Relevant bibliographies by topics / Hypoxic translation

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic 'Hypoxic translation'

Author: Grafiati
Published: 28 June 2021
Last updated: 15 February 2022

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Journal articles on the topic "Hypoxic translation"

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Melanson, Gaelan, Sara Timpano, and James Uniacke. "The eIF4E2-Directed Hypoxic Cap-Dependent Translation Machinery Reveals Novel Therapeutic Potential for Cancer Treatment." Oxidative Medicine and Cellular Longevity 2017 (2017): 1–12. http://dx.doi.org/10.1155/2017/6098107.

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Hypoxia is an aspect of the tumor microenvironment that is linked to radiation and chemotherapy resistance, metastasis, and poor prognosis. The ability of hypoxic tumor cells to achieve these cancer hallmarks is, in part, due to changes in their gene expression profiles. Cancer cells have a high demand for protein synthesis, and translational control is subsequently deregulated. Various mechanisms of translation initiation are active to improve the translation efficiency of select transcripts to drive cancer progression. This review will focus on a noncanonical cap-dependent translation initiation mechanism that utilizes the eIF4E homolog eIF4E2, a hypoxia-activated cap-binding protein that is implicated in hypoxic cancer cell migration, invasion, and tumor growth in mouse xenografts. A historical perspective about eIF4E2 and its various aliases will be provided followed by an evaluation of potential therapeutic strategies. The recent successes of disabling canonical translation and eIF4E with drugs should highlight the novel therapeutic potential of targeting the homologous eIF4E2 in the treatment of hypoxic solid tumors.
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Blais, Jaime D., Vasilisa Filipenko, Meixia Bi, Heather P. Harding, David Ron, Costas Koumenis, Bradly G. Wouters, and John C. Bell. "Activating Transcription Factor 4 Is Translationally Regulated by Hypoxic Stress." Molecular and Cellular Biology 24, no. 17 (September 1, 2004): 7469–82. http://dx.doi.org/10.1128/mcb.24.17.7469-7482.2004.

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ABSTRACT Hypoxic stress results in a rapid and sustained inhibition of protein synthesis that is at least partially mediated by eukaryotic initiation factor 2α (eIF2α) phosphorylation by the endoplasmic reticulum (ER) kinase PERK. Here we show through microarray analysis of polysome-bound RNA in aerobic and hypoxic HeLa cells that a subset of transcripts are preferentially translated during hypoxia, including activating transcription factor 4 (ATF4), an important mediator of the unfolded protein response. Changes in mRNA translation during the unfolded protein response are mediated by PERK phosphorylation of the translation initiation factor eIF2α at Ser-51. Similarly, PERK is activated and is responsible for translational regulation under hypoxic conditions, while inducing the translation of ATF4. The overexpression of a C-terminal fragment of GADD34 that constitutively dephosphorylates eIF2α was able to attenuate the phosphorylation of eIF2α and severely inhibit the induction of ATF4 in response to hypoxic stress. These studies demonstrate the essential role of ATF4 in the response to hypoxic stress, define the pathway for its induction, and reveal that GADD34, a target of ATF4 activation, negatively regulates the eIF2α-mediated inhibition of translation. Taken with the concomitant induction of additional ER-resident proteins identified by our microarray analysis, this study suggests an important integrated response between ER signaling and the cellular adaptation to hypoxic stress.
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Mao, Xianrong R., and C. Michael Crowder. "Protein Misfolding Induces Hypoxic Preconditioning via a Subset of the Unfolded Protein Response Machinery." Molecular and Cellular Biology 30, no. 21 (August 23, 2010): 5033–42. http://dx.doi.org/10.1128/mcb.00922-10.

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ABSTRACT Prolonged cellular hypoxia results in energy failure and ultimately cell death. However, less-severe hypoxia can induce a cytoprotective response termed hypoxic preconditioning (HP). The unfolded protein response pathway (UPR) has been known for some time to respond to hypoxia and regulate hypoxic sensitivity; however, the role of the UPR, if any, in HP essentially has been unexplored. We have shown previously that a sublethal hypoxic exposure of the nematode Caenorhabditis elegans induces a protein chaperone component of the UPR (L. L. Anderson, X. Mao, B. A. Scott, and C. M. Crowder, Science 323:630-633, 2009). Here, we show that HP induces the UPR and that the pharmacological induction of misfolded proteins is itself sufficient to stimulate a delayed protective response to hypoxic injury that requires the UPR pathway proteins IRE-1, XBP-1, and ATF-6. HP also required IRE-1 but not XBP-1 or ATF-6; instead, GCN-2, which is known to suppress translation and induce an adaptive transcriptional response under conditions of UPR activation or amino acid deprivation, was required for HP. The phosphorylation of the translation factor eIF2α, an established mechanism of GCN-2-mediated translational suppression, was not necessary for HP. These data suggest a model where hypoxia-induced misfolded proteins trigger the activation of IRE-1, which along with GCN-2 controls an adaptive response that is essential to HP.
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Cho, Sung-Yup, Seungun Lee, Jeonghun Yeom, Hyo-Jun Kim, Jin-Haeng Lee, Ji-Woong Shin, Mee-ae Kwon, et al. "Transglutaminase 2 mediates hypoxia-induced selective mRNA translation via polyamination of 4EBPs." Life Science Alliance 3, no. 3 (February 19, 2020): e201900565. http://dx.doi.org/10.26508/lsa.201900565.

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Hypoxia selectively enhances mRNA translation despite suppressed mammalian target of rapamycin complex 1 activity, contributing to gene expression reprogramming that promotes metastasis and survival of cancer cells. Little is known about how this paradoxical control of translation occurs. Here, we report a new pathway that links hypoxia to selective mRNA translation. Transglutaminase 2 (TG2) is a hypoxia-inducible factor 1–inducible enzyme that alters the activity of substrate proteins by polyamination or crosslinking. Under hypoxic conditions, TG2 polyaminated eukaryotic translation initiation factor 4E (eIF4E)-bound eukaryotic translation initiation factor 4E-binding proteins (4EBPs) at conserved glutamine residues. 4EBP1 polyamination enhances binding affinity for Raptor, thereby increasing phosphorylation of 4EBP1 and cap-dependent translation. Proteomic analyses of newly synthesized proteins in hypoxic cells revealed that TG2 activity preferentially enhanced the translation of a subset of mRNA containing G/C-rich 5′UTRs but not upstream ORF or terminal oligopyrimidine motifs. These results indicate that TG2 is a critical regulator in hypoxia-induced selective mRNA translation and provide a promising molecular target for the treatment of cancers.
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Connor, John H., Christine Naczki, Costas Koumenis, and Douglas S. Lyles. "Replication and Cytopathic Effect of Oncolytic Vesicular Stomatitis Virus in Hypoxic Tumor Cells In Vitro and In Vivo." Journal of Virology 78, no. 17 (September 1, 2004): 8960–70. http://dx.doi.org/10.1128/jvi.78.17.8960-8970.2004.

