Relevant bibliographies by topics / Integrin modulation

Contents

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

Academic literature on the topic 'Integrin modulation'

Author: Grafiati
Published: 2 November 2024

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Journal articles on the topic "Integrin modulation"

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Hughes, Paul E., and Martin Pfaff. "Integrin affinity modulation." Trends in Cell Biology 8, no. 9 (September 1998): 359–64. http://dx.doi.org/10.1016/s0962-8924(98)01339-7.

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Martin-Bermudo, Maria D., Olga M. Dunin-Borkowski, and Nicholas H. Brown. "Modulation of Integrin Activity is Vital for Morphogenesis." Journal of Cell Biology 141, no. 4 (May 18, 1998): 1073–81. http://dx.doi.org/10.1083/jcb.141.4.1073.

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Cells can vary their adhesive properties by modulating the affinity of integrin receptors. The activation and inactivation of integrins by inside-out mechanisms acting on the cytoplasmic domains of the integrin subunits has been demonstrated in platelets, lymphocytes, and keratinocytes. We show that in the embryo, normal morphogenesis requires the α subunit cytoplasmic domain to control integrin adhesion at the right times and places. PS2 integrin (αPS2βPS) adhesion is normally restricted to the muscle termini, where it is required for attaching the muscles to the ends of other muscles and to specialized epidermal cells. Replacing the wild-type αPS2 with mutant forms containing cytoplasmic domain deletions results in the rescue of the majority of defects associated with the absence of the αPS2 subunit, however, the mutant PS2 integrins are excessively active. Muscles containing these mutant integrins make extra muscle attachments at aberrant positions on the muscle surface, disrupting the muscle pattern and causing embryonic lethality. A gain- of-function phenotype is not observed in the visceral mesoderm, showing that regulation of integrin activity is tissue-specific. These results suggest that the αPS2 subunit cytoplasmic domain is required for inside-out regulation of integrin affinity, as has been seen with the integrin αIIbβ3.
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Tozer, Eileen Collins, Paul E. Hughes, and Joseph C. Loftus. "Ligand binding and affinity modulation of integrins." Biochemistry and Cell Biology 74, no. 6 (December 1, 1996): 785–98. http://dx.doi.org/10.1139/o96-085.

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Integrins are cell adhesion receptors that mediate cell–cell and cell–extracellular matrix interactions. The extracellular domains of these receptors possess binding sites for a diverse range of protein ligands. Ligand binding is divalent cation dependent and involves well-defined motifs in the ligand. Integrins can dynamically regulate their affinity for ligands (inside-out signaling). This ability to rapidly modulate their affinity state is key to their involvement in such processes as cell migration and platelet aggregation. This review will focus on two aspects of integrin function: first, on the molecular basis of ligand–integrin interactions and, second, on the underlying mechanisms controlling the affinity state of integrins for their ligands.Key words: integrins, ligand binding, affinity modulation.
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Ashe, Hilary L. "Modulation of BMP signalling by integrins." Biochemical Society Transactions 44, no. 5 (October 15, 2016): 1465–73. http://dx.doi.org/10.1042/bst20160111.

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The bone morphogenetic protein (BMP) pathway is a major conserved signalling pathway with diverse roles in development and homeostasis. Given that cells exist in three-dimensional environments, one important area is to understand how the BMP pathway operates within such complex cellular environments. The extracellular matrix contains information regarding tissue architecture and its mechanical properties that is transmitted to the cell via integrin receptors. In this review, I describe various examples of modulation of the BMP pathway by integrins. In the case of the Drosophila embryo and some cell line-based studies, integrins have been found to enhance BMP responses through different mechanisms, such as enhancement of BMP ligand–receptor binding and effects on Smad phosphorylation or stability. In these contexts, BMP-dependent activation of integrins is a common theme. However, I also discuss examples where integrins inhibit the BMP pathway, highlighting the context-dependent nature of integrin–BMP cross-talk.
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Huang, Jing, Lance C. Bridges, and Judith M. White. "Selective Modulation of Integrin-mediated Cell Migration by Distinct ADAM Family Members." Molecular Biology of the Cell 16, no. 10 (October 2005): 4982–91. http://dx.doi.org/10.1091/mbc.e05-03-0258.

