Relevant bibliographies by topics / Eif6

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Academic literature on the topic 'Eif6'

Author: Grafiati
Published: 14 December 2024

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Journal articles on the topic "Eif6"

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Smolle, Maria Anna, Piotr Czapiewski, Sylwia Lapińska-Szumczyk, Hanna Majewska, Anna Supernat, Anna Zaczek, Wojciech Biernat, Nicole Golob-Schwarzl, and Johannes Haybaeck. "The Prognostic Significance of Eukaryotic Translation Initiation Factors (eIFs) in Endometrial Cancer." International Journal of Molecular Sciences 20, no. 24 (December 6, 2019): 6169. http://dx.doi.org/10.3390/ijms20246169.

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Whilst the role of eukaryotic translation initiation factors (eIFs) has already been investigated in several human cancers, their role in endometrial cancer (EC) is relatively unknown. In the present retrospective study, 279 patients with EC (1180 samples) were included (mean age: 63.0 years, mean follow-up: 6.1 years). Samples were analysed for expression of 7 eIFs subunits (eIF2α, eIF3c, eIF3h, eIF4e, eIF4g, eIF5, eIF6) through immunohistochemistry and western blotting. Fifteen samples of healthy endometrium served as controls. Density and intensity were assessed and mean combined scores (CS) calculated for each patient. Upon immunohistochemistry, median eIF5 CS were significantly higher in EC as compared with non-neoplastic tissue (NNT, p < 0.001), whilst median eIF6 CS were significantly lower in EC (p < 0.001). Moreover, eIF5 (p = 0.002), eIF6 (p = 0.032) and eIF4g CS (p = 0.014) were significantly different when comparing NNT with EC grading types. Median eIF4g CS was higher in type II EC (p = 0.034). Upon western blot analysis, eIF4g (p < 0.001), peIF2α (p < 0.001) and eIF3h (p < 0.05) were significantly overexpressed in EC, while expression of eIF3c was significantly reduced in EC as compared with NNT (p < 0.001). The remaining eIFs were non-significant. Besides tumour stage (p < 0.001) and patient’s age (p < 0.001), high eIF4g CS-levels were independently associated with poor prognosis (HR: 1.604, 95%CI: 1.037–2.483, p = 0.034). The other eIFs had no prognostic significance. Notably, the independent prognostic significance of eIF4g was lost when adding tumour type. Considering the difficulties in differentiating EC type I and II, eIF4g may serve as a novel prognostic marker indicating patient outcome.
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Wang, Xiaoyan, Guangchao Xu, Fangyingnan Zhang, Yating Wei, Jiawen Deng, Lan Mu, Jinqing He, et al. "eIF6 modulates skin wound healing by upregulating keratin 6B." Stem Cells Translational Medicine 13, no. 11 (October 15, 2024): 1101–12. http://dx.doi.org/10.1093/stcltm/szae064.

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Abstract Eukaryotic translation initiation factor 6 (eIF6) plays a crucial role in 60S ribosome biogenesis and protein translation, as well as in hypertrophic scar formation, but its potential role in epithelialization is still poorly understood. Herein, we found that eIF6 negatively correlated with the wound healing process. Mice with genetically knockdown eIF6 (eIF6+/−) showed faster re-epithelization as shown by the longer tongue of the newly formed epidermis. Furthermore, eIF6 ablation accelerated the wound healing process by targeting basal keratinocytes in the eIF6 keratinocyte-conditional knockout (eIF6f/+; Krt5-Cre+) mice. Mechanistically, keratin 6B, an important wound-activated protein, was significantly upregulated in eIF6f/+; Krt5-Cre+ mice skin as proved by RNA-seq, western immunoblots, and immunofluorescence staining. Moreover, an elevated level of KRT6B and accelerated proliferative capacity were also observed in stable knockdown eIF6 HaCaT cells. Taken together, eIF6 downregulation could accelerate epithelialization by upregulating KRT6B expression and promoting keratinocyte proliferation. Our results for the first time indicate that eIF6 might be a novel target to regulate re-epithelialization.
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Jivotovskaya, Antonina V., Leoš Valášek, Alan G. Hinnebusch, and Klaus H. Nielsen. "Eukaryotic Translation Initiation Factor 3 (eIF3) and eIF2 Can Promote mRNA Binding to 40S Subunits Independently of eIF4G in Yeast." Molecular and Cellular Biology 26, no. 4 (February 15, 2006): 1355–72. http://dx.doi.org/10.1128/mcb.26.4.1355-1372.2006.

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ABSTRACT Recruitment of the eukaryotic translation initiation factor 2 (eIF2)-GTP-Met-tRNAi Met ternary complex to the 40S ribosome is stimulated by multiple initiation factors in vitro, including eIF3, eIF1, eIF5, and eIF1A. Recruitment of mRNA is thought to require the functions of eIF4F and eIF3, with the latter serving as an adaptor between the ribosome and the 4G subunit of eIF4F. To define the factor requirements for these reactions in vivo, we examined the effects of depleting eIF2, eIF3, eIF5, or eIF4G in Saccharomyces cerevisiae cells on binding of the ternary complex, other initiation factors, and RPL41A mRNA to native 43S and 48S preinitiation complexes. Depleting eIF2, eIF3, or eIF5 reduced 40S binding of all constituents of the multifactor complex (MFC), comprised of these three factors and eIF1, supporting a mechanism of coupled 40S binding by MFC components. 40S-bound mRNA strongly accumulated in eIF5-depleted cells, even though MFC binding to 40S subunits was reduced by eIF5 depletion. Hence, stimulation of the GTPase activity of the ternary complex, a prerequisite for 60S subunit joining in vitro, is likely the rate-limiting function of eIF5 in vivo. Depleting eIF2 or eIF3 impaired mRNA binding to free 40S subunits, but depleting eIF4G led unexpectedly to accumulation of mRNA on 40S subunits. Thus, it appears that eIF3 and eIF2 are more critically required than eIF4G for stable binding of at least some mRNAs to native preinitiation complexes and that eIF4G has a rate-limiting function at a step downstream of 48S complex assembly in vivo.
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Harish, Kavya Meena, Poonam Roshan, Aparna Biswas, Stella Anagnos, Riley Luebbers, and Sofia Origanti. "Abstract 7078: Targeting eIF6 to modulate ribosomal subunit association dynamics in cancers." Cancer Research 84, no. 6_Supplement (March 22, 2024): 7078. http://dx.doi.org/10.1158/1538-7445.am2024-7078.

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Abstract Deregulation of ribosomal subunit levels and accessibility are hallmarks of cancer. Eukaryotic translation initiation factor 6 (eIF6) is a key regulator of ribosomal subunit association that is over expressed in many cancers including lung, colon, ovarian and breast cancers, and deregulation of eIF6 is correlated with a poor cancer prognosis. Association of eIF6 with 60S is critical for 60S assembly. However, eIF6 must be released from 60S prior to translation to permit inter subunit interactions between 60S and 40S and to facilitate the formation of translationally proficient 80S monosome. Release of eIF6 is deregulated in the ribosomopathy- Shwachman Diamond Syndrome that is predisposed to leukemias. Also, loss of eIF6 markedly delays tumorigenesis without affecting normal growth, which presents eIF6 as a viable therapeutic target. A potential therapeutic strategy is to target the eIF6 and 60S ribosomal interaction interface. Through biophysical analyses we had identified residues that are critical for the interaction between eIF6 and 60S ribosomal subunit. We show that targeting these key residues in the eIF6-60S interaction interface markedly delays colonic cancer growth and inhibits protein synthesis. Furthermore, we show that the levels of other eIFs and the release factors: SBDS, and EFL1-GTPase are unaltered in the mutant cells suggesting that the translational inhibition is primarily attributed to the deregulation of eIF6. Interestingly, targeting eIF6 leads to an upregulation of p53 independent of the DNA damage response, suggesting that ribosomal stress contributes to the stabilization of p53. Previously, it was shown that translation of Cdc42 was upregulated by eIF6 to promote invasiveness. However, Cdc42 levels were unaltered in the mutant cells. Future studies will determine the mRNA substrates that are translationally deregulated in the mutants. We will also determine the effect of disrupting eIF6 function in inhibiting tumor growth and progression in vivo. Category: MCB, Subcategory: MCB07-Gene regulation sub classification: Translational Control Citation Format: Kavya Meena Harish, Poonam Roshan, Aparna Biswas, Stella Anagnos, Riley Luebbers, Sofia Origanti. Targeting eIF6 to modulate ribosomal subunit association dynamics in cancers [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2024; Part 1 (Regular Abstracts); 2024 Apr 5-10; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2024;84(6_Suppl):Abstract nr 7078.
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Golob-Schwarzl, Nicole, Christina Wodlej, Florian Kleinegger, Margit Gogg-Kamerer, Anna Maria Birkl-Toeglhofer, Johannes Petzold, Ariane Aigelsreiter, Michael Thalhammer, Young Nyun Park, and Johannes Haybaeck. "Eukaryotic translation initiation factor 6 overexpression plays a major role in the translational control of gallbladder cancer." Journal of Cancer Research and Clinical Oncology 145, no. 11 (October 4, 2019): 2699–711. http://dx.doi.org/10.1007/s00432-019-03030-x.