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ABSTRACT Tumor hypoxia presents an obstacle to the effectiveness of most antitumor therapies, including treatment with oncolytic viruses. In particular, an oncolytic virus must be resistant to the inhibition of DNA, RNA, and protein synthesis that occurs during hypoxic stress. Here we show that vesicular stomatitis virus (VSV), an oncolytic RNA virus, is capable of replication under hypoxic conditions. In cells undergoing hypoxic stress, VSV infection produced larger amounts of mRNA than under normoxic conditions. However, translation of these mRNAs was reduced at earlier times postinfection in hypoxia-adapted cells than in normoxic cells. At later times postinfection, VSV overcame a hypoxia-associated increase in α subunit of eukaryotic initiation factor 2 (eIF-2α) phosphorylation and initial suppression of viral protein synthesis in hypoxic cells to produce large amounts of viral protein. VSV infection caused the dephosphorylation of the translation initiation factor eIF-4E and inhibited host translation similarly under both normoxic and hypoxic conditions. VSV produced progeny virus to similar levels in hypoxic and normoxic cells and showed the ability to expand from an initial infection of 1% of hypoxic cells to spread through an entire population. In all cases, virus infection induced classical cytopathic effects and apoptotic cell death. When VSV was used to treat tumors established in nude mice, we found VSV replication in hypoxic areas of these tumors. This occurred whether the virus was administered intratumorally or intravenously. These results show for the first time that VSV has an inherent capacity for infecting and killing hypoxic cancer cells. This ability could represent a critical advantage over existing therapies in treating established tumors.
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Hettiarachchi, Gaya K., Upendra K. Katneni, Ryan C. Hunt, Jacob M. Kames, John C. Athey, Haim Bar, Zuben E. Sauna, Joseph R. McGill, Juan C. Ibla, and Chava Kimchi-Sarfaty. "Translational and transcriptional responses in human primary hepatocytes under hypoxia." American Journal of Physiology-Gastrointestinal and Liver Physiology 316, no. 6 (June 1, 2019): G720—G734. http://dx.doi.org/10.1152/ajpgi.00331.2018.

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The liver is the primary source of a large number of plasma proteins and plays a critical role in multiple biological processes. Inadequate oxygen supply characterizing various clinical settings such as liver transplantation exposes the liver to hypoxic conditions. Studies assessing hypoxia-induced global translational changes in liver are lacking. Here, we employed a recently developed ribosome-profiling technique to assess global translational responses of human primary hepatocytes exposed to acute hypoxic stress (1% O2) for the short term. In parallel, transcriptome profiling was performed to assess mRNA expression changes. We found that translational responses appeared earlier and were predominant over transcriptional responses. A significant decrease in translational efficiency of several ribosome genes indicated translational inhibition of new ribosome protein synthesis in hypoxia. Pathway enrichment analysis highlighted altered translational regulation of MAPK signaling, drug metabolism, oxidative phosphorylation, and nonalcoholic fatty liver disease pathways. Gene Ontology enrichment analysis revealed terms related to translation, metabolism, angiogenesis, apoptosis, and response to stress. Transcriptional induction of genes encoding heat shock proteins was observed within 30 min of hypoxia. Induction of genes encoding stress response mediators, metabolism regulators, and proangiogenic proteins was observed at 240 min. Despite the liver being the primary source of coagulation proteins and the implicated role of hypoxia in thrombosis, limited differences were observed in genes encoding coagulation-associated proteins. Overall, our study demonstrates the predominance of translational regulation over transcription and highlights differentially regulated pathways or biological processes in short-term hypoxic stress responses of human primary hepatocytes.NEW & NOTEWORTHY The novelty of this study lies in applying parallel ribosome- and transcriptome-profiling analyses to human primary hepatocytes in hypoxia. To our knowledge, this is the first study to assess global translational responses using ribosome profiling in hypoxic hepatocytes. Our results demonstrate the predominance of translational responses over transcriptional responses in early hepatic hypoxic stress responses. Furthermore, our study reveals multiple pathways and specific genes showing altered regulation in hypoxic hepatocytes.
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Ron, David, and Alan G. Hinnebusch. "Targeting Translation in Hypoxic Tumors." ACS Chemical Biology 1, no. 3 (April 2006): 145–48. http://dx.doi.org/10.1021/cb600125y.

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Lang, Kenneth J. D., Andreas Kappel, and Gregory J. Goodall. "Hypoxia-inducible Factor-1α mRNA Contains an Internal Ribosome Entry Site That Allows Efficient Translation during Normoxia and Hypoxia." Molecular Biology of the Cell 13, no. 5 (May 2002): 1792–801. http://dx.doi.org/10.1091/mbc.02-02-0017.

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HIF-1α is the regulated subunit of the HIF-1 transcription factor, which induces transcription of a number of genes involved in the cellular response to hypoxia. The HIF-1α protein is rapidly degraded in cells supplied with adequate oxygen but is stabilized in hypoxic cells. Using polysome profile analysis, we found that translation of HIF-1α mRNA in NIH3T3 cells is spared the general reduction in translation rate that occurs during hypoxia. To assess whether the 5′UTR of the HIF-1α mRNA contains an internal ribosome entry site (IRES), we constructed a dicistronic reporter with the HIF-1α 5′UTR inserted between two reporter coding regions. We found that the HIF-1α 5′UTR promoted translation of the downstream reporter, indicating the presence of an IRES. The IRES had activity comparable to that of the well-characterized c-myc IRES. IRES activity was not affected by hypoxic conditions that caused a reduction in cap-dependent translation, and IRES activity was less affected by serum-starvation than was cap-dependent translation. These data indicate that the presence of an IRES in the HIF-1α 5′UTR allows translation to be maintained under conditions that are inhibitory to cap-dependent translation.
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Vumbaca, Frank, Kathryn N. Phoenix, Daniel Rodriguez-Pinto, David K. Han, and Kevin P. Claffey. "Double-Stranded RNA-Binding Protein Regulates Vascular Endothelial Growth Factor mRNA Stability, Translation, and Breast Cancer Angiogenesis." Molecular and Cellular Biology 28, no. 2 (November 26, 2007): 772–83. http://dx.doi.org/10.1128/mcb.02078-06.

