Relevant bibliographies by topics / Eps15L1

Academic literature on the topic 'Eps15L1'

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Published: 9 March 2023
Last updated: 10 March 2023

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Journal articles on the topic "Eps15L1"

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Milesi, Cinzia, Paola Alberici, Benedetta Pozzi, Amanda Oldani, Galina V. Beznoussenko, Andrea Raimondi, Blanche Ekalle Soppo, et al. "Redundant and nonredundant organismal functions of EPS15 and EPS15L1." Life Science Alliance 2, no. 1 (January 28, 2019): e201800273. http://dx.doi.org/10.26508/lsa.201800273.

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EPS15 and its homologous EPS15L1 are endocytic accessory proteins. Studies in mammalian cell lines suggested that EPS15 and EPS15L1 regulate endocytosis in a redundant manner. However, at the organismal level, it is not known to which extent the functions of the two proteins overlap. Here, by exploiting various constitutive and conditional null mice, we report redundant and nonredundant functions of the two proteins. EPS15L1 displays a unique nonredundant role in the nervous system, whereas both proteins are fundamental during embryo development as shown by the embryonic lethality of -Eps15/Eps15L1-double KO mice. At the cellular level, the major process redundantly regulated by EPS15 and EPS15L1 is the endocytosis of the transferrin receptor, a pathway that sustains the development of red blood cells and controls iron homeostasis. Consequently, hematopoietic-specific conditional Eps15/Eps15L1-double KO mice display traits of microcytic hypochromic anemia, due to a cell-autonomous defect in iron internalization.
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Guo, Mengbiao, Zhen-Dong Xiao, Zhiming Dai, Ling Zhu, Hang Lei, Li-Ting Diao, and Yuanyan Xiong. "The landscape of long noncoding RNA-involved and tumor-specific fusions across various cancers." Nucleic Acids Research 48, no. 22 (December 4, 2020): 12618–31. http://dx.doi.org/10.1093/nar/gkaa1119.

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Abstract The majority of the human genome encodes long noncoding RNA (lncRNA) genes, critical regulators of various cellular processes, which largely outnumber protein-coding genes. However, lncRNA-involved fusions have not been surveyed and characterized yet. Here, we present a systematic study of the lncRNA fusion landscape across cancer types and identify >30 000 high-confidence tumor-specific lncRNA fusions (using 8284 tumor and 6946 normal samples). Fusions positively correlated with DNA damage and cancer stemness and were specifically low in microsatellite instable (MSI)-High or virus-infected tumors. Moreover, fusions distribute differently among cancer molecular subtypes, but with shared enrichment in tumors that are microsatellite stable (MSS), with high somatic copy number alterations (SCNA), and with poor survival. Importantly, we find a potentially new mechanism, mediated by enhancer RNAs (eRNA), which generates secondary fusions that form densely connected fusion networks with many fusion hubs targeted by FDA-approved drugs. Finally, we experimentally validate functions of two tumor-promoting chimeric proteins derived from mRNA-lncRNA fusions, KDM4B–G039927 and EPS15L1–lncOR7C2–1. The EPS15L1 fusion protein may regulate (Gasdermin E) GSDME, critical in pyroptosis and anti-tumor immunity. Our study completes the fusion landscape in cancers, sheds light on fusion mechanisms, and enriches lncRNA functions in tumorigenesis and cancer progression.
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Ma, Jie, Li Zhang, Hai-Rong Bian, Zheng-Guo Lu, Lian Zhu, Ping Yang, Zhao-Chong Zeng, and Zuo-Lin Xiang. "A Noninvasive Prediction Nomogram for Lymph Node Metastasis of Hepatocellular Carcinoma Based on Serum Long Noncoding RNAs." BioMed Research International 2019 (July 1, 2019): 1–14. http://dx.doi.org/10.1155/2019/1710670.

