Готові списки джерел за темами / LIM domain

Добірка наукової літератури з теми "LIM domain"

Автор: Grafiati

Опубліковано: 4 червня 2021

Оновлено: 4 лютого 2022

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Статті в журналах з теми "LIM domain":

Matthews, Jacqueline M., Mugdha Bhati, Vanessa J. Craig, Janet E. Deane, Cy Jeffries, Christopher Lee, Amy L. Nancarrow, Daniel P. Ryan, and Margaret Sunde. "Competition between LIM-binding domains." Biochemical Society Transactions 36, no. 6 (November 19, 2008): 1393–97. http://dx.doi.org/10.1042/bst0361393.

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LMO (LIM-only) and LIM-HD (LIM-homeodomain) proteins form a family of proteins that is required for myriad developmental processes and which can contribute to diseases such as T-cell leukaemia and breast cancer. The four LMO and 12 LIM-HD proteins in mammals are expressed in a combinatorial manner in many cell types, forming a transcriptional ‘LIM code’. The proteins all contain a pair of closely spaced LIM domains near their N-termini that mediate protein–protein interactions, including binding to the ∼30-residue LID (LIM interaction domain) of the essential co-factor protein Ldb1 (LIM domain-binding protein 1). In an attempt to understand the molecular mechanisms behind the LIM code, we have determined the molecular basis of binding of LMO and LIM-HD proteins for Ldb1LID through a series of structural, mutagenic and biophysical studies. These studies provide an explanation for why Ldb1 binds the LIM domains of the LMO/LIM-HD family, but not LIM domains from other proteins. The LMO/LIM-HD family exhibit a range of affinities for Ldb1, which influences the formation of specific functional complexes within cells. We have also identified an additional LIM interaction domain in one of the LIM-HD proteins, Isl1. Despite low sequence similarity to Ldb1LID, this domain binds another LIM-HD protein, Lhx3, in an identical manner to Ldb1LID. Through our and other studies, it is emerging that the multiple layers of competitive binding involving LMO and LIM-HD proteins and their partner proteins contribute significantly to cell fate specification and development.

Breen, Joseph J., Alan D. Agulnick, Heiner Westphal, and Igor B. Dawid. "Interactions between LIM Domains and the LIM Domain-binding Protein Ldb1." Journal of Biological Chemistry 273, no. 8 (February 20, 1998): 4712–17. http://dx.doi.org/10.1074/jbc.273.8.4712.

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Shang, Ming-Mei, Husain A. Talukdar, Jennifer J. Hofmann, Colin Niaudet, Hassan Foroughi Asl, Rajeev K. Jain, Aranzazu Rossignoli, et al. "Lim Domain Binding 2." Arteriosclerosis, Thrombosis, and Vascular Biology 34, no. 9 (September 2014): 2068–77. http://dx.doi.org/10.1161/atvbaha.113.302709.

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El Omari, Kamel, Sarah J. Hoosdally, Kapil Tuladhar, Dimple Karia, Paresh Vyas, Roger Patient, Catherine Porcher, and Erika J. Mancini. "Structure of the leukemia oncogene LMO2: implications for the assembly of a hematopoietic transcription factor complex." Blood 117, no. 7 (February 17, 2011): 2146–56. http://dx.doi.org/10.1182/blood-2010-07-293357.

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Abstract The LIM only protein 2 (LMO2) is a key regulator of hematopoietic stem cell development whose ectopic expression in T cells leads to the onset of acute lymphoblastic leukemia. Through its LIM domains, LMO2 is thought to function as the scaffold for a DNA-binding transcription regulator complex, including the basic helix-loop-helix proteins SCL/TAL1 and E47, the zinc finger protein GATA-1, and LIM-domain interacting protein LDB1. To understand the role of LMO2 in the formation of this complex and ultimately to dissect its function in normal and aberrant hematopoiesis, we solved the crystal structure of LMO2 in complex with the LID domain of LDB1 at 2.4 Å resolution. We observe a largely unstructured LMO2 kept in register by the LID binding both LIM domains. Comparison of independently determined crystal structures of LMO2 reveals large movements around a conserved hinge between the LIM domains. We demonstrate that such conformational flexibility is necessary for binding of LMO2 to its partner protein SCL/TAL1 in vitro and for the function of this complex in vivo. These results, together with molecular docking and analysis of evolutionarily conserved residues, yield the first structural model of the DNA-binding complex containing LMO2, LDB1, SCL/TAL1, and GATA-1.

NAGATA, Kyoko, Kazumasa OHASHI, Neng YANG, and Kensaku MIZUNO. "The N-terminal LIM domain negatively regulates the kinase activity ofLIM-kinase 1." Biochemical Journal 343, no. 1 (September 24, 1999): 99–105. http://dx.doi.org/10.1042/bj3430099.