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ABSTRACT Vascular endothelial growth factor (VEGF) is a key angiogenic factor expressed under restricted nutrient and oxygen conditions in most solid tumors. The expression of VEGF under hypoxic conditions requires transcription through activated hypoxia-inducible factor 1 (HIF-1), increased mRNA stability, and facilitated translation. This study identified double-stranded RNA-binding protein 76/NF90 (DRBP76/NF90), a specific isoform of the DRBP family, as a VEGF mRNA-binding protein which plays a key role in VEGF mRNA stability and protein synthesis under hypoxia. The DRBP76/NF90 protein binds to a human VEGF 3′ untranslated mRNA stability element. RNA interference targeting the DRBP76/NF90 isoform limited hypoxia-inducible VEGF mRNA and protein expression with no change in HIF-1-dependent transcriptional activity. Stable repression of DRBP76/NF90 in MDA-MB-435 breast cancer cells demonstrated reduced polysome-associated VEGF mRNA levels under hypoxic conditions and reduced mRNA stability. Transient overexpression of the DRBP76/NF90 protein increased both VEGF mRNA and protein levels synthesized under normoxic and hypoxic conditions. Cells with stable repression of the DRBP76/NF90 isoform showed reduced tumorigenic and angiogenic potential in an orthotopic breast tumor model. These data demonstrate that the DRBP76/NF90 isoform facilitates VEGF expression by promoting VEGF mRNA loading onto polysomes and translation under hypoxic conditions, thus promoting breast cancer growth and angiogenesis in vivo.
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Ivanova, Iglika G., Catherine V. Park, and Niall S. Kenneth. "Translating the Hypoxic Response—the Role of HIF Protein Translation in the Cellular Response to Low Oxygen." Cells 8, no. 2 (February 1, 2019): 114. http://dx.doi.org/10.3390/cells8020114.

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Hypoxia-Inducible Factors (HIFs) play essential roles in the physiological response to low oxygen in all multicellular organisms, while their deregulation is associated with human diseases. HIF levels and activity are primarily controlled by the availability of the oxygen-sensitive HIFα subunits, which is mediated by rapid alterations to the rates of HIFα protein production and degradation. While the pathways that control HIFα degradation are understood in great detail, much less is known about the targeted control of HIFα protein synthesis and what role this has in controlling HIF activity during the hypoxic response. This review will focus on the signalling pathways and RNA binding proteins that modulate HIFα mRNA half-life and/or translation rate, and their contribution to hypoxia-associated diseases.
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Dissertations / Theses on the topic "Hypoxic translation"

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Perera, Joseph Kishan Rex. "The eIF4E2-Mediated Hypoxic Protein Synthesis Complex Permits Tumourigenesis in Several Genetically Distinct Cancers." Thesis, Université d'Ottawa / University of Ottawa, 2013. http://hdl.handle.net/10393/26198.

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Identifying exploitable differences between cancer cells and normal cells has been ongoing since the dawn of cancer therapeutics. This task has proven difficult due to the complex genetic makeup of cancers. Tumours, however, share a low oxygen (hypoxic) microenvironment that selects for malignant cancer cells. It has recently been shown that cells switch from eIF4E to eIF4E2-mediated protein synthesis during periods of hypoxia, similar to those found in tumour cores. We hypothesize that this hypoxic translation complex is required for cell survival in hypoxia and can be targeted by inhibiting the eIF4E2 cap-binding protein. Here, we show that genetically diverse cancer cells require the cap-binding protein eIF4E2 for their growth, proliferation, and resistance to apoptosis in hypoxia, but not in normoxia. Furthermore, in vitro and in vivo eIF4E2-depleted tumour models cannot grow or sustain hypoxic regions without the reintroduction of exogenous eIF4E2. Thus, tumour cells could be targeted over somatic cells by selectively inhibiting their protein synthesis machinery, much like the function of antibiotics that revolutionized medicine.
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Kasti, M. "Experimental neuroinflammation : a study of hypoxia and protein translation." Thesis, University College London (University of London), 2013. http://discovery.ucl.ac.uk/1413014/.

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Multiple sclerosis is a chronic inflammatory disease of the CNS associated with widespread primary demyelination and axonal degeneration. The mechanisms underlying the expression of neurological deficits are incompletely understood. Recent histological findings are consistent with a view that active MS lesions may be hypoxic (i.e. suffer a low oxygen concentration). For example, inflammatory ‘Pattern III’ MS lesions express hypoxia inducible factor-1a (HIF-1a), a master regulator of genes whose function is to bias a cell for survival under hypoxic conditions. Hypoxia also results in a number of other consequences designed to limit energy expenditure, including the inhibition of protein translation by the phosphorylation of the eukaryotic initiation factor (eIF-2a), and the formation of stress granules (SGs). Both hypoxia and the inhibition of protein synthesis could cause neurological deficits and thus contribute to the neurological deficits of MS. The aim of the present study is to explore experimental models of MS for evidence of a) hypoxia and b) inhibition of protein translation. The experimental models of inflammatory demyelinating lesions were induced either by the intraspinal injection of lipopolysaccharide (LPS) into the rat dorsal column (LPS-DC, focal lesion), or by immunization of rats or mice to induce experimental autoimmune encephalomyelitis (EAE, disseminated lesions). Animals were examined daily for the expression of any neurological deficit, and tissue hypoxia was detected during life by the systemic administration of pimonidazole, a marker for hypoxia, several hours before termination. Tissue was taken at different stages of lesion development (1-28 days post injection) and examined immunohistochemically for the presence of hypoxia, determined by the expression of binding for pimonidazole, and for the inhibition of protein translation by examining the expression of eIF-2a and SGs. Other markers of disease activity were also examined, including a marker of microglial/macrophage activation (ED-1), HIF-1a, and glucose transporter-1 (GLUT-1). In LPS lesions, labelling for pimonidazole was most intense at the site of injection, 24 hours later. In EAE, labelling for pimonidazole was present as early as 2 days post immunization, but it was expressed more strongly when animals were exhibiting a neurological deficit, subsiding thereafter. In animals injected with LPS, eIF-2a and SGs were expressed most intensely 24 hours post LPS injection, localised to the spinal motor neurons. In EAE, eIF-2a and SGs were expressed in spinal motor neurons, and in cerebellar neurons, at the onset of neurological deficits. These findings reveal for the first time that inflammatory demyelinating lesions are associated with the presence of tissue hypoxia and markers of the inhibition of protein synthesis. It appears that these phenomena may contribute to the expression of neurological deficits, opening new opportunities for therapy.
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Magagnin, Michaël Gaston Pietro. "Cellular adaptation to hypoxia and reoxygenation through gene specific mRNA translation." [Maastricht : Maastricht : Maastricht University] ; University Library, Universiteit Maastricht [host], 2008. http://arno.unimaas.nl/show.cgi?fid=12817.

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Liang, Manfei. "Molecular mechanisms of translational control under hypoxia in Drosophila melanogaster." Doctoral thesis, Universite Libre de Bruxelles, 2021. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/327261.