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Background and Objectives. Lymph node metastasis (LNM) is common in hepatocellular carcinoma (HCC). In order to intervene HCC LNM in advance, we developed a prediction nomogram based on serum long noncoding RNA (lncRNA). Methods. Serum samples from 242 HCC patients were gathered and randomly enrolled into the training and validation cohorts. LncRNAs screened out from microarray were quantified with qRT-PCR. Univariate and multivariate analyses were applied for screening independent risk factors. A prediction nomogram was ultimately developed for HCC LNM. The nomogram was estimated by discrimination and calibration tests in the validation cohort. The effects of the candidate lncRNA on the malignant phenotypes of HCC cells were further explored by wound healing assay and colony formation assay. Results. ENST00000418803, lnc-ZNF35-4:1, lnc-EPS15L1-2:1, BCLC stage, and vascular invasion were selected as components of the nomogram according to the adjusted multivariate analysis. The nomogram effectively predicted the HCC LNM risk among the cohorts with suitable calibration fittings and displayed high discrimination with C-index of 0.89 and 0.85. Moreover, the abnormally high expression of lnc-EPS15L1-2:1 in HCC cell lines showed significant carcinogenic effects. Conclusions. The noninvasive nomogram may provide more diagnostic basis for treatments of HCC. The biomarkers identified can bring new clues to basic researches.
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Seiler, Christoph, Nichole Gebhart, Yong Zhang, Susan A. Shinton, Yue-sheng Li, Nicola L. Ross, Xingjun Liu, et al. "Mutagenesis Screen Identifies agtpbp1 and eps15L1 as Essential for T lymphocyte Development in Zebrafish." PLOS ONE 10, no. 7 (July 10, 2015): e0131908. http://dx.doi.org/10.1371/journal.pone.0131908.

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Roxrud, Ingrid, Camilla Raiborg, Nina Marie Pedersen, Espen Stang, and Harald Stenmark. "An endosomally localized isoform of Eps15 interacts with Hrs to mediate degradation of epidermal growth factor receptor." Journal of Cell Biology 180, no. 6 (March 24, 2008): 1205–18. http://dx.doi.org/10.1083/jcb.200708115.

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Down-regulation of activated and ubiquitinated growth factor (GF) receptors by endocytosis and subsequent lysosomal degradation ensures attenuation of GF signaling. The ubiquitin-binding adaptor protein Eps15 (epidermal growth factor receptor [EGFR] pathway substrate 15) functions in endocytosis of such receptors. Here, we identify an Eps15 isoform, Eps15b, and demonstrate its expression in human cells and conservation across vertebrate species. Although both Eps15 and Eps15b interact with the endosomal sorting protein Hrs (hepatocyte growth factor–regulated tyrosine kinase substrate) in vitro, we find that Hrs specifically binds Eps15b in vivo (whereas adaptor protein 2 preferentially interacts with Eps15). Although Eps15 mainly localizes to clathrin-coated pits at the plasma membrane, Eps15b localizes to Hrs-positive microdomains on endosomes. Eps15b overexpression, similarly to Hrs overexpression, inhibits ligand-mediated degradation of EGFR, whereas Eps15 is without effect. Similarly, depletion of Eps15b but not Eps15 delays degradation and promotes recycling of EGFR. These results indicate that Eps15b is an endosomally localized isoform of Eps15 that is present in the Hrs complex via direct Hrs interaction and important for the sorting function of this complex.
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Gu, Wenjin, Apurva Bhangale, Molly E. Heft Neal, Josh D. Smith, Collin Brummel, Jonathan B. McHugh, Matthew E. Spector, Ryan E. Mills, and J. Chad Brenner. "Analysis of Human Papilloma Virus Content and Integration in Mucoepidermoid Carcinoma." Viruses 14, no. 11 (October 26, 2022): 2353. http://dx.doi.org/10.3390/v14112353.

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Mucoepidermoid Carcinomas (MEC) represent the most common malignancies of salivary glands. Approximately 50% of all MEC cases are known to harbor CRTC1/3-MAML2 gene fusions, but the additional molecular drivers remain largely uncharacterized. Here, we sought to resolve controversy around the role of human papillomavirus (HPV) as a potential driver of mucoepidermoid carcinoma. Bioinformatics analysis was performed on 48 MEC transcriptomes. Subsequent targeted capture DNA sequencing was used to annotate HPV content and integration status in the host genome. HPV of any type was only identified in 1/48 (2%) of the MEC transcriptomes analyzed. Importantly, the one HPV16+ tumor expressed high levels of p16, had high expression of HPV16 oncogenes E6 and E7, and displayed a complex integration pattern that included breakpoints into 13 host genes including PIK3AP1, HIPI, OLFM4,SIRT1, ARAP2, TMEM161B-AS1, and EPS15L1 as well as 9 non-genic regions. In this cohort, HPV is a rare driver of MEC but may have a substantial etiologic role in cases that harbor the virus. Genetic mechanisms of host genome integration are similar to those observed in other head and neck cancers.
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Essa, Bothaina, Mona Al-Sharif, Mohamed Abdo, Liana Fericean, and Ahmed Ateya. "New Insights on Nucleotide Sequence Variants and mRNA Levels of Candidate Genes Assessing Resistance/Susceptibility to Mastitis in Holstein and Montbéliarde Dairy Cows." Veterinary Sciences 10, no. 1 (January 3, 2023): 35. http://dx.doi.org/10.3390/vetsci10010035.