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Abstract Background Gallbladder cancer (GBC) is a rare neoplasia of the biliary tract with high mortality rates and poor prognosis. Signs and symptoms of GBC are not specific and often arise at late stage of disease. For this reason, diagnosis is typically made when the cancer is already in advanced stages, and prognosis for survival is less than 5 years in 90% of cases. Biomarkers to monitor disease progression and novel therapeutic alternative targets for these tumors are strongly required. Commonly, dysregulated protein synthesis contributes to carcinogenesis and cancer progression. In this case, protein synthesis directs translation of specific mRNAs, and, in turn, promotes cell survival, invasion, angiogenesis, and metastasis of tumors. In eukaryotes, protein synthesis is regulated at its initiation, which is a rate-limiting step involving eukaryotic translation initiation factors (eIFs). We hypothesize that eIFs represent crossroads in the development of GBC, and might serve as potential biomarkers. The study focus was the role of eIF6 (an anti-association factor for the ribosomal subunits) in GBC. Methods In human GBC samples, the expression of eIF6 was analyzed biochemically at the protein (immunohistochemistry, immunoblot analyses) and mRNA levels (qRT-PCR). Results High levels of eIF6 correlated with shorter overall survival in biliary tract cancer (BTC) patients (n = 28). Immunohistochemical data from tissue microarrays (n = 114) demonstrated significantly higher expression levels of eIF6 in GBC compared to non-neoplastic tissue. Higher eIF6 expression on protein (immunoblot) and mRNA (qRT-PCR) level was confirmed by analyzing fresh frozen GBC patient samples (n = 14). Depletion of eIF6 (using specific siRNA-mediated knockdown) in Mz-ChA-2 and TFK-1 cell lines inhibited cell proliferation and induced apoptosis. Conclusion Our data indicates that eIF6 overexpression plays a major role in the translational control of GBC, and indicates its potential as a new biomarker and therapeutic target in GBC.
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Schatz, Christoph, Susanne Sprung, Volker Schartinger, Helena Codina-Martínez, Matt Lechner, Mario Hermsen, and Johannes Haybaeck. "Dysregulation of Translation Factors EIF2S1, EIF5A and EIF6 in Intestinal-Type Adenocarcinoma (ITAC)." Cancers 13, no. 22 (November 11, 2021): 5649. http://dx.doi.org/10.3390/cancers13225649.

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Intestinal-type adenocarcinoma (ITAC) is a rare cancer of the nasal cavity and paranasal sinuses that occurs sporadically or secondary to exposure to occupational hazards, such as wood dust and leather. Eukaryotic translation initiation factors have been described as promising targets for novel cancer treatments in many cancers, but hardly anything is known about these factors in ITAC. Here we performed in silico analyses, evaluated the protein levels of EIF2S1, EIF5A and EIF6 in tumour samples and non-neoplastic tissue controls obtained from 145 patients, and correlated these results with clinical outcome data, including tumour site, stage, adjuvant radiotherapy and survival. In silico analyses revealed significant upregulation of the translation factors EIF6 (ITGB4BP), EIF5, EIF2S1 and EIF2S2 (p < 0.05) with a higher arithmetic mean expression in ITAC compared to non-neoplastic tissue (NNT). Immunohistochemical analyses using antibodies against EIF2S1 and EIF6 confirmed a significantly different expression at the protein level (p < 0.05). In conclusion, this work identifies the eukaryotic translation initiation factors EIF2S1 and EIF6 to be significantly upregulated in ITAC. As these factors have been described as promising therapeutic targets in other cancers, this work identifies candidate therapeutic targets in this rare but often deadly cancer.
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Pesce, Elisa, Annarita Miluzio, Lorenzo Turcano, Claudia Minici, Delia Cirino, Piera Calamita, Nicola Manfrini, et al. "Discovery and Preliminary Characterization of Translational Modulators that Impair the Binding of eIF6 to 60S Ribosomal Subunits." Cells 9, no. 1 (January 10, 2020): 172. http://dx.doi.org/10.3390/cells9010172.

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Eukaryotic initiation factor 6 (eIF6) is necessary for the nucleolar biogenesis of 60S ribosomes. However, most of eIF6 resides in the cytoplasm, where it acts as an initiation factor. eIF6 is necessary for maximal protein synthesis downstream of growth factor stimulation. eIF6 is an antiassociation factor that binds 60S subunits, in turn preventing premature 40S joining and thus the formation of inactive 80S subunits. It is widely thought that eIF6 antiassociation activity is critical for its function. Here, we exploited and improved our assay for eIF6 binding to ribosomes (iRIA) in order to screen for modulators of eIF6 binding to the 60S. Three compounds, eIFsixty-1 (clofazimine), eIFsixty-4, and eIFsixty-6 were identified and characterized. All three inhibit the binding of eIF6 to the 60S in the micromolar range. eIFsixty-4 robustly inhibits cell growth, whereas eIFsixty-1 and eIFsixty-6 might have dose- and cell-specific effects. Puromycin labeling shows that eIF6ixty-4 is a strong global translational inhibitor, whereas the other two are mild modulators. Polysome profiling and RT-qPCR show that all three inhibitors reduce the specific translation of well-known eIF6 targets. In contrast, none of them affect the nucleolar localization of eIF6. These data provide proof of principle that the generation of eIF6 translational modulators is feasible.
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Harish, Kavya Meena, Aparna Biswas, Poonam Roshan, and Sofia Origanti. "Abstract 3719: Targeting the eIF6 and 60S ribosomal subunit interaction interface in cancers." Cancer Research 83, no. 7_Supplement (April 4, 2023): 3719. http://dx.doi.org/10.1158/1538-7445.am2023-3719.

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Abstract Translational control is integral to cancer initiation and progression. A subset of translation initiation factors are deregulated in cancers to facilitate their rampant growth and proliferation. Eukaryotic translation initiation factor 6 (eIF6) is one such factor that is over expressed in many cancers including lung, colon, ovarian and breast cancers, and deregulation of eIF6 is correlated with a poor cancer prognosis. Association of eIF6 with 60S is critical for 60S assembly. However, eIF6 must be released from 60S prior to translation to permit inter subunit interactions between 60S and 40S and to facilitate the formation of translationally proficient 80S complex. Release of eIF6 is deregulated in the ribosomopathy- Shwachman Diamond Syndrome that is predisposed to leukemias. Also, loss of eIF6 markedly delays tumorigenesis without affecting normal growth, which presents eIF6 as a viable therapeutic target. A potential therapeutic strategy is to target the eIF6 and 60S ribosomal interaction interface. Through extensive biophysical analyses, we had identified residues that are critical for the interaction between eIF6 and 60S ribosomal subunit. We show that targeting these key residues in the eIF6-60S interaction interface markedly delays colonic cancer growth and inhibits protein synthesis. Interestingly, targeting eIF6 leads to an upregulation of p53 independent of the DNA damage response, suggesting that ribosomal stress contributes to the stabilization of p53. Future studies will determine the mRNA targets that are translationally deregulated by inactivation of eIF6. We will also determine the effect of targeting eIF6 function in inhibiting tumor growth and progression in vivo. Citation Format: Kavya Meena Harish, Aparna Biswas, Poonam Roshan, Sofia Origanti. Targeting the eIF6 and 60S ribosomal subunit interaction interface in cancers. [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2023; Part 1 (Regular and Invited Abstracts); 2023 Apr 14-19; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2023;83(7_Suppl):Abstract nr 3719.
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Oyarbide, Usua, Valentino Bezzerri, Morgan Staton, Christian Boni, Arish Shah, Marco Cipolli, Eliezer Calo, and Seth J. Corey. "Eif6 Dosage Alleviates Activation of the Tp53 Pathway in Sbds-Deficient Cells: A Mechanism for Somatic Genetic Rescue in Shwachman-Diamond Syndrome." Blood 144, Supplement 1 (November 5, 2024): 4090. https://doi.org/10.1182/blood-2024-209812.