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Adaptation to variations in oxygen concentration is a conserved mechanism in all metazoans as this process is central for the maintenance of cell and tissue homeostasis. Two major and highly conserved processes contribute to hypoxia-induced gene reprogramming. The first one relies on the transcriptional activation of gene expression by the Hypoxia Inducible Factors (HIFs) leading to the upregulation of a large panel of genes. The second one corresponds to a strong modification of the translation program. While the mechanisms underlying HIF-dependent transcriptional activation have been well characterized, the ones governing translation reprogramming are only partially understood. 
To uncover how mRNA translation takes place at low oxygen tension, we used Drosophila as our research model since both Drosophila flies and S2 cells are highly resistant to low O2. We first demonstrate that several genes are efficiently translated under hypoxia in Drosophila S2 cells. By a gene reporter-based approach, we demonstrate that Ldh mRNA 3’UTR is sufficient to promote reporter mRNA association to polysomes in hypoxia. A deletion analysis of Ldh 3’UTR leads to the identification of a ACAAA-rich sequence important for polysomal association and translation in hypoxia.Cap-binding factors play a key role in controlling translational initiation. We have shown that the cap-binding translation initiation factor eIF4EHP (4EHP) plays a dual role on translation under hypoxic conditions. Despite having a general repressive function on global translation under normoxic and hypoxic conditions, we demonstrated that 4EHP also positively controls the translation of specific mRNAs under hypoxia. Inactivation of 4ehp reduces LDH protein synthesis and impairs reporter mRNA translation in hypoxia. Deletion of 4ehp inhibites the translation of several candidate genes harboring a ACAAA motif in 3’UTR under hypoxia, suggesting that 4EHP is required for hypoxic translation of mRNAs carrying ACAAA-rich motifs. Most interestingly, we observed that 4EHP is strongly enriched in polysomal fractions in hypoxia, further supporting a role of this initiation factor in hypoxic translation. The reduction of 4ehp expression also impairs Drosophila development under hypoxic conditions. Taken together, our results indicate that specific mRNAs can bypass the translational blockade imposed by hypoxic conditions. This process is controlled by mRNA 3’UTR “CA” rich element and is positively regulated by the translation initiation factor 4EHP.
L'adaptation aux variations de la concentration en oxygène est un mécanisme conservé chez tous les métazoaires car ce processus est central pour le maintien de l'homéostasie cellulaire et tissulaire. Deux processus hautement conservés contribuent à la reprogrammation génétique induite par l'hypoxie. Le premier repose sur l'activation transcriptionnelle de l'expression génique par les facteurs inductibles de l'hypoxie (HIF) conduisant à l’induction d'un large panel de gènes. Le second correspond à une forte modification du programme traductionnel. Alors que les mécanismes sous-jacents à l'activation transcriptionnelle dépendante de HIF ont été bien caractérisés, ceux qui régissent la reprogrammation de la traduction ne sont que partiellement compris.Pour découvrir comment la traduction de l'ARNm se déroule à faible tension d'oxygène, nous avons utilisé la drosophile comme modèle d’étude, car les mouches Drosophila melanogaster et les cellules S2 issue de cet organisme sont très résistantes à de faibles teneurs en O2. Nous avons tout d’abord démontré que plusieurs gènes sont efficacement traduits en hypoxie dans les cellules S2 de drosophile. Par une approche basée sur l’utilisation de gènes rapporteurs, nous avons démontré que la région 3’ Non traduite (3’UTR) de l’ARNm Ldh est suffisante pour promouvoir l’association de l’ARNm du rapporteur aux polysomes en conditions hypoxiques. Une analyse par délétion de la région 3’UTR de l’ARNm Ldh a conduit à l’identification d’une séquence riche en ACAAA importante pour l’association polysomale et la traduction en hypoxie. La reconnaissance de la coiffe joue un rôle clé dans le contrôle de l'initiation de la traduction Nous avons montré que le facteur d'initiation de la traduction eIF4EHP (4EHP), qui se lie à la coiffe, joue un double rôle sur la traduction dans des conditions hypoxiques. Bien qu'il ait une fonction répressive sur la traduction générale dans des conditions normoxiques et hypoxiques, nous avons démontré que 4EHP contrôle aussi positivement la traduction d'ARNm spécifiques dans des conditions hypoxiques. L'inactivation de 4ehp réduit la synthèse de la protéine LDH et altère la traduction de l'ARNm rapporteur contenant la partir 3’UTR du messager Ldh en hypoxie. La délétion de 4ehp peut atténuer la traduction de plusieurs gènes candidats contenant un motif ACAAA dans leur région 3’UTR 3' en hypoxie, ce qui suggère que 4EHP est nécessaire pour la traduction hypoxique des ARNm portant des motifs riches en ACAAA. De façon intéressante, nous avons observé que 4EHP est fortement enrichi dans les fractions polysomales en hypoxie, ce qui confirme le rôle de ce facteur d'initiation dans la traduction en hypoxie. La réduction de l'expression de 4ehp altère également le développement de la Drosophile dans des conditions hypoxiques. Ensemble, nos résultats indiquent que des ARNm spécifiques peuvent contourner le blocage traductionnel imposé par les conditions hypoxiques. Ce processus est contrôlé par l'élément riche en "CA" situé dans la partie 3'UTR de l’ARNm et est régulé positivement par le facteur d'initiation de la traduction 4EHP.
Doctorat en Sciences
info:eu-repo/semantics/nonPublished
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Sikarwar, Anurag Singh. "Post-translational modifications of thromboxane receptor G-protein alpha q complex in hypoxic PPHN." American Thoracic Society, 2014. http://hdl.handle.net/1993/31664.

