Relevant bibliographies by topics / CSK

Academic literature on the topic 'CSK'

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Published: 4 June 2021
Last updated: 1 February 2022

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Journal articles on the topic "CSK"

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Nagy, Zoltan, Jun Mori, Vanesa-Sindi Ivanova, Alexandra Mazharian, and Yotis A. Senis. "Interplay between the tyrosine kinases Chk and Csk and phosphatase PTPRJ is critical for regulating platelets in mice." Blood 135, no. 18 (April 30, 2020): 1574–87. http://dx.doi.org/10.1182/blood.2019002848.

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Abstract The Src family kinases (SFKs) Src, Lyn, and Fyn are essential for platelet activation and also involved in megakaryocyte (MK) development and platelet production. Platelet SFKs are inhibited by C-terminal Src kinase (Csk), which phosphorylates a conserved tyrosine in their C-terminal tail, and are activated by the receptor-type tyrosine phosphatase PTPRJ (CD148, DEP-1), which dephosphorylates the same residue. Deletion of Csk and PTPRJ in the MK lineage in mice results in increased SFK activity, but paradoxically hypoactive platelets resulting from negative feedback mechanisms, including upregulation of Csk homologous kinase (Chk) expression. Here, we investigate the role of Chk in platelets, functional redundancy with Csk, and the physiological consequences of ablating Chk, Csk, and PTPRJ in mice. Platelet count was normal in Chk knockout (KO) mice, reduced by 92% in Chk;Csk double KO (DKO) mice, and partially rescued in Chk;Csk;Ptprj triple KO (TKO) mice. Megakaryocyte numbers were significantly increased in both DKO and TKO mice. Phosphorylation of the inhibitory tyrosine of SFKs was almost completely abolished in DKO platelets, which was partially rescued in Src and Fyn in TKO platelets. This residual phosphorylation was abolished by Src inhibitors, revealing an unexpected mechanism in which SFKs autoinhibit their activity by phosphorylating their C-terminal tyrosine residues. We demonstrate that reduced inhibitory phosphorylation of SFKs leads to thrombocytopenia, with Csk being the dominant inhibitor in platelets and Chk having an auxiliary role. PTPRJ deletion in addition to Chk and Csk ameliorates the extent of thrombocytopenia, suggesting targeting it may have therapeutic benefits in such conditions.
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Sabe, H., M. Okada, H. Nakagawa, and H. Hanafusa. "Activation of c-Src in cells bearing v-Crk and its suppression by Csk." Molecular and Cellular Biology 12, no. 10 (October 1992): 4706–13. http://dx.doi.org/10.1128/mcb.12.10.4706.

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The protein product of the CT10 virus, p47gag-crk (v-Crk), which contains Src homology region 2 (SH2) and 3 (SH3) domains but lacks a kinase domain, is believed to cause an increase in cellular protein tyrosine phosphorylation. A candidate tyrosine kinase, Csk (C-terminal Src kinase), has been implicated in c-Src Tyr-527 phosphorylation, which negatively regulates the protein tyrosine kinase of pp60c-src (c-Src). To investigate how c-Src kinase activity is regulated in vivo, we first looked at whether v-Crk can activate c-Src kinase. We found that cooverexpression of v-Crk and c-Src caused elevation of c-Src kinase activity, resulting in an increase of tyrosine phosphorylation of cellular proteins and morphological transformation of rat 3Y1 fibroblasts. v-Crk and c-Src complexes were not detected, although v-Crk bound to a variety of tyrosine-phosphorylated proteins in cells overexpressing v-Crk and c-Src. Overexpression of Csk in these transformed cells caused reversion to normal phenotypes and also reduced the level of c-Src kinase activity. However, Csk did not cause reversion of cells transformed by v-Src or c-Src527F, in which Tyr-527 was changed to Phe. These results strongly suggest that Csk acts on Tyr-527 of c-Src and suppresses c-Src kinase activity in vivo. Because Csk can suppress transformation by cooverexpression of v-Crk and c-Src, we suggest that v-Crk causes activation of c-Src in vivo by altering the phosphorylation state of Tyr-527.
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Sabe, H., M. Okada, H. Nakagawa, and H. Hanafusa. "Activation of c-Src in cells bearing v-Crk and its suppression by Csk." Molecular and Cellular Biology 12, no. 10 (October 1992): 4706–13. http://dx.doi.org/10.1128/mcb.12.10.4706-4713.1992.

