María Laura García Bermejo - Academia.edu (original) (raw)

Papers by María Laura García Bermejo

A monoclonal antibody against-GSDMB (AbGB) that was previously characterized by our group (1) and... more A monoclonal antibody against-GSDMB (AbGB) that was previously characterized by our group (1) and an irrelevant mouse IgG of the same isotype (IgG2b, kindly provided by the Antibody Unit-CNIO, Spain) were purified on a Hi-trap Protein G column (GE Healthcare, UK) and quantified spectrophotometrically (NanoDrop® 2000, Thermo-Fisher Scientific). The AbGB was labeled fluorescently using the FITC Fast Conjugation Kit (Abcam) according to the manufacturer's instructions. Additionally, the whole amino acid sequences of the gasdermin B isoform3 was obtained from the Uniprot database (2). From the FASTA query sequence, the secondary and tertiary structures, as well as the solvent accessibility and disordered regions, were predicted using RaptorX (3). Two different algorithms were used to predict B-Cell Epitopes, ABCPred (4) based on a neural network and COBEPro (5). Nanocarrier preparation and characterization Nanocapsules (NCs) and nanoemulsions (NEs, used as control) were obtained by spontaneous emulsion. Briefly, an oil phase, composed of a 1:1 ratio (v/v) of the triglyceride Miglyol® 812 and the surfactant Polysorbate® 80. For NCs preparation 8 volumes of an aqueous phase that was composed of hyaluronic acid (HA) conjugated to a dodecylamide functionalized C12 carbon chain and PEG-15 hydroxystearate (Solutol®HS15) was added to, and mixed by magnetic stirring. As such, the final concentration of HA in the NCs was 0.5 mg/ml. The purified AbGB antibody was adsorbed to the surface of the NCs by a physical procedure based on two strategies: (i) electrostatic interactions between the positively charged AbGB (protonated AbGB+) and the negatively charged HA coating; and, (ii) hydrophobic forces, using AbGB close to its isoelectric point (neutral AbGB). Protonated AbGB+ was prepared by acidification in a sodium acetate/acetic acid buffer (pH 3.8) until a final pH of 4.5 was reached. Neutral AbGB (pH 7.4) and protonated AbGB+ (pH 4.5) were associated with the surface of NCs by incubating 150 µL of NCs (10 mg) with 5, 10 and 25 µg of the antibody per mg of NCs at 4 o C with mild horizontal shaking. The irrelevant IgG was also loaded onto NCs through hydrophobic forces. The size, polydispersion index (PDI), and surface charge of the NCs and AbGB-NCs were measured by dynamic light scattering (DLS) and laser Doppler anemometry (Nano-ZS instrument, Malvern, UK). The

Frontiers in Molecular Biosciences

Personalised medicine (PM) presents a great opportunity to improve the future of individualised h... more Personalised medicine (PM) presents a great opportunity to improve the future of individualised healthcare. Recent advances in -omics technologies have led to unprecedented efforts characterising the biology and molecular mechanisms that underlie the development and progression of a wide array of complex human diseases, supporting further development of PM. This article reflects the outcome of the 2021 EATRIS-Plus Multi-omics Stakeholder Group workshop organised to 1) outline a global overview of common promises and challenges that key European stakeholders are facing in the field of multi-omics research, 2) assess the potential of new technologies, such as artificial intelligence (AI), and 3) establish an initial dialogue between key initiatives in this space. Our focus is on the alignment of agendas of European initiatives in multi-omics research and the centrality of patients in designing solutions that have the potential to advance PM in long-term healthcare strategies.