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Shwachman-Diamond syndrome (SDS) is characterized by skeletal abnormalities, pancreatic insufficiency, and neutropenia, with an increased risk of developing myelodysplastic syndromes (MDS) and acute myeloid leukemia (AML). Nearly all cases of SDS are caused by biallelic mutations in the SBDS gene, which is critical for ribosome assembly. SBDS interacts with EFL1 to remove EIF6 from the 60S ribosomal subunit, facilitating ribosome formation in the cytoplasm. Research using mouse and zebrafish models has shown that Sbds deficiency activates the tumor suppressor protein Tp53, leading to developmental abnormalities and tissue-specific defects. TP53 biallelic mutations have been found in SDS patients with MDS/AML, suggesting a survival advantage for these mutations. SBDS deficiency is also linked to acquired deletions of chromosome 20q, where the EIF6 gene is located, or somatic mutations in EIF6. These changes, which have been termed somatic genetic rescue, are thought to compensate for the ribosome assembly defect in SDS and lower the risk of MDS/AML. Yet the mechanism of somatic genetic rescue has not been characterized. We created sbds-null zebrafish that exhibited Eif6 accumulation, changes in levels of ribosome proteins, and activation of Tp53 pathways. We have generated an eif6 knockout (KO) line which died earlier (~7-10 days post-fertilization) than the sbds KO line (~15 days post-fertilization). To determine the role of a Eif6 dose effect, we generated zebrafish mutants with low Eif6 protein expression (10% of the wildtype). Surprisingly, we observed that these eif6 hypomorph mutants survived to adulthood. Polysome profiling revealed significant reductions in the 80S monosomes and 40S ribosomal subunits in the eif6 KO at 5 dpf. However, the eif6 hypomorph mutants displayed polysome profiles similar to the eif6 wild type. We crossed the eif6 KO or hypomorph mutants with sbds-null fish and analyzed their phenotypic and molecular characteristics. In the sbds-null background, expression of eif6+/- significantly but partially extended their survival at 15 days post fertilization. The eif6 hypomorph mutants also increased larvae survival at 20 days post fertilization with Mendelian ratios. Low Eif6 levels did not rescue neutropenia in Sbds-deficient zebrafish. Notably, the eif6 hypomorph mutants in sbds-null background reduced the expression of Tp53-dependent targets (e.g., cdkn1a, bax, and puma). SDS patient-derived cell lines also showed accumulation of EIF6, TP53, and CDKN1A (p21). Knocking down EIF6 significantly decreased CDKN1A mRNA levels. These observations support the hypothesis that low levels of Eif6 mitigate Tp53 pathway activation and partially alleviate cellular stress in Sbds-deficient cells. These findings highlight the complex relationships between SBDS, EIF6, TP53, and stress responses in the pathogenesis of SDS. EIF6 dosage determines the degree of intracellular stress mediated by TP53, which may explain the somatic genetic rescue in SDS and the decreased risk for malignant transformation. Understanding these mechanisms will aid in developing therapeutic strategies for SDS. In addition, this partial dosage effect suggests additional stress pathways that are unlikely to be TP53-dependent. We are currently identifying TP53-independent mechanisms.
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De Marco, N., C. Campanella, and R. Carotenuto. "In X. laevis embryos high levels of the anti-apoptotic factor p27BBP/eIF6 are stage-dependently found in BrdU and TUNEL-reactive territories." Zygote 19, no. 2 (July 27, 2010): 157–63. http://dx.doi.org/10.1017/s0967199410000213.

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Summaryp27BBP/eIF6 (β4 binding protein/eukaryotic initiation factor 6) is a highly conserved protein necessary for cell life. In adult eIF6 mice, a 50% decrease in the protein levels in all tissues is accompanied by a reduction in cell proliferation only in the liver, fat cells and cultured fibroblasts. During X. laevis embryogenesis expression of p27BBP/eIF6 is abundant in high proliferative territories. However, in Xenopus cell proliferation appears unaffected following p27BBP/eIF6 over-expression or down-regulation. Indeed, p27BBP/eIF6 is an anti-apoptotic factor acting upstream of Bcl2 that reduces endogenous apoptosis. We studied p27BBP/eIF6 protein localization in wild type embryos and compared it to proliferation and apoptosis. At the beginning of embryogenesis, high levels of p27BBP/eIF6, proliferation and apoptosis overlap. In later development stages high proliferation levels are present in the same regions where higher p27BBP/eIF6 expression is observed, while apoptosis does not appear specifically concentrated in the same sites. The higher presence of p27BBP/eIF6 would appear related to an increased need of apoptosis control in the regions where cell death is essential for normal development.
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Dissertations / Theses on the topic "Eif6"

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RUSSO, ARIANNA. "Increasing Eukaryotic Initiation Factor (eIF6) gene dosage stimulates global translation and induces a transcriptional and metabolic rewiring that blocks Programmed Cell Death." Doctoral thesis, Università del Piemonte Orientale, 2018. http://hdl.handle.net/11579/97190.

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SCAGLIOLA, ALESSANDRA. "EIF6 PHOSPHORYLATION ON SER235 IS REQUIRED FOR MAMMALIAN DEVELOPMENT AND FOR T-CELL LYMPHOMAGENESIS, ESTABLISHING A FUNCTIONAL NETWORK BETWEEN TRANSLATION AND SENESCENCE." Doctoral thesis, Università degli Studi di Milano, 2019. http://hdl.handle.net/2434/631917.

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Deregulated translation control is a hallmark of human cancers and is critical for tumorigenesis downstream of multiple oncogenic signaling pathways. eIF6 is an oncogenic translation factor, which regulates the initiation phase of translation controlling active 80S complex formation. eIF6 depletion and dephosphorylation slow cell growth and cell transformation in vitro and protect from tumor development in mice. eIF6 activation is mTORC1-independent and driven by PKCβ mediated phosphorylation on Ser235. Intriguingly, both eIF6 overexpression and PKC hyperactivation are found in T-cell lymphomas, such as in Anaplastic Large Cell Lymphoma (ALCL). We hypothesized that eIF6 phosphorylation drives T cell lymphomagenesis and mammalian development. We used a conditional eIF6SA KI mouse model in which Ser235 is replaced by an Ala. We discovered that homozygous point mutation (eIF6SA/SA) is lethal after gastrulation. Heterozygous mice (eIF6SA/+) are viable but resistant to NPM-ALK induced lymphomagenesis. The survival of eIF6SA/SA NPM-ALK mice is significantly increased and the appearance of lymphoma is delayed up to 6 months. Surprisingly, ex vivo eIF6SA/SA NPM-ALK primary thymocytes have a striking senescence-like phenotype. Similarly, in vitro generated eIF6SA/SA MEFs show a markedly reduced proliferation and increased senescence. This phenotype is completely rescued by transducing eIF6wt, but not by eIF6SA. In eIF6SA/SA MEFs, the direct interaction between mutant eIF6SA protein with the 60S ribosomal subunit surface is extremely increased, suggesting that 60S viability, required for active translation, could be compromised. In conclusion, our work demonstrates for the first time that eIF6 phosphorylation on Ser235 is essential for mammalian development, cell homeostasis and is rate-limiting for T-cell lymphomagenesis in vivo. Finally, we suggest that the translational control driven by eIF6 activity induces cellular premature senescence, resulting in a protective mechanism against tumor progression.
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Bertrand, Alexis. "Caractérisation fonctionnelle de mutations somatiques compensatrices d'elF6 dans le contexte du syndrome de Shwachman- Diamond." Electronic Thesis or Diss., université Paris-Saclay, 2024. http://www.theses.fr/2024UPASL089.