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The protein product of the CT10 virus, p47gag-crk (v-Crk), which contains Src homology region 2 (SH2) and 3 (SH3) domains but lacks a kinase domain, is believed to cause an increase in cellular protein tyrosine phosphorylation. A candidate tyrosine kinase, Csk (C-terminal Src kinase), has been implicated in c-Src Tyr-527 phosphorylation, which negatively regulates the protein tyrosine kinase of pp60c-src (c-Src). To investigate how c-Src kinase activity is regulated in vivo, we first looked at whether v-Crk can activate c-Src kinase. We found that cooverexpression of v-Crk and c-Src caused elevation of c-Src kinase activity, resulting in an increase of tyrosine phosphorylation of cellular proteins and morphological transformation of rat 3Y1 fibroblasts. v-Crk and c-Src complexes were not detected, although v-Crk bound to a variety of tyrosine-phosphorylated proteins in cells overexpressing v-Crk and c-Src. Overexpression of Csk in these transformed cells caused reversion to normal phenotypes and also reduced the level of c-Src kinase activity. However, Csk did not cause reversion of cells transformed by v-Src or c-Src527F, in which Tyr-527 was changed to Phe. These results strongly suggest that Csk acts on Tyr-527 of c-Src and suppresses c-Src kinase activity in vivo. Because Csk can suppress transformation by cooverexpression of v-Crk and c-Src, we suggest that v-Crk causes activation of c-Src in vivo by altering the phosphorylation state of Tyr-527.
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Li, Leiming, Masaya Okura, and Akira Imamoto. "Focal Adhesions Require Catalytic Activity of Src Family Kinases To Mediate Integrin-Matrix Adhesion." Molecular and Cellular Biology 22, no. 4 (February 15, 2002): 1203–17. http://dx.doi.org/10.1128/mcb.22.4.1203-1217.2002.

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ABSTRACT Members of the Src family of tyrosine kinases function to phosphorylate focal adhesion (FA) proteins. To explore the overlapping functions of Src kinases, we have targeted Csk, a negative regulator of the Src family, to FA structures. Expression of FA-targeted Csk (FA-Csk) effectively reduced the active form (nonphosphorylated at the C-terminal regulatory tyrosine) of Src members in the cell. We found that fibroblasts expressing FA-Csk lost integrin-mediated adhesion. Activated Src (SrcY529F) as well as activation of putative Src signaling mediators (Fak, Cas, Crk/CrkL, C3G, and Rap1) blocked the effect of FA-Csk in a manner dependent on Rap1. SrcY529F also inhibited activated Ras-induced cell detachment but failed to rescue detachment caused by an activated mutant of Raf1 (Raf-BXB) that Rap1 cannot inhibit. Although normal spreading onto fibronectin was restored by the β1 integrin affinity-activating antibody TS2/16 in cells expressing FA-Csk or Raf-BXB, FAs were lost in these cells. On the other hand, Rap1 activation could restore FAs in cells expressing FA-Csk. Activation of the executioner caspase, caspase 3, is essential for many forms of apoptosis. While a caspase 3 inhibitor (Z-DEVD-FMK) inhibited cell detachment triggered by activation of caspase 8, this inhibitor had no effect on cell detachment caused by FA-Csk. Likewise, overexpression of an activated Akt made cells resistant to the effect of caspase 8 activation, but not to the effect of FA-Csk. It is therefore likely that the primary cause of cell rounding and detachment induced by FA-Csk involves dysfunction of FAs rather than caspase-mediated apoptosis that may result from possible loss of survival signals mediated by Src family kinases. We suggest that endogenous Src family kinases are essential for FAs through activation of Rap1 in fibroblasts.
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Yamaguchi, N., Y. Nakayama, T. Urakami, S. Suzuki, T. Nakamura, T. Suda, and N. Oku. "Overexpression of the Csk homologous kinase (Chk tyrosine kinase) induces multinucleation: a possible role for chromosome-associated Chk in chromosome dynamics." Journal of Cell Science 114, no. 9 (May 1, 2001): 1631–41. http://dx.doi.org/10.1242/jcs.114.9.1631.