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A major factor in the propagation of an infectious disease is host genetics. In this study, 180 dairy cows (90 of each breed: Holstein and Montbéliarde) were used. Each breed’s tested dairy cows were divided into two groups of comparable size (45 cows each), mastitis-free and mastitis-affected groups. Each cow’s jugular vein was punctured to obtain blood samples for DNA and RNA extraction. In the examined Holstein and Montbéliarde dairy cows, single nucleotide polymorphisms (SNPs) related with mastitis resistance/susceptibility were found in the RASGRP1, NFkB, CHL1, MARCH3, PDGFD, MAST3, EPS15L1, C1QTNF3, CD46, COX18, NEURL1, PPIE, and PTX3 genes. Chi-square analysis of identified SNPs revealed a significant difference in gene frequency between mastitic and healthy cows. Except for CHL1, mastitic dairy cows of two breeds had considerably higher mRNA levels of the examined genes than did healthy ones. Marker-assisted selection and monitoring of dairy cows’ susceptibility to mastitis may be accomplished through the use of discovered SNPs and changes in the gene expression profile of the studied genes. These findings also point to a possible method for reducing mastitis in dairy cows through selective breeding of animals using genetic markers linked to an animal’s ability to resist infection.
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Umair, M., A. Ullah, S. Abbas, F. Ahmad, S. Basit, and W. Ahmad. "First direct evidence of involvement of a homozygous loss-of-function variant in the EPS15L1 gene underlying split-hand/split-foot malformation." Clinical Genetics 93, no. 3 (January 25, 2018): 699–702. http://dx.doi.org/10.1111/cge.13152.

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Bens, Susanne, Andrea Haake, Holger Tönnies, Inga Vater, Ulrich Stephani, Paul-Martin Holterhus, Reiner Siebert, and Almuth Caliebe. "A de novo 1.1Mb microdeletion of chromosome 19p13.11 provides indirect evidence for EPS15L1 to be a strong candidate for split hand split foot malformation." European Journal of Medical Genetics 54, no. 5 (September 2011): e501-e504. http://dx.doi.org/10.1016/j.ejmg.2011.05.004.

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Doria, Margherita, Anna Elisabetta Salcini, Emanuela Colombo, Tristram G. Parslow, Pier Giuseppe Pelicci, and Pier Paolo Di Fiore. "The Eps15 Homology (Eh) Domain-Based Interaction between Eps15 and Hrb Connects the Molecular Machinery of Endocytosis to That of Nucleocytosolic Transport." Journal of Cell Biology 147, no. 7 (December 27, 1999): 1379–84. http://dx.doi.org/10.1083/jcb.147.7.1379.

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The Eps15 homology (EH) module is a protein–protein interaction domain that establishes a network of connections involved in various aspects of endocytosis and sorting. The finding that EH-containing proteins bind to Hrb (a cellular cofactor of the Rev protein) and to the related protein Hrbl raised the possibility that the EH network might also influence the so-called Rev export pathway, which mediates nucleocytoplasmic transfer of proteins and RNAs. In this study, we demonstrate that Eps15 and Eps15R, two EH-containing proteins, synergize with Hrb and Hrbl to enhance the function of Rev in the export pathway. In addition, the EH-mediated association between Eps15 and Hrb is required for the synergistic effect. The interaction between Eps15 and Hrb occurs in the cytoplasm, thus pointing to an unexpected site of action of Hrb, and to a possible role of the Eps15–Hrb complex in regulating the stability of Rev.
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Dissertations / Theses on the topic "Eps15L1"

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MILESI, CINZIA. "REDUNDANT AND NON-REDUNDANT ROLES OF THE ENDOCYTIC ADAPTOR PROTEINS EPS15 AND EPS15L1 IN MAMMALS." Doctoral thesis, Università degli Studi di Milano, 2017. http://hdl.handle.net/2434/466637.