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LIM-kinase 1 (LIMK1, where LIM is an acronym of the three gene products Lin-11, Isl-1 and Mec-3) is a serine/threonine kinase that phosphorylates cofilin and regulates actin cytoskeletal reorganization. LIMK1 contains two LIM domains and a PDZ (an acronym of the three proteins PSD-95, Dlg and ZO-1) domain in the N-terminal half and a kinase domain in the C-terminal half. In this study we examined the role of the extra-catalytic region in the regulation of kinase activity of LIMK1. Limited proteolysis of LIMK1 resulted in the production of the 35-40-kDa kinase core fragments with 3.5-5.5-fold increased kinase activity. The LIMK1 mutants with deleted LIM domains (δLIM) or conserved cysteines in the two LIM domains replaced with glycines (dmLIMK1) had 3-7-fold higher kinase activitiesin vitro, compared with the wild-type LIMK1. The C-terminal kinase fragment of LIMK1 bound to the LIM domain but not to the PDZ domain. Furthermore, the LIM fragment dose-dependently inhibited the kinase catalytic activity of the kinase core fragment of LIMK1. Taken together, these results suggest that the N-terminal LIM domain negatively regulates the kinase activity of LIMK1 by direct interaction with the C-terminal kinase domain. In addition, expression of the δLIM mutant in cultured cells induced punctate accumulation of actin filaments, an event distinct from the pattern of actin organization induced by expression of the wild-type LIMK1, suggesting that the LIM domain plays a role in the function of LIMK1in vivo.

Winkelman, Jonathan D., Caitlin A. Anderson, Cristian Suarez, David R. Kovar, and Margaret L. Gardel. "Evolutionarily diverse LIM domain-containing proteins bind stressed actin filaments through a conserved mechanism." Proceedings of the National Academy of Sciences 117, no. 41 (September 28, 2020): 25532–42. http://dx.doi.org/10.1073/pnas.2004656117.

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The actin cytoskeleton assembles into diverse load-bearing networks, including stress fibers (SFs), muscle sarcomeres, and the cytokinetic ring to both generate and sense mechanical forces. The LIM (Lin11, Isl- 1, and Mec-3) domain family is functionally diverse, but most members can associate with the actin cytoskeleton with apparent force sensitivity. Zyxin rapidly localizes via its LIM domains to failing SFs in cells, known as strain sites, to initiate SF repair and maintain mechanical homeostasis. The mechanism by which these LIM domains associate with stress fiber strain sites (SFSS) is not known. Additionally, it is unknown how widespread strain sensing is within the LIM protein family. We identify that the LIM domain-containing region of 18 proteins from the Zyxin, Paxillin, Tes, and Enigma proteins accumulate to SFSS. Moreover, the LIM domain region from the fission yeast protein paxillin like 1 (Pxl1) also localizes to SFSS in mammalian cells, suggesting that the strain sensing mechanism is ancient and highly conserved. We then used sequence and domain analysis to demonstrate that tandem LIM domains contribute additively, for SFSS localization. Employing in vitro reconstitution, we show that the LIM domain-containing region from mammalian zyxin and fission yeast Pxl1 binds to mechanically stressed F-actin networks but does not associate with relaxed actin filaments. We propose that tandem LIM domains recognize an F-actin conformation that is rare in the relaxed state but is enriched in the presence of mechanical stress.

Jurata, L. W., and G. N. Gill. "Functional analysis of the nuclear LIM domain interactor NLI." Molecular and Cellular Biology 17, no. 10 (October 1997): 5688–98. http://dx.doi.org/10.1128/mcb.17.10.5688.

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LIM homeodomain and LIM-only (LMO) transcription factors contain two tandemly arranged Zn2+-binding LIM domains capable of mediating protein-protein interactions. These factors have restricted patterns of expression, are found in invertebrates as well as vertebrates, and are required for cell type specification in a variety of developing tissues. A recently identified, widely expressed protein, NLI, binds with high affinity to the LIM domains of LIM homeodomain and LMO proteins in vitro and in vivo. In this study, a 38-amino-acid fragment of NLI was found to be sufficient for the association of NLI with nuclear LIM domains. In addition, NLI was shown to form high affinity homodimers through the amino-terminal 200 amino acids, but dimerization of NLI was not required for association with the LIM homeodomain protein Lmxl. Chemical cross-linking analysis revealed higher-order complexes containing multiple NLI molecules bound to Lmx1, indicating that dimerization of NLI does not interfere with LIM domain interactions. Additionally, NLI formed complexes with Lmx1 on the rat insulin I promoter and inhibited the LIM domain-dependent synergistic transcriptional activation by Lmx1 and the basic helix-loop-helix protein E47 from the rat insulin I minienhancer. These studies indicate that NLI contains at least two functionally independent domains and may serve as a negative regulator of synergistic transcriptional responses which require direct interaction via LIM domains. Thus, NLI may regulate the transcriptional activity of LIM homeodomain proteins by determining specific partner interactions.

te Velthuis, Aartjan J. W., and Christoph P. Bagowski. "PDZ and LIM Domain-Encoding Genes: Molecular Interactions and their Role in Development." Scientific World JOURNAL 7 (2007): 1470–92. http://dx.doi.org/10.1100/tsw.2007.232.