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The Csk family of non-receptor-type tyrosine kinases consists of Csk and the Csk homologous kinase Chk. Each enzyme suppresses the catalytic activity of Src family kinases by phosphorylating their C-terminal negative regulatory tyrosine residues. Ectopic and transient expression of Chk in COS-1 cells showed nuclear localization of Chk and growth inhibition. To further explore the role of Chk in cell growth, we overexpressed Chk in human immature myeloid KMT-2 cells. Chk overexpression brought about growth retardation and aberrant chromosome movement leading to multinucleation, and these events were accompanied by insufficient formation of mitotic spindles. In vitro kinase assays showed that Chk overexpression suppressed the tyrosine kinase activity of Lyn, a member of the Src family, immunoprecipitated from Triton X-100 lysates. Subcellular fractionation studies revealed that fractions of Chk and Lyn, resistant to Triton X-100 solubilization, are associated with mitotic chromosome scaffolds and spindles. Chk overexpression induced a decrease in autophosphorylation of Lyn and concomitant changes in levels of tyrosine phosphorylation of proteins associated with both fractions. These results indicate that Chk, Lyn and the tyrosine-phosphorylated proteins localize to mitotic chromosomes and spindles, suggesting that Chk-dependent tyrosine phosphorylation, presumably through Lyn, may be involved in chromosome dynamics.
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Howell, B. W., and J. A. Cooper. "Csk suppression of Src involves movement of Csk to sites of Src activity." Molecular and Cellular Biology 14, no. 8 (August 1994): 5402–11. http://dx.doi.org/10.1128/mcb.14.8.5402.

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Csk phosphorylates Src family members at a key regulatory tyrosine in the C-terminal tail and suppresses their activities. It is not known whether Csk activity is regulated. To examine the features of Csk required for Src suppression, we expressed Csk mutants in a cell line with a disrupted csk gene. Expression of wild-type Csk suppressed Src, but Csk with mutations in the SH2, SH3, and catalytic domains did not suppress Src. An SH3 deletion mutant of Csk was fully active against in vitro substrates, but two SH2 domain mutants were essentially inactive. Whereas Src repressed by Csk was predominantly perinuclear, the activated Src in cells lacking Csk was localized to structures resembling podosomes. Activated mutant Src was also in podosomes, even in the presence of Csk. When Src was not active, Csk was diffusely located in the cytosol, but when Src was active, Csk colocalized with activated Src to podosomes. Csk also localizes to podosomes of cells transformed by an activated Src that lacks the major tyrosine autophosphorylation site, suggesting that the relocalization of Csk is not a consequence of the binding of the Csk SH2 domain to phosphorylated Src. A catalytically inactive Csk mutant also localized with Src to podosomes, but SH3 and SH2 domain mutants did not, suggesting that the SH3 and SH2 domains are both necessary to target Csk to places where Src is active. The failure of the catalytically active SH3 mutant of Csk to regulate Src may be due to its inability to colocalize with active Src.
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Howell, B. W., and J. A. Cooper. "Csk suppression of Src involves movement of Csk to sites of Src activity." Molecular and Cellular Biology 14, no. 8 (August 1994): 5402–11. http://dx.doi.org/10.1128/mcb.14.8.5402-5411.1994.

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Csk phosphorylates Src family members at a key regulatory tyrosine in the C-terminal tail and suppresses their activities. It is not known whether Csk activity is regulated. To examine the features of Csk required for Src suppression, we expressed Csk mutants in a cell line with a disrupted csk gene. Expression of wild-type Csk suppressed Src, but Csk with mutations in the SH2, SH3, and catalytic domains did not suppress Src. An SH3 deletion mutant of Csk was fully active against in vitro substrates, but two SH2 domain mutants were essentially inactive. Whereas Src repressed by Csk was predominantly perinuclear, the activated Src in cells lacking Csk was localized to structures resembling podosomes. Activated mutant Src was also in podosomes, even in the presence of Csk. When Src was not active, Csk was diffusely located in the cytosol, but when Src was active, Csk colocalized with activated Src to podosomes. Csk also localizes to podosomes of cells transformed by an activated Src that lacks the major tyrosine autophosphorylation site, suggesting that the relocalization of Csk is not a consequence of the binding of the Csk SH2 domain to phosphorylated Src. A catalytically inactive Csk mutant also localized with Src to podosomes, but SH3 and SH2 domain mutants did not, suggesting that the SH3 and SH2 domains are both necessary to target Csk to places where Src is active. The failure of the catalytically active SH3 mutant of Csk to regulate Src may be due to its inability to colocalize with active Src.
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Lee, Byeong-Chel, Shalom Avraham, Akira Imamoto, and Hava Karsenty Avraham. "Identification of the nonreceptor tyrosine kinase MATK/CHK as an essential regulator of immune cells using Matk/CHK-deficient mice." Blood 108, no. 3 (August 1, 2006): 904–7. http://dx.doi.org/10.1182/blood-2005-12-4885.