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Le syndrome de Shwachman Diamond (SDS) est une ribosomopathie génétique rare entraînant une altération de la synthèse protéique associée à de nombreux symptômes, notamment une insuffisance médullaire et une neutropénie pouvant évoluer vers un syndrome de myélodysplasie ou une leucémie myéloïde aiguë. Les mutations bialléliques du gène SBDS sont responsables de plus de 90 % des cas de SDS et nous avons récemment identifié des mutations bialléliques EFL1 comme une nouvelle cause génétique de SDS. SBDS et EFL1 évincent le facteur elF6 de la sous-unité ribosomale pré60S, permettant à cette dernière d'interagir avec la sous-unité 40S pour former le ribosome mature 80S. L'acquisition naturelle d'événements génétiques somatiques au fil du temps participe au développement des maladies liées à l'âge et au développement des cancers. Cependant, dans les maladies mendéliennes, ces événements peuvent, dans de rares cas, contrer l'effet délétère de la mutation germinale et conférer un avantage sélectif aux cellules somatiquement modifiées, un phénomène appelé sauvetage génétique somatique (SGR). Nous avons récemment montré que plusieurs événements génétiques somatiques affectantl'expression ou la fonction d'elF6 sont fréquemment détectés dans les clones sanguins de patients atteints de SDS mais pas chez les individus sains, suggérant un mécanisme de SGR. Alors que la plupart de ces mutations somatiques induisent une déstabilisation de elF6 ou une haploinsuffisance d'EIF6, une mutation récurrente (N106S) n'affecte pas l'expression/stabilité d'elF6 mais réduit sa capacité à interagir avec la sous-unité 60S. Afin d'étudier plus en détail les conséquences fonctionnelles de l'haploinsuffisance de EIF6 et de la mutation N106S dans un contexte de SDS, j'ai introduit via CRISPR/Cas9 ces mutations dans des lignées fibroblastiques immortalisées de patients SDS et de contrôle. Ces modèles cellulaires originaux ont permis de déterminer l'impact de la mutation N106S sur la la localisation et la fonction d'elF6 mais aussi de préciser les effets de ces mutations sur plusieurs aspects du « fitness » cellulaire, notamment la biogenèse des ribosomes, le taux de traduction et la prolifération cellulaire. Dans l'ensemble, le développement de ce modèle a aidé à caractériser comment la mutation N106S et l'haploinsuffisance somatique de elF6 confèrent un avantage sélectif dans les cellules déficientes en SBDS ou EFL1
Shwachman Diamond syndrome (SDS) is a rare genetic ribosomopathy leading to impaired protein synthesis, which causes numerous symptoms including bone marrow failure and neutropenia that can evolve to myelodysplasia syndrome or acute myeloid leukaemia. Biallelic mutations in the SBDS gene are responsible of above 90% of the SDS cases and we recently identified biallelic EFL1 mutations as a novel cause of SDS. SBDS together with EFL1 remove the anti-association factor elF6 from the pre60S ribosomal subunit, allowing its interaction with the 40S subunit to form the mature ribosome 80S. Natural acquisition of somatic genetic events over time participâtes to age-related diseases and cancer development. However, in Mendelian diseases these events can, in rare case, counteract the deleterious effect of the germline mutation and provide a sélective advantage to the somatically modified cells, a phenomenon dubbed Somatic Genetic Rescue (SGR). We recently showed that several somatic genetic events affecting the expression or function of elF6 are frequently detected in blood clones from SDS patients but not in healthy individuals, suggesting a mechanism of SGR. While most of these somatic mutations induce elF6 destabilization or EIF6 haploinsufficiency, one récurrent mutation (N106S) did not affect the expression of elF6 but rather impact its ability to interact with the 60S subunit. In order to further investigate the functional conséquences of ElF6 haploinsufficiency and N106S mutation in a context of SDS, I introduced via CRISPR/Cas9 these mutations in immortalized fibroblastic cell line from SDS patients and control. These original cellular models hâve made it possible to détermine the impact of the N106S mutation on the localisation and function of elF6 and also to clarify the effects of these mutations on several aspects of cellular fitness, in particular ribosome biogenesis, translation rate and cell prolifération. Overall, the development of these cellular models has helped to characterise how the somatic N106S mutation and elF6 haploinsufficiency confer a sélective advantage in cells déficient in SBDS or EFL1
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Crespillo, Casado Ana. "The eIF2 phosphatase : characterization and modulation." Thesis, University of Cambridge, 2018. https://www.repository.cam.ac.uk/handle/1810/283601.

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Cellular needs are fulfilled by the combined activity of functional proteins. Consequently, cells are equipped with a complex proteostatic network that controls protein production in response to cellular requisites. Thereby, protein synthesis is induced or attenuated depending on the particular cellular conditions. One of the mechanisms to control protein synthesis is the phosphorylation of eIF2, which triggers the so-called Integrated Stress Response (ISR). Kinases that sense stresses induce the phosphorylation of eIF2, which, on the one hand, attenuates global rates of protein synthesis and, on the other hand, activates the expression of specific proteins that help to alleviate the stress. One of the proteins preferentially expressed during the ISR is PPP1R15A, a regulatory subunit of Protein Phosphatase 1 (PP1). The PP1/PPP1R15A holophosphatase dephosphorylates eIF2 and terminates the ISR once the stresses are resolved. Hence, eIF2 kinases and phosphatases work together to control levels of phosphorylated eIF2. Maintaining the right balance between the activity of these kinases and phosphatases is important, as is seen by the correlation between their perturbance and the appearance of certain cellular malfunctions or diseases. However, affecting this balance has been also suggested to have beneficial effects. For example, genetic interference with the PPP1R15A regulatory subunit is proposed to confer protection to mice and cells under ER-stress conditions. This observation led to the search for compounds with the ability to modulate the ISR, in particular, by acting on the eIF2 phosphatases. Three compounds (Salubrinal, Guanabenz and Sephin1) have been proposed as eIF2 phosphatase inhibitors with potential use as therapeutic tools in protein misfolding diseases. However, their precise mechanism of action and their direct effect on the enzyme remains an open question. This thesis focuses on the in vitro reconstitution of the eIF2 phosphatase, which served as a platform for characterizing the enzyme (in terms of its structure, activity and assembly) and for studying the proposed inhibitors. This report details key structural features of the PPP1R15/PP1 holophosphatase, the discovery of a cellular cofactor of the enzyme and the conclusions obtained after analysing the effect of its proposed inhibitors. It also includes the development of several in vitro assays, which could potentially be used to screen libraries of compounds in search for modulators of the enzyme.
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Murphy, Patrick. "Characterisation of critical interactions between translation factors eIF2 and eIF2B." Thesis, University of Manchester, 2013. https://www.research.manchester.ac.uk/portal/en/theses/characterisation-of-critical-interactions-between-translation-factors-eif2-and-eif2b(9138d7c8-34b1-4489-8048-a2ac45ef8533).html.

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Eukaryotic translation initiation is a complex and highly regulated process involving the ribosome, mRNA and proteins called eukaryotic initiation factors (eIFs). The overall aim of translation initiation is to position the ribosome at the initiation codon of the mRNA. eIF2, in its GTP-bound conformation, binds the initiator tRNA (Met-tRNAiMet) and delivers it to the 40S ribosomal subunit. When the anticodon of the tRNA is bound to the initiation codon, the GTP on eIF2 is hydrolysed to GDP. The guanine nucleotide exchange factor (GEF) eIF2B regenerates eIF2-GTP. eIF2 and eIF2B are multisubunit/multidomain protein complexes. Because information regarding the interface between each complex is limited, particularly the interface on the eIF2γ subunit, which binds the guanine-nucleotides and Met-tRNAiMet, interactions between the minimal GEF domain of eIF2Bε, εGEF, and eIF2 were mapped using mutagenesis and an in vitro cysteine cross-linking approach, with the cross-linker Mts-Atf-Biotin. Site-directed mutagenesis (SDM) was used to mutate five N-terminal and five C-terminal surface-exposed εGEF residues to cysteines. The mutant alleles were analysed in Saccharomyces cerevisiae and it was found that the gcd6-R574C allele was lethal and the gcd6-T572C was Gcd-. Further gcd6-R574 mutant alleles were also found to be lethal in yeast but expressed in vivo.εGEF-R574C has dramatically reduced GEF activity in vitro and binding assays showed that this mutant has significantly reduced affinity for eIF2. The εGEF-T572C and εGEF-S576C mutants also have severe and minor eIF2-binding defects respectively, while the C-terminal εGEF-Cys mutants have slightly reduced affinity for eIF2. The N-terminal εGEF-Cys mutants cross-link specifically to eIF2γ, while the C-terminal εGEF-Cys mutants interact predominantly with eIF2β. From the data obtained in this study, we propose a new model for eIF2B-mediated guanine-nucleotide exchange that reduces the importance of eIF2β and suggests εGEF resembles other GEFs in binding primarily to its G protein partner eIF2γ.
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Guillon, Laurent. "Etude des facteurs du démarrage de la traduction eIF5B et eIF3." Phd thesis, Ecole Polytechnique X, 2008. http://pastel.archives-ouvertes.fr/pastel-00004650.