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PDZ/LIM genes encode a group of proteins that play very important, but diverse, biological roles. They have been implicated in numerous vital processes, e.g., cytoskeleton organization, neuronal signaling, cell lineage specification, organ development, and oncogenesis.In mammals, there are ten genes that encode for both a PDZ domain, and one or several LIM domains: four genes of the ALP subfamily (ALP, Elfin, Mystique, and RIL), three of the Enigma subfamily (Enigma, Enigma Homolog, and ZASP), the two LIM kinases (LIMK1 and LIMK2), and the LIM only protein 7 (LMO7). Functionally, all PDZ and LIM domain proteins share an important trait, i.e., they can associate with and/or influence the actin cytoskeleton.We review here the PDZ and LIM domain—encoding genes and their different gene structures, their binding partners, and their role in development and disease. Emphasis is laid on the important questions: why the combination of a PDZ domain with one or more LIM domains is found in such a diverse group of proteins, and what role the PDZ/LIM module could have in signaling complex assembly and localization.Furthermore, the current knowledge on splice form specific expression and the function of these alternative transcripts during vertebrate development will be discussed, since another source of complexity for the PDZ and LIM domain—encoding proteins is introduced by alternative splicing, which often creates different domain combinations.

Schmeichel, K. L., and M. C. Beckerle. "Molecular dissection of a LIM domain." Molecular Biology of the Cell 8, no. 2 (February 1997): 219–30. http://dx.doi.org/10.1091/mbc.8.2.219.

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LIM domains are novel sequence elements that are found in more than 60 gene products, many of which function as key regulators of developmental pathways. The LIM domain, characterized by the cysteine-rich consensus CX2CX16-23HX2CX2CX2CX16-21 CX2-3(C/H/ D), is a specific mental-binding structure that consists of two distinct zinc-binding subdomains. We and others have recently demonstrated that the LIM domain mediates protein-protein interactions. However, the sequences that define the protein-binding specificity of the LIM domain had not yet been identified. Because structural studies have revealed that the C-terminal zinc-binding module of a LIM domain displays a tertiary fold compatible with nucleic acid binding, it was of interest to determine whether the specific protein-binding activity of a LIM domain could be ascribed to one of its two zinc-binding subdomains. To address this question, we have analyzed the protein-binding capacity of a model LIM peptide, called zLIM1, that is derived from the cytoskeletal protein zyxin. These studies demonstrate that the protein-binding function of zLIM1 can be mapped to sequences contained within its N-terminal zinc-binding module. The C-terminal zinc-binding module of zLIM1 may thus remain accessible to additional interactive partners. Our results raise the possibility that the two structural subdomains of a LIM domain are capable of performing distinct biochemical functions.

Brown, Michael C., Joseph A. Perrotta, and Christopher E. Turner. "Serine and Threonine Phosphorylation of the Paxillin LIM Domains Regulates Paxillin Focal Adhesion Localization and Cell Adhesion to Fibronectin." Molecular Biology of the Cell 9, no. 7 (July 1998): 1803–16. http://dx.doi.org/10.1091/mbc.9.7.1803.

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We have previously shown that the LIM domains of paxillin operate as the focal adhesion (FA)-targeting motif of this protein. In the current study, we have identified the capacity of paxillin LIM2 and LIM3 to serve as binding sites for, and substrates of serine/threonine kinases. The activities of the LIM2- and LIM3-associated kinases were stimulated after adhesion of CHO.K1 cells to fibronectin; consequently, a role for LIM domain phosphorylation in regulating the subcellular localization of paxillin after adhesion to fibronectin was investigated. An avian paxillin-CHO.K1 model system was used to explore the role of paxillin phosphorylation in paxillin localization to FAs. We found that mutations of paxillin that mimicked LIM domain phosphorylation accelerated fibronectin-induced localization of paxillin to focal contacts. Further, blocking phosphorylation of the LIM domains reduced cell adhesion to fibronectin, whereas constitutive LIM domain phosphorylation significantly increased the capacity of cells to adhere to fibronectin. The potentiation of FA targeting and cell adhesion to fibronectin was specific to LIM domain phosphorylation as mutation of the amino-terminal tyrosine and serine residues of paxillin that are phosphorylated in response to fibronectin adhesion had no effect on the rate of FA localization or cell adhesion. This represents the first demonstration of the regulation of protein localization through LIM domain phosphorylation and suggests a novel mechanism of regulating LIM domain function. Additionally, these results provide the first evidence that paxillin contributes to “inside-out” integrin-mediated signal transduction.