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A disintegrin and a metalloprotease (ADAM) family members have been implicated in many biological processes. Although it is recognized that recombinant ADAM disintegrin domains can interact with integrins, little is known about ADAM-integrin interactions in cellular context. Here, we tested whether ADAMs can selectively regulate integrin-mediated cell migration. ADAMs were expressed in Chinese hamster ovary cells that express defined integrins (α4β1, α5β1, or both), and cell migration on full-length fibronectin or on its α4β1 or α5β1 binding fragments was studied. We found that ADAMs inhibit integrin-mediated cell migration in patterns dictated by the integrin binding profiles of their isolated disintegrin domains. ADAM12 inhibited cell migration mediated by the α4β1 but not the α5β1 integrin. ADAM17 had the reciprocal effect; it inhibited α5β1- but not α4β1-mediated cell migration. ADAM19 and ADAM33 inhibited migration mediated by both α4β1 and α5β1 integrins. A point mutation in the ADAM12 disintegrin loop partially reduced the inhibitory effect of ADAM12 on cell migration on the α4β1 binding fragment of fibronectin, whereas mutations that block metalloprotease activity had no effect. Our results indicate that distinct ADAMs can modulate cell migration mediated by specific integrins in a pattern dictated, at least in part, by their disintegrin domains.
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Mahabeleshwar, Ganapati H., Juhua Chen, Weiyi Feng, Payaningal R. Somanath, Olga V. Razorenova, and Tatiana V. Byzova. "Integrin affinity modulation in angiogenesis." Cell Cycle 7, no. 3 (February 2008): 335–47. http://dx.doi.org/10.4161/cc.7.3.5234.

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Woods, Anne, and John R. Couchman. "Integrin Modulation by Lateral Association." Journal of Biological Chemistry 275, no. 32 (May 4, 2000): 24233–36. http://dx.doi.org/10.1074/jbc.r000001200.

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Sethi, Tariq, Mark H. Ginsberg, Julian Downward, and Paul E. Hughes. "The Small GTP-binding Protein R-Ras Can Influence Integrin Activation by Antagonizing a Ras/Raf-initiated Integrin Suppression Pathway." Molecular Biology of the Cell 10, no. 6 (June 1999): 1799–809. http://dx.doi.org/10.1091/mbc.10.6.1799.

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The rapid modulation of ligand-binding affinity (“activation”) is a central property of the integrin family of cell adhesion receptors. The small GTP-binding protein Ras and its downstream effector kinase Raf-1 suppress integrin activation. In this study we explored the relationship between Ras and the closely related small GTP-binding protein R-Ras in modulating the integrin affinity state. We found that R-Ras does not seem to be a direct activator of integrins in Chinese hamster ovary cells. However, we observed that GTP-bound R-Ras strongly antagonizes the Ras/Raf-initiated integrin suppression pathway. Furthermore, this reversal of the Ras/Raf suppressor pathway does not seem to be via a competition between Ras and R-Ras for common downstream effectors or via an inhibition of Ras/Raf-induced MAP kinase activation. Thus, R-Ras and Ras may act in concert to regulate integrin affinity via the activation of distinct downstream effectors.
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Yu, Tao, Xing Wu, Kiran B. Gupta, and Dennis F. Kucik. "Affinity, lateral mobility, and clustering contribute independently to β2-integrin-mediated adhesion." American Journal of Physiology-Cell Physiology 299, no. 2 (August 2010): C399—C410. http://dx.doi.org/10.1152/ajpcell.00039.2009.

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Affinity changes and avidity modulation both contribute to activation of β2-integrin-mediated adhesion, an essential, early step in inflammation. Avidity modulation, defined as an increase in adhesiveness independent of integrin conformational changes, might be due to integrin clustering, motion, or both. Increased integrin diffusion upon leukocyte activation has been demonstrated, but whether it is proadhesive in itself, or just constitutes a mechanism for integrin clustering, remains unclear. To understand the proadhesive effects of integrin affinity changes, clustering, and motion, an experimental system was devised to separate them. Clustering and integrin motion together were induced by cytochalasin D (CD) without inducing high-affinity; integrin motion could then be frozen by fixation; and high affinity was induced independently by Mn2+. Adhesion was equivalent for fixed and unfixed cells except following pretreatment with CD or Mn2+, which increased adhesion for both. However, fixed cells were less adhesive than unfixed cells after CD, even though integrin clustering was similar. A simple explanation is that CD induces both clustering and integrin motion, fixation then stops motion on fixed cells, but integrins continue to diffuse on unfixed cells, increasing the kinetics of integrin/ICAM-1 interactions to enhance adhesion. Affinity changes are then independent of, and additive to, avidity effects.
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Anderson, M. J., Z. Q. Shi, and S. L. Zackson. "Proteolytic disruption of laminin-integrin complexes on muscle cells during synapse formation." Molecular and Cellular Biology 16, no. 9 (September 1996): 4972–84. http://dx.doi.org/10.1128/mcb.16.9.4972.