Journal of Investigational Allergy and Clinical Immunology

At the beginning of the Pandemia of SARS-CoV-2, different types of skin lesions were described in... more At the beginning of the Pandemia of SARS-CoV-2, different types of skin lesions were described in patients during the infection period [1]. The first reports of cutaneous manifestations described 6 patterns of skin lesions: maculopapular exanthems, urticarial exanthems, vesicular exanthems, erythema multiforme, cutaneous vasculitis and chilblain-like lesions [2]. Many of this patients were exposed to different treatments and to date, there is no clear understanding on whether some of this skin lesions presented during the so-called "first wave" could be secondary to drug hypersensitivity. We conducted a prospective, observational and descriptive study which main objective was to determine if drug hypersensitivity could be a cause of skin lesions in patients admitted to our hospital due to SARS-CoV-2 infection during the months of march to may 2020. A total of 72 patients with skin lesions were admited to the Allergology and/or Dermatology Department (see supplementary material) during this period of time. Out of this 72 patients, 37 presented possible drug implication following the algorithm of the spanish pharmacovigilance system (ASPS) [4], which evaluates the possible implication of a drug reaction as a cause of the skin lesions. All of these patients had received treatment with azithromycin, hydroxychloroquine, lopinavir/ritonavir and/or betalactam antibiotics. Of the 37 patients, 16 patients consented in continuing the study. The types of lesions observed and reported by histology were maculopapular exanthem (n=5), urticarial exanthem (n=5), vesicular exanthem (n=4), cutaneous vasculitis (n=1) and chilblain-like lesion (n=1). The mean of days since beginning of treatment to skin manifestations was 7.5 days (1-15 days). No patient presented an immediate type reaction during their treatment.

Frontiers in Immunology, 2022

BackgroundCOVID‐19 can generate a broad spectrum of severity and symptoms. Many studies analysed ... more BackgroundCOVID‐19 can generate a broad spectrum of severity and symptoms. Many studies analysed the determinants of severity but not among some types of symptoms. More importantly, very few studies analysed patients highly exposed to the virus that nonetheless remain uninfected.MethodsWe analysed serum levels of ACE2, Angiotensin II and anti-Spike antibodies in 2 different cohorts at high risk of viral exposure, highly exposed but uninfected subjects, either high risk health care workers or persons cohabiting with infected close relatives and seropositive patients with symptoms. We tested the ability of the sera of these subjects to neutralize lentivirus pseudotyped with the Spike-protein.ResultsWe found that the serum levels of ACE2 are significantly higher in highly exposed but uninfected subjects. Moreover, sera from this seronegative persons can neutralize SARS-CoV-2 infection in cellular assays more strongly that sera from non-exposed negative controls eventhough they do not h...

Introduction & Objectives: Despite a significant reduction in metabolism at low temperatures, the... more Introduction & Objectives: Despite a significant reduction in metabolism at low temperatures, the remaining cellular activity requires oxygen. ATP depletion under hypothermic conditions results in cellular injury, irreversible damage and graft loss. Hypothermic machine perfusion (HMP) have improved early graft function. Oxygen during ischemia may exacerbate injury through the production of harmful ROS. The objective is to compare oxygenated HMP (OxHMP) with HMP alone in a porcine model of donation after circulatory death. Materials & Methods: Left kidney of female commercial breed pigs was exposed to 30 minutes of warm ischemia, via vascular clamping and randomized to Ox-HMP vs. HMP (LifePort® kidney transporter). O2 supply was achieved via brief initial (30 min) bubble surface oxygenation. Endpoints considered were miRNA expression in perfusate by real-time PCR; creatinine (Cr) at days 1 and 3 post-KT; graft survival; pO2, lactate and LDH perfusate levels. Lipid peroxidation as an indirect measure of oxidative stress was determined by malondialdehyde (MDA) assay in kidney biopsies pre and post-perfusion. ATP generation was determined in primary cultures of proximal tubule cells from kidney biopsies pre and post perfusion by using XF technology by Seahorse®. Results: 19 animals were included for miRNAS, lipid peroxidation and perfusate composition analysis. 15 animals were finally transplanted (OxHMP=4; HMP=11) and functional and survival data examined. Cr at days 1 (6.5 (1.3)) vs. 7.1 ((5.8) p=0.106) and 3 (12.5 (10.4)) vs. 16.5 ((12.2) p=0.400) were lower in the OxHMP group (nS). Mean survival was 7.

Transplantation Proceedings, 2019

MicroRNAs (miRNAs) are post-transcriptional regulators that have emerged as promising biomarkers ... more MicroRNAs (miRNAs) are post-transcriptional regulators that have emerged as promising biomarkers in kidney transplantation. Quantification of miRNAs can be analyzed by means of biological normalization. The purpose of normalization is to remove technical variation in data, which is not related to the biological changes under investigation. Proper normalization is critical for the correct analysis and interpretation of results. Material and Methods. A prospective cohort study was conducted on graft dysfunction in kidney transplantation from expanded criteria donors. After RNA extraction quantitative real-time polymerase chain reaction was performed. The exogenous spike-in normalization was used as technical normalization. Relative expression was calculated using the 2-DDCt method and UniSp2 spike-in was used as reference for normalization. Results obtained were further analyzed by the application of the mean expression value that uses the calculated mean of all miRNAs in a given sample. Results. The mean expression value approach confirmed the significance of a subset of the miRNAs previously identified for delayed graft function development and composed by miRNAs miR-486-5p, miR-144-3p, miR-142-5p, and miR-144-5p. Conclusions. MicroRNAs are becoming increasingly important as biomarkers in multiple disease processes including kidney transplantation. Perfusion fluid, particularly during hypothermic machine perfusion, provides a valuable pretransplantation source for identification of organ viability biomarkers. Although there is no clear consensus concerning the normalization technique, the mean expression value method shows the better normalization strategy.