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Abstract Matk/CHK knockout mice were reported to show no apparent phenotypic abnormalities. This was thought to be due to the homologous kinase Csk that compensates for Matk/CHK. Here, we present the first evidence that the nonreceptor tyrosine kinase, Matk/CHK, is an important modulator of immune cell signaling. We found that the frequency of primitive hematopoietic cells, the side population c-kit+ Lin– Sca-1+ (SPKLS) cells, in Matk/CHK–/– mice was increased 2.2-fold compared with the control mice. Moreover, Matk/CHK deficiency led to significantly higher pre–B cell colony formation following IL-7 stimulation. Interestingly, when mice received the in vivo antigen challenge of TNP-ovalbumin followed by restimulation, the Matk/CHK–/– lymph node and spleen cells produced significantly lower IFN-γ levels compared with the respective wild-type cells. Our study indicates that Matk/CHK is not functionally redundant with Csk, and that this tyrosine kinase plays an important role as a regulator of immunologic responses.
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Chong, Yuh-Ping, Terrence D. Mulhern, and Heung-Chin Cheng. "C-terminal Src kinase (CSK) and CSK-homologous kinase (CHK)—endogenous negative regulators of Src-family protein kinases." Growth Factors 23, no. 3 (January 2005): 233–44. http://dx.doi.org/10.1080/08977190500178877.

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Zagozdzon, Radoslaw, Rafal Kaminski, Yigong Fu, Wei Fu, Cecile Bougeret, and Hava Karsenty Avraham. "Csk homologous kinase (CHK), unlike Csk, enhances MAPK activation via Ras-mediated signaling in a Src-independent manner." Cellular Signalling 18, no. 6 (June 2006): 871–81. http://dx.doi.org/10.1016/j.cellsig.2005.07.016.

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Dissertations / Theses on the topic "CSK"

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Thomas, R. M. "Csk is an important negative regulator of phagocyte responsiveness in vivo : characterisation of myeloid cell-specific Csk deficiency in mice by conditional mutagenesis (Cre/loxP)." Thesis, University College London (University of London), 2007. http://discovery.ucl.ac.uk/1445173/.