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To explore whether a neural modulation of muscle integrins' extracellular ligand interactions contributes to synapse induction, we compared the distributions of beta1-integrins and basal lamina proteins on Xenopus myotomal myocytes developing in culture. beta1-Integrins formed numerous organized aggregates scattered over the entire muscle surface, with particularly dense accumulations at specialized sites resembling myotendinous and neuromuscular junctions. Integrin aggregates on muscle cells differed from those on surrounding fibroblasts and epithelial cells, both in their lack of response to cross-linking by multivalent ligands and in their consistent association with the cells' own extracellular matrices. Muscle integrin clusters were usually associated with congruent basal lamina accumulations containing laminin and a heparan sulfate proteoglycan (HSPG), sometimes including fibronectin and vitronectin acquired from the surrounding medium. Immediately prior to synaptic differentiation, any existing laminin and HSPG accumulations along the path of cell contact were eliminated, disrupting otherwise stable laminin-integrin complexes. This apparently proteolytic modulation of integrins' extracellular ligand interactions was soon followed by the accumulation of new congruent accumulations of laminin and HSPG in the developing synaptic basal lamina. Combining these results with earlier findings, we consider the possibility that postsynaptic differentiation is induced, at least in part, by the proteolytic disruption of integrin-ligand complexes at sites of nerve-muscle contact.
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Dissertations / Theses on the topic "Integrin modulation"

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Buttery, Robert Christians. "Integrin affinity modulation and lung cancer." Thesis, University of Edinburgh, 2006. http://hdl.handle.net/1842/29025.

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Recent work has shown that the transmembrane protein CD98 is able to influence the affinity with which β1 integrins bind to extracellular ligands. The first part of this thesis presents confocal microscopy and co-immunoprecipitation experiments that confirm the physical juxtaposition of the two proteins within the cell membrane, suggesting a direct functional link between the two. It also demonstrated that cross-linking CD98 stimulates both phosphoinositide 3-kinase intracellular signalling and increased β1 integrin-dependent cellular adhesion. Because of the role of CD98 in integrin affinity modulation, the immunohistochemical expression of CD98 and its ligand, galectin-3, was studied in a variety of human ling diseases including lung cancers. The major finding of this work was a striking distinction between high expression of galectin-3 in non-small cell lung cancer and low expression in small cell lung cancer. This may hag significant implications for the differing clinical behaviours of these two groups of cancers. The final section of this thesis returns to describe experiments aimed at defining the molecular regulators of integrin affinity more clearly. A genetic screen of a cDNA library was undertaken to identify candidate genes coding for proteins able to rescue integrins from the low affinity state induced by the small signalling protein H-Ras. This identified a candidate cDNA 480, recognised to be part of a novel gene Nessie, which codes for a large protein with multiple transmembrane domains. Both 480 and Nessie appear to have the ability to rescue integrin affinity from H-Ras suppression.
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Coppolino, Marc Gabriel. "Modulation of integrin function by calreticulin." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp02/NQ35131.pdf.

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Elliott, Paul Anthony. "Integrin affinity modulation and survival signalling." Thesis, University of Edinburgh, 2008. http://hdl.handle.net/1842/4393.

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Integrins are heterodimeric transmembrane proteins that provide a bi-directional link between the cell’s internal biological mechanisms and the extracellular environment. During inside-out signalling, intracellular messages converge on the integrin cytoplasmic domain to induce a conformational change. This is transmitted to the extracellular domain where it results in an alteration in affinity for integrin ligands such as fibronectin and laminin. In this way the cell has developed the ability to modulate the critical functions of adhesion and cell movement. In outside-in signalling, the integrin performs a more complex function than simple adhesion; upon binding to ligand, the integrin extracellular domain undergoes a conformational change which is transmitted to the cytoplasmic domain. This alters the integrin’s cytoplasmic domain affinity for intracellular signalling proteins and results in the activation of intracellular second messenger pathways. In this way, the extracellular milieu is able to influence intracellular signalling including those involved in apoptosis. This thesis demonstrates data which provide original insights into bi-directional integrin signalling: Inside-out signalling: Constitutively active Notch1 increases β3-integrin affinity and abrogates Hras-mediated integrin suppression without increasing expression of β3- integrin. Dominant-Negative Rras blocks Notch-mediated integrin activation and Notch1-mediated reversal of Hras and Raf-mediated integrin suppression and this is independent of erk phosphorylation. Notch1 induces Rras activation. Functional adhesion assays confirm that Notch1IC increases K562 adhesion in a β1-integrin dependent manner and this is abrogated by Dominant-Negative Rras. This data supports a mechanism in which Notch1 increases integrin affinity via activation of Rras. Outside-in signalling: Evidence is presented demonstrating that extracellular matrix proteins, laminin and fibronectin, activate β1-integrins to protect SCLC cells against the apoptotic effects of etoposide and ionizing radiation via PI3Kinase activation. This occurs in two ways: 1) PI3Kinase-dependent β1-integrin signalling resulting in phosphorylation of Bad and reduced caspase-9 cleavage and 2) a β1-integrinmediated over-riding of etoposide and radiotherapy-induced cell cycle S phase delay and G2/M arrest. β1-integrin-mediated outside-in survival signalling was investigated further in the in vivo setting; MatrigelTM, a basement membrane product rich in extracellular matrix proteins, promoted SCLC xenograft survival and growth in a β1-integrin and tyrosine kinase-dependent manner. This data provides novel insights into the critical functions that integrins play in adhesion and survival signalling.
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Lad, Yatishkumar. "Integrin affinity modulation by Ras signalling molecules." Thesis, University of Edinburgh, 2002. http://hdl.handle.net/1842/24800.