Neuropharmacology, 2016

Cannabinoid CB 1 receptor, the molecular target of endocannabinoids and cannabis active component... more Cannabinoid CB 1 receptor, the molecular target of endocannabinoids and cannabis active components, is one of the most abundant metabotropic receptors in the brain. Cannabis is widely used for both recreational and medicinal purposes. Despite the ever-growing fundamental roles of microRNAs in the brain, the possible molecular connections between the CB 1 receptor and microRNAs are surprisingly unknown. Here, by using reporter gene constructs that express interaction sequences for microRNAs in human SH-SY5Y neuroblastoma cells, we show that CB 1 receptor activation enhances the expression of several microRNAs, including let-7d. This was confirmed by measuring hsa-let-7d expression levels. Accordingly, knocking-down CB 1 receptor in zebrafish reduced dre-let-7d levels, and knocking-out CB 1 receptor in mice decreased mmu-let-7d levels in the cortex, striatum and hippocampus. Conversely, knocking-down let-7d increased CB 1 receptor mRNA expression in zebrafish, SH-SY5Y cells and primary striatal neurons. Likewise, in primary striatal neurons chronically exposed to a cannabinoid or opioid agonist, a let-7d-inhibiting sequence facilitated not only cannabinoid or opioid signaling but also cannabinoid/opioid cross-signaling. Taken together, these findings provide the first evidence for a bidirectional link between the CB 1 receptor and a microRNA, namely let-7d, and thus unveil a new player in the complex process of cannabinoid action.

Journal of Diabetes Research, 2013

The role of diabetic nephropathy in the outcome of acute renal injury (AKI) is not well defined. ... more The role of diabetic nephropathy in the outcome of acute renal injury (AKI) is not well defined. Herein we evaluate the outcome of lipopolysaccharide- (LPS-) induced AKI in streptozotocin-induced diabetes, as well as the potential role of Hypoxia Inducible Factor (HIF-1α) in this condition. Although 6 h after LPS injection all mice developed a decrease in renal function, proteinuric diabetic mice showed a better recovery of this parameter throughout the study (72 h). Both HIF-1αand vascular endothelium growth factor (VEGF) were found to be upregulated in diabetic mice. After LPS injection, all animals showed an upregulation of these factors, although it was higher in the diabetic group. Glycated albumin (GA) was found to upregulate HIF-1αin HK-2 cells, which resulted in increased production of VEGF. Interestingly, LPS cooperated with GA to induce HIF-1αupregulation. In conclusion, diabetic mice display a better recovery of AKI after experimental endotoxemia. Moreover, these animals ...

Zenodo (CERN European Organization for Nuclear Research), Dec 31, 2021

Nature Communications, 2020

Pancreatic cancer stem cells (PaCSCs) drive pancreatic cancer tumorigenesis, chemoresistance and ... more Pancreatic cancer stem cells (PaCSCs) drive pancreatic cancer tumorigenesis, chemoresistance and metastasis. While eliminating this subpopulation of cells would theoretically result in tumor eradication, PaCSCs are extremely plastic and can successfully adapt to targeted therapies. In this study, we demonstrate that PaCSCs increase expression of interferon-stimulated gene 15 (ISG15) and protein ISGylation, which are essential for maintaining their metabolic plasticity. CRISPR-mediated ISG15 genomic editing reduces overall ISGylation, impairing PaCSCs self-renewal and their in vivo tumorigenic capacity. At the molecular level, ISG15 loss results in decreased mitochondrial ISGylation concomitant with increased accumulation of dysfunctional mitochondria, reduced oxidative phosphorylation (OXPHOS) and impaired mitophagy. Importantly, disruption in mitochondrial metabolism affects PaCSC metabolic plasticity, making them susceptible to prolonged inhibition with metformin in vivo. Thus, IS...

