PHDs) inhibiting HIF (FIH)]. These sensors regulate activity HIF, a transcriptional complex central homeostasis. In well oxygenated cells, PHDs hydroxylate HIFα subunits, thereby targeting them for proteasomal degradation. contrast, acute inhibits PHDs, leading stabilisation. However, here we...
Nuclear factor kappa B (NF-kappa B) plays a critical role in the regulation of number genes. NF-kappa is heterodimer 50- and 65-kDa subunits sequestered cytoplasm complexed to inhibitory protein I B. Following stimulation cells, dissociates from B, allowing its translocation nucleus, where it carries out transactivation function. The precise mechanism controlling activation involvement members kinase C (PKC) family isotypes have previously been investigated. It was found that phorbol...
The zeta isoform of protein kinase C (zeta PKC) has been shown to be involved in the maturation Xenopus oocytes and mitogenic signaling fibroblasts. PKC also regulates important transcription factor nuclear kappa B, most probably by phosphorylation inhibitory molecule I B. mechanisms that control activity are still poorly characterized. This is not activated diacylglycerol but potently stimulated vitro products phosphatidylinositol 3-kinase (PI 3-kinase), which suggests at least one critical...
Hypoxia stabilizes HIF-1alpha (Hypoxia Inducible Factor-1alpha), which then triggers the expression of several genes involved in many aspects cancer progression, including metabolic adaptation, cell survival and angiogenesis. The aim our study was to evaluate impact CA IX (carbonic anhydrase IX) (one its target genes) on prognosis treatment outcome patients with breast cancer. Because extreme O2-dependent instability protein, we first validated staining using xenograft tumours that were...
In melanocytes and melanoma cells alpha-melanocyte stimulating hormone (alpha-MSH), via the cAMP pathway, elicits a large array of biological responses that control melanocyte differentiation influence development or susceptibility. this work, we show transcriptionally activates Hif1a gene in cell-specific manner increases expression functional hypoxia-inducible factor 1alpha (HIF1alpha) protein resulting stimulation Vegf expression. Interestingly, report melanocyte-specific transcription...
During progression of type 2 diabetes, pancreatic β cells are subjected to sustained metabolic overload. We postulated that this state mediates a hypoxic phenotype driven by hypoxia-inducible factor-1α (HIF-1α) and treatment with the HIF-1α inhibitor PX-478 would improve cell function. Our studies showed protein was present in diabetic mouse models. In islets high glucose metabolism, emergence intracellular Ca2+ oscillations at low concentration abnormally basal release insulin were...
Stability of the vascular endothelial growth factor (VEGF) mRNA is tightly regulated through its 3′-untranslated region (3′-UTR). Here, we demonstrate that VEGF levels are increased by anisomycin, a strong activator stress-activated protein kinases. Hence, induction inhibited SB202190, an inhibitor JNK and p38/HOG kinase. Furthermore, expression in cells overexpress increase stability. We show two different approaches anisomycin exerts effect on 3′-UTR. First, using vitro degradation assay,...