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In this thesis I have sought to understand the mechanism by which H-Ras and its effectors modulate integrin affinity. H-Ras is a member of the Ras superfamily of small GTP binding proteins. Expression of the constitutively active variant of H-Ras (Ras G12V) within an integrin affinity reporter system (αβ-py cells) reduced integrin affinity (suppressed integrin). Ras effector mutants revealed that integrin suppression is mediated by Raf-dependent and Raf-independent signalling pathways. Raf-independent signalling pathways activated by Ral-GEFs and PI3-kinase were not recognisable for integrin suppression. An active variant of R-Ras (R-Ras G38V) reversed integrin suppression by both Raf-dependent and - independent pathways, indicating that these pathways may converge at a point proximal to the integrin. Raf initiates a protein signalling cascade leading to ERK activation that is responsible for many of the Ras/Raf-dependent biological functions. However, Raf-dependent integrin suppression was insensitive to MEK inhibition with the PD098059 compound. A novel Raf mutant (T481A) that fails to bind to MEK was also capable of mediating integrin suppression in the absence of ERK activation. Surprisingly, Raf-BxB T481A-mediated integrin suppression was sensitive to expression of MKP-1. Taken together it is proposed that Raf may mediate integrin suppression via a MEK-independent pathway that may utilise a member of the MAP kinase superfamily. In conclusion, integrin suppression by Ras is mediated by both Raf-independent and dependent pathways. Signalling by Raf may utilise components other than those present in the classical Ras to ERK protein cascade.
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El-Aouni, Chiraz. "In Vivo modulation of integrin linked kinase using transgenic mice." Diss., lmu, 2006. http://nbn-resolving.de/urn:nbn:de:bvb:19-61756.

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van, Wieringen Tijs. "Intra- and Extracellular Modulation of Integrin-directed Connective Tissue Cell Contraction." Doctoral thesis, Uppsala universitet, Institutionen för medicinsk biokemi och mikrobiologi, 2009. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-102349.

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All blood vessels in the microvasculature are embedded in loose connective tissue, which regulates the transport of fluid to and from tissues. The intersti-tial fluid pressure (IFP) is one of the forces that control this transport. A lowering of IFP in vivo results in an increased transport of fluid from the circulation into the underhydrated connective tissues, resulting in edema formation. During homeostasis, contractile connective tissue cells exert a tension on the connective tissue fibrous network by binding with β1 in-tegrins, thereby actively controlling IFP. During inflammation, the IFP is lowered but platelet-derived growth factor (PDGF)-BB induces an IFP nor-malization dependent on integrin αVβ3. We demonstrate that extracellular proteins from Streptococcus equi subspecies equi modulated cell-mediated and integrin αVβ3-directed collagen gel contraction in vitro. One of these proteins, the collagen- and fibronectin binding FNE, stimulated contraction by a process dependent on fibronectin synthesis. This study identified a pos-sible novel virulence mechanism for bacteria based on the ability of bacteria to modulate the edema response. Another protein, the collagen-binding pro-tein CNE, inhibited contraction and this led to the identification of sites in collagen monomers that potentially are involved in connecting αVβ3 to the collagen network. PDGF-BB and prostaglandin E1 (PGE1) stimulate and inhibit collagen gel contraction in vitro and normalize and lower IFP, respec-tively. We showed that these agents affected both similar and different sets of actin-binding proteins. PDGF-BB stimulated actin cytoskeleton dynamics whereas PGE1 inhibited processes dependent on cytoskeletal motor and adhesive functions, suggesting that these different activities may partly ex-plain the contrasting effects of PGE1 and PDGF-BB on contraction and IFP. Mutation of the phosphatidylinositol 3’-kinase (PI3K), but not phospholipase C (PLC)γ activation site, rendered cells unable to respond to PDGF-BB in contraction and in activation of the actin binding and severing protein cofilin. Ability to activate cofilin after PDGF-BB stimulation correlated with ability to respond to PDGF-BB in contraction, suggesting a role for cofilin in this process downstream of PDGF receptor-activated PI3K. Many proteins can modulate contraction either by affecting the extracellular matrix and cell adhesions or by altering cytoskeletal dynamics. Knowledge on how these proteins might influence IFP is likely to be of clinical importance for treat-ment of inflammatory conditions including anaphylaxis, septic shock and also carcinoma growth.
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Walsh, Erin. "Crossreactivity of alpha9beta1 integrin with p75NTR in modulation of proinvasive activities of glioma cells." Diss., Temple University Libraries, 2011. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/143048.