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Le démarrage de la traduction est un processus central dans toute cellule. L'étude des protéines assistant le ribosome pour réaliser cette étape, les facteurs de démarrage (Initiation Factors Ifs), permet d'obtenir des informations sur les mécanismes moléculaires complexes assurant la fidélité et l'efficacité du démarrage. La comparaison des jeux de facteurs protéiques dans les trois règnes du monde vivant a permis de mettre en évidence la présence de trois facteurs universellement conservés. Parmi ceux-ci, le facteur eucaryotique/archéen e/aIF5B, homologue au facteur bactérien IF2, stimule l'association des sous-unités ribosomales au même titre que chez les Bactéries. Néanmoins, l'universalité du facteur est limitée par l'absence d'interaction reportée entre le facteur e/aIF5B et l'ARNt initiateur alors que cette liaison est parfaitement caractérisée chez les Bactéries. Une partie de ce travail de thèse a permis d'étendre la similitude fonctionnelle entre les facteurs en mettant en évidence une liaison de l'ARNt initiateur méthionylé par le facteur e/aIF5B. Cette liaison présente des caractéristiques identiques à celle de l'ARNt initiateur méthionylé et formylé par le facteur bactérien IF2. Une deuxième partie du travail de thèse a concerné le facteur eIF3, le plus complexe du système de démarrage chez les Eucaryotes. Ce complexe de 13 sous-unités chez l'humain et de 5 sous-unités chez la levure n'a pas d'équivalent dans les autres domaines du vivant bien qu'il joue un rôle central et essentiel chez les Eucaryotes. La compréhension de ses fonctions est néanmoins fortement limitée par le manque d'information à l'échelle moléculaire sur les interactions entre les sous-unités le composant et avec ses autres facteurs partenaires. De plus, le facteur s'avère être impliqué dans de nombreux cancers, ce qui étend l'intérêt de son étude. Mon travail a permis de développer une bibliothèque de vecteurs permettant de coexprimer les différentes sous-unités ou des formes stabilisées des sous-unités du facteur eIF3 de levure chez la Bactérie Escherichia coli. La purification des sous-unités isolées et de différents sous-complexes nous permet d'envisager la résolution de la structure du facteur et de son organisation par une approche alliant la cristallographie et la microscopie électronique.
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Wang, Xiaoshan. "Regulation of eIF3-Paip1 interaction by extracellular stimuli and phosphorylation status." Thesis, McGill University, 2010. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=86958.

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The tertiary interaction of poly(A)-binding protein (PABP), with eukaryotic translation initiation factor 4G (eIF4G) and 3'poly(A) tail of mRNA acts to stimulate translation initiation. Subsequently, the interaction of PABP-interacting protein 1 (Paip1) with PABP and eukaryotic translation initiation factor 3 (eIF3) (via the eIF3g subunit) further stimulates translation. Here, we demonstrate that the interaction of eIF3 and Paip1 is regulated by the presence of amino acids through an mTORC1 dependent signaling pathway. This interaction is inhibited by addition of mTORC1 signaling pathway inhibitors; such as rapamycin and wortmannin. Paip1 binds to eIF3g and this subunit can be phosphorylated on either Thr41 or Ser42. However, we find that phosphorylation on these sites is not stimulated by amino acids, nor does it act to enhance eIF3-Paip1 interaction. On the other hand, we show that S6 ribosomal protein kinase (S6K) positively regulates the interaction of eIF3 and Paip1 and we propose that S6K acts as a putative kinase for eIF3. The studies of the regulation of eIF3-Paip1 interaction will lead to better understanding the translation process.
L'interaction tertiaire entre la protéine PABP (poly(A)-binding protein), le facteur d'initiation de la traduction eucaryote 4G (eIF4G), et la queue poly(A) des ARN messagers, stimule l'initiation de la traduction. De plus, l'interaction entre la protéine qui interagit avec PABP, Paip1 (PABP-interacting protein 1), et le facteur d'initiation de la traduction eucaryote 3 (eIF3) (par sa sous-unité g), induit la traduction de façon plus élevée. Dans cette thèse, nous démontrons que l'interaction entre l'eIF3 et Paip1 est régulée par la présence d'acides aminées, et que cette interaction est dépendante de la voie signalétique contrôlée par mTORC1. En effet, les inhibiteurs de cette voie signalétique comme la rapamycin et la wortmannin bloquent l'interaction. Comme Paip1 s'attache directement à la sous-unité g de l'eIF3 et que cette dernière peut être phosphorylée sur la thréonine 41 ou la sérine 42, nous avons étudié le rôle la phosphorylation de eIF3g sur l'interaction entre les deux protéines. Nous démontrons que cette phosphorylation n'est pas stimulée par l'addition d'acides aminées et qu'elle n'induit pas une plus grande interaction entre eIF3 et Paip1. Par contre, nous observons que la kinase S6K (S6 ribosomal protein kinase), régule de façon positive l'interaction entre eIF3 et Paip1, et nous suggérons que cette kinase agit sur eIF3. Cette étude sur les rôles et actions de eIF3 et Paip1 aide à de plus grandes connaissances sur la régulation de l'initiation de la traduction eucaryote.
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Chamot, Danuta. "Translation initiation factor 5A (eIF-5A) in plants /." [S.l.] : [s.n.], 1993. http://www.ub.unibe.ch/content/bibliotheken_sammlungen/sondersammlungen/dissen_bestellformular/index_ger.html.

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Reber-Brochocka, Krystyna Barbara. "Charakterisierung genomischer Klone des Proteinsnythese-Initiationsfaktors eIF-4A /." [S.l : s.n.], 1986. http://www.ub.unibe.ch/content/bibliotheken_sammlungen/sondersammlungen/dissen_bestellformular/index_ger.html.

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Eshaque, Bithi. "Characterization of Eukaryotic Translation Initiation Factor 5A isoforms (eIF-5A1 & eIF-5A2) using human cell lines as a model system." Thesis, University of Waterloo, 2006. http://hdl.handle.net/10012/1218.

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Eukaryotic translation initiation factor 5A (eIF-5A) is the only known cellular protein that contains the post-translationally derived amino acid, hypusine. Initially, eIF-5A was named as a translation initiation factor because of its capability to stimulate the formation of methionyl-puromycin, which mimics the first peptide bond formation during protein synthesis, under in vitro conditions. Subsequently, however, this proposed function of eIF-5A has been questioned because a similar effect on translation was not observed in situ. Moreover, eIF-5A appears not to be required for general protein synthesis. Rather, there is evidence that it facilitates the translation of specific subsets of mRNAs required for cell proliferation as well as apoptosis.

There are two isoforms of eIF-5A in the human genome which have designated eIF-5A1 and eIF-5A2. The objective of the present study was to gain an increased understanding of the roles of eIF-5A1 and eIF-5A2 during apoptosis and cell proliferation using human cell lines as a model system. Apoptosis was induced by treating the cells with Actinomycin D or sodium nitroprusside (SNP), which initiate programmed cell death by different mechanisms. It was observed for both normal and cancer cells that eIF-5A1 protein is up-regulated during apoptosis induced by Actinomycin D or SNP, whereas eIF-5A1 mRNA is constitutively expressed and does not change in abundance during this treatment. The up regulation of eIF-5A1 protein levels in the absence of a corresponding up-regulation in eIF-5A1 mRNA suggests that eIF-5A1 may be post-transcriptionally regulated. Moreover, eIF-5A1 protein up-regulation was stronger in normal cells than in cancer cells. By contrast, eIF-5A2 protein was below detection levels during apoptosis in both normal and cancer cells, although the corresponding transcript was detectable by semi-quantitative RT-PCR. This is attributable to inefficient translation of eIF-5A2 mRNA.

The effects of eIF-5A1 and eIF-5A2 on cell proliferation were examined by modulating the levels of serum in cultures of UACC-1598 cells, which are ovarian cancer cells that express high levels of both isoforms of eIF-5A. Serum starvation, which induces cell cycle arrest and ensuing apoptosis, followed by the re-addition of serum had no effect on the transcript levels of either eIF-5A1 or eIF-5A2. However, eIF-5A1 and eIF-5A2 proteins were both up-regulated within 24 hours of the initiation of serum starvation, and this coincided temporally with the onset of apoptosis as measured by TUNEL and a subsequent decline in viable cells.

The data indicate that eIF-5A1 and eIF-5A2 are both post-transcriptionally regulated and that they have functionally redundant roles in apoptosis.
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Books on the topic "Eif6"

1

Eiff, W. von. Wilhelm von Eiff (1890-1943). Freiburg: Augustinermuseum, 1990.

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Sasayama, Haruo. Nihon kodai eifu seido no kenkyū. Tōkyō: Tōkyō Daigaku Shuppankai, 1985.