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Дисертації з теми "LIM domain":

Tuladhar, Kapil. "Lim-only domain proteins in developmental haematopoiesis." Thesis, University of Oxford, 2012. http://ora.ox.ac.uk/objects/uuid:d6b73e89-7095-402f-9d9f-4d7837a4db00.

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The production of adult blood initiates from the haematopoietic stem cell (HSC). This clinically important cell has the capacity to maintain all blood lineages throughout the lifetime of an organism. HSCs emerge de novo from the haemogenic endothelium in the ventral wall of the embryonic dorsal aorta, from where they go on to seed adult sites of haematopoiesis. We have shown that Lmo4a is required for the emergence of HSCs in the zebrafish, and go on to demonstrate that Lmo4a regulates expression of the critical transcription factor, gata2a. Strikingly, both over- and under-expression of gata2a in the dorsal aorta severely diminishes HSC production. The LIM-only domain protein Lmo4 has previously been shown to interact with the known haematopoietic regulator, Ldb1. Together with our collaborators, we have identified novel binding partners of Lmo4 in mouse erythroleukaemic cells. Our functional analysis shows that many of these partners are also necessary for HSC emergence, thus revealing several new potential regulators of HSC formation. Given that these proteins were identified in an in vitro model of definitive erythropoiesis, it is remarkable that they also appear to act together in vivo at the level of HSC formation, and our data suggests that a transcriptional complex containing Lmo4 and these partners may directly repress gata2a. The related protein Lmo2 is also known to bind Ldb1. Together with Scl, Lmo2 is a master regulator of the haemangioblast programme. We have been utilising this activity, together with recent structural studies, to identify functionally important residues in the Lmo2 molecule. As a cell’s transcriptional programme drives both normal and pathological development, and misexpression of both Lmo2 and Lmo4 is involved in a variety of oncogenic states, the work presented in this thesis is likely to inform efforts to develop therapeutically relevant reagents.

Jurata, Linda Wagner. "Identification and analysis of the nuclear LIM domain interactor NLI /." Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 1998. http://wwwlib.umi.com/cr/ucsd/fullcit?p9904815.

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Diefenbacher, Markus Elmar. "The transcriptional co-activator function of the LIM-domain protein nTrip6." Eggenstein-Leopoldshafen Forschungszentrum Karlsruhe GmbH, 2010. http://d-nb.info/1002907535/34.

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Gu, Wenchao. "Exploring the roles of LIM domain binding proteins in zebrafish development." Thesis, University of Oxford, 2014. http://ora.ox.ac.uk/objects/uuid:54f520f6-170a-480a-a195-1a0739055031.

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As some of the most important and widely utilised intercellular signalling molecules, transforming growth factor βs (TGFβs) play critical roles in normal development and in human disease. Establishing appropriate levels of signalling involves positive and negative feedback, driven by the same signal transduction components, but whether or how the two are distinguished has not previously been understood. Here we show that LIM domain binding proteins (Ldbs) drive the Smad6/7-mediated negative feedback of TGFβ signalling, but they are not required for the ligand-driven positive feedback or other downstream transcriptional activation. In Ldb-deficient zebrafish embryos, the homeostasis of TGFβ signalling is perturbed. As a consequence, signalling of TGFβ family members, Nodal and BMP, is stably enhanced, giving rise to excess mesoderm and endoderm, an effect that can be rescued by reducing Nodal and BMP. Later in development, conditional ldb2a knockdown causes defective vascular, angiogenic and haemogenic development, likely also by elevating TGFβ signalling. Thus, Ldbs control the homeostatic regulation of TGFβ signalling and therefore play critical roles in diverse developmental processes.

Klaavuniemi, T. (Tuula). "PDZ-LIM domain proteins and α-actinin at the muscle Z-disk". Doctoral thesis, University of Oulu, 2006. http://urn.fi/urn:isbn:9514282647.