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Biology
Ph.D.
Gliomas are the most common and difficult to treat tumors of the central nervous system. Current treatments often fail to slow progression of disease due to the high invasive nature of glioma leading to a high percentage of recurrence. Our previous studies have demonstrated that the levels of alpha; 9 beta; 1 integrin found on high grade glioma were significantly increased in comparison to normal brain tissue where the levels were negligible. We also found that interaction between alpha; 9 beta; 1 integrin and nerve growth factor (NGF) plays a major role in progression of experimental tumor. Another receptor for NGF the common neurotrophin receptor p75NTR is also overexpressed in high grade glioma. p75NTR forms a high affinity complex with the specific NGF receptor, TrkA leading to an increase in cell proliferation and survival. In the absence of an association, p75NTR is involved in transferring pro-apoptotic signals through the JNK pathway. We have found that the α 9 integrin subunit of α 9 β 1 forms a stable, cation independent complex with p75NTR on the cell membrane of glioma both in vitro using glioma derived immortalized cells lines and in vivo using glioma tissue. The co-expression of p75NTR with α 9 β 1 integrin led to optimization of integrin-dependent cellular activities such as cell survival, proliferation, and migration. Co-expression of p75NTR was also required for implanted glioma cells to migrate in a glioma-like perivascular manner away from the site of implantation as was seen in the in vivo quail chorioallantoic membrane assay.
Temple University--Theses
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Coyer, Sean R. "Modulation of cell adhesion strengthening by nanoscale geometries at the adhesive interface." Diss., Georgia Institute of Technology, 2010. http://hdl.handle.net/1853/34763.

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Cell adhesion to extracellular matrices (ECM) is critical to many cellular processes including differentiation, proliferation, migration, and apoptosis. Alterations in adhesive mechanisms are central to the behavior of cells in pathological conditions including cancer, atherosclerosis, and defects in wound healing. Although significant progress has been made in identifying molecules involved in adhesion, the mechanisms that dictate the generation of strong adhesive forces remain poorly understood. Specifically, the role of nanoscale geometry of the adhesive interface in integrin recruitment and adhesion forces remains elusive due to limitations in the techniques available for engineering cell adhesion environments. The objective of this project was to analyze the role of nanoscale geometry in cell adhesion strengthening to ECM. Our central hypothesis was that adhesive interactions are regulated by integrin clusters whose recruitment is determined by the nanoscale geometry of the adhesive interface and whose heterogeneity in size, spacing, and orientation modulates adhesion strength. The objective of this project was accomplished by 1) developing an experimental technique capable of producing nanoscale patterns of proteins on surfaces for cell adhesion arrays, 2) assessing the regulation of integrin recruitment by geometry of the adhesive interface, and 3) determining the functional implications of adhesive interface geometry by systematically analyzing the adhesion strengthening response to nanoscale patterns of proteins. A printing technique was developed that patterns proteins into features as small as 90nm with high contrast and high reproducibility. Cell adhesion arrays were produced by directly immobilizing proteins into patterns on mixed-SAMs surfaces with a protein-resistant background. Colocalization analysis of integrin recruitment to FN patterns demonstrated a concentrating effect of bound integrins at pattern sizes with areas equivalent to small nascent focal adhesions. At adhesion areas below 333 × 333 nm2, the frequency of integrin recruitment events decreased significantly indicating a threshold size for integrin clustering. Functionally, pattern sizes below the threshold were unable to participate in generation of adhesion strength. In contrast, patterns between the threshold and micron sizes showed a relationship between adhesion strength and area of individual adhesion points, independent of the total available adhesion area. These studies introduce a robust platform for producing nanoscale patterns of proteins in biologically relevant geometries. Results obtained using this approach yielded new insights on the role of nanoscale organization of the adhesive interface in modulating adhesion strength and integrin recruitment.
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Lygoe, Kate Alexandra. "Modulation of the myofibroblast phenotype is via the interaction of extracellular matrix proteins with integrin receptors." Thesis, University College London (University of London), 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.411053.

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Hönig, Ellena [Verfasser], and Ralf [Akademischer Betreuer] Jacob. "Modulation der β1-Integrin-Lokalisation an der apikalen Plasmamembran durch Galektin-3 / Ellena Hönig ; Betreuer: Ralf Jacob." Marburg : Philipps-Universität Marburg, 2017. http://d-nb.info/1129358348/34.

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Books on the topic "Integrin modulation"

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Schöning, Michael. Beeinflussung des metastatischen Potentials von Kolon-Karzinomzellen durch Modulation von Integrin-Rezeptoren. [s.l.]: [s.n.], 1998.