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Eps15 and Eps15L1 are two endocytic adaptor proteins involved in both clathrin-dependent and clathrin-independent endocytosis of receptor tyrosine kinases. Due to their homology, Eps15 and Eps15L1 are thought to be redundant in several cellular processes. Their redundancy, however, has never been demonstrated in in vivo model systems. Our laboratory has generated genetically engineered mice to unravel the physiological functions of Eps15 and Eps15L1. We found that Eps15-KO (knockout) mice were healthy and fertile, while Eps15L1-KO mice died at birth because of neural defects, showing the specific function of Eps15L1 in neuronal development. Importantly, Eps15/Eps15L1-DKO (double knockout) mice had a more severe phenotype, dying at midgestation, suggesting redundancy in one or more fundamental developmental programs. The aim of this thesis project was to investigate redundant and non-redundant roles of Eps15 and Eps15L1, with the final goal to unmask the underlying causes of embryo lethality of Eps15/Eps15L1-DKO mice. Since Eps15/Eps15L1-DKO mice displayed a Notch loss-of-function phenotype, accompanied by a downregulation of Notch target genes, our initial hypothesis was that Eps15 and Eps15L1 were redundantly required in the regulation of the Notch signalling. To address this issue, we set-up a co-culture model system to recapitulate Notch signalling. In detail, we used MEFs (mouse embryonic fibroblasts) derived from Eps15- and Eps15L1-KO mice as a model system for the signal-sending cell and we co-cultured them with CHO (chinese hamster ovary) cells expressing the Notch receptor, as signal receiving cells. We found that Eps15L1, but not Eps15, played a non-redundant role in Notch signalling activation. This finding indicated that impaired Notch signalling was not responsible for the more severe phenotype observed in Eps15/Eps15L1-DKO mice compared to single KO mice. Whether Eps15 and Eps15L1 are required in signal-receiving cells will be addressed, using MEFs as a model for the signal-receiving cell. We found that angiogenesis was seriously compromised in Eps15/Eps15L1-DKO mice and, therefore, hypothesized that impaired vascular development might be the major cause of midgestation lethality of these mice. To address this issue, we generated cDKO (conditional Eps15/Eps15L1-DKO mice), which lack Eps15 and Eps15L1 in endothelial and hematopoietic cells. We found that cDKO mice displayed vascular defects but did not recapitulate the severe phenotype of constitutive DKO mice. This finding indicated that impaired angiogenesis was not the major lethality cause of constitutive DKO mice. However, by in vitro studies in endothelial cells, we found that Eps15 and Eps15L1 redundantly regulated VEGFR-2 turnover, thus indicating a possible cell-autonomous function of the proteins in vascular homeostasis, even if not sufficient to cause embryo lethality when functionally impaired. Previous in vitro studies have demonstrated a role for Eps15 and Eps15L1 in the CDE (clathrin-dependent endocytosis) of EGFR (epidermal growth factor receptor) and TfR (transferrin receptor). To confirm this role in a clean background, we used MEFs as a model system. By using radioactive assays, we found that Eps15 and Eps15L1 redundantly regulate the CDE of TfR. Indeed, in DKO cells, the Ke (endocytic rate constant) of the TfR was reduced to ~50% and, as a consequence, surface levels of TfR were increased, while single KO cells showed only a minor, if any, defect. Moreover, in DKO cells, we found that the number of AP-2-positive structures (which label clathrin-structures that form during CDE) was increased, but the structures were significantly smaller in size. Whether the maturation of clathrin-coated structures is altered in DKO cells will be addressed by live imaging studies. Next, we asked whether the role of Eps15 and Eps15L1 in TfR internalization had a physiological relevance in vivo. In detail, since TfR is essential for the biology of erythroid cells, we investigated whether erythroid development was impaired in cDKO mice, lacking Eps15 and Eps15L1 in endothelial and hematopoietic cells. We found that these mice suffered from microcytic hypochromic anemia: RBCs (red blood cells) had reduced MCV (mean corpuscular volume) and high RDW (red blood cell distribution width, index of anisocytosis), and reticulocyte counts were higher. These findings suggest that Eps15 and Eps15L1 redundantly regulate erythroid development. However, since cDKO mice did not recapitulate the severe phenotype of constitutive DKO mice, altered erythroid development per se was not the only cause of the early lethality of constitutive DKO mice. Further studies are required to investigate whether altered development of Eps15/Eps15L1-DKO erytroid cells correlates with increased surface levels of TfR and reduced iron uptake. These findings, combined with previous data generated in our laboratory, highlight that Eps15 and Eps15L1 regulate several cellular processes, both in a redundant and in a non-redundant manner. Functional impairment of these processes, together with other unexplored processes, might addictively contribute to the DKO phenotype.
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Lucano, C. "A NOVEL ROLE OF THE ENDOCYTIC ADAPTOR PROTEINS EPS15 AND EPS15L1 IN THE REGULATION OF NOTCH SIGNALING." Doctoral thesis, Università degli Studi di Milano, 2015. http://hdl.handle.net/2434/263596.