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Abstract The Z-disk is a sophisticated structure that connects adjacent sarcomeres in striated muscle myofibrils. α-Actinin provides strength to the Z-disks by crosslinking the actin filaments of adjacent sarcomeres. α-Actinin is an antiparallel homodimer, composed of an N-terminal actin binding domain (ABD), the central rod domain, and two pairs of C-terminal EF-hands. The PDZ-LIM domain proteins interact with α-actinin at the Z-disk. Of these proteins, only the actinin-associated LIM protein (ALP), Z-band alternatively spliced PDZ-containing protein (ZASP/Cypher) and C-terminal LIM protein (CLP36) have a ZASP/Cypher-like (ZM) motif consisting of 26-27 conserved residues in the internal region between the PDZ and LIM domains. The aim of this work was to understand the molecular interplay between the ZM-motif containing members of the PDZ-LIM proteins and α-actinin. To unveil the biological relevance of the interaction between the PDZ-LIM proteins and α-actinin, naturally occurring human ZASP/Cypher mutations were analyzed. Two interaction sites were found between ALP, CLP36 and α-actinin using recombinant purified proteins in surface plasmon resonance (SPR) analysis. The PDZ domain of ALP and CLP36 recognized the C-terminus of α-actinin, whereas the internal regions bound to the rod domain. Further characterization showed that the ALP internal region adopts and extended conformation when interacting with α-actinin and that the ZM-motif partly mediated the interaction, but did not define the entire interaction area. ZASP/Cypher also interacted and competed with ALP in binding to the rod domain. The internal fragments containing the ZM-motif were important for co-localization of ALP and ZASP/Cypher with α-actinin at the Z-disks and on stress fibers. The absence of ALP and ZASP/Cypher in focal contacts indicates that other interacting molecules, for instance vinculin and integrin, may compete in binding to the rod in these areas or additional proteins are required in targeting to these locations. The co-localization of the ZASP/Cypher with α-actinin could be released by disrupting the stress fibers leading to an accumulation of α-actinin in the cell periphery, whereas ZASP/Cypher was not in these areas. This suggests that an intact cytoskeleton is important for ZASP/Cypher interaction with α-actinin. Earlier studies have shown that mutations in the ZASP/Cypher internal region are associated with muscular diseases. These mutations, however, did not affect ZASP/Cypher co-localization with α-actinin or the stability of ZASP/Cypher proteins. The Z-disk possesses a stretch sensor, which is involved in triggering hypertrophic growth as a compensatory mechanism to increased workloads. α-Actinin is a docking site of molecules that are involved in hypertrophic signaling cascades mediated by calsarcin-calcineurin and protein kinase C (PKC) isoforms. The internal interaction site may be involved in targeting PKCs, which bind to the LIM domains of ZASP/Cypher, to the Z-disks. The similar location of the internal interaction site with calsarcin on the rod suggests that ZASP/Cypher, ALP and CLP36 may regulate calsarcin-mediated hypertrophic signaling.

Diefenbacher, Markus Elmar [Verfasser]. "The transcriptional co-activator function of the LIM-domain protein nTrip6 / Markus Elmar Diefenbacher." Eggenstein-Leopoldshafen : Forschungszentrum Karlsruhe GmbH, 2010. http://d-nb.info/1002907535/34.

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Khurana, Bharat. "Characterization of DLIM1, a novel cytoskeleton-associated LIM domain containing protein of Dictyostelium discoideum." [S.l. : s.n.], 2000. http://deposit.ddb.de/cgi-bin/dokserv?idn=961945737.

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Proeschel, Christoph Johann Wolfgang. "The cloning and characterisation of Lnk-1 : a novel LIM-domain containing protein kinase." Thesis, University College London (University of London), 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.294778.

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Diefenbacher, Markus Elmar [Verfasser], and A. [Akademischer Betreuer] Cato. "The transcriptional co-activator function of the LIM-domain protein nTrip6 / Markus Elmar Diefenbacher. Betreuer: A. Cato." Karlsruhe : KIT-Bibliothek, 2009. http://d-nb.info/1014222877/34.

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Banthien, Nils [Verfasser]. "The four-and-a-half-LIM-domain Protein FHL2 is a novel regulator of pulmonary fibrosis / Nils Banthien." Gießen : Universitätsbibliothek, 2020. http://d-nb.info/1216142955/34.

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Книги з теми "LIM domain":

Khalīl, Saʻd Muḥammad. Nazʻ al-milkīyah lil-manfaʻah al-ʻāmmah: Bayna al-sharīʻah wa-al-qānūn. [Cairo]: Dār al-Salām lil-Ṭibāʻah wa-al-Nashr wa-al-Tawzīʻ wa-al-Tarjamah, 1993.

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Nāṣir, Muḥammad al-Ḥājj. al- Islām wa-intizāʻ al-milk lil-maṣlaḥah al-ʻāmmah. [Rabat]: al-Mamlakah al-Maghribīyah, Wizārat al-Awqāf wa-al-Shuʼūn al-Islāmīyah, 1991.

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Druet, Olivier. The Lin-Ni's problem for mean convex domains. Providence, R.I: American Mathematical Society, 2011.