BMC nephrology, Jan 24, 2007

Mercuric chloride (HgCl2) induces an autoimmune nephritis in the Brown Norway (BN) rats character... more Mercuric chloride (HgCl2) induces an autoimmune nephritis in the Brown Norway (BN) rats characterized by anti-glomerular basement membrane antibodies (anti-GBM Ab) deposition, proteinuria and a severe interstitial nephritis, all evident at day 13 of the disease. We assessed the effects of all-trans retinoic acid (at-RA) in this experimental model. At-RA is a vitamin A metabolite which has shown beneficial effects on several nephropathies, even though no clear targets for at-RA were provided. We separated animals in four different experimental groups (HgCl2, HgCl2+at-RA, at-RA and vehicle). From each animal we collected, at days 0 and 13, numerous biological samples: urine, to measure proteinuria by colorimetry; blood to determine VLA-4 expression by flow citometry; renal tissue to study the expression of VCAM-1 by Western blot, the presence of cellular infiltrates by immunohistochemistry, the IgG deposition by immunofluorescence, and the cytokines expression by RT-PCR. Additionally,...

Oncogene, 2019

Pancreatic ductal adenocarcinoma (PDAC) is an inherently chemoresistant tumor. Chemotherapy leads... more Pancreatic ductal adenocarcinoma (PDAC) is an inherently chemoresistant tumor. Chemotherapy leads to apoptosis of cancer cells, and in previous studies we have shown that tumor-associated macrophage (TAM) infiltration increases following chemotherapy in PDAC. Since one of the main functions of macrophages is to eliminate apoptotic cells, we hypothesized that TAMs phagocytose chemotherapy-induced apoptotic cells and secrete factors, which favor PDAC chemoresistance. To test this hypothesis, primary human PDAC cultures were treated with conditioned media (CM) from monocyte-derived macrophage cultures incubated with apoptotic PDAC cells (MØ Apop CM). MØ Apop CM pretreatment rendered naïve PDAC cells resistant to Gemcitabine-or Abraxane-induced apoptosis. Proteomic analysis of MØ Apop CM identified YWHAZ/14-3-3 protein zeta/delta (14-3-3ζ), a major regulator of apoptotic cellular pathways, as a potential mediator of chemoresistance, which was subsequently validated in patient transcriptional datasets, serum samples from PDAC patients and using recombinant 14-3-3ζ and inhibitors thereof. Moreover, in mice bearing orthotopic PDAC tumors, the antitumor potential of Gemcitabine was significantly enhanced by elimination of TAMs using clodronate liposomes or by pharmacological inhibition of the Axl receptor tyrosine kinase, a 14-3-3ζ interacting partner. These data highlight a unique regulatory mechanism by which chemotherapy-induced apoptosis acts as a switch to initiate a protumor/antiapoptotic mechanism in PDAC via 14-3-3ζ/Axl signaling, leading to phosphorylation of Akt and activation of cellular prosurvival mechanisms. The data presented therefore challenge the idea that apoptosis of tumor cells is therapeutically beneficial, at least when immune sensor cells, such as macrophages, are present.

Journal of Hepatology, 2014

Background and Aims: Integrins bind to the extracellular matrix and mediate the interaction betwe... more Background and Aims: Integrins bind to the extracellular matrix and mediate the interaction between cells and the matrix. b1integrin is a major integrin affecting proliferation and apoptosis. Our aim was to define the function of b1-integrin in hepatocytes. Methods: b1-integrin in the hepatocytes was deleted using transgenic mice carrying albumin attached to cre-recombinase in b1-integrin-floxed mice. Matings over two generation resulted in conditional knockout mice in which b1-integrin was deleted in the hepatocytes only. Results: These showed 77% decrease in b1-integrin mRNA and protein expression in liver and parenchymal-cell fractions. Interestingly, histologic evaluation was consistent with fibrosis development, whereby a significant increase in a-SMA+ cells and protein as well as a 4-fold increase in collagen I and IV protein expression (by Western and IHC) were found. In vitro studies revealed increased collagen I mRNA production and responsiveness to TGF-b by the isolated hepatic stellate cells, but the difference between cells isolated from knockout and control mice diminished with time in culture. This suggests the presence of a stimulatory effect in vivo but not in vitro. Indeed, the most dramatic changes were a 4-fold decrease in TGF-b mRNA associated with a 2-fold increase in active TGF-b protein both in liver lysates and cultured knockout hepatocytes. This was not associated, as one would expect, by increased TGF-bRII expression or increased SMAD3phosphorylation. Conclusions: Taken together, these data suggest that b1-integrin expression in hepatocytes is required for normal TGF-b dynamics and that it normally suppresses a profibrotic TGF-b signal. Thus, b1-integrin in the hepatocytes serves to diminish fibrosis development.