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Eps15 and Eps15L1 are endocytic adaptor proteins involved in both clathrin-mediated and clathrin-independent endocytosis of receptor tyrosine kinases. Eps15/Eps15L1 double knockout mice are embryonic lethal and display a Notch loss-of-function phenotype, accompanied by downregulation of Notch target genes. The Notch pathway is an evolutionary conserved signal transduction pathway that regulates multiple aspects of the development of multicellular organisms. Notch signaling activation requires direct contact between a signal-sending cell, expressing the ligand, and a signal-receiving cell, expressing the receptor. Both Notch ligands and receptors are transmembrane proteins, tightly regulated by endocytosis and membrane trafficking. Given these premises, the overall aim of this thesis was to understand whether Eps15 and Eps15L1 have a direct role in the regulation of Notch signaling, and, if so, whether this regulation takes place in the signal-receiving cell or in the signal-sending cell. Our final goal was to understand the molecular mechanisms by which Eps15 and Eps15L1 affect Notch signaling. To investigate the role of Eps15 and Eps15L1 in Notch signaling, we set-up a co-culture model system composed of the signal-sending cell OP9-Dll1 that overexpresses the ligand Dll1, and the signal-receiving cell C2C12-Notch1 that overexpresses the receptor Notch1. To assess the role of Eps15 and Eps15L1 in Notch signaling regulation, we developed an in vitro Notch transactivation reporter assay based on our co-culture model system. We observed no reduction in Notch activity after knockdown (KD) of Eps15 or Eps15L1 in the signal-receiving cell, indicating that the two proteins do not have a role in the regulation of Notch receptors. However, when we performed KD of Eps15 and/or Eps15L1 in the signal-sending cell, we observed a 40-50% reduction in Notch activity. This reduction was observed for all the Notch ligands tested, Dll1, Dll4, Jag1 and Jag2, indicating that Eps15 and Eps15L1 have a general role in the modulation of Notch ligand activity/signaling. Since Eps15 and Eps15L1 are known to act in combination with Epsin, a fundamental regulator of Notch ligand internalization, we investigated whether removal of Eps15 and Eps15L1 from the signal-sending cell affected the early steps of Dll1 endocytosis. To do so, we set-up a Dll1 internalization assay to measure induced or constitutive Dll1 endocytosis. Using this assay, we observed a strong reduction in Dll1 endocytosis following KD of known endocytic regulators of Notch ligands, Epsin and Mindbomb1. However, we did not detect any alterations in Dll1 internalization after KD of Eps15, Eps15L1 or both Eps15 and Eps15L1, indicating that the two proteins do not participate in the regulation of the early steps of Notch ligand endocytosis, both induced and constitutive. Eps15 and Eps15L1 have also been implicated in endocytic recycling. Therefore, we asked whether a recycling function of Eps15/Esp15L1 could be involved in Notch ligand regulation. We attempted to assess Dll1 recycling in OP9-Dll1 cells, however, results suggested that Dll1 does not undergo significant recycling in our experimental conditions, therefore a change of strategy will be necessary. We also assessed Dll1 localization in plasma membrane lipid rafts following KD of Eps15 and Eps15L1, but did not score any change in ligand membrane localization. In conclusion, we showed that Eps15 and Eps15L1 are key regulators of Notch ligands in the signal-sending cell. However, in contrast to their known role as endocytic adaptors, the two proteins do not appear to be involved in the early steps of Dll1 endocytosis. Given that Eps15 and Eps15L1 have been implicated in other pathways and cellular processes, such as recycling, secretion, degradation, cell-matrix adhesion and cell-cell connection, it is possible that Eps15/Esp15L1 might mediate Notch ligand regulation through one of these other pathways. However, the precise molecular mechanisms by which Eps15 and Eps15L1 regulate Dll1 activity remain to be defined, and will be the focus of future studies.
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Wairkar, Yogesh P. "The role of Eps15 in vesicle recycling at neuromuscular junctions of Drosophila melanogaster." Thesis, University of Cambridge, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.615848.