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Canada Mortgage and Housing Corporation., ed. Exterior insulation and finish systems (EIFS). Ottawa: Canada Mortgage and Housing Corporation, 2004.

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Elfed-Owens, Prydwen. Ysgol yr Eifl, Trefor, Caernarfon, Gwynedd LL54 5LU: Inspection under section 10 of the Schools Inspection Act 1996 : school number: 661/2111 : date of inspection: 7-9 October 2002 = Ysgol yr Eifl, Trefor, Caernarfon, Gwynedd LL54 5LU : arolygiad dan adran 10 Deddf Arolygu Ysgolion 1996 : rhif yr ysgol: 661/2111 : dyddiad arolygiad: 7-9 Hydref 2002. [Cardiff]: Estyn, 2002.

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Nelson, PE, and RE Kroll, eds. Exterior Insulation Finish Systems (EIFS): Materials, Properties, and Performance. 100 Barr Harbor Drive, PO Box C700, West Conshohocken, PA 19428-2959: ASTM International, 1996. http://dx.doi.org/10.1520/stp1269-eb.

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1953-, Nelson Peter E., Kroll Richard E. 1942-, American Society for Testing and Materials., and International Symposium on Exterior Insulation and Finish Systems (2nd : 1995 : Denver, Colo.), eds. Exterior insulation finish systems (EIFS): Materials, properties, and performance. West Conshohocken, PA: ASTM, 1996.

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Nelson, Peter E., and Bill Egan, eds. Exterior Insulation and Finish Systems (EIFS): Performance, Progress and Innovation. 100 Barr Harbor Drive, PO Box C700, West Conshohocken, PA 19428-2959: ASTM International, 2016. http://dx.doi.org/10.1520/stp1585-eb.

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financial systems and corporate performance (Project) European integration. European integration, financial systems and corporate performance (EIFC) working paper. Maastricht, the Netherlands: United Nations University, Institute for New Technologies, 2001.

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Environmental Studies Research Funds (Canada), Canada Oil and Gas Lands Administration., and CANATEC Consultants Ltd, eds. Beaufort sea: Ice design criteria : acquisition of data on EIFs. [Ottawa]: Environmental Studies Research Funds, 1992.

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Canada Mortgage and Housing Corporation., ed. Exterior insulation and finish systems (EIFS): Problems, causes and solutions. [Ottawa]: CMHC, 2000.

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Book chapters on the topic "Eif6"

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Biffo, Stefano, Daniela Brina, and Stefania Oliveto. "eIF6." In Translation and Its Regulation in Cancer Biology and Medicine, 233–40. Dordrecht: Springer Netherlands, 2014. http://dx.doi.org/10.1007/978-94-017-9078-9_11.

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Biswas, Arunima, Avik Choudhuri, and Umadas Maitra. "TIF6 (eIF6)." In Encyclopedia of Signaling Molecules, 5437–44. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_615.

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Gonçalves, João, Helena Soares, Norman L. Eberhardt, Sarah C. R. Lummis, David R. Soto-Pantoja, David D. Roberts, Umadas Maitra, et al. "TIF6 (eIF6)." In Encyclopedia of Signaling Molecules, 1859–66. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_615.

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Hershey, John W. B. "eIF3." In Translation and Its Regulation in Cancer Biology and Medicine, 173–94. Dordrecht: Springer Netherlands, 2014. http://dx.doi.org/10.1007/978-94-017-9078-9_8.

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Choudhuri, Avik, Anirban Ray, Arunima Biswas, and Umadas Maitra. "eIF3." In Encyclopedia of Signaling Molecules, 1–10. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4614-6438-9_101984-1.

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Maitra, Umadas, and Romit Majumdar. "TIF5 (eIF5)." In Encyclopedia of Signaling Molecules, 5430–37. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_614.

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Gonçalves, João, Helena Soares, Norman L. Eberhardt, Sarah C. R. Lummis, David R. Soto-Pantoja, David D. Roberts, Umadas Maitra, et al. "TIF5 (eIF5)." In Encyclopedia of Signaling Molecules, 1853–59. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_614.

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Newton, Mark J., and Eric Smith. "EIFS Mesh Coating Improvements." In Exterior Insulation and Finish Systems (EIFS): Performance, Progress and Innovation, 237–47. 100 Barr Harbor Drive, PO Box C700, West Conshohocken, PA 19428-2959: ASTM International, 2016. http://dx.doi.org/10.1520/stp158520140107.

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Aktas, Bertal H., and Ting Chen. "The eIF2 Complex and eIF2α." In Translation and Its Regulation in Cancer Biology and Medicine, 195–221. Dordrecht: Springer Netherlands, 2014. http://dx.doi.org/10.1007/978-94-017-9078-9_9.

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Taylor, A. Judson. "Successful Strategies for EIFS Over-Cladding." In Exterior Insulation and Finish Systems (EIFS): Performance, Progress and Innovation, 88–112. 100 Barr Harbor Drive, PO Box C700, West Conshohocken, PA 19428-2959: ASTM International, 2016. http://dx.doi.org/10.1520/stp158520140114.

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Conference papers on the topic "Eif6"

1

Scagliola, A., A. Miluzio, S. Faienza, S. Oliveto, M. Fedeli, P. Dellabona, C. Voena, R. Chiarle, and S. Biffo. "PO-130 SER235 residue drives eIF6 oncogenic activity in NPM-ALK induced T cell lymphomagenesis." In Abstracts of the 25th Biennial Congress of the European Association for Cancer Research, Amsterdam, The Netherlands, 30 June – 3 July 2018. BMJ Publishing Group Ltd, 2018. http://dx.doi.org/10.1136/esmoopen-2018-eacr25.171.

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Merali, Salim, Oscar Perez-Leal, and Carlos Barrero. "Abstract 4554: Downstream effects of rigosertib (ON 01910.Na) in cancer cells involves impairment of protein translation via eIF2 and eIF4." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-4554.

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Zou, Guang, Kian Banisoleiman, and Arturo González. "Development of Probabilistic Fracture Mechanics Method for Fatigue Life Prediction Based on EIFS Concept." In ASME 2017 36th International Conference on Ocean, Offshore and Arctic Engineering. American Society of Mechanical Engineers, 2017. http://dx.doi.org/10.1115/omae2017-61994.

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A problem with fracture mechanics (FM) based fatigue analysis is that reliable information on initial crack/flaw size is often hard to obtain. Also, FM method can’t be applied directly to welded joints with relatively small initial flaws and long crack initiation life. This paper proposes a novel probabilistic FM method based on the equivalent initial flaw size (EIFS) concept. The initial crack size is substituted with EIFS to take both the crack initiation and propagation life into account. Three methods are tested to obtain mean value of EIFS: calibrating to S-N curves, Kitagawa-Takahashi (KT) diagram and fitting to test data. The obtained EIFSs are evaluated by comparing the predicted fatigue lives and crack evolutions with S-N curves and test crack evolution data. The suggested procedure is to derive the mean value of EIFS from S-N curves and the coefficient of variation from KT diagram.
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Johnson, W. S., A. C. Wilson, and S. Highsmith. "Equivalent Initial Flaw Size Distribution Determination for Gas Turbine Blades Based Upon Inspection Data." In ASME Turbo Expo 2005: Power for Land, Sea, and Air. ASMEDC, 2005. http://dx.doi.org/10.1115/gt2005-69124.

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A fracture mechanics-based methodology is presented for determining equivalent initial flaw size (EIFS) distributions from field inspection data accounting for different service histories of fracture critical components. The EIFS distribution based on inspection data from a subset of the fleet allows for an assessment of initial material/manufacturing quality and enables a probabilistic fracture mechanics-based fatigue life prediction for the fleet as a whole. The methodology is demonstrated on an industrial gas turbine blade experiencing in-service cracking.
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Newman, James C., and Balkrishna S. Annigeri. "Fatigue-Life Prediction Method Based on Small-Crack Theory in an Engine Material." In ASME 2011 Turbo Expo: Turbine Technical Conference and Exposition. ASMEDC, 2011. http://dx.doi.org/10.1115/gt2011-45644.