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Whilst the recruitment of phagocytic leukocytes is fundamental to the innate response against pathogenic infection, the inappropriate mobilisation of their cytotoxic potential can also lead to fatal tissue injury. To determine the contribution of Csk, a negative regulator of Src family kinases, to the regulation of phagocyte recruitment and activation in vivo, mice lacking Csk in the myeloid lineage were generated using conditional mutagenesis (cre/loxP). This Csk deficiency resulted in acute multifocal inflammation in skin and lung, accompanied by extramedullary haematopoiesis in the spleen and liver, and increased myelopoiesis in bone marrow. Animals were protected from the disease in a microbiologically controlled environment, but remained hypersensitive to LPS-induced shock. Csk-deficient granulocytes showed enhanced spontaneous and ligand-induced degranulation accompanied by hyperinduction of integrins. Hyperresponsiveness was associated with hyperadhesion and impaired migratory responses in vitro. Biochemical studies revealed spontaneous accumulation of tyrosine-phosphorylated proteins, including hyperphosphorylation of key signalling proteins including Syk and paxillin. These data support a breakdown of the activation threshold set by Csk. Thus, Csk is critical in preventing premature granulocyte recruitment through enforcing the requirement for ligand engagement while supporting the migratory capacity of activated cells through negative regulation of cell adhesion. To address the incomplete Cre mediated deletion of floxed genes in vivo, a genetic approach to elevate Cre recombinase gene expression was developed. Whilst manipulation of regulatory elements including promoter, enhancer, and untranslated regions has yielded enhanced and sustained expression in vitro, this has been difficult to achieve in vivo. Here, it is reported that construction of artificial exons through insertion of short heterologous intron sequences into the open reading frames of the Cre recombinase and enhanced green fluorescent protein results in functional expression accompanied by a 30-fold increase in transcription levels in vitro. Furthermore, green fluorescence levels were enhanced five-fold in cell lines and enhanced considerably in the rat brain after transduction with a herpes simplex virus-based vector. These data define a method of improving both the level and duration of recombinant gene expression, in addition to and independently of surrounding regulatory elements. Significantly, the method should help to increase Cre recombinase expression from weak or transiently expressed promoters thus overcoming an important limitation of Cre/loxP technology incomplete deletion. Furthermore, this method may also be applicable in gene therapy to obtain sustained and effective expression of recombinant proteins in vivo.
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Correia, Lúcio José Herculano. "CSK: uma abordagem para estruturação de kernel de tempo real em componentes." Universidade Federal de São Carlos, 2004. https://repositorio.ufscar.br/handle/ufscar/520.

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Made available in DSpace on 2016-06-02T19:06:02Z (GMT). No. of bitstreams: 1 DissLJHC.pdf: 911507 bytes, checksum: 0af483c56c4aeb6304f9100fe71cccb9 (MD5) Previous issue date: 2004-05-27
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Generally, operating systems offer a set of services through primitives that are used on demand by applications. Similarly, software components implement and provide services through well-defined interfaces, which are reused in different software projects of a problem domain. Based upon this similarity, it is researched the reuse of software components in real time operating systems projects. It is presented CSK (Computer Structured Kernel) approach for structuring a real time kernel with software components. The approach is divided in two phases. In the first one software components are built from the legacy code and documentation of a preexisting kernel. In the second one, that kernel is rebuilt by reusing the produced components. A case study applies CSK to real time kernel Virtuoso.
Sistemas operacionais em geral oferecem um conjunto de serviços através de primitivas, as quais são utilizadas sob demanda pelas aplicações. Similarmente, componentes de software implementam e disponibilizam serviços através de interfaces bem definidas, sendo reutilizados em diferentes projetos de software de um domínio de problema. Baseado nesta similaridade, é pesquisado o reuso de componentes de software na área de tempo-real, nos projetos de sistemas operacionais. É apresentada uma abordagem para a estruturação de kernels de tempo-real utilizando componentes de software, denominada CSK (Component Structured Kernel). Esta abordagem é dividida em duas grandes fases. Na primeira fase, constroem-se os componentes a partir do código legado e da documentação de um kernel já existente. Na segunda fase é feita a reestruturação do kernel, através do reúso de componentes. Um estudo de caso aplica a abordagem CSK ao kernel Virtuoso.
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Ayrapetov, Marina K. "Structural and functional studies of the Csk and Src family protein tyrosine kinases /." View online ; access limited to URI, 2006. http://0-wwwlib.umi.com.helin.uri.edu/dissertations/dlnow/3225312.

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Lee, Sungsoo. "Functional and structural study of the protein tyrosine kinase CSK, as a model system /." View online ; access limited to URI, 2005. http://0-wwwlib.umi.com.helin.uri.edu/dissertations/dlnow/3188063.

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Lau, Yuu Seng, and lauje@rocketmail com. "Techniques in Secure Chaos Communication." RMIT University. Electrical and Computer Engineering, 2006. http://adt.lib.rmit.edu.au/adt/public/adt-VIT20070116.151025.