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Shah, Claudio S. [Verfasser]. "Structural and mechanistic analysis of membrane remodeling by Eps15-homology domain-containing protein 2 / Claudio S. Shah." Berlin : Freie Universität Berlin, 2013. http://d-nb.info/1044891912/34.

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POUPON, VIVIANE. "Etude du role de la proteine eps15 dans les phases precoces de l'endocytose dependante de la clathrine." Paris 6, 2000. http://www.theses.fr/2000PA066536.

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Nos travaux anterieurs ont etablis qu'eps15 est associe au complexe ap-2, un acteur central des puits recouverts de clathrine, ainsi que son role indispensable dans la voie d'endocytose dependante de la clathrine. Le but de ce travail a ete de mieux comprendre la fonction d'eps15. Deux approches complementaires ont ete utilisees. D'une part, nous avons tente de caracteriser de nouveaux partenaires pour eps15. L'utilisation de proteines recombinantes derivees d'eps15 a permis de caracteriser une proteine de 48 kd liant son domaine central. Nous avons clone cette proteine par purification, microsequencage et criblage des banques d'est. Cette nouvelle proteine caracterise une famille d'acyl-coa thioesterase tres conservee au cours de l'evolution que nous avons localise dans les mitochondries, ce qui nous a pousse a abandonner l'etude de son role dans l'endocytose. D'autre part, nous avons etudie les mecanismes d'adressage d'eps15 dans les puits recouverts. L'analyse de la distribution intracellulaire de mutants d'eps15 a demontre que sa localisation au sein des puits resulte d'une collaboration de son domaine n-terminal avec le domaine de liaison au complexe ap-2. Le fait que l'adressage d'eps15 dans les puits recouverts ne soit pas simplement du a sa liaison a ap-2 suggere un role actif d'eps15 dans le recrutement d'ap-2, hypothese en accord avec le fait que des mutants d'eps15 inhibent l'assemblage des puits. Enfin, l'analyse systematique de la localisation intracellulaire de l'ensemble des mutants d'eps15, nous a permis de mettre en evidence l'existence d'un nouveau domaine fonctionnel. Ce domaine, localise dans les 50 derniers acides amines, a toutes les caracteristiques d'un signal d'export nucleaire, suggerant qu'eps15 serait capable de naviguer entre le cytosol et le noyau. Cette observation permet d'integrer les donnees initiales identifiant eps15 comme substrat du recepteur de l'egf et de proposer une double fonction dans l'endocytose et la signalisation.
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Bélanger, Catherine. "The Parkinson's disease gene, Parkin, ubiquitinates the endocytic accessory protein Eps15 and regulates endocytosis of the epidermal growth factor receptor /." Thesis, McGill University, 2006. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=101705.

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Mutations in the parkin gene are responsible for an early-onset autosomal-recessive form of Parkinson's disease. Parkin is an E3 ubiquitin ligase that acts in the covalent attachment of the small protein ubiquitin to substrate proteins. Although many parkin substrates have been identified, none can fully account for the relatively specific death of the dopaminergic neurons in the substantia nigra that occurs in Parkinson's disease. Using an assay that reconstitutes the ubiquitination reaction completely in vitro, I found that not all disease-associated mutations affected parkin's ligase activity. I used this assay to test a potential parkin substrate identified in our lab, the endocytic accessory protein Eps15, which specifically interacts with parkin in a regulated fashion. I found that parkin directly ubiquitinates Eps15 in vitro. Eps15 ubiquitination is known to occur during the process of ligand-induced downregulation of the epidermal growth factor receptor. I found that overexpressing parkin in COS-7 cells inhibited the first step of this process, namely, receptor internalization. These findings add to the knowledge of how pathogenic mutations affect parkin function, and identify a novel role for parkin as a regulator of ligand-induced downregulation of the epidermal growth factor receptor.
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Tsushima, Hanako. "A study of the interactors of Eps15 homology domain and the role of the EH network in the model system of Caenorhabditis elegans." Thesis, Open University, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.497396.