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Introduction: Persistent pulmonary hypertension of the newborn (PPHN) is associated with an elevated thromboxane to prostacyclin ratio, pulmonary artery (PA) hyperreactivity and hypersensitivity. Thromboxane receptor (TP), coupling with G-protein Gαq causes pulmonary vasoconstriction; whereas prostacyclin receptor (IP), coupling with Gαs, causes vasodilation and TP phosphorylation via adenylyl cyclase (AC)-cAMP-protein kinase A (PKA), desensitizes TP. Both TP phosphorylation and Gαq palmitoylation play major roles in regulation of signaling through the TP-Gαq complex. We hypothesized that increased Gαq palmitoylation and decreased AC activity could cause hypoxic TP hyperresponsiveness. We studied the impact of hypoxia on selected post-translational modifications of the receptor-G-protein complex, determining TP vasoconstriction: Gαq palmitoylation, TP phosphorylation and upstream AC activity. Methods: Force responses to thromboxane mimetic U46619, palmitoylation inhibition by 2-bromopalmitate (2-BP) and AC activation (forskolin) were studied by myography in hypoxic PPHN and control newborn swine pulmonary artery. Ca2+ mobilization was studied by fluorescent calcium indicators fura-2AM in pulmonary myocytes (PASMC), and fluo-4NW in HEK293 cells. Effects of hypoxia on Gαq palmitoylation were studied by metabolic labeling. Gαq cysteines and TP serines were mutated to determine sites of post-translational modifications. Protein expression and receptor-G-protein coupling were studied by Western blot and co-immunoprecipitation. PKA activity was assayed; and AC activity quantified. Results: Hypoxia increases Gαq palmitoylation, without increasing total palmitate uptake. Palmitoylation inhibition decreases U46619-stimulated force generation as well as Ca2+ mobilization in PPHN PA rings and hypoxic PASMC. Mutation of palmitoylable cysteine and palmitoylation inhibition proportionately decrease U46619-mediated Ca2+ mobilization in HEK293 cells. TP serine phosphorylation is decreased by hypoxia due to decreased PKA activity; this causes TP hypersensitivity and hyper-reactivity. Serine 324 of TPα is the target of PKA-mediated desensitization. AC activator-induced relaxation is reduced in PPHN PA. Basal and receptor-stimulated AC activity are decreased in hypoxic PASMC. Decreased AC activity is not due to decreased AC expression, ATP availability nor increased Gαi activation. Conclusion: Increased Gαq palmitoylation plays a role in TPα hyper-responsiveness in hypoxic PPHN. Hypoxia also reduces responses to agents acting through AC, unleashing TP-mediated vasoconstriction. Reactivation of pulmonary AC might be useful therapeutically to promote vasodilation and TP desensitization.
October 2016
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Staudacher, Jonas Jaromir [Verfasser]. "Bedeutung des endoplasmatischen Retikulums für die mRNA Translation unter Hypoxie / Jonas Jaromir Staudacher." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2016. http://d-nb.info/1082237574/34.

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Staudacher, Jonas [Verfasser]. "Bedeutung des endoplasmatischen Retikulums für die mRNA Translation unter Hypoxie / Jonas Jaromir Staudacher." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2016. http://d-nb.info/1082237574/34.

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Rispal, Delphine. "Etude des facteurs impliqués dans la terminaison de la traduction et la dégradation des ARNm chez Saccaromyces cerevisiae." Thesis, Paris 11, 2011. http://www.theses.fr/2011PA112128.

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Au cours de mon travail de thèse j’ai étudié la relation entre les facteurs participant à la terminaison de la traduction et ceux participant à la dégradation des ARNm chez S. cerevisiae.D’une part, je me suis intéressée au facteur Tpa1, caractérisé pour son rôle dans la terminaison de la traduction et la stabilité des ARNm chez S. cerevisiae et dont l’homologue chez S. pombe, Ofd1, participe au contrôle de la réponse hypoxique. Je me suis basée sur la structure de ce facteur, établie par nos collaborateurs pour comprendre plus précisément la fonction moléculaire de Tpa1 et rechercher des similitudes avec sa fonction chez S. pombe.Tpa1 est composée de deux domaines de type DSBH dont le premier, contenant le site catalytique, présente des homologies structurales avec la famille des prolyl-hydroxylases.Nous avons reproduit l’effet de la protéine Tpa1 sur la translecture in vivo et montré que son site catalytique prédit, ainsi que la présence des deux domaines étaient nécessaires pour cette activité. Nous avons aussi observé que Tpa1 inhibait par un mécanisme inconnu le facteur de transcription Hap1, qui régule des gènes en fonction de la quantité d’oxygène. Basé sur l’existence d’un inhibiteur d’Ofd1 chez S. pombe, nous avons ensuite montré qu’Ett1 (l’homologue de cet inhibiteur chez S. cerevisiae) avait un rôle similaire à Tpa1 dans la translecture. Une étude structurale collaborative d’Ett1 a mis en évidence une région conservée, se liant à une molécule de sulfate et à un ligand inconnu. Cette région est importante pour la translecture. Cependant, le substrat de Tpa1 reste pour l’instant inconnu comme les rôles précis de Tpa1 et Ett1 dans la terminaison de la traduction et dans la réponse à l’hypoxie.D’autre part, j’ai étudié le processus de NMD, particulièrement en me focalisant sur le mécanisme de discrimination entre un codon stop précoce (PTC) et un codon stop normal, et en analysant également la modification post-traductionnelle d’un facteur central du NMD, Upf1. Nous avons mis en évidence, qu’en plus de la région aval, la région en amont du PTCparticipait à sa reconnaissance. Nous avons testé plusieurs hypothèses sur le rôle de cette région, qui ont confirmé son rôle sans permettre de démontrer un mécanisme définitif. En parallèle, l’étude de la protéine Upf1 s’est concentrée sur ses modifications posttraductionnelles, particulièrement par phosphorylation. En effet, une telle modification est importante chez son homologue humain. Nous avons pu confirmer l’existence d’une forme modifiée et démontrer que celle-ci était localisée entre les acides aminés 153 et 971. Cette modification s’est avérée être très labile ce qui n’a pas permis de confirmer qu’il s’agissait d’une phosphorylation, ni de la cartographier plus précisément
During my PhD thesis, I analyzed the relation between factors that participate intranslation termination and those participating in mRNA decay in yeast S. cerevisiae.First, I focused on Tpa1, that had been proposed to participate in translationtermination and mRNA decay in S. cerevisiae, and whose homologue in S. pombe, Ofd1,participates to the control of hypoxic response. Based on the structure of Tpa1, established byour collaborators, I performed functional analysis to understand more precisely the molecularfunction of Tpa1 and similarities with its role in S. pombe. Tpa1 is composed of two DSBHdomains; the first, which contains the catalytic site, has structural homologies with the familyof prolyl-hydroxylase. We could reproduce the effect of Tpa1 on stop codon readthrough invivo and we showed that the predicted catalytic site and the presence of the two domains ofTpa1 were necessary for its activity. We also showed that Tpa1 inhibited one factor, Hap1,implicated in regulation of gene expression by oxygen. The existence of an inhibitor of Ofd1in S. pombe, allowed the identification of Ett1 (its homologue in S. cerevisiae). We showedthat Ett1 has a role similar to the one of Tpa1 in translational readthrough. A collaborativestructural and functional study of Ett1 revealed a conserved region, which binds a sulfate ion,and an unknown ligand. This region is important for the readthrough. However, thesubstrate(s) of Tpa1 remain(s) for the moment unknown, and the precise roles of Tpa1 andEtt1 in translation termination and in response to hypoxia remain to be deciphered.I also analyzed the NMD process by focusing more particularly on the mechanism thatallows the discrimination between a normal stop and a PTC (premature termination codon)and on the analysis of the post-translational modification of an important factor for the NMD,Upf1. This study revealed that, not only the region downstream of the PTC but also theupstream region participates to its recognition. We have tested several hypotheses on the roleof this upstream region, which confirmed its implication but did not reveal a definitivemechanism. In parallel, we started the study of the post-translational modifications of Upf1,and more particularly by phosphorylation. Indeed, the phosphorylation of Upf1 in human isvery important for the NMD process. We could confirm the presence of a modified form ofyeast Upf1 and we have demonstrated that it was localized between amino acids 153 and 971.This modification appeared to be highly labile. This prevented us to confirm definitively thatit was really a phosphorylation and to cartography precisely its location
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Joshi, Shrinidh Ashokkumar. "Hypoxic Regulation of Angiotensin-Converting Enzyme 2 and Mas Receptor in Hematopoietic Stem/Progenitor Cells: A Translational Study." Diss., North Dakota State University, 2018. https://hdl.handle.net/10365/28961.