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In today's climate of increased criminal attacks on the privacy of personal or confidential data over digital communication systems, a more secure physical communication link is required. Chaotic signals which have bifurcation behavior (depending on some initial condition) can readily be exploited to enhance the security of communication systems. A chaotic generator produces disordered sequences that provide very good auto- and cross- correlation properties similar to those of random white noise. This would be an important feature in multiple access environments. These sequences are used to scramble data in spread spectrum systems as they can produce low co-channel interference, hence improve the system capacity and performance. The chaotic signal can be created from only a single mathematical relationship and is neither restricted in length nor is repetitive/ cyclic. On the other hand, with the progress in digital signal processing and digital hardware, there has been an increased interest in using adaptive algorithms to improve the performance of digital systems. Adaptive algorithms provide the system with the ability to self-adjust its coefficients according to the signal condition, and can be used with linear or non-linear systems; hence, they might find application in chaos communication. There has been a lot of literature that proposed the use of LMS adaptive algorithm in the communication arena for a variety of applications such as (but not limited to): channel estimation, channel equalization, demodulation, de-noising, and beamforming. In this thesis, we conducted a study on the application of chaos theory in communication systems as well as the application of adaptive algorithms in chaos communication. The First Part of the thesis tackled the application of chaos theory in com- munication. We examined different types of communication techniques utilizing chaos theory. In particular, we considered chaos shift keying (CSK) and mod- ified kind of logistic map. Then, we applied space-time processing and eigen- beamforming technique to enhance the performance of chaos communication. Following on, we conducted a study on CSK and Chaos-CDMA in conjunction with multi-carrier modulation (MCM) techniques such as OFDM (FFT/ IFFT) and wavelet-OFDM. In the Second Part of the thesis, we tried to apply adaptivity to chaos com- munication. Initially, we presented a study of multi-user detection utilizing an adaptive algorithm in a chaotic CDMA multi-user environment, followed by a study of adaptive beamforming and modified weight-vector adaptive beam- forming over CSK communication. At last, a study of modified time-varying adaptive filtering is presented and a conventional adaptive filtering technique is applied in chaotic signal environment. Twelve papers have been published during the PhD candidature, include two journal papers and ten refereed conference papers.
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Baumeister, Ulf. "Identifizierung der zytosolischen Kinase CSK als Bindungspartner von VE-Cadherin Auswirkung dieser Assoziation auf das Zellwachstum /." [S.l. : s.n.], 2004. http://deposit.ddb.de/cgi-bin/dokserv?idn=97146720X.

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Gregorieff, Alexander. "Determinants of the Csk-PEP complex and translational regulation of suppressor of cytokine signalling (SOCS)-1." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape7/PQDD_0017/MQ55063.pdf.

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Lieser, Scot A. "Mechanistic characterization of Csk the role of structural transitions and inter-domain crosstalk in enzyme function /." Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2007. http://wwwlib.umi.com/cr/ucsd/fullcit?p3277705.

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Thesis (Ph. D.)--University of California, San Diego, 2007.
Title from first page of PDF file (viewed October 10, 2007). Available via ProQuest Digital Dissertations. Vita. Includes bibliographical references (p. 143-153).
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Seet, Siong Leng Henry. "Analysis of noncoherent orthogonal modulation for mobile computing." Thesis, Monterey, California. Naval Postgraduate School, 2010. http://hdl.handle.net/10945/55206.

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Wireless communication is employed to connect mobile computers in a networked environment for information exchange. In a tactical space, sensors and computers typically need to operate on-the-move while transmitting data over both short and long distances in different terrain and conditions. The wireless communication is thus susceptible to effects of Doppler shift and channel fading. In addition, when security and anti jamming features are required, such as frequency-hopping techniques, then coherent signal detection is difficult and noncoherent modulation is used instead. Our study will focus on the bit error rate (BER) performance analysis of noncoherent orthogonal modulation, specifically M-ary frequency-shift keying (MFSK) and code-shift keying (CSK) modulation, in both additive white Gaussian noise (AWGN) and for a Rayleigh fading channel with Doppler shift. The potential applications include communications between mobile computer-sensor devices, such as a mobile ground control station maintaining a datalink with UAV.
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Lin, Xiaofeng. "Probing the regulatory mechanisms of protein tyrosine kinases, using C-terminal SRC kinase (CSK) as a model system /." View online ; access limited to URI, 2005. http://0-wwwlib.umi.com.helin.uri.edu/dissertations/dlnow/3188064.

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Books on the topic "CSK"

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name, No. The CDK-activating kinase (CAK). Georgetown, TX: Landes Bioscience, 2003.

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Tournier, Laurent. GREP et InDesign CS3/CS4. Paris: Dunod, 2009.