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Epsl5 homology (EH) domain-containing proteins have been implicated in diverse intracellular signalling pathways, such as endocytosis, actin cytoskeleton organization, nucleo-cytosolic shuttling and mitogenic signalling. However, the extent of the protein-protein interactions mediated by the EH domain at the level of a whole organism has not yet been addressed. This project aims to gain an overview of the EH network in a model system, C. elegans, by identifying interactors of all EH-domain containing proteins present in C. elegans. Five genes encode EH proteins in the C. elegans genome and the isolated EH domains were used to screen a C. elegans cDNA library using the Yeast Two Hybrid system. The validation of the putative interactions was carried out by in vitro pull-down assays. The biological relevance of the interactions was tested genetically using C elegans as a model system. The genetic interactions were monitored using available mutants for four of the five EH encoding genes, in which the genes of the putative interactors were knocked-down by RNA interference.
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Lin, Amy Wei Pey. "Regulation of glutamatergic AMPA receptor stability and trafficking by ubiquitination." Thesis, 2013. https://hdl.handle.net/2144/13152.

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AMPA-type glutamate receptors (AMPARs) play a critical role in mediating the majority of fast excitatory synaptic transmission in the brain, where alterations in receptor expression, distribution and trafficking have been shown to underlie synaptic plasticity and higher brain function. However, the molecular mechanisms regulating AMPAR surface expression and turnover are still not fully understood. We report that mammalian AMPARs are subject to post-translational modification by ubiquitin, and identify Nedd4 as the E3 ligase responsible for mediating this process. AMPAR ubiquitination enhanced receptor degradation and reduced AMPAR cell-surface expression; conversely, inhibition of proteasomal activity caused AMPAR accumulation. Using site-directed mutagenesis we replaced each of four lysine residues available as putative ubiquitination sites on the AMPAR subunit GluA1 C-terminal with an arginine and identified critical residues for ubiquitination and receptor degradation. Consistent with the role of protein ubiquitination, lysine mutation reduced the efficiency of AMPAR endocytosis. We further investigated the molecular mechanisms involved in the internalization of ubiquitinated AMPARs. We find that the endocytic adaptor protein Eps15 plays a critical role in this process. siRNA-mediated suppression or overexpression of Eps15 results in changes in AMPAR surface expression. Eps15 interaction with AMPARs requires Nedd4-mediated GluA1 ubiquitination along with the ubiquitin interacting motif (UIM) of Eps15. Consistent with ubiquitination-mediated receptor internalization, knockdown of Eps15 suppresses GluA1 internalization of wild-type GluA1, but not a mutant GluA1 lacking ubiquitination sites, indicating a crucial role for Eps15 in the trafficking of ubiquitinated AMPARs. These findings reveal novel regulatory mechanisms in the control of glutamate receptor amount and distribution dynamics, which are key factors implicated in higher brain functions and neurological disorders.
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Book chapters on the topic "Eps15L1"

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van Delft, Sanne, Arie J. Verkleij, and Paul M. P. van Bergen en Henegouwen. "A function for Eps15 in EGF-receptor endocytosis?" In Molecular Mechanisms of Signalling and Membrane Transport, 151–61. Berlin, Heidelberg: Springer Berlin Heidelberg, 1997. http://dx.doi.org/10.1007/978-3-642-60799-8_10.

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van Delft, Sanne, Arie J. Verkleij, and Paul M. P. van Bergen en Henegouwen. "A Function for EGF-Induced Eps15 Ubiquitination in Endocytosis." In Lipid and Protein Traffic, 85–94. Berlin, Heidelberg: Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/978-3-642-51463-0_7.

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"Eps15 Interacting Protein." In Encyclopedia of Signaling Molecules, 1604. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_101151.

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Conference papers on the topic "Eps15L1"

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Jagannathan, N. Suhas, Christopher W. V. Hogue, and Lisa Tucker-Kellogg. "De novo ensemble modeling suggests that AP2-binding to disordered regions can increase steric volume of Epsin but not Eps15." In Pacific Symposium on Biocomputing 2020. WORLD SCIENTIFIC, 2019. http://dx.doi.org/10.1142/9789811215636_0017.

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You might also be interested in the extended bibliographies on the topic 'Eps15L1' for particular source types:
Journal articles
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