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Chander, Ashok Coil. Integrin-Linked Kinase, ECM Composition, and Substrate Rigidity Regulate Focal Adhesion - Actin Coupling, Modulating Survival, Proliferation and Migration: Towards a Biophysical Cancer Biomarker. [New York, N.Y.?]: [publisher not identified], 2012.

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Coppolino, Marc Gabriel. Modulation of integrin function by calreticulin. 1998.

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Carmeliet, G. Modulation of B1 Integrin Function During Neurite Outgrowth. Leuven University Press, 1994.

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Leone, Dino. Tamoxifen-inducible glia-specific cre mice for somatic mutagenesis in oligodendrocytes and schwann cells and [beta]1-integrin regulates neural progenitor maintenance through modulation of growth factor signaling. 2003.

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Kintzel, Claudia. Expression, Modulation und funktionelle Bedeutung von Integrinen auf Kolonkarzinomzellinien. 1993.

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Yust, Jason. Tonal Structure. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780190696481.003.0003.

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The concept of tonal structure is intimately associated with the person of Heinrich Schenker, but ultimately in order to enter dialogue with Schenker the theory of tonal structure must take the place of “Schenkerian analysis” in our discourse. A number of useful principles of tonal structure may be derived from Schenker’s theory: Schenkerian notation agrees with the network representation for temporal structure, and linear progressions are a good starting point for a tonal structure discovery procedure. The theory of the Ursatz, however, cannot be understood as an empirical claim but rather as a collection of grammatical norms. Also, Schenker’s dismissal of the concept of key is disputed, and a theory of tonal structure to which keys and modulation are integral is presented.
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Book chapters on the topic "Integrin modulation"

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Leitinger, Birgit. "DDRs: Binding Properties, Cell Adhesion and Modulation of Integrin Function." In Discoidin Domain Receptors in Health and Disease, 3–21. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-6383-6_1.

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Wright, Samuel D. "Integrin Modulating Factor and the Regulation of Leukocyte Integrins." In Cellular Adhesion, 25–35. Boston, MA: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4615-2466-3_2.

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Mousa, Shaker A., and Paul J. Davis. "Integrin Antagonists and Angiogenesis." In Angiogenesis Modulations in Health and Disease, 119–41. Dordrecht: Springer Netherlands, 2013. http://dx.doi.org/10.1007/978-94-007-6467-5_11.

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Eckert, J. "Structure Modulation and Nanocrystallization of Metallic Glasses: How to Tune Mechanical Properties." In Structural Integrity, 352–53. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-91989-8_81.

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Iacob, Nicusor, Ioan-Alexandru Ivan, Gabriel Schinteie, Claudiu Locovei, Mihai Burdusel, and Victor Kuncser. "Modulation of Water Jets by Detonation of Shaped Charges, for Penetration of Metallic Structures." In Structural Integrity, 489–96. Cham: Springer Nature Switzerland, 2024. http://dx.doi.org/10.1007/978-3-031-49723-0_37.

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Defilippi, Paola, Chiarella Bozzo, Massimo Geuna, Paola Rossino, Lorenzo Silengo, and Guido Tarone. "Modulation of extracellular matrix receptors (integrins) on human endothelial cells by cytokines." In Experientia Supplementum, 193–97. Basel: Birkhäuser Basel, 1992. http://dx.doi.org/10.1007/978-3-0348-7001-6_29.

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Bazan, Nicolas G., and Anasheh Halabi. "Docosahexaenoic Acid Signalolipidomics in the Homeostatic Modulation of Photoreceptor/Retinal Pigment Epithelial Cell Integrity During Oxidative Stress." In Studies on Retinal and Choroidal Disorders, 141–63. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-61779-606-7_7.

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Whittle, Brendan J. R. "Relationship between Sensory Neuropeptides and other Local Vasoactive Mediators in Modulating Gastric Mucosal Integrity." In Advances in Experimental Medicine and Biology, 147–56. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4899-0744-8_13.

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Ito, Makoto, Motohiro Tani, and Yukihiro Yoshimura. "Neutral Ceramidase as an Integral Modulator for the Generation of S1P and S1P-Mediated Signaling." In Sphingolipid Biology, 183–96. Tokyo: Springer Japan, 2006. http://dx.doi.org/10.1007/4-431-34200-1_13.

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Trikha, Mohit, and Kenneth V. Honn. "Role of 12-Lipoxygenase and Protein Kinase C in Modulating the Activation State of the Integrin αIIbβ3 on Human Tumor Cells." In Advances in Experimental Medicine and Biology, 55–60. Boston, MA: Springer US, 1997. http://dx.doi.org/10.1007/978-1-4899-1813-0_8.