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CSI. Chichester: Wiley-Blackwell, 2010.

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Kompare, Derek. CSI. Oxford, UK: Wiley-Blackwell, 2010. http://dx.doi.org/10.1002/9781444328028.

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Muraḷi, Mērlapāka. Cek. Vijayavāḍa: Navajyōti Pablikēṣans, 1991.

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MacLaverty, Bernard. Csl. Harmondsworth: Penguin, 1985.

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Photoshop CS5++: Adobe creative suite 5 design standard, Photoshop CS5, InDesign CS5, Illustrator CS5. Toronto: Software News, 2011.

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E, Shuman James, and Reding Elizabeth Eisner, eds. The Web collection revealed: Adobe Flash CS4, Dreamweaver CS4, & Photoshop CS4. Clifton Park, NY: Delmar Cengage Learning, 2010.

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Eisner, Reding Elizabeth, ed. The design collection revealed: Adobe InDesign CS4, Photoshop CS4 & Illustrator CS4. Clifton Park, NY: Delmar, 2010.

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Eisner, Reding Elizabeth, ed. The design collection revealed: Adobe InDesign CS5, Photoshop CS5, Illustrator CS5. Clifton Park, NY: Delmar Cengage Learning, 2011.

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Book chapters on the topic "CSK"

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Okada, Masato. "Csk." In Encyclopedia of Signaling Molecules, 1210–14. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_264.

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van Roy, Frans, Volker Nimmrich, Anton Bespalov, Achim Möller, Hiromitsu Hara, Jacob P. Turowec, Nicole A. St. Denis, et al. "Csk." In Encyclopedia of Signaling Molecules, 458–63. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_264.

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van Roy, Frans, Volker Nimmrich, Anton Bespalov, Achim Möller, Hiromitsu Hara, Jacob P. Turowec, Nicole A. St. Denis, et al. "CSK-Homologous Kinase." In Encyclopedia of Signaling Molecules, 463–72. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_185.

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Cheng, Heung-Chin, Gahana Advani, Mohammed Iqbal Hossain, Nadia L. Y. Ng, Ya Chee Lim, Anderly C. Chüeh, Mohd Aizuddin Kamaruddin, and Yuh-Ping Chong. "CSK-Homologous Kinase." In Encyclopedia of Signaling Molecules, 1215–30. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_185.

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Cheng, Heung-Chin, Gahana Advani, Mohammed Iqbal Hossain, Nadia LY Ng, Ya Chee Lim, Anderly C. Chüeh, Mohd Aizuddin Kamaruddin, and Yuh-Ping Chong. "CSK-Homologous Kinase." In Encyclopedia of Signaling Molecules, 1–17. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4614-6438-9_185-1.

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Shang, Ying. "Performance of Chirp CSK for Integrated Wideband Communication." In Advances in Intelligent Systems and Computing, 666–73. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-53980-1_98.

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Chen, Yaohui, Dun Wang, Siyuan Chen, Wencong Ma, Dongjun Li, and Qijia Dong. "Research on Receiving Method of Code Shift Keying (CSK) Signal." In China Satellite Navigation Conference (CSNC) 2020 Proceedings: Volume III, 298–309. Singapore: Springer Singapore, 2020. http://dx.doi.org/10.1007/978-981-15-3715-8_28.

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Yan, Tao, Ying Wang, Tian Li, Ye Tian, Lang Bian, and Yansong Meng. "Low Complexity Acquisition and Tracking Methods for CSK Modulated Signals." In Lecture Notes in Electrical Engineering, 193–202. Singapore: Springer Singapore, 2021. http://dx.doi.org/10.1007/978-981-16-3146-7_19.

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Barreto, Sara, and Damien Lacroix. "Quantification of CSK Mechanics and Deformation in Relation to Cellular Functioning." In Frontiers of Biomechanics, 181–93. Singapore: Springer Singapore, 2018. http://dx.doi.org/10.1007/978-981-10-8075-3_10.

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Georgescu, Alexandru, Adrian V. Gheorghe, Marius-Ioan Piso, and Polinpapilinho F. Katina. "CSG: Towards CSI Research." In Critical Space Infrastructures, 321–43. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-12604-9_13.