Journal of Biological Chemistry, 2000

Phorbol esters, the activators of protein kinase C (PKC), induce apoptosis in androgen-sensitive ... more Phorbol esters, the activators of protein kinase C (PKC), induce apoptosis in androgen-sensitive LNCaP prostate cancer cells. The role of individual PKC isozymes as mediators of this effect has not been thoroughly examined to date. To study the involvement of the novel isozyme PKC␦, we used a replication-deficient adenovirus (PKC␦AdV), which allowed for a tightly controlled expression of PKC␦ in LNCaP cells. A significant reduction in cell number was observed after infection of LNCaP cells with PKC␦AdV. Overexpression of PKC␦ markedly enhanced the apoptotic effect of phorbol 12myristate 13-acetate in LNCaP cells. PKC␦-mediated apoptosis was substantially reduced by the pan-caspase inhibitor z-VAD and by Bcl-2 overexpression. Importantly, and contrary to other cell types, PKC␦-mediated apoptosis does not involve its proteolytic cleavage by caspase-3, suggesting that allosteric activation of PKC␦ is sufficient to trigger apoptosis in LNCaP cells. In addition, phorbol ester-induced apoptosis was blocked by a kinase-deficient mutant of PKC␦, supporting the concept that PKC␦ plays an important role in the regulation of apoptotic cell death in LNCaP prostate cancer cells.

Experimental Cell Research, 2006

Sublethal renal ischemia induces tubular epithelium damage and kidney dysfunction. Using NRK-52E ... more Sublethal renal ischemia induces tubular epithelium damage and kidney dysfunction. Using NRK-52E rat proximal tubular epithelial cells, we have established an in vitro model, which includes oxygen and nutrients deprivation, to study the proximal epithelial cell response to ischemia. By means of this system, we demonstrate that confluent NRK-52E cells lose monolayer integrity and detach from collagen IV due to: (i) actin cytoskeleton reorganization; (ii) Rac1 and RhoA activity alterations; (iii) Adherens junctions (AJ) and Tight junctions (TJ) disruption, involving redistribution but not degradation of E-cadherin, β-catenin and ZO-1; (iv) focal adhesion complexes (FAC) disassembly, entangled by mislocalization of paxillin and FAK dephosphorylation. Reactive oxygen species (ROS) are generated during the deprivation phase and rapidly balanced at recovery involving MnSOD induction, among others. The use of antioxidants (NAC) prevented FAC disassembly by blocking paxillin redistribution and FAK dephosphorylation, without abrogating AJ or TJ disruption. In spite of this, NAC did not show any protective effect on cell detachment. H 2 O 2 , as a pro-oxidant treatment, supported the contribution of ROS in tubular epithelial cell-matrix but not cell-cell adhesion alterations. In conclusion, ROS-mediated FAC disassembly was not sufficient for the proximal epithelial cell shedding in response to sublethal ischemia, which also requires intercellular adhesion disruption.

Biochemical Pharmacology, 2000

The phorbol ester tumor promoters and related analogs are widely used as potent activators of pro... more The phorbol ester tumor promoters and related analogs are widely used as potent activators of protein kinase C (PKC). The phorbol esters mimic the action of the lipid second messenger diacylglycerol (DAG). The aim of this commentary is to highlight a series of important and controversial concepts in the pharmacology and regulation of phorbol ester receptors. First, phorbol ester analogs have marked differences in their biological properties. This may be related to a differential regulation of PKC isozymes by distinct analogs. Moreover, it seems that marked differences exist in the ligand recognition properties of the C1 domains, the phorbol ester/DAG binding sites in PKC isozymes. Second, an emerging theme that we discuss here is that phorbol esters also target receptors unrelated to PKC isozymes, a concept that has been largely ignored. These novel receptors lacking kinase activity include chimaerins (a family of Rac-GTPase-activating proteins), RasGRP (a Ras exchange factor), and Unc-13/Munc-13 (a family of proteins involved in exocytosis). Unlike the classical and novel PKCs, these "non-kinase" phorbol ester receptors possess a single copy of the C1 domain. Interestingly, each receptor class has unique pharmacological properties and biochemical regulation. Lastly, it is well established that phorbol esters and related analogs can translocate each receptor to different intracellular compartments. The differential pharmacological properties of the phorbol ester receptors can be exploited to generate specific agonists and antagonists that will be helpful tools to dissect their cellular function.

Journal of Biological Chemistry, 2000

We examined the activation of the p38 mitogen-activated protein kinase (p38-MAPK) pathway by the ... more We examined the activation of the p38 mitogen-activated protein kinase (p38-MAPK) pathway by the G protein-coupled receptor agonists, endothelin-1 and phenylephrine in primary cultures of cardiac myocytes from neonatal rat hearts. Both agonists increased the phosphorylation (activation) of p38-MAPK by ‫ف‬ 12-fold. A p38-MAPK substrate, MAPK-activated protein kinase 2 (MAPKAPK2), was activated approximately fourfold and 10 M SB203580, a p38-MAPK inhibitor, abolished this activation. Phosphorylation of the MAPKAPK2 substrate, heat shock protein 25/27, was also increased. Using selective inhibitors, activation of the p38-MAPK pathway by endothelin-1 was shown to involve protein kinase C but not G i /G o nor the extracellularly responsive kinase (ERK) pathway. SB203580 failed to inhibit the morphological changes associated with cardiac myocyte hypertrophy induced by endothelin-1 or phenylephrine between 4 and 24 h. However, it decreased the myofibrillar organization and cell profile at 48 h. In contrast, inhibition of the ERK cascade with PD98059 prevented the increase in myofibrillar organization but not cell profile. These data are not consistent with a role for the p38-MAPK pathway in the immediate induction of the morphological changes of hypertrophy but suggest that it may be necessary over a longer period to maintain the response. Key words: hypertrophy • cardioprotection • mitogenactivated protein kinases • adrenergic agonists • endothelin-1 T he p38-MAPKs, extracellularly responsive kinases (ERKs) 1 and stress-activated protein kinases/c-Jun NH 2-terminal kinases (SAPKs/JNKs) constitute the three best-characterized subgroups of the mitogen-activated protein kinase (MAPK) superfamily (reviewed by

PLoS ONE, 2010

When oxygen becomes limiting, cells reduce mitochondrial respiration and increase ATP production ... more When oxygen becomes limiting, cells reduce mitochondrial respiration and increase ATP production through anaerobic fermentation of glucose. The Hypoxia Inducible Factors (HIFs) play a key role in this metabolic shift by regulating the transcription of key enzymes of glucose metabolism. Here we show that oxygen regulates the expression of the muscle glycogen synthase (GYS1). Hypoxic GYS1 induction requires HIF activity and a Hypoxia Response Element within its promoter. GYS1 gene induction correlated with a significant increase in glycogen synthase activity and glycogen accumulation in cells exposed to hypoxia. Significantly, knockdown of either HIF1a or GYS1 attenuated hypoxia-induced glycogen accumulation, while GYS1 overexpression was sufficient to mimic this effect. Altogether, these results indicate that GYS1 regulation by HIF plays a central role in the hypoxic accumulation of glycogen. Importantly, we found that hypoxia also upregulates the expression of UTP:glucose-1-phosphate urydylyltransferase (UGP2) and 1,4-a glucan branching enzyme (GBE1), two enzymes involved in the biosynthesis of glycogen. Therefore, hypoxia regulates almost all the enzymes involved in glycogen metabolism in a coordinated fashion, leading to its accumulation. Finally, we demonstrated that abrogation of glycogen synthesis, by knock-down of GYS1 expression, impairs hypoxic preconditioning, suggesting a physiological role for the glycogen accumulated during chronic hypoxia. In summary, our results uncover a novel effect of hypoxia on glucose metabolism, further supporting the central importance of metabolic reprogramming in the cellular adaptation to hypoxia.

Frontiers in Molecular Biosciences

Journal of Investigational Allergy and Clinical Immunology

Frontiers in Immunology, 2022

Transplantation Proceedings, 2019

Neuropharmacology, 2016

Journal of Diabetes Research, 2013

Zenodo (CERN European Organization for Nuclear Research), Dec 31, 2021

Nature Communications, 2020

BMC nephrology, Jan 24, 2007

Oncogene, 2019

Journal of Hepatology, 2014

Journal of Biological Chemistry, 2000

Experimental Cell Research, 2006

Biochemical Pharmacology, 2000

Journal of Biological Chemistry, 2000

PLoS ONE, 2010