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Plasticity effects and crack-closure modeling of small fatigue cracks were used on a Ti-6Al-4V alloy to calculate fatigue lives under various constant-amplitude loading conditions (negative to positive stress ratios, R) on notched and un-notched specimens. Fatigue test data came from a high-cycle-fatigue study by the U.S. Air Force and a metallic materials properties handbook. A crack-closure model with a cyclic-plastic-zone-corrected effective stress-intensity factor range and equivalent-initial-flaw-sizes (EIFS) were used to calculate fatigue lives using only crack-growth-rate data. For un-notched specimens, EIFS values were 25-μm; while for notched specimens, the EIFS values ranged from 6 to 12 μm for positive stress ratios and 25-μm for R = −1 loading. Calculated fatigue lives under a wide-range of constant-amplitude loading conditions agreed fairly well with the test data from low- to high-cycle fatigue conditions.
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Chiarelli, Federico, Barbora Kudzmanaite, Giorgio Cacciaguerra Ranghieri, and Miguel Alvarez-Rodriguez. "The EIF monitoring mechanism." In ICEGOV 2020: 13th International Conference on Theory and Practice of Electronic Governance. New York, NY, USA: ACM, 2020. http://dx.doi.org/10.1145/3428502.3428627.

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Zhang, Wei, Huili Liu, Qiang Wang, and Shan Jiang. "Fatigue Life Prediction Using Strain Intensity Factor and Equivalent Initial Flaw Size." In ASME 2016 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2016. http://dx.doi.org/10.1115/imece2016-66505.

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In this paper, an effective approach is developed to evaluate fatigue life of smooth specimens of 316 austenitic stainless steel under the fully reversed loading condition based on strain intensity factor and the equivalent initial flaw size (EIFS) concept. The strain intensity factor is indicated to be a better driving parameter to correlate with the fatigue crack growth rate, especially for the fully reversed load condition and the low cycle fatigue region. EIFS is an effective approach to account for complex process of the crack initiation and small crack propagation, which can be calculated by correlating the fatigue limit strain with fatigue threshold strain intensity factor. The fatigue limit strain is obtained from experimental data by analyzing the asymptotic behavior of the fatigue life curve. The driving force of crack growth is expressed in strain intensity factor. Then the fatigue life could be calculated by integrating the crack growth rate from integral lower limit EIFS to integral upper limit critical crack length ac. The experimental data of 316 austenitic stainless steel are employed to validate the proposed model. The good agreements are observed. It has shown that strain-intensity-factor-based approach could be a good method for fatigue life evaluation.
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Tuan, Chia-Wei, Ho-Ting Wu, and Mei-Ting Chaung. "A new EIFS strategy for IEEE 802.11e wireless LANs." In the International Conference. New York, New York, USA: ACM Press, 2008. http://dx.doi.org/10.1145/1506270.1506279.

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Kalogirou, Victoria, Antonis Stasis, and Yannis Charalabidis. "Adapting national interoperability frameworks beyond EIF 3.0." In ICEGOV 2020: 13th International Conference on Theory and Practice of Electronic Governance. New York, NY, USA: ACM, 2020. http://dx.doi.org/10.1145/3428502.3428536.

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Liu, Yongming, and Sankaran Mahadevan. "An Efficient Method for Equivalent Initial Flaw Size (EIFS) Calculation." In 49th AIAA/ASME/ASCE/AHS/ASC Structures, Structural Dynamics, and Materials Conference
16th AIAA/ASME/AHS Adaptive Structures Conference
10t. Reston, Virigina: American Institute of Aeronautics and Astronautics, 2008. http://dx.doi.org/10.2514/6.2008-1761.

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Reports on the topic "Eif6"

1

Chamovitz, Daniel A., and Albrecht G. Von Arnim. eIF3 Complexes and the eIF3e Subunit in Arabidopsis Development and Translation Initiation. United States Department of Agriculture, September 2009. http://dx.doi.org/10.32747/2009.7696545.bard.

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The original working hypothesis of our proposal was that The “e” subunit of eIF3 has multiple functions from both within the nucleus and in the cytoplasm. Within this model, we further hypothesized that the “e” subunit of eIF3 functions in translation as a repressor. We proposed to test these hypotheses along the following specific aims: 1) Determine the subcellular localization of the interaction between eIF3e and other eIF3 subunits, or the COP9 signalosome. 2) Elucidate the biological significance of the varied subcellular localizations of eIF3e through generating Arabidopsis eIF3e alleles with altered subcellular localization. 3.) Purify different eIF3e complexes by tandem affinity purification (TAP). 4) Study the role of eIF3e in translational repression using both in vitro and in planta assays. eIF3 is an evolutionarily ancient and essential component of the translational apparatus in both the plant and animal kingdoms. eIF3 is the largest, and in some ways the most mysterious, of the translation factors. It is a multi-subunit protein complex that has a structural/scaffolding role in translation initiation. However, despite years of study, only recently have differential roles for eIF3 in the developmental regulation of translation been experimentally grounded. Furthermore, the roles of individual eIF3 subunits are not clear, and indeed some, such as the “e” subunit may have roles independent of translation initiation. The original three goals of the proposal were technically hampered by a finding that became evident during the course of the research – Any attempt to make transgenic plants that expressed eIF3e wt or eIF3e variants resulted in seedling lethality or seed inviability. That is, it was impossible to regenerate any transgenic plants that expressed eIF3e. We did manage to generate plants that expressed an inducible form of eIF3e. This also eventually led to lethality, but was very useful in elucidating the 4th goal of the research (Yahalom et al., 2008), where we showed, for the first time in any organism, that eIF3e has a repressory role in translation. In attempt to solve the expression problems, we also tried expression from the native promoter, and as such analyzed this promoter in transgenic plants (Epel, 2008). As such, several additional avenues were pursued. 1) We investigated protein-protein interactions of eIF3e (Paz-Aviram et al., 2008). 2) The results from goal #4 led to a novel hypothesis that the interaction of eIF3e and the CSN meets at the control of protein degradation of nascent proteins. In other words, that the block in translation seen in csn and eIF3e-overexpressing plants (Yahalom et al., 2008) leads to proteasome stress. Indeed we showed that both over expression of eIF3e and the csn mutants lead to the unfolded protein response. 3) We further investigated the role of an additional eIF3 subunit, eIF3h, in transalational regulation in the apical meristem (Zhou et al., 2009). Epel, A. (2008). Characterization of eIF3e in the model plant Arabidopsis thaliana. In Plant Sciences (Tel Aviv, Tel Aviv University). Paz-Aviram, T., Yahalom, A., and Chamovitz, D.A. (2008). Arabidopsis eIF3e interacts with subunits of the ribosome, Cop9 signalosome and proteasome. Plant Signaling and Behaviour 3, 409-411. Yahalom, A., Kim, T.H., Roy, B., Singer, R., von Arnim, A.G., and Chamovitz, D.A. (2008). Arabidopsis eIF3e is regulated by the COP9 signalosome and has an impact on development and protein translation. Plant J 53, 300-311. Zhou, F., Dunlap, J.R., and von Arnim, A.G. The translation initiation factor subunit eIF3h is .1 involved in Arabidopsis shoot apical meristem maintenance and auxin response. (submitted to Development).
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2

Carbary, Lawrence D., Laura L. Perkins, Roland Serino, Bill Preston, and Jan Kosny. Contributing to Net Zero Building: High Energy Efficient EIFS Wall Systems. Office of Scientific and Technical Information (OSTI), January 2014. http://dx.doi.org/10.2172/1116737.

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3

Chamovitz, Daniel, and Albrecht Von Arnim. Translational regulation and light signal transduction in plants: the link between eIF3 and the COP9 signalosome. United States Department of Agriculture, November 2006. http://dx.doi.org/10.32747/2006.7696515.bard.