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Conference papers on the topic "CSK"

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Liping Du, Xiangyi Hu, Ying Li, and Guifen Zhao. "A CSK based SSL handshake protocol." In 2009 IEEE International Conference on Network Infrastructure and Digital Content (IC-NIDC 2009). IEEE, 2009. http://dx.doi.org/10.1109/icnidc.2009.5360980.

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Ndjiongue, A. R., H. C. Ferreira, and Telex M. N. Ngatched. "Constellation design for cascaded MPSK-CSK systems." In 2017 IEEE International Conference on Communications Workshops (ICC Workshops). IEEE, 2017. http://dx.doi.org/10.1109/iccw.2017.7962627.

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Singh, Ravinder, Timothy O'Farrell, and John P. R. David. "Performance evaluation of IEEE 802.15.7 CSK physical layer." In 2013 IEEE Globecom Workshops (GC Wkshps). IEEE, 2013. http://dx.doi.org/10.1109/glocomw.2013.6825133.

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Sugimoto, Toru, Tsuyoshi Arai, and Hiroshi Inai. "Performance evaluation of CSK spread spectrum Boomerang system." In 2008 International Symposium on Information Theory and Its Applications (ISITA). IEEE, 2008. http://dx.doi.org/10.1109/isita.2008.4895473.

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Ju, DongWook, Guisik Kim, Soowoong Jeong, and Sangkeun Lee. "Frequency decomposition-based tracking for improving a CSK tracker." In 2016 IEEE International Conference on Consumer Electronics - Asia (ICCE-Asia). IEEE, 2016. http://dx.doi.org/10.1109/icce-asia.2016.7804820.

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Caparra, Gianluca, and Nicola Laurenti. "On the Use of CSK for GNSS Anti-Spoofing." In 2018 9th ESA Workshop on Satellite Navigation Technologies and European Workshop on GNSS Signals and Signal Processing (NAVITEC). IEEE, 2018. http://dx.doi.org/10.1109/navitec.2018.8642661.

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Han, Chunyan, and Fengquan Man. "Noise Performance Analysis of Chaotic Coherent CSK Communication System." In 2010 International Conference on Computational Intelligence and Software Engineering (CiSE). IEEE, 2010. http://dx.doi.org/10.1109/cise.2010.5676923.

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Ndjiongue, A. R., Thokozani Shongwe, H. C. Ferreira, T. M. Nkouatchah Ngatched, and A. J. Han Vinck. "Cascaded PLC-VLC Channel Using OFDM and CSK Techniques." In GLOBECOM 2015 - 2015 IEEE Global Communications Conference. IEEE, 2014. http://dx.doi.org/10.1109/glocom.2014.7417129.

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Ndjiongue, A. R., Thokozani Shongwe, H. C. Ferreira, T. M. Nkouatchah Ngatched, and A. J. Han Vinck. "Cascaded PLC-VLC Channel Using OFDM and CSK Techniques." In 2015 IEEE Global Communications Conference (GLOBECOM). IEEE, 2015. http://dx.doi.org/10.1109/glocom.2015.7417129.

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Lombardi, Nunzia, Rino Lorusso, and Giovanni Milillo. "Accuracy of high resolution CSK interferometric Digital Elevation Models." In IGARSS 2015 - 2015 IEEE International Geoscience and Remote Sensing Symposium. IEEE, 2015. http://dx.doi.org/10.1109/igarss.2015.7326438.

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Reports on the topic "CSK"

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Lee, Byeong-Chei. Csk Homologous Kinase, a Potential Regulator of CXCR4-mediated Breast Cancer Cell Metastasis. Fort Belvoir, VA: Defense Technical Information Center, August 2010. http://dx.doi.org/10.21236/ada538886.

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Lee, Byeong-Chel. Csk Homologous Kinase, a Potential Regulator of CXCR4-Medicated Breast Cancer Cell Metastasis. Fort Belvoir, VA: Defense Technical Information Center, August 2011. http://dx.doi.org/10.21236/ada554270.

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Zagozdzon, Radoslaw, and Hava Avraham. Effects of Csk Homologous Kinase Overexpression on HER2/Neu-Mediated Signal Transduction Pathways in Breast Cancer Cells. Fort Belