Background: During myocardial ischemia, hypoxia-inducible factors are stabilized and provide protection from ischemia and reperfusion injury. Recent studies show that myocyte-specific hypoxia-inducible factor 2A promotes myocardial ischemia tolerance through induction of epidermal growth factor, amphiregulin. Here, the authors hypothesized that hypoxia-inducible factor 2A may enhance epidermal growth factor receptor 1 (ERBB1) expression in the myocardium that could interface between growth factors and its effect on providing tolerance to ischemia and reperfusion injury. Methods: Human myocardial tissues were obtained from ischemic heart disease patients and normal control patients to compare ERBB1 expression. Myocyte-specific Hif2a or ErbB1 knockout mice were generated to observe the effect of Hif2a knockdown in regulating ERBB1 expression and to examine the role of ERBB1 during myocardial ischemia and reperfusion injury. Results: Initial studies of myocardial tissues from patients with ischemic ...
Definition of hypoxia-inducible factor 1, alpha subunit in the Definitions.net dictionary. Meaning of hypoxia-inducible factor 1, alpha subunit. What does hypoxia-inducible factor 1, alpha subunit mean? Information and translations of hypoxia-inducible factor 1, alpha subunit in the most comprehensive dictionary definitions resource on the web.
... skin of mice influences vascular resistance and it is correlated with homeostatic regulation of nitric oxide synthesis. 34). On the other hand, HIF-2 deletion in keratinocytes (= 10) considerably reduced basal systolic (103 mmHg) and diastolic (82 mmHg) stresses, leading to systemic hypotension. Fig. 3. Murine keratinocyte manifestation of HIF-1/-2 subunits modulates systemic blood circulation pressure. (< 0.01) and diastolic (111 mmHg vs. 89 mmHg, < 0.01) bloodstream stresses were significantly increased in day time 14 in Ang-IICtreated WT mice in comparison with vehicle-treated settings (Fig. S6= 7) there is a significant upsurge in both systolic (187 mm/Hg vs. 170 mm/Hg) and diastolic (138 mmHg vs. 119 mmHg) bloodstream stresses weighed against littermate settings (Fig. 4= 7), where substantial safety against Ang-IICinduced hypertension was noticed, with attenuation in both systolic and diastolic ...
The vascular endothelial growth factors (VEGF) plays major roles during tumor development. VEGF expression is regulated by the transcription factor HIF (hypoxia inducible factor) which is very sensitive to oxygene variations. We will show here that HIF1alpha is today a good prognostic and diagnostic marker for an increasing number of cancers from various origins. Furthermore, the reduction of the expression or the activity of HIF1alpha impairs tumour angiogenesis and subsequently growth. Altogether, these results suggest that HIF1alpha could be an interesting target in cancer therapy.
accepted 12 December 2013. Abstract. Background: Lymphomas are B and/or T cell clonal neoplasms in various states of differentiation, characteristically compromising lymph nodes. They are constituted by B and T lymphocytes that reach the node by chemokine-mediated recruitment including CXCL13. Hypoxia-inducible transcription factor (HIF-1α) plays a role in cellular adaptation to oxygen concentration changes. It also regulates expression of chemokines such as CXCL12, CCL20, and CCL5 as well as some of their receptors such as CCR7 and CXCR4.. Methods: We performed in silico analysis of the CXCL13 promoter, pharmacologic modulation of HIF-1α activity and, using reporter plasmids, site-directed mutation and DNA-protein interaction analysis we analyzed the relation between HIF-1α activity and CXCL13 expression. Moreover, we did tissue microarray and immunohistochemistry to see the expression of HIF-1α and CXCL13.. Results: This study detected three possible HIF-1α binding sites suggesting that ...
intestinal epithelial cells (IECs) present in the metabolic state of low oxygen tension is called "physiological hypoxia." An important factor in maintaining intestinal homeostasis is a transcription factor hypoxia-inducible factor (HIF), which is stabilized under hypoxic conditions and mediate the homeostatic response to low oxygen tension IEC. To identify the target HIF transcription in IEC, chromatin immunoprecipitation (CHIP) is performed in Caco-2 IECs using HIF-1α […]. ...
Title: Hypoxia Inducible Factor-1 as a Therapeutic Target in Cerebral Ischemia. VOLUME: 4 ISSUE: 3. Author(s):Penelope Aguilera, Edgar Vazquez-Contreras, Carlos Daniel Gomez-Martínez and Maria Elena Chanez Cardenas. Affiliation:Laboratorio de Patologia Vascular Cerebral, Instituto Nacional de Neurologia y Neurocirugia Manuel Velasco Suarez. Av Insurgentes Sur 3877, Mexico D.F. 14269, Mexico.. Keywords:Hypoxia inducible factor, ischemic preconditioning, prolyl hydroxylase, cerebral ischemia. Abstract: Cerebral ischemia is the third leading cause of death in industrialized countries and an important health system problem with no efficient treatment to date. The reduction in oxygen and glucose supply triggers a cascade of events such as excitotoxicity, oxidative stress, inflammation, apoptosis, and an adjustment of the gene expression program. The hypoxia inducible factor-1 (HIF-1) is a transcription factor that mediates the adaptive responses to the reduction in oxygen availability. HIF-1 ...
The transcription factor hypoxia-inducible factor 1 (HIF1), which regulates oxygen homeostasis, is activated by stabilisation of the HIF1α subunit under low-oxygen conditions. Several studies have hinted that HIF1 might also have a role in cell adhesion and motility; now, Roser Buscà and colleagues (p. 2992) establish that HIF1 is important in keratinocyte migration during wound healing. The authors previously used an in vitro scratch-wound assay to show that several targets of HIF1 were upregulated in keratinocyte sheets in response to wounding, and they now show that HIF1α protein levels increase under the same conditions. Moreover, they demonstrate that HIF1α stabilisation is regulated by the PI3K-Akt pathway and, unusually, occurs under normoxic conditions. When HIF1α is depleted by siRNA, keratinocyte migration is impaired; additionally, HIF1α depletion abolishes the scratch-wound-dependent upregulation of the ECM protein laminin-332 (which is important in wound healing). The authors ...
Mitochondria have various essential functions in metabolism and in determining cell fate during apoptosis. In addition, mitochondria are also important nodes in a number of signaling pathways. For example, mitochondria can modulate signals transmitted by second messengers such as calcium. Because mitochondria are also major sources of reactive oxygen species (ROS), they can contribute to redox signaling-for example, by the production of ROS such as hydrogen peroxide that can reversibly modify cysteine residues and thus the activity of target proteins. Mitochondrial ROS production is thought to play a role in hypoxia signaling by stabilizing the oxygen-sensitive transcription factor hypoxia-inducible factor-1α. New evidence has extended the mechanism of mitochondrial redox signaling in cellular responses to hypoxia in interesting and unexpected ways. Hypoxia altered the microtubule-dependent transport of mitochondria so that the organelles accumulated in the perinuclear region, where they ...
When oxygen is limiting, cells adjust their metabolism through the transcription factors hypoxia-inducible factors (HIFs). Loss of function of VHL, a protein necessary to maintain the low abundance of HIFs under normoxic conditions, results in constitutively active HIFs and contributes to some forms of cancer, in particular clear cell renal carcinoma (ccRCC). Li et al. found through metabolomic analysis that primary human ccRCCs had higher glucose metabolism but lower gluconeogenesis than matched normal kidney tissue. The tumors universally had reduced or undetectable amounts of the enzyme fructose-1,6-bisphosphatase 1 (FBP1). Knockdown of endogenous FBP1 enhanced the proliferation of HK-2 cells, a proximal tubule cell line. Ectopic expression of FBP1 (to amounts similar to those in HK-2 cells) in a ccRCC line inhibited tumor growth when xenografted in mice and inhibited anchorage-dependent and anchorage-independent growth in culture. Ectopic expression of FBP1 in ccRCC cells reduced glycolysis ...
The HIF signaling pathway is a crucial way in which tumors can circumvent the constraints of regions of low oxygen (hypoxia) to induce angiogenesis and maintain proliferation. The oxygen regulated subunit of the transcription factor hypoxia-inducible factor 1 (HIF1), HIF1αlpha, is a positive factor in tumor growth and its expression has been correlated with poor patient prognosis in a number of settings.. We here present in vitro and in vivo data for a novel series of orally available small-molecule HIF signaling modulators that show nanomolar inhibition of the HIF signaling pathway in addition to potent anti-proliferative activity against a large number of cell lines derived from solid and blood tumors (EC50 in the range 1-100nM). Phenotypically, the compounds elicit an initial G2/M arrest, followed by the induction of caspase-3/7 and the onset of apoptosis.. The in vitro results also translate into in vivo animal models. The lead compounds from the series show efficacy in tumor xenograft ...
TY - JOUR. T1 - Effects of aging and hypoxia-inducible factor-1 activity on angiogenic cell mobilization and recovery of perfusion after limb ischemia. AU - Bosch-Marce, Marta. AU - Okuyama, Hiroaki. AU - Wesley, Jacob B.. AU - Sarkar, Kakali. AU - Kimura, Hideo. AU - Liu, Ye V.. AU - Zhang, Huafeng. AU - Strazza, Marianne. AU - Rey, Sergio. AU - Savino, Lindsey. AU - Zhou, Yi Fu. AU - McDonald, Karin R.. AU - Na, Youn. AU - Vandiver, Scott. AU - Rabi, Alireza. AU - Shaked, Yuval. AU - Kerbel, Robert. AU - LaVallee, Theresa. AU - Semenza, Gregg L.. PY - 2007/12/1. Y1 - 2007/12/1. N2 - Ischemia is a stimulus for production of angiogenic cytokines that activate local vascular cells and mobilize angiogenic cells to the circulation. These responses are impaired in elderly patients with peripheral arterial disease. Hypoxia-inducible factor (HIF)-1 mediates adaptive responses to ischemia, including production of angiogenic cytokines. In this study, we demonstrate that aging and HIF-1 loss-of-function ...
The kidneys are exposed to hypoxic conditions during development. Hypoxia-inducible factor (HIF), an important mediator of the response to hypoxia, is believed to have an important role in development. However, the relationship between HIF and branching morphogenesis has not been elucidated clearly. In this study, we examined whether HIF regulates kidney development. We harvested kidneys from day 13 rat embryos (E13K5) and cultured the organs under normoxic (20% 02/5% CO2) or hypoxic (5% 02/5% CO2) conditions. We evaluated the kidneys based on morphology and gene expression. El3K5 cultured under hypoxic conditions had significantly more ureteric bud (UB) branching than the E13Ks cultured under normoxic conditions. In addition, the mRNA levels of GDNF and GDNF receptor (GFR-alpha l), increased under hypoxic conditions in E13K5. When we cultured E13Ks( with the HIF-1 alpha inhibitor digoxin or with siRNA targeting HIF-l alpha under hypoxic conditions, we did not observe increased UB branching. In ...
The phosphatidylinositol 3-kinase (PI3K) signaling pathway has inherent oncogenic potential. It is up-regulated in diverse human cancers by either a gain of function in PI3K itself or in its downstream target Akt or by a loss of function in the negative regulator PTEN. However, the complete consequences of this up-regulation are not known. Here we show that insulin and epidermal growth factor or an inactivating mutation in the tumor suppressor PTEN specifically increase the protein levels of hypoxia-inducible factor (HIF) 1alpha but not of HIF-1beta in human cancer cell lines. This specific elevation of HIF-1alpha protein expression requires PI3K signaling. In the prostate carcinoma-derived cell lines PC-3 and DU145, insulin- and epidermal growth factor-induced expression of HIF-1alpha was inhibited by the PI3K-specific inhibitors LY294002 and wortmannin in a dose-dependent manner. HIF-1beta expression was not affected by these inhibitors. Introduction of wild-type PTEN into the PTEN-negative ...
The hypoxia-mediated response of tumours is a major determining factor in growth and metastasis. Understanding tumour biology under hypoxic conditions is crucial for the development of antiangiogenic therapy. Using one of the largest cohorts of rectal adenocarcinomas to date, this study investigated hypoxia-inducible factor-1 alpha (HIF-1 alpha) and HIF-2 alpha protein expression in relation to rectal cancer recurrence and cancer-specific survival. Patients (n = 90) who had undergone surgery for rectal adenocarcinoma, with no prior neoadjuvant therapy or metastatic disease, and for whom adequate follow-up data were available were selected. Microvessel density (MVD), HIF-1 alpha and HIF-2 alpha expressions were assessed immunohistologically with the CD34 antibody for vessel identification and the NB100-131B and NB100-132D3 antibodies for HIF-1 alpha and HIF-2 alpha, respectively. In a multifactorial analysis, results were correlated with tumour stage, recurrence rate and long-term survival. ...
Synthesis and biological evaluation of meta-carborane-containing phenoxyacetanilides as inhibitors of hypoxia-inducible factor (HIF)-1 transcriptional activitySynthesis and biological evaluation of meta-carborane-containing phenoxyacetanilides as inhibitors of hypoxia-inducible factor (HIF)-1 transcriptional activity ...
A great many aspects of the anatomy and physiology of large animals are constrained by the need to match oxygen supply to cellular metabolism and appear likely to involve the regulation of gene expression by oxygen. Some insight into possible underlying mechanisms has been provided by studies of erythropoietin, a haemopoietic growth factor which stimulates red cell production in response to hypoxia. Studies of hypoxia-inducible cis-acting sequences from the erythropoietin gene have led to the recognition of a widespread transcriptional response to hypoxia based on the activation of a DNA-binding complex termed hypoxia-inducible factor-1 (HIF-1). Perturbation of the transcriptional response by particular transition metal ions, iron chelators and certain redox-active agents have suggested a specific oxygen sensing mechanism, perhaps involving a haem protein in a flavoprotein/cytochrome system. In addition to erythropoietin, HIF-1-responsive genes include examples with functions in cellular energy
EGLN1_HUMAN] Cellular oxygen sensor that catalyzes, under normoxic conditions, the post-translational formation of 4-hydroxyproline in hypoxia-inducible factor (HIF) alpha proteins. Hydroxylates a specific proline found in each of the oxygen-dependent degradation (ODD) domains (N-terminal, NODD, and C-terminal, CODD) of HIF1A. Also hydroxylates HIF2A. Has a preference for the CODD site for both HIF1A and HIF1B. Hydroxylated HIFs are then targeted for proteasomal degradation via the von Hippel-Lindau ubiquitination complex. Under hypoxic conditions, the hydroxylation reaction is attenuated allowing HIFs to escape degradation resulting in their translocation to the nucleus, heterodimerization with HIF1B, and increased expression of hypoxy-inducible genes. EGLN1 is the most important isozyme under normoxia and, through regulating the stability of HIF1, involved in various hypoxia-influenced processes such as angiogenesis in retinal and cardiac functionality.[3] [4] [5] [6] [7] ...
A key adaptation to environmental hypoxia is an increase in erythropoiesis, driven by the hormone erythropoietin (EPO) through what is traditionally thought to be primarily a renal response. However, both neurons and astrocytes (the largest subpopulation of glial cells in the CNS) also express EPO following ischemic injury, and this response is known to ameliorate damage to the brain. To investigate the role of glial cells as a component of the systemic response to hypoxia, we created astrocyte-specific deletions of the murine genes encoding the hypoxia-inducible transcription factors HIF-1α and HIF-2α and their negative regulator von Hippel-Lindau (VHL) as well as astrocyte-specific deletion of the HIF target gene Vegf. We found that loss of the hypoxic response in astrocytes does not cause anemia in mice but is necessary for approximately 50% of the acute erythropoietic response to hypoxic stress. In accord with this, erythroid progenitor cells and reticulocytes were substantially reduced in ...
Gene therapy techniques were used to insert a peptide into cultures of human cancer cells that blocked their ability to use the enzyme Hypoxia-inducible factor-1, a heterodimeric transcription factor that enables cell survival under low oxygen conditions by altering the transcription of over 300 genes. Hypoxia inducible factor-1 (HIF-1) is a heterodimeric transcription factor that acts as the master regulator of cellular response to reduced oxygen levels, thus playing a key role in the adaptation, survival, and progression of tumors. There is significant evidence that inhibition of HIF-1 would be beneficial for cancer therapy, since tumor cells must thrive in a microenvironment characterized by lack of oxygen. In previous work, investigators at the University of Southampton (United Kingdom) discovered a cyclic hexapeptide (cyclo-CLLFVY) that inhibited the HIF-1alpha/HIF-1beta protein-protein interaction in vitro and prevented HIF-1-mediated hypoxia-response signaling in cells. This cyclic peptide was
Hypoxia-inducible factor 1 (HIF-1) is found in mammalian cells cultured under reduced O2 tension and is necessary for transcriptional activation mediated by the erythropoietin gene enhancer in hypoxic cells. We show that both HIF-1 subunits are basic-helix-loop-helix proteins containing a PAS domain, defined by its presence in the Drosophila Per and Sim proteins and in the mammalian ARNT and AHR proteins. HIF-1 alpha is most closely related to Sim. HIF-1 beta is a series of ARNT gene products, which can thus heterodimerize with either HIF-1 alpha or AHR. HIF-1 alpha and HIF-1 beta (ARNT) RNA and protein levels were induced in cells exposed to 1% O2 and decayed rapidly upon return of the cells to 20% O2, consistent with the role of HIF-1 as a mediator of transcriptional responses to hypoxia.. ...
TY - JOUR. T1 - Up-regulation of gene expression by hypoxia is mediated predominantly by hypoxia-inducible factor 1 (HIF-1). AU - Greijer, A.E.. AU - Groep, van der, P.. AU - Kemming, D.. AU - Shvarts, A.. AU - Semenza, G.L.. AU - Meijer, G.A.. AU - Wiel, van de, M.A.. AU - Belien, J.A.M.. AU - Diest, van, P.J.. AU - Wall, van der, E.. PY - 2005. Y1 - 2005. U2 - 10.1002/path.1778. DO - 10.1002/path.1778. M3 - Article. C2 - 15906272. VL - 206. SP - 291. EP - 304. JO - Journal of Pathology. JF - Journal of Pathology. SN - 0022-3417. IS - 3. ER - ...
FSH stimulation of granulosa cells (GCs) results in increased hypoxia-inducible factor (HIF)-1alpha protein levels and HIF-1 activity that is necessary for up-regulation of certain FSH target genes including vascular endothelial growth factor. We report that the role of the phosphatidylinositol (PI)-3-kinase/AKT pathway in increasing HIF-1alpha protein in FSH-stimulated GCs extends beyond an increase in mammalian target of rapamycin-stimulated translation. FSH increases phosphorylation of the AKT target mouse double-minute 2 (MDM2); a phosphomimetic mutation of MDM2 is sufficient to induce HIF-1 activity. The PI3-kinase/AKT target forkhead box-containing protein O subfamily 1 (FOXO1) also effects the accumulation of HIF-1alpha as evidenced by the ability of a constitutively active FOXO1 mutant to inhibit the induction by FSH of HIF-1alpha protein and HIF-1 activity. Activation of the PI3-kinase/AKT pathway in GCs by IGF-I is sufficient to induce HIF-1alpha protein but surprisingly not HIF-1 activity.
Poorly oxygenated ( hypoxic) tumors are frequently more aggressive compared to corresponding tumors that are better oxygenated. Adaptation to hypoxia is primarily mediated by two closely related hypoxia inducible transcription factor complexes, HIF-1 and HIF-2, which become stabilized and activated at low oxygen levels. Whether HIF-1 and HIF-2 have different roles in tumorigenesis is an open question and an issue we discuss. With focus on HIF-2, we summarize reported phenotypical changes of HIF genetic models and HIF expression patterns during normal development, in adult non - malignant tissues and in tumors. We further address the much - discussed subject of target gene preferences between HIF-1 and HIF-2, given that both transcription factors bind to the same DNA motif. Finally, we also discuss the observations that the oxygen - sensitive HIF-2 alpha subunit is accumulated and active under non - hypoxic conditions as exemplified by HIF-2 alpha expressing tumor macrophages and neuroblastoma ...
Hypoxia-inducible factor-1alpha is a critical mediator of hypoxia induced apoptosis in cardiac H9c2 and kidney epithelial HK-2 cells. . Biblioteca virtual para leer y descargar libros, documentos, trabajos y tesis universitarias en PDF. Material universiario, documentación y tareas realizadas por universitarios en nuestra biblioteca. Para descargar gratis y para leer online.
References for Abcams Recombinant Human HIF-1 alpha protein (ab48734). Please let us know if you have used this product in your publication
Tumour progression is characterized by massive cellular proliferation associated with alterations of the tumour microenvironment. Hence, the tumour microenvironment is considered to be of great...
Clinical studies using oxygen-sensitive electrodes provided evidence that human tumors contain regions of low pO2. Tumor hypoxia correlates with poor prognosis after treatment (3 , 51) . Recent efforts concentrated on this unique feature of solid tumors to develop antitumor strategies, including the production of drugs that are toxic under hypoxic conditions or the generation of hypoxia-inducible vectors containing concatamerized HRE sites. These vectors activate toxin production under hypoxic conditions (for review, see Ref. 6 ). However, the role of HIF-1α in tumorigenesis is still controversial. Our study provides new information concerning the implication of HIF-1α in tumor growth, vasculogenesis, apoptosis, and differentiation. We generated teratocarcinomas in nude mice by injecting HIF-1α+/+ and HIF-1α−/− ES cells. In agreement with previous publications on HIF-1α-deficient ES cells (52) and on transformed mouse embryonic fibroblasts (52) , our results show that HIF-1α+/+ tumors ...
In the present era of ever-increasing antibiotic resistance and increasingly complex and immunosuppressed patient populations, physicians and
HIF-3 alpha (hypoxia-inducible factor 3-alpha/ HIF3A) represents an isoform of HIF-alpha subunits which heterodimerize with stable beta subunit (HIF-beta) for the regulation of HIF target genes through binding to hypoxia response elements/HRE in the promoter regions.
The hypoxia inducible factor-1 (HIF-1), a heterodimer composed of HIF-1alpha and HIF-1beta, is activated in response to low oxygen tension and serves as the master regulator for cells to adapt to hypoxia. HIF-1 is usually considered to be regulated via degradation of its a-subunit. Recent findings, however, point to the existence of alternative mechanisms of HIF-1 regulation which appear to be important for down-regulating HIF-1 under prolonged and severe oxygen depletion. The aims of my Ph.D. thesis, therefore, were to further elucidate mechanisms involved in such down-regulation of HIF-1. The first part of the thesis addresses the impact of the severity and duration of oxygen depletion on HIF-1alpha protein accumulation and HIF-1 transcriptional activity. A special focus was put on the influence of the transcription factor p53 on HIF-1. I found that p53 only accumulates under prolonged anoxia (but not hypoxia), thus limiting its influence on HIF-1 to severe hypoxic conditions. At low ...
The hypoxia inducible factor-1 (HIF-1), a heterodimer composed of HIF-1alpha and HIF-1beta, is activated in response to low oxygen tension and serves as the master regulator for cells to adapt to hypoxia. HIF-1 is usually considered to be regulated via degradation of its a-subunit. Recent findings, however, point to the existence of alternative mechanisms of HIF-1 regulation which appear to be important for down-regulating HIF-1 under prolonged and severe oxygen depletion. The aims of my Ph.D. thesis, therefore, were to further elucidate mechanisms involved in such down-regulation of HIF-1. The first part of the thesis addresses the impact of the severity and duration of oxygen depletion on HIF-1alpha protein accumulation and HIF-1 transcriptional activity. A special focus was put on the influence of the transcription factor p53 on HIF-1. I found that p53 only accumulates under prolonged anoxia (but not hypoxia), thus limiting its influence on HIF-1 to severe hypoxic conditions. At low ...
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This study explored the possibility that upregulation of Hypoxia Inducible Factor-1 (Hif-1)-responsive genes in Human Umbilical Vein Endothelial Cells (HUVEC) would promote and stabilize HUVEC formation into inchoate vascular beds within artificial collagen gels. This experiment was designed to explore the above possibility by sub-cloning Hif-1α, the related chimeric construct Hif-1α/VP16, and the marker gene dsRed into retroviral expression vectors, producing retroviral vectors containing these genes, and stably transducing HUVEC using these retroviruses. Transduced HUVEC were to be observed in cell culture as well as after implantation into artificial collagen gels that have previously supported vascular bed formation by HUVEC. Our results show, preliminarily, that HUVEC transduced with Hif-1α/VP16 go into cell-cycle arrest. Attempts to transduce HUVEC with Hif-1α failed to achieve high enough transduction efficiency to determine the cells angiogenic potential. This study concluded that more
Hypoxia inducible factor-1 (HIF-1) is a key regulator in hypoxia. It has been suggested to be a critical regulator of neurological outcomes following ischemic s...
Inflammation is a primary response to injury and or infection, allowing the body to eliminate pathogens and/or damaged tissue and to initiate repair processes. Low oxygen levels, or hypoxia, is a key feature of inflamed tissue and is due to damage to the local vasculature and increased oxygen consumption by pathogens and infiltrating immune cells. In addition to being a feature of inflammation, hypoxia also induces and regulates the inflammatory response by inducing the release of inflammatory cytokines, directing immune cell infiltration, and tuning the responses of the immune cells themselves. These effects are largely mediated by a family of hypoxia-inducible transcription factors (HIFs), which serve as the master regulators of cellular responses to inadequate oxygenation and HIFs and their regulatory factors are now emerging as therapeutic targets in a number of disease states. Reviews in this series discuss the roles of hypoxia and HIFs in the regulation of inflammatory pathways, immune ...
Inflammation is a primary response to injury and or infection, allowing the body to eliminate pathogens and/or damaged tissue and to initiate repair processes. Low oxygen levels, or hypoxia, is a key feature of inflamed tissue and is due to damage to the local vasculature and increased oxygen consumption by pathogens and infiltrating immune cells. In addition to being a feature of inflammation, hypoxia also induces and regulates the inflammatory response by inducing the release of inflammatory cytokines, directing immune cell infiltration, and tuning the responses of the immune cells themselves. These effects are largely mediated by a family of hypoxia-inducible transcription factors (HIFs), which serve as the master regulators of cellular responses to inadequate oxygenation and HIFs and their regulatory factors are now emerging as therapeutic targets in a number of disease states. Reviews in this series discuss the roles of hypoxia and HIFs in the regulation of inflammatory pathways, immune ...
Inflammation is a primary response to injury and or infection, allowing the body to eliminate pathogens and/or damaged tissue and to initiate repair processes. Low oxygen levels, or hypoxia, is a key feature of inflamed tissue and is due to damage to the local vasculature and increased oxygen consumption by pathogens and infiltrating immune cells. In addition to being a feature of inflammation, hypoxia also induces and regulates the inflammatory response by inducing the release of inflammatory cytokines, directing immune cell infiltration, and tuning the responses of the immune cells themselves. These effects are largely mediated by a family of hypoxia-inducible transcription factors (HIFs), which serve as the master regulators of cellular responses to inadequate oxygenation and HIFs and their regulatory factors are now emerging as therapeutic targets in a number of disease states. Reviews in this series discuss the roles of hypoxia and HIFs in the regulation of inflammatory pathways, immune ...
Inflammation is a primary response to injury and or infection, allowing the body to eliminate pathogens and/or damaged tissue and to initiate repair processes. Low oxygen levels, or hypoxia, is a key feature of inflamed tissue and is due to damage to the local vasculature and increased oxygen consumption by pathogens and infiltrating immune cells. In addition to being a feature of inflammation, hypoxia also induces and regulates the inflammatory response by inducing the release of inflammatory cytokines, directing immune cell infiltration, and tuning the responses of the immune cells themselves. These effects are largely mediated by a family of hypoxia-inducible transcription factors (HIFs), which serve as the master regulators of cellular responses to inadequate oxygenation and HIFs and their regulatory factors are now emerging as therapeutic targets in a number of disease states. Reviews in this series discuss the roles of hypoxia and HIFs in the regulation of inflammatory pathways, immune ...
Inflammation is a primary response to injury and or infection, allowing the body to eliminate pathogens and/or damaged tissue and to initiate repair processes. Low oxygen levels, or hypoxia, is a key feature of inflamed tissue and is due to damage to the local vasculature and increased oxygen consumption by pathogens and infiltrating immune cells. In addition to being a feature of inflammation, hypoxia also induces and regulates the inflammatory response by inducing the release of inflammatory cytokines, directing immune cell infiltration, and tuning the responses of the immune cells themselves. These effects are largely mediated by a family of hypoxia-inducible transcription factors (HIFs), which serve as the master regulators of cellular responses to inadequate oxygenation and HIFs and their regulatory factors are now emerging as therapeutic targets in a number of disease states. Reviews in this series discuss the roles of hypoxia and HIFs in the regulation of inflammatory pathways, immune ...
Inflammation is a primary response to injury and or infection, allowing the body to eliminate pathogens and/or damaged tissue and to initiate repair processes. Low oxygen levels, or hypoxia, is a key feature of inflamed tissue and is due to damage to the local vasculature and increased oxygen consumption by pathogens and infiltrating immune cells. In addition to being a feature of inflammation, hypoxia also induces and regulates the inflammatory response by inducing the release of inflammatory cytokines, directing immune cell infiltration, and tuning the responses of the immune cells themselves. These effects are largely mediated by a family of hypoxia-inducible transcription factors (HIFs), which serve as the master regulators of cellular responses to inadequate oxygenation and HIFs and their regulatory factors are now emerging as therapeutic targets in a number of disease states. Reviews in this series discuss the roles of hypoxia and HIFs in the regulation of inflammatory pathways, immune ...
Inflammation is a primary response to injury and or infection, allowing the body to eliminate pathogens and/or damaged tissue and to initiate repair processes. Low oxygen levels, or hypoxia, is a key feature of inflamed tissue and is due to damage to the local vasculature and increased oxygen consumption by pathogens and infiltrating immune cells. In addition to being a feature of inflammation, hypoxia also induces and regulates the inflammatory response by inducing the release of inflammatory cytokines, directing immune cell infiltration, and tuning the responses of the immune cells themselves. These effects are largely mediated by a family of hypoxia-inducible transcription factors (HIFs), which serve as the master regulators of cellular responses to inadequate oxygenation and HIFs and their regulatory factors are now emerging as therapeutic targets in a number of disease states. Reviews in this series discuss the roles of hypoxia and HIFs in the regulation of inflammatory pathways, immune ...
Insight into Hypoxia Tolerance in Cowpea Bruchid: Metabolic Repression and Heat Shock Protein Regulation via Hypoxia-Inducible Factor 1. . Biblioteca virtual para leer y descargar libros, documentos, trabajos y tesis universitarias en PDF. Material universiario, documentación y tareas realizadas por universitarios en nuestra biblioteca. Para descargar gratis y para leer online.
As well documented,15 the overall activity of HIF-1 is determined by the level of intracellular HIF-1α. In the past decade, the mechanisms of HIF-1α regulation have become a field of intense research and much information concerning it has been gained. In this study, we show that differentiation-inducing concentrations of ATRA rapidly increase HIF-1α protein but not its mRNA during the induced differentiation of both NB4 and U937 cells. ATRA also significantly increased the accumulation of HIF-1α protein induced by tetracycline withdrawal in engineered U937 cells, in which expression of HIF-1α mRNA was not under the control of the endogenous promoter of HIF-1α gene. Of note, NB4 and U937 cells presented different dynamic courses of changes in HIF-1α protein levels: the increase of HIF-1α protein was rapid but transitory in ATRA-treated NB4 cells, while ATRA induced a lasting increase of HIF-1α protein in U937 cells. All these observations indicate that ATRA accumulates HIF-1α protein ...
Scientists revealed that CD55 is a novel target of hypoxia-inducible factor HIF-2α in neuroblastoma (NB) cells. They showed that HIF-2α expression is sufficient to sustain stem-like features of NB cells, whereas CD55 protein upon HIF-2α expression contributes to growth of colonies and to invasion of cells, but not to stemness features. [Oncogenesis ...
Reactome is pathway database which provides intuitive bioinformatics tools for the visualisation, interpretation and analysis of pathway knowledge.
The tumor immune response is in a dynamic balance between antitumor mechanisms, which serve to decrease cancer growth, and the protumor inflammatory response, which increases immune tolerance, cell survival, and proliferation. Hypoxia and expression of HIF-1α and HIF-2α are characteristic features of all solid tumors. HIF signaling serves as a major adaptive mechanism in tumor growth in a hypoxic microenvironment. HIFs represent a critical signaling node in the switch to protumorigenic inflammatory responses through recruitment of protumor immune cells and altered immune cell effector functions to suppress antitumor immune responses and promote tumor growth through direct growth-promoting cytokine production, angiogenesis, and ROS production. Modulating HIF function will be an important mechanism to dampen the tumor-promoting inflammatory response and inhibit cancer growth.. ...
Biotinylated peptides derived from the HIF-1α oxygen-dependent degradation domain Biotin-Ahx-DLDLEALAPYIPADDDFQL or a hydroxylated control peptide Biotin-Ahx-DLDLEALAP[OH]YIPADDDFQL are immobilized on streptavidin-coated microplate. Tissue samples are homogenized in our tissue extraction buffer. Supernatants of the tissue homogenates are mixed with proprietary reaction buffer and incubated in the microplate. Peptide hydroxylation is recognized by a rabbit antibody specific for HIF-1α [Hydroxy Pro564] peptide, and detected with a donkey anti-rabbit HRP-conjugated secondary antibody. Upon the addition of the TMB substrate, the intensity of color is proportional to the activity of PHD2 in the samples. Positive and negative controls allow for assay quality assurance ...
In embryonic stem (ES) cell tumors, the hypoxia-inducible transcription factor, HIF- 1[alpha], has been shown to be a tumor suppressor, and HIF-1[alpha]-expressing cells have been shown to localize preferentially in vivo ...
Sigma-Aldrich offers abstracts and full-text articles by [Christian Hanna, Susan C Hubchak, Xiaoyan Liang, Benaya Rozen-Zvi, Paul T Schumacker, Tomoko Hayashida, H William Schnaper].