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The COP9 signalosome (CSN) is an eight-subunit protein complex that is highly conserved among eukaryotes. Genetic analysis of the signalosome in the plant model species Arabidopsis thaliana has shown that the signalosome is a repressor of light dependent seedling development as mutant Arabidopsis seedlings that lack this complex develop in complete darkness as if exposed to light. These mutant plants die following the seedling stage, even when exposed to light, indicating that the COP9 signalosome also has a central role in the regulation of normal photomorphogenic development. The biochemical mode of action of the signalosome and its position in eukaryotic cell signaling pathways is a matter of controversy and ongoing investigation, and recent results place the CSN at the juncture of kinase signaling pathways and ubiquitin-mediated protein degradation. We have shown that one of the many CSN functions may relate to the regulation of translation through the interaction of the CSN with its related complex, eukaryotic initiation factor (eIF3). While we have established a physical connection between eIF3 subunits and CSN subunits, the physiological and developmental significance of this interaction is still unknown. In an effort to understand the biochemical activity of the signalosome, and its role in regulating translation, we originally proposed to dissect the contribution of "h" subunit of eIF3 (eIF3h) along the following specific aims: (i) Isolation and phenotypic characterization of an Arabidopsis loss-of-function allele for eIF3h from insertional mutagenesis libraries; (ii) Creation of designed gain and loss of function alleles for eIF3h on the basis of its nucleocytoplasmic distribution and its yeast-two-hybrid interactions with other eIF3 and signalosome partner proteins; (iii) Determining the contribution of eIF3h and its interaction with the signalosome by expressing specific mutants of eIF3h in the eIF3h- loss-of function background. During the course of the research, these goals were modified to include examining the genetic interaction between csn and eif3h mutations. More importantly, we extended our effort toward the genetic analysis of mutations in the eIF3e subunit, which also interacts with the CSN. Through the course of this research program we have made several critical scientific discoveries, all concerned with the apparent diametrically opposed roles of eIF3h and eIF3e. We showed that: 1) While eIF3e is essential for growth and development, eIF3h is not essential for growth or basal translation; 2) While eIF3e has a negative role in translational regulation, eIF3h is positively required for efficient translation of transcripts with complex 5' UTR sequences; 3) Over-accumulation of eIF3e and loss-of-function of eIF3h both lead to cop phenotypes in dark-grown seedlings. These results were published in one publication (Kim et al., Plant Cell 2004) and in a second manuscript currently in revision for Embo J. Are results have led to a paradigm shift in translation research – eIF3 is now viewed in all systems as a dynamic entity that contains regulatory subuits that affect translational efficiency. In the long-term agronomic outlook, the proposed research has implications that may be far reaching. Many important plant processes, including developmental and physiological responses to light, abiotic stress, photosynthate, and hormones operate in part by modulating protein translation [23, 24, 40, 75]. Translational regulation is slowly coming of age as a mechanism for regulating foreign gene expression in plants, beginning with translational enhancers [84, 85] and more recently, coordinating the expression of multiple transgenes using internal ribosome entry sites. Our contribution to understanding the molecular mode of action of a protein complex as fundamental as eIF3 is likely to lead to advances that will be applicable in the foreseeable future.
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von Arnim, Albrecht G. Eukaryotic initiation factor 3 (eIF3) and 5’ mRNA leader sequences as agents of translational regulation in Arabidopsis. Final report. Office of Scientific and Technical Information (OSTI), February 2015. http://dx.doi.org/10.2172/1169186.

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5

Maxwell, J. Integrated Information Support System (IISS). Volume 4. IISS System. Part 6. Enterprise Integration Framework (EIF) for Aerospace. Fort Belvoir, VA: Defense Technical Information Center, September 1990. http://dx.doi.org/10.21236/ada252446.

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6

Chamovitz, Daniel, and Xing-Wang Deng. Morphogenesis and Light Signal Transduction in Plants: The p27 Subunit of the COP9-Complex. United States Department of Agriculture, 1997. http://dx.doi.org/10.32747/1997.7580666.bard.

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Plants monitor environmental signals and modulate their growth and development in a manner optimal for the prevailing light conditions. The mechanisms by which plants transduce light signals and integrate them with other environmental and developmental signals to regulate plant pattern development are beginning to be unraveled. A large body of knowledge has accumulated regarding the roles of specific photoreceptors in perceiving light signals, and about the downstream developmental responses responding to light (Batschauer, 1999; Chamovitz and Deng, 1996; Deng and Quail, 1999). Still, little is know about the molecular mechanisms connecting the photoreceptors to development, and how these developmental pathways are integrated with additional developmental regulatory pathways to modulate growth. The multi-subunit protein complex COP9 signalosome (previously referred to as the "COP9 complex") has a central role in mediating the light control of plant development, and in general developmental regulation. Arabidopsis mutants that lack this complex develop photomorphogenically even in the absence of light signals (reviewed in Chamovitz and Deng 1996, 1997). Various genetic studies have indicated that the COP9 signalosome acts at the nexus of upstream signals transduced from the individual photoreceptors, and specific downstream signaling pathways. Thus the COP9 signalosome was hypothesized to be a master repressor of photomorphogenesis, and that light acts to abrogate this repression. However, the COP9 signalosome has roles beyond the regulation of photomorphogenesis as all mutants lacking this complex die following early seedling development, and an essentially identical complex has also been detected in animal systems (Chamovitz and Deng, 1995; Seeger et al., 1998; Wei et al., 1998). Our long term objective is to determine the role of the COP9 signalosome in controlling plant development. In this research project we showed that this complex contains at least eight subunits (Karniol et al., 1998; Serino et al., 1999) and that the 27 kD subunit is encoded by the FUS5 locus (Karniol et al., 1999). The FUS5 subunit also has a role extraneous to the COP9 signalosome, and differential kinase activity has been implicated in regulating FUSS and the COP9 signalosome (Karniol et al., 1999). We have also shown that the COP9 signalosome may work together with the translational-regulator eIF3. Our study of the COP9 signalosome is one of the exciting examples of plant science leading the way to discoveries in basic animal science (Chamovitz and Deng, 1995; Karniol and Chamovitz, 2000; Wei and Deng, 1999).
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7

Chejanovsky, Nor, and Suzanne M. Thiem. Isolation of Baculoviruses with Expanded Spectrum of Action against Lepidopteran Pests. United States Department of Agriculture, December 2002. http://dx.doi.org/10.32747/2002.7586457.bard.

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Our long-term goal is to learn to control (expand and restrict) the host range of baculoviruses. In this project our aim was to expand the host range of the prototype baculovirus Autographa cali/arnica nuclear polyhedrosis virus (AcMNPV) towards American and Israeli pests. To achieve this objective we studied AcMNPV infection in the non-permissive hosts L. dispar and s. littoralis (Ld652Y and SL2 cells, respectively) as a model system and the major barriers to viral replication. We isolated recombinant baculoviruses with expanded infectivity towards L. dispar and S. littoralis and tested their infectivity towards other Lepidopteran pests. The restricted host range displayed by baculoviruses constitutes an obstacle to their further implementation in the control of diverse Lepidopteran pests, increasing the development costs. Our work points out that cellular defenses are major role blocks to AcMNPV replication in non- and semi-permissive hosts. Therefore a major determinant ofbaculovirus host range is the ability of the virus to effectively counter cellular defenses of host cells. This is exemplified by our findings showing tliat expressing the viral gene Ldhrf-l overcomes global translation arrest in AcMNPV -infected Ld652Y cells. Our data suggests that Ld652Y cells have two anti-viral defense pathways, because they are subject to global translation arrest when infected with AcMNPV carrying a baculovirus apoptotic suppressor (e.g., wild type AcMNPV carryingp35, or recombinant AcMNPV carrying Opiap, Cpiap. or p49 genes) but apoptose when infected with AcMNPV-Iacking a functional apoptotic suppressor. We have yet to elucidate how hrf-l precludes the translation arrest mechanism(s) in AcMNPV-infected Ld652Y cells. Ribosomal profiles of AcMNPV infected Ld652Y cells suggested that translation initiation is a major control point, but we were unable to rule-out a contribution from a block in translation elongation. Phosphorylation of eIF-2a did not appear to playa role in AcMNPV -induced translation arrest. Mutagenesis studies ofhrf-l suggest that a highly acidic domain plays a role in precluding translation arrest. Our findings indicate that translation arrest may be linked to apoptosis either through common sensors of virus infection or as a consequence of late events in the virus life-cycle that occur only if apoptosis is suppressed. ~ AcMNPV replicates poorly in SL2 cells and induces apoptosis. Our studies in AcMNPV - infected SL2ceils led us to conclude that the steady-state levels of lEI (product of the iel gene, major AcMNPV -transactivator and multifunctional protein) relative to those of the immediate early viral protein lEO, playa critical role in regulating the viral infection. By increasing the IEl\IEO ratio we achieved AcMNPV replication in S. littoralis and we were able to isolate recombinant AcMNPV s that replicated efficiently in S. lifforalis cells and larvae. Our data that indicated that AcMNPV - infection may be regulated by an interaction between IE 1 and lED (of previously unknown function). Indeed, we showed that IE 1 associates with lED by using protein "pull down" and immunoprecipitation approaches High steady state levels of "functional" IE 1 resulted in increased expression of the apoptosis suppressor p35 facilitating AcMNPV -replication in SL2 cells. Finally, we determined that lED accelerates the viral infection in AcMNPV -permissive cells. Our results show that expressing viral genes that are able to overcome the insect-pest defense system enable to expand baculovirus host range. Scientifically, this project highlights the need to further study the anti-viral defenses of invertebrates not only to maximi~e the possibilities for manipulating baculovirus genomes, but to better understand the evolutionary underpinnings of the immune systems of vertebrates towards virus infection.
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