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Naqʻāwī, Ḥāmid. al- Jadīd fī qānūn al-intizāʻ lil-maṣlaḥah al-ʻumūmīyah: Al-Qānūn ʻadad 26 li-sanat 2003 al-muʼarrakh fī 14 Afrīl 2003. 8-ме вид. Ḥammām Sūsah: Dār al-Mīzān lil-Nashr, 2003.

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al-Laṭīf, Muḥammad ʻAbd. Nazʻ al-milkīyah lil-manfaʻah al-ʻāmmah: Dirāsah taʼṣīlīyah muqāranah. [Cairo]: Dār al-Nahḍah al-ʻArabīyah, 1988.

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Egypt. Qānūn raqm 10 li-sanat 1990: Bi-shaʼn nazʻ milkīyat al-ʻaqārāt lil-manfaʻah al-ʻāmmah wa-lāʼiḥatuhu al-tanfīdhīyah. 8-ме вид. al-Qāhirah: al-Hayʼah al-ʻĀmmah li-Shuʼūn al-Maṭābiʻ al-Amīrīyah, 1992.

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Nāṣir, Muḥammad al-Ḥājj. al- Islām wa-intizāʻ al-milk lil-maṣlaḥah al-ʻāmmah. [Rabat]: al-Mamlakah al-Maghrabīyah, Wizārat al-Awqāf wa-al-Shuʾūn al-Islāmīyah, 1991.

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Ṭuʻmah, Khālid. al-Tajribah al-Kuwaytīyah fī nazʻ al-milkīyah: Dirāsah sharʻīyah qānūnīyah ʻan nazʻ al-milkīyah lil-manfaʻah al-ʻāmmah fī Dawlat al-Kuwayt. 8-ме вид. al-Kuwayt: Khālid Ṭuʻmah, 2009.

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Egypt. Qānūn raqm 577 li-sanat 1954: Bi-shaʼn nazʻ milkīyat al-ʻaqārāt lil-manfaʻah al-ʻāmmah aw al-taḥsīn, mutaḍamminan mudhakkiratahu al-īḍāḥīyah, al-qarārat al-mutaʻalliqah bi-nazʻ al-milkīyah. 8-ме вид. al-Qāhirah: al-Hayʼah al-ʻĀmmah li-Shuʼūn al-Maṭābiʻ al-Amīrīyah, 1990.

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Roos, Guy. Systèmes triples de Jordan et domaines symétriques. Paris: Hermann, 1992.

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Частини книг з теми "LIM domain":

Pantelis, D., J. Kirfel, R. Büttner, A. Hirner, and J. C. Kalff. "Role of four and one half LIM domain protein FHL2 on intestinal anastomotic healing." In Deutsche Gesellschaft für Chirurgie, 9–10. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-642-00625-8_4.

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Schessl, Joachim. "Scapuloperoneal Disorders and Reducing Body Myopathy Associated with the Four and Half LIM Domain Protein 1." In Muscle Disease, 175–77. Oxford, UK: John Wiley & Sons, Ltd, 2013. http://dx.doi.org/10.1002/9781118635469.ch19.

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Jurata, L. W., and G. N. Gill. "Structure and Function of LIM Domains." In Protein Modules in Signal Transduction, 75–113. Berlin, Heidelberg: Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/978-3-642-80481-6_4.

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Greene, Robert E., Kang-Tae Kim, and Steven G. Krantz. "Lie Groups Realized as Automorphism Groups." In The Geometry of Complex Domains, 135–59. Boston: Birkhäuser Boston, 2011. http://dx.doi.org/10.1007/978-0-8176-4622-6_5.

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Kaneyuki, Soji. "Semisimple Graded Lie Algebras." In Analysis and Geometry on Complex Homogeneous Domains, 107–26. Boston, MA: Birkhäuser Boston, 2000. http://dx.doi.org/10.1007/978-1-4612-1366-6_9.

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Wolf, Joseph A. "Compact Subvarieties in Flag Domains." In Lie Theory and Geometry, 577–96. Boston, MA: Birkhäuser Boston, 1994. http://dx.doi.org/10.1007/978-1-4612-0261-5_22.

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Roos, Guy. "Volume of Bounded Symmetric Domains and Compactification of Jordan Triple Systems." In Lie Groups and Lie Algebras, 249–59. Dordrecht: Springer Netherlands, 1998. http://dx.doi.org/10.1007/978-94-011-5258-7_16.

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Kelly, A. A. "Benedicamus Domino." In Liam O’Flaherty The Collected Stories, 23–27. New York: Palgrave Macmillan US, 1999. http://dx.doi.org/10.1007/978-1-137-07257-3_5.

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Fiorelli, Manuel, Armando Stellato, John P. McCrae, Philipp Cimiano, and Maria Teresa Pazienza. "LIME: The Metadata Module for OntoLex." In The Semantic Web. Latest Advances and New Domains, 321–36. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-18818-8_20.