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Conference papers on the topic "Integrin modulation"

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Kireev, Arseny Y., Nikolai S. Laskavyi, and Anton A. Zhuravlev. "Experimental Study of an Integral-Optical Modulator Based on a Mach-Zehnder Interferometer with Increased Modulation Depth." In 2024 IEEE 25th International Conference of Young Professionals in Electron Devices and Materials (EDM), 970–73. IEEE, 2024. http://dx.doi.org/10.1109/edm61683.2024.10615119.

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Isichenko, Andrei, Andrew Kortyna, Nitesh Chauhan, Jiawei Wang, Mark W. Harrington, Judith Olson, and Daniel J. Blumenthal. "Tunable 778 nm Integrated Brillouin Laser Probe for a Rubidium Two-Photon Optical Atomic Clock." In CLEO: Science and Innovations, SM1R.7. Washington, D.C.: Optica Publishing Group, 2024. http://dx.doi.org/10.1364/cleo_si.2024.sm1r.7.

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We demonstrate a frequency-controllable 778 nm integrated Brillouin laser with 40 Hz fundamental and 5 kHz integral linewidths maintained over >10 kHz modulation. Stabilization to a rubidium two-photon transition results in stability 2e-13 at 100s.
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Lee, Hee Doo, Michael Y. Park, Ok‐Hee Jeon, and Doo‐Sik Kim. "Abstract B42: Modulation of integrin‐mediated cell adhesion by ADAM15 disintegrin‐like domain." In Abstracts: AACR International Conference on Frontiers in Cancer Prevention Research‐‐ Dec 6–9, 2009; Houston, TX. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1940-6207.prev-09-b42.

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Geraghty, Terese D., Anugraha Rajagopalan, Rabail Aslam, and Vineet Gupta. "Abstract PR4: Modulation of integrin CD11b as a novel therapeutic strategy against lung cancer." In Abstracts: AACR Special Conference on Tumor Immunology and Immunotherapy; November 17-20, 2019; Boston, MA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/2326-6074.tumimm19-pr4.

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Dagnino, Lina, and Ernest Ho. "Abstract 1249: Modulation of epidermal growth factor induction of migration by integrin-linked kinase." 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.am2012-1249.

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Ek-Rylander, Barbro, and Goran Andersson. "MODULATION OF OSTEOCLAST ADHESION AND MIGRATION ON PHOSPHORYLATED OSTEOPONTIN (OPN) BY TARTRATE-RESISTANT ACID PHOSPHATASE (TRAP)." In 3rd International Conference on Osteopontin and SIBLING (Small Integrin-Binding Ligand, N-linked Glycoprotein) Proteins, 2002. TheScientificWorld Ltd, 2002. http://dx.doi.org/10.1100/tsw.2002.234.

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Barlow, LaMont, Rebecca Meyer, Ethan Shelkey, Bishoy Faltas, and Mark Rubin. "Abstract 5941: Integrin signaling modulation demonstrates potential therapeutic strategy in bladder cancer using three-dimensional organoid culture." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-5941.

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Ashkar, Samy, Sandra Pavao, and Georg F. Weber. "MODULATION OF CELL ATTACHMENT AND MIGRATION BY OSTEOPONTIN THROUGH DIFFERENTIAL ACTIVATION OF PKC ALPHA, BETA1, AND EPSILON." In 3rd International Conference on Osteopontin and SIBLING (Small Integrin-Binding Ligand, N-linked Glycoprotein) Proteins, 2002. TheScientificWorld Ltd, 2002. http://dx.doi.org/10.1100/tsw.2002.333.

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El-Kurdi, Mohammed S., J. Scott Van Epps, Robert J. Toth, Douglas W. Hamilton, Chuanyue Wu, Jeffrey S. Vipperman, and David A. Vorp. "Regulation of Cell Adhesion and De-Adhesion Proteins in Veins Perfused Under Arterial Conditions Ex-Vivo." In ASME 2004 International Mechanical Engineering Congress and Exposition. ASMEDC, 2004. http://dx.doi.org/10.1115/imece2004-61531.