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Vascular disease is the leading cause of mortality and morbidity in the western world, and account for the 1 of every 3 death?s in the US, but a cure for vascular disease is yet to be realized. Hematopoietic stem progenitor cells (HSPCs) are mobilized from bone marrow and have the innate propensity to accelerate vascular repair by reendothelialization and revascularization of ischemic areas. The vasoreparative ability of HSPCs is largely due to their capacity to home to the areas of hypoxia and their sensitivity to hypoxia plays a critical role in the vasoreparative functions of these cells. The discovery of vasoreparative potential of HSPCs resulted in a breakthrough approach of cell-based therapies for the treatment of ischemic vascular diseases. However, success of this approach is essentially dependent on the number of cells that could be collected from an individual. Therefore, novel mechanism-based strategies are needed to enhance the outcomes of autologous cell-based therapies in poor mobilizers and older adults. Recent evidence of a potential role of the vasoprotective axis of the renin angiotensin system (RAS) in HSPCs functions offers a breakthrough. Angiotensin-(1-7), the primary mediator of the protective functions which acts on Mas receptor (MasR), is generated by angiotensin converting enzyme-2 (ACE2). In this study, we tested the effects of hypoxia on stimulation of vasoreparative potential of HSPCs and in upregulation of ACE2 and MasR. Importantly, we delineated the molecular mechanism of hypoxic exposure in regulation of ACE2 and MasR in a HIF1?- dependent manner and hypoxic exposure induced shedding of the membrane bound ACE2 in HSPCs. We used luciferase, a reporter assay, cell-based assays, gene/protein expression studies and pharmacological strategies in human and mouse HSPCs to test our hypotheses. To verify the biological significance of hypoxia, we performed in vivo studies in mice and humans, which recapitulated the in vitro observations on vascular protective axis of RAS in HSPCs. Collectively, these studies provided mechanistic insights into hypoxic regulation of vascular protective axis of RAS in HSPCs and also provided compelling evidence for the clinical use of hypoxia as a promising approach for enhancing the vasoreparative outcomes of cell-based therapies.
American Heart Association grant, 13SDG16960025
National Institutes of Health, National institute of Aging (NIA), 1R01AG056881
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Godet, Anne-Claire. "Régulation de la traduction des facteurs de croissance (lymph)angiogéniques et rôle de l'ARN non codant NEAT1 lors du stress hypoxique." Thesis, Toulouse 3, 2020. http://www.theses.fr/2020TOU30061.

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La traduction est une étape de l'expression des gènes fortement régulée. Lorsque la cellule est stressée, cela bloque la synthèse protéique globale tout en activant la traduction de certains ARNm par des mécanismes alternatifs. L'un de ces mécanismes implique des structures de l'ARNm, les IRES (Internal Ribosome Entry Sites), qui permettent un recrutement de la machinerie de traduction indépendamment de l'extrémité 5' coiffée de l'ARNm. L'activité des IRES est régulée par des facteurs appelés ITAF (IRES trans-acting factor). Le stress hypoxique survient dans différentes pathologies comme l'ischémie cardiaque et le cancer. Pour répondre rapidement à ce stress, les cellules produisent des facteurs de croissance (lymph)angiogéniques qui stimulent la formation de vaisseaux sanguins et lymphatiques. Cela permet de reperfuser la zone lésée dans le cœur ischémique, ou de stimuler la croissance tumorale et la dissémination métastatique dans le cancer. Mon projet de thèse porte sur l'identification d'ITAF contrôlant la traduction des ARNm de ces facteurs de croissance lors de l'hypoxie. La première partie de ma thèse s'est focalisée sur la régulation de la traduction dans les cardiomyocytes hypoxiques. Une étude semi-globale a montré que les gènes de la (lymph)angiogenèse sont régulés majoritairement au niveau traductionnel, alors que tous les ARNm connus pour posséder des IRES sont recrutés plus activement dans les polysomes lors du stress. Nous avons montré que les IRES d'ARNm des familles FGF (fibroblast growth factor) et VEGF (vascular endothelial growth factor) sont tous activés lors de l'hypoxie précoce alors que les IRES d'ARNm non liés à la (lymph)angiogenèse sont activés plus tardivement. Enfin, nous avons identifié un nouvel ITAF, la vasohibine (VASH1), qui active spécifiquement l'IRES du FGF1, mais pas les autres IRES testés. Une analyse par PCR array indique cependant que VASH1 est capable d'inhiber ou de stimuler la traduction de nombreux autres ARNm. La recherche d'un mécanisme global d'activation des IRES des FGF et VEGF fait l'objet du deuxième chapitre de ma thèse. VASH1 n'étant pas un ITAF commun, j'ai recherché d'autres candidats. Je suis partie de l'observation qu'un autre ITAF identifié précédemment au laboratoire, p54nrb, est un composant essentiel du paraspeckle, un corps nucléaire formé en cas de stress. Nous avons émis l'hypothèse que d'autres composants du paraspeckle pourraient être des ITAFs, en particulier le long ARN non codant NEAT1 sur lequel repose sa formation. J'ai établi une corrélation entre l'induction de NEAT1 et l'activation de l'IRES du FGF1 lors de l'hypoxie. De plus, la déplétion de NEAT1 entraine une inactivation de l'IRES, suggérant que cet ARN non codant est un ITAF. J'ai mis en évidence qu'une autre protéine du paraspeckle, PSPC1, est également un ITAF. Une analyse de la composition de l'IRESome par spectrométrie de masse m'a permis d'identifier trois candidats supplémentaires : hnRNPM, rps2 et Nucléoline. Ayant élargi cette étude aux autres IRES étudiés dans le chapitre 1, nous avons démontré que p54nrb et PSPC1 sont capables d'activer plusieurs IRES alors que l'ARN non codant NEAT1, est un ITAF activateur de tous les IRES testés. NEAT1 paraît donc être la clé de l'activation des IRES, et donne au paraspeckle la fonction nouvelle de plateforme d'assemblage de l'IRESome dans les cardiomyocytes en réponse à l'hypoxie. Dans un troisième chapitre, nous avons élargi l'étude à d'autres types cellulaires, les carcinomes mammaires métastatiques et non-métastatiques 4T1et 67NR. NEAT1 est induit en corrélation avec l'activation de l'IRES du FGF1 lorsque ces cellules sont soumises à l'hypoxie, suggérant que le rôle de NEAT1 et du paraspeckle dans le contrôle de la traduction concerne l'hypoxie tumorale comme l'ischémie. Ainsi, ces travaux de thèse révèlent le grand potentiel de NEAT1 en tant que nouvelle cible thérapeutique
Translation is a highly regulated step of gene expression. During cellular stress, global protein synthesis is blocked but translation of specific subsets of mRNAs is activated by alternative mechanisms. One of these mechanisms involves an RNA structure called IRES (Internal Ribosome Entry Site), that enables the recruitment of the translational machinery in a 5' cap-independent manner. IRES activity is regulated by factors called ITAF (IRES trans-acting factor). Hypoxic stress occurs in different pathologies such as cardiac ischemia and cancer. In response to stress, the cell produces (lymph)angiogenic growth factors that stimulate blood and lymphatic vessel formation, allowing reperfusion of the injured area in ischemic heart, or stimulation of tumor growth and metastatic spread in cancer. My thesis project is focused on identification of ITAF-controlled translation of (lymph)angiogenic growth factor mRNAs during hypoxia. The first part of my thesis addresses translational regulation in hypoxic cardiomyocytes. A semi-global study showed that (lymph)angiogenic genes are mostly regulated at the translational level. Furthermore IRESs of mRNAs coding (lymph)angiogenic growth factors are activated in early hypoxia while IRESs of mRNAs non-related to (lymph)angiogenesis are activated later. Finally, we have identified a new ITAF, vasohibin (VASH1), that specifically activates the FGF1 IRES, but not the other IRES tested. A PCR array study indicates however that VASH1 is able to inhibit or stimulate translation of numerous mRNAs. Identification of a global mechanism of FGF and VEGF IRES activation is the main focus of the second chapter of my thesis. Considering that VASH1 is not a common ITAF, I searched for new candidates. I started from the observation that another ITAF previously identified in the laboratory, P54nrb, is also a component of the paraspeckle, a nuclear body formed during cellular stress. We make the hypothesis that other paraspeckle components could be ITAFs, particularly the backbone of the paraspeckle, the long non-coding RNA NEAT1. I established a correlation between NEAT1 induction in hypoxia and FGF1 IRES activation in cardiomyocytes. Moreover, NEAT1 depletion leads to inactivation of the FGF1 IRES, suggesting that NEAT1 is an ITAF. I also highlighted that another paraspeckle component, PSPC1, has an ITAF function. Analysis of IRESsome composition by mass spectrometry allowed me to identify three other candidates: hnRNPM, Rps2 and nucleolin. We then expanded the study to the other IRESs studied in chapter 1 and demonstrated that P54nrb and PSPC1 are able to activate several IRES whilst the non-coding RNA NEAT1 is a positive ITAF of all tested IRES. Thus NEAT1 seems to be the key of IRES activation, and confers on the paraspeckle the novel function of assembly platform for IRESsome formation in cardiomyocytes during hypoxia. In a third chapter, we investigated the same way in other cellular types, metastatic and non metastatic mammary carcinoma 4T1 and 67NR. NEAT1 is induced in correlation with FGF1 IRES activation when the cells are subjected to hypoxia, suggesting that the role of NEAT1 in translational control can be associated to tumoral hypoxia as well as to ischemia. Thus, this work reveal the unique potential of NEAT1 as a therapeutic target
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Books on the topic "Hypoxic translation"