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Faraut, Jacques. "Invariant Cones in a Lie Algebra and Complex Semi-groups." In Analysis and Geometry on Complex Homogeneous Domains, 19–32. Boston, MA: Birkhäuser Boston, 2000. http://dx.doi.org/10.1007/978-1-4612-1366-6_3.

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Тези доповідей конференцій з теми "LIM domain":

Sommer, J., C. Dorn, R. Weiskirchen, and C. Hellerbrand. "Expression and Function of Four-and-a-Half LIM-domain protein 2 (FHL2) in Hepatic Fibrosis." In 36. Jahrestagung der Deutschen Arbeitsgemeinschaft zum Studium der Leber. Georg Thieme Verlag KG, 2020. http://dx.doi.org/10.1055/s-0039-3402114.

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Sommer, J., and C. Hellerbrand. "Expression and Function of Four-and-a-Half LIM-domain protein 2 (FHL2) in Hepatocellular Carcinoma." In 36. Jahrestagung der Deutschen Arbeitsgemeinschaft zum Studium der Leber. Georg Thieme Verlag KG, 2020. http://dx.doi.org/10.1055/s-0039-3402218.

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Bian, Minglei, Yang Liao, Monicah Njogu, Rebecca Schmidt, Rie Takahashi, Zandra Walton, and Amy H. Tang. "Abstract 5049: SIAH2 E3 ligase targets LIM-domain proteins for degradation to modulate focal adhesion and cell motility." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-5049.

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Venkitachalam, Srividya, Fu-Yu Chueh, and Chao-Lan Yu. "Abstract 4008: Nuclear localization of Lymphocyte-specific protein tyrosine kinase (Lck) and its role in regulating LIM domain only 2 (LMO2) gene." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-4008.

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Tang, Amy H., Yang Liao, Rebecca L. Schmidt, Zandra E. Walton, and Rie Takahashi. "Abstract A88: SIAH2-mediated proteolysis of LIM domain proteins induces invasion and metastasis in response to oncogenic K-RAS activation in human pancreatic cancer cells." In Abstracts: AACR Special Conference on Pancreatic Cancer: Progress and Challenges; June 18-21, 2012; Lake Tahoe, NV. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.panca2012-a88.

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Ming Lim, Tong, and Lee Sai Peck. "Extended Object Languages for The Extolware Persistent Framework." In InSITE 2004: Informing Science + IT Education Conference. Informing Science Institute, 2004. http://dx.doi.org/10.28945/2832.

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Users interact with a database system through a set of database languages and this makes designing database languages a very challenging task to a computer software engineer. A set of well-defined database languages must be easy to learn, easy to understand and powerful enough to capture semantic of a problem domain. This paper discusses design issues of a proposed database language, namely Extended Object Language or EOL for short, for an Extolware Persistent Object framework (Lim & Lee, 1997, 1998, 1999, 2001, 2002a, 2002b, 2002c) that provide wrapping services for relational database systems and multidimensional database systems (DataPro, 1996; IBM Corp., 2001; Informix Software Inc., 2001a, 2001b). This research examines SQL3 (Fortier, 1999) and ODL/OQL (Cattell & Barry, 1999) with an overview of their language constructs and operators that support object-oriented requirements as stated in Object Data Management Group (ODMG) object model. Next, a discussion on the Extended Object Language (EOL) and its language constructs are examined. This is followed by a close examination of new database operators and constructs introduced into EOL. A design overview and evaluation of these database languages are examined. A summary on these languages is presented at the end of the paper with conclusion and further research plans.

Lee, Eunjin, David Braines, Mitchell Stiffler, Adam Adam Hudler, and Daniel Harborne. "Developing the sensitivity of LIME for better machine learning explanation." In Artificial Intelligence and Machine Learning for Multi-Domain Operations Applications, edited by Tien Pham. SPIE, 2019. http://dx.doi.org/10.1117/12.2520149.

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Colicchio, Giuseppina, Claudio Lugni, Marilena Greco, and Odd M. Faltinsen. "Dynamic Domain Decomposition Strategy Coupling Lattice Boltzmann Methods With Finite Differences Approximations of the Navier-Stokes Equations to Study Bodies in Current." In ASME 2015 34th International Conference on Ocean, Offshore and Arctic Engineering. American Society of Mechanical Engineers, 2015. http://dx.doi.org/10.1115/omae2015-42195.