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Failure of veins employed as arterial bypass grafts via intimal hyperplasia (IH) often occurs within 5 years after implantation, requiring re-operation in 60% of all cases1. IH is characterized by de-adhesion, followed by migration of medial and adventitial smooth muscle cells (SMCs) and myofibroblasts into the intima, where they demonstrate uncontrolled proliferation. It is thought that this process may be induced by the abrupt exposure of the veins to the dynamic mechanical environment of the arterial circulation2. Veins are much thinner walled and more distensible than arteries. Therefore, the SMCs within the vein wall are exposed to significantly higher levels of stress and strain than they are accustomed2. The tissue responds to this perceived injury by thickening, which is thought to be an attempt to return the stress and strain to venous levels. However, when this response is uncontrolled it can over-compensate, leading to stenosis instead of the desired thickening or “arterialization” of the vein segment. Cellular de-adhesion, which refers to a change from a state of stronger adherence to a state of weaker adherence, is involved in the earliest response and therefore was the focus of this study. While there are many important proteins involved in the regulation of cellular adhesion, we focus our attention here to matricellular proteins, which function as adaptors and modulators of cell-matrix interactions3,4, and intracellular adhesion proteins, which have been shown to localize to cellular focal adhesion sites5,6. Tenascin-C (TN-C), thrombospondin-1,2 (TSP), and secreted protein acidic and rich in cysteine (SPARC) are matricellular proteins that exhibit highly regulated expression during development and cellular injury7. Mitogen inducible gene 2 (Mig-2) and integrin linked kinase (ILK) are intracellular proteins involved in cellular shape modulation5 and integrin-mediated signal transduction8, respectively. It is well known that many intracellular and extracellular matrix proteins are regulated by mechanical stress9,10. The purpose of this work was to explore the hypothesis that intact vein segments exposed to arterial hemodynamics will alter their expression of TN-C, TSP, SPARC, Mig-2 and ILK within 24 hours. This may induce a modulation of the level of cell adhesion, which could contribute to IH.
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DeBeer, D., E. Usadi, and S. R. Hartmann. "Ultrafast modulations in time-delayed four-wave mixing experiments." In OSA Annual Meeting. Washington, D.C.: Optica Publishing Group, 1988. http://dx.doi.org/10.1364/oam.1988.me5.

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Two transient time-delayed four-wave mixing experiments have been performed on the Na D doublet and modulations of 1.9 ps and 980 as have been observed. These periods correspond to the difference and sum frequencies of the two Na D lines. Both experiments were performed using 7-ns pulses of light with frequency components at each of the D-line transitions. The effects of superimposition-state modulations are observed in the integrated TDFWM signal as a function of the time delay. As the time delay is varied, the lowest diffraction order mixing signal is modulated. Higher diffraction order mixing signals contain modulation components at integral multiples of the beat frequency.
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Reports on the topic "Integrin modulation"

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Philosoph-Hadas, Sonia, Peter B. Kaufman, Shimon Meir, and Abraham H. Halevy. Inhibition of the Gravitropic Shoot Bending in Stored Cut Flowers Through Control of Their Graviperception: Involvement of the Cytoskeleton and Cytosolic Calcium. United States Department of Agriculture, December 2005. http://dx.doi.org/10.32747/2005.7586533.bard.

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Original objectives: The basic goal of the present project was to study the mechanism involved in shoot graviperception and early transduction, in order to determine the sequence of events operating in this process. This will enable to control the entire process of gravity-induced differential growth without affecting vertical growth processes essential for development. Thus, several new postulated interactions, operating at the perception and early transduction stages of the signaling cascade leading to auxin-mediated bending, were proposed to be examined in snapdragon spikes and oat shoot pulvini, according to the following research goals: 1) Establish the role of amyloplasts as gravireceptors in shoots; 2) Investigate gravity-induced changes in the integrity of shoot actin cytoskeleton (CK); 3) Study the cellular interactions among actin CK, statoliths and cell membranes (endoplasmic reticulum - ER, plasma membrane - PM) during shoot graviperception; 4) Examine mediation of graviperception by modulations of cytosolic calcium - [Ca2+]cyt, and other second messengers (protein phosphorylation, inositol 1,4,5-trisphosphate - IP3). Revisions: 1) Model system: in addition to snapdragon (Antirrhinum majus L.) spikes and oat (Avena sativa) shoot pulvini, the model system of maize (Zea mays) primary roots was targeted to confirm a more general mechanism for graviperception. 2) Research topic: brassinolide, which were not included in the original plan, were examined for their regulatory role in gravity perception and signal transduction in roots, in relation to auxin and ethylene. Background to the topic: The negative gravitropic response of shoots is a complex multi-step process that requires the participation of various cellular components acting in succession or in parallel. Most of the long-lasting studies regarding the link between graviperception and cellular components were focused mainly on roots, and there are relatively few reports on shoot graviperception. Our previous project has successfully characterized several key events occurring during shoot bending of cut flowers and oat pulvini, including amyloplast displacement, hormonal interactions and differential growth analysis. Based on this evidence, the present project has focused on studying the initial graviperception process in flowering stems and cereal shoots. Major conclusions and achievements: 1) The actin and not the microtubule (MT) CK is involved in the graviperception of snapdragon shoots. 2) Gravisensing, exhibited by amyloplast displacement, and early transduction events (auxin redistribution) in the gravitropic response of snapdragon spikes are mediated by the acto-myosin complex. 3) MTs are involved in stem directional growth, which occurs during gravitropism of cut snapdragon spikes, but they are not necessary for the gravity-induced differential growth. 4) The role of amyloplasts as gravisensors in the shoot endodermis was demonstrated for both plant systems. 5) A gravity-induced increase in IP.
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