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Hackett, Peter H., Peter D. Wagner, and Robert C. Roach. Hypoxia: Translation in Progress. Springer, 2018.

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Hackett, Peter H., Peter D. Wagner, and Robert C. Roach. Hypoxia: Translation in Progress. Springer, 2016.

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Stocchetti, Nino, and Marco Carbonara. Pharmacologic Neuroprotection. Edited by David L. Reich, Stephan Mayer, and Suzan Uysal. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190280253.003.0002.

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Acute cerebral injury sets into motion a cascade of deleterious biochemical events that cause further neuronal damage and amplify deleterious effects. This cascade develops over time and potentially may be attenuated or limited by pharmacologic manipulation. The neuroprotective properties of several molecules have been clearly demonstrated in experimental models of various pathologies. Based on these findings, many promising compounds have been tested in clinical trials. Large randomized controlled trials, however, have repeatedly failed to provide evidence of clinical efficacy. The authors present an overview of neuroprotective agents studied in traumatic brain injury, subarachnoid hemorrhage, ischemic stroke, and hypoxic-ischemic encephalopathy in adults due to cardiac arrest. They review the molecular mechanisms involved in secondary neuronal injury and how drugs targeting these mechanisms have been evaluated in clinical trials. Finally, the chapter briefly analyzes the possible reasons for repeated failures in translating experimental success into clinical benefit.
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Book chapters on the topic "Hypoxic translation"

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Li, Lu-Ping, Bradley Hack, Erdmann Seeliger, and Pottumarthi V. Prasad. "MRI Mapping of the Blood Oxygenation Sensitive Parameter T2* in the Kidney: Basic Concept." In Methods in Molecular Biology, 171–85. New York, NY: Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-0978-1_10.

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AbstractThe role of hypoxia in renal disease and injury has long been suggested but much work still remains, especially as it relates to human translation. Invasive pO2 probes are feasible in animal models but not for human use. In addition, they only provide localized measurements. Histological methods can identify hypoxic tissue and provide a spatial distribution, but are invasive and allow only one-time point. Blood oxygenation level dependent (BOLD) MRI is a noninvasive method that can monitor relative oxygen availability across the kidney. It is based on the inherent differences in magnetic properties of oxygenated vs. deoxygenated hemoglobin. Presence of deoxyhemoglobin enhances the spin–spin relaxation rate measured using a gradient echo sequence, known as R2* (= 1/T2*). While the key interest of BOLD MRI is in the application to humans, use in preclinical models is necessary primarily to validate the measurement against invasive methods, to better understand physiology and pathophysiology, and to evaluate novel interventions. Application of MRI acquisitions in preclinical settings involves several challenges both in terms of logistics and data acquisition. This section will introduce the concept of BOLD MRI and provide some illustrative applications. The following sections will discuss the technical issues associated with data acquisition and analysis.This chapter is based upon work from the COST Action PARENCHIMA, a community-driven network funded by the European Cooperation in Science and Technology (COST) program of the European Union, which aims to improve the reproducibility and standardization of renal MRI biomarkers. This introduction chapter is complemented by two separate chapters describing the experimental procedure and data analysis.
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Yi, Tingfang, and Gerhard Wagner. "Translation in Cancer at Hypoxia." In Translation and Its Regulation in Cancer Biology and Medicine, 421–32. Dordrecht: Springer Netherlands, 2014. http://dx.doi.org/10.1007/978-94-017-9078-9_20.