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A Domain-Decomposition (DD) strategy is proposed for problems involving regions with slow variations of the flow (A) and others where the fluid features undergo rapid changes (B), like in the case of steady current past bodies with pronounced local unsteadiness connected with the vortex shedding from the structures. For an efficient and accurate solution of such problems, the DD couples a Finite Difference solver of the Navier-Stokes equations (FD-NS) with a Multiple Relaxation Time Lattice Boltzmann method (MRT-LBM). Regions A are handled by FD-NS, while zones B are solved by MRT-LBM and the two solvers exchange information within a strong coupling strategy. Present DD strategy is able to deal with a dynamic change of the sub-domains topology. This feature is needed when regions with vorticity shed from the body vary in time for a more flexible and reliable solution strategy. Its performances in terms of accuracy and efficiency have been successfully assessed by comparing the hybrid solver against a full FD-NS solution and experimental data for a 2D circular cylinder in an impulsively started flow.

Peña, Blanca, and Aaron McDougall. "An Investigation Into the Limitations of the Panel Method and the Gap Effect for a Fixed and a Floating Structure Subject to Waves." In ASME 2016 35th International Conference on Ocean, Offshore and Arctic Engineering. American Society of Mechanical Engineers, 2016. http://dx.doi.org/10.1115/omae2016-54121.

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The wave-induced motions of vessels moored next to a fixed object and open to the sea impact the operability of many offshore operations, and should be assessed in order to avoid accidents and catastrophes. When analysing vessels moored by a fixed object (e.g. quay-side or platform), time domain simulations have shown numeric instabilities resulting in unreliable outcomes. The origin of the numerical instability might lie in the hydrodynamic added mass and wave radiation damping. This is typically calculated using potential flow methods and influenced by the existence of standing waves in the gap between the two bodies. For certain frequencies, these give negative values, potentially causing instabilities in non-linear (coupled) time domain simulations. In these cases, the vessel can behave unexpectedly, generating energy rather than dissipating it. As such, certain simulations have been disregarded as they are unlikely to accurately represent real-life scenarios. This paper investigates and compares added mass and damping using two different tools and studies the gap effect when conducting diffraction analysis using 3D panel methods. The work covers a literature study into potential theory, multibody analysis, Computational Fluid Dynamics (CFD) and lid techniques. This is followed by a study conducted using both panel method and CFD analyses. The results from both approaches have been compared, showing interesting information and the necessity of researching more into the problem addressed in this paper.

Moze, Mathieu, Jocelyn Sabatier, and Alain Oustaloup. "LMI Tools for Stability Analysis of Fractional Systems." In ASME 2005 International Design Engineering Technical Conferences and Computers and Information in Engineering Conference. ASMEDC, 2005. http://dx.doi.org/10.1115/detc2005-85182.

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The main point when dealing with Linear Matrix Inequalities (LMI) is convexity. However, with state space representation of fractional systems, the stability domain for a fractional order 0 < ν < 1 is not convex. The classical stability condition thus cannot be extended to fractional systems. In this paper, three LMI based methods are used to characterize stability. The first is based on the second Lyapunov method and provides a sufficient but non-necessary condition. The second and new method provides a sufficient and necessary condition, and is based on a geometric analysis of a fractional system stability domain. The third method is more conventional but involves non strict LMI. A comparison of the first two methods is provided.

Звіти організацій з теми "LIM domain":

Cachalia, Firoz, and Jonathan Klaaren. Digitalisation, the ‘Fourth Industrial Revolution’ and the Constitutional Law of Privacy in South Africa: Towards a public law perspective on constitutional privacy in the era of digitalisation. Digital Pathways at Oxford, July 2021. http://dx.doi.org/10.35489/bsg-dp-wp_2021/04.

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In this working paper, our focus is on the constitutional debates and case law regarding the right to privacy, adopting a method that is largely theoretical. In an accompanying separate working paper, A South African Public Law Perspective on Digitalisation in the Health Sector, we employ the analysis developed here and focus on the specific case of digital technologies in the health sector. The topic and task of these papers lie at the confluence of many areas of contemporary society. To demonstrate and apply the argument of this paper, it would be possible and valuable to extend its analysis into any of numerous spheres of social life, from energy to education to policing to child care. In our accompanying separate paper, we focus on only one policy domain – the health sector. Our aim is to demonstrate our argument about the significance of a public law perspective on the constitutional right to privacy in the age of digitalisation, and attend to several issues raised by digitalisation’s impact in the health sector. For the most part, we focus on technologies that have health benefits and privacy costs, but we also recognise that certain technologies have health costs and privacy benefits. We also briefly outline the recent establishment (and subsequent events) in South Africa of a contact tracing database responding to the COVID-19 pandemic – the COVID-19 Tracing Database – a development at the interface of the law enforcement and health sectors. Our main point in this accompanying paper is to demonstrate the value that a constitutional right to privacy can bring to the regulation of digital technologies in a variety of legal frameworks and technological settings – from public to private, and from the law of the constitution to the ‘law’ of computer coding.