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Feng, Zhong-Ping, and Hong-Shuo Sun. "ATP-Sensitive Potassium Channels (KATP) Play a Role in Hypoxic Preconditioning Against Neonatal Hypoxic-Ischemic Brain Injury." In Springer Series in Translational Stroke Research, 185–201. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-45345-3_7.

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Chen, Chunhua, and Changman Zhou. "Hypoxia-Inducible Factor: A New Hope to Counteract Stroke." In Translational Stroke Research, 175–88. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-9530-8_8.

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Karunakaran, C., T. Madasamy, M. Pandiaraj, Niroj K. Sethy, and Kalpana Bhargava. "Electrochemical Biosensors for Hypoxia Markers." In Translational Research in Environmental and Occupational Stress, 93–107. New Delhi: Springer India, 2014. http://dx.doi.org/10.1007/978-81-322-1928-6_9.

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Bhattacharya, Rahul, and M. P. Kaushik. "Hypoxia in Acute Chemical Emergencies: Toxicity, Mechanism, and Treatment." In Translational Research in Environmental and Occupational Stress, 229–42. New Delhi: Springer India, 2014. http://dx.doi.org/10.1007/978-81-322-1928-6_19.

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Dimova, Elitsa Y., and Thomas Kietzmann. "Hypoxia-Inducible Factors: Post-translational Crosstalk of Signaling Pathways." In Methods in Molecular Biology, 215–36. Totowa, NJ: Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60761-738-9_13.

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Navarrete-Opazo, A., E. A. Dale, and Gordon S. Mitchell. "Therapeutic Potential of Intermittent Hypoxia: Lessons from Respiratory Motor Plasticity." In Translational Research in Environmental and Occupational Stress, 31–42. New Delhi: Springer India, 2014. http://dx.doi.org/10.1007/978-81-322-1928-6_4.

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Serebrovskaya, T. V. "Lessons from a 20-Year Investigation of Intermittent Hypoxia: Principles and Practices." In Translational Research in Environmental and Occupational Stress, 267–74. New Delhi: Springer India, 2014. http://dx.doi.org/10.1007/978-81-322-1928-6_22.

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Mishra, Aastha, and M. A. Qadar Pasha. "HIF-1 and EGLN1 Under Hypobaric Hypoxia: Regulation of Master Regulator Paradigm." In Translational Research in Environmental and Occupational Stress, 81–91. New Delhi: Springer India, 2014. http://dx.doi.org/10.1007/978-81-322-1928-6_8.

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Conference papers on the topic "Hypoxic translation"

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Brady, Lauren K., Rohil Shekher, Vladimir Popov, Mircea Ivan, Milan Radovich, and Constantinos Koumenis. "Abstract 733: Analysis of the hypoxic transcriptome in cells and solid tumors reveals a novel spliced isoform of the key regulator of mRNA translation, eIF2B5." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-733.

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Woo, Jong Kyu, and Ho-Young Lee. "Abstract 217: Modulation of Hsp90 chaperone activity by hypoxic condition: Hypoxia stimulates ARD1-mediated Hsp90 post-translational modification." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-217.

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Giblin, John, Krvılcım Kiliҫ, John Jiang, Anderson Chen, Baoqiang Li, Sava Sakadžić, Anna Devor, and David A. Boas. "Long-Term Monitoring of Capillary Flow to Measure Hypoxic Effects of Capillary Flow Disruptions." In Clinical and Translational Biophotonics. Washington, D.C.: OSA, 2020. http://dx.doi.org/10.1364/translational.2020.jtu3a.37.

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Noor, Siti Noor Fazliah Mohd, Maria Azevedo, Hasmaliza Mohamad, and Hélène Autefage. "Hypoxia-mimicking bioactive glass regenerative effects on dental stem cells." In TRANSLATIONAL CRANIOFACIAL CONFERENCE 2016 (TCC 2016): Proceedings of the 1st Translational Craniofacial Conference 2016. Author(s), 2016. http://dx.doi.org/10.1063/1.4968864.

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Zhou, B., O. Larsson, M. Peterson, J. Smith, PB Bitterman, and DH Inbgar. "Transcriptional and Translational Profiling in Hypoxic Alveolar Epithelial Cells." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a1875.

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Sun, Jessica D., Qian Liu, Dharmendra Ahluwalia, Yan Wang, Fanying Meng, Deepthi Bhupathi, John G. Curd, Mark D. Matteucci, and Charles P. Hart. "Abstract A22: Hypoxia-dependent antitumor activity of TH-302, a hypoxia-activated prodrug, in preclinical pancreatic xenograft models." In Abstracts: AACR International Conference on Translational Cancer Medicine-- Jul 11-14, 2010; San Francisco, CA. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1078-0432.tcmusa10-a22.

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Zhou, Bing, Dan H. Fan, Wayne Xu, Ola Larsson, Mark S. Peterson, Jen Smith, Peter B. Bitterman, and David H. Ingbar. "GENOME-WIDE ANALYSIS OF TRANSLATIONAL-REGULATED GEGE In Hypoxic Alveolar Epithelial Cells." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a6795.

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Cheng, Yuping, and Teik C. Lim. "Dynamics of Hypoid Gear Transmission With Non-Linear Time-Varying Mesh." In ASME 2000 International Design Engineering Technical Conferences and Computers and Information in Engineering Conference. American Society of Mechanical Engineers, 2000. http://dx.doi.org/10.1115/detc2000/ptg-14432.

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Abstract A new generalized 14 degrees-of-freedom dynamic model with coupled translation-rotation effect is developed for simulating the nonlinear vibratory response of hypoid geared rotor systems. The model incorporates the load-dependant time-varying mesh characteristic vectors due to tooth load sharing and profile modifications, backlash non-linearity, and off line-of-action friction forces. Based on the 3-dimensional tooth contact analysis results, the quasi-static mesh characteristics that describe the translation-rotation and rotation-rotation force couplings are obtained for use in the dynamic formulation. The three-dimensional representations of the mesh vectors, normal and friction forces, and moments generated at the mesh interface are also included in the proposed study. Tooth separation and the occurrence of jump phenomenon observed in the predicted frequency response functions are analyzed.
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Simon, M. Celeste. "Abstract IA5-3: HIFs, hypoxia, and tumor progression." In Abstracts: AACR International Conference on Translational Cancer Medicine-- Jul 11-14, 2010; San Francisco, CA. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1078-0432.tcmusa10-ia5-3.

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Garmy-Susini, Barbara H., Francoise Pujol, Loic Van den Berghe, and Anne-Catherine Prats. "Abstract 3482: Hypoxia induces translational regulation of lymphangiogenic growth factors." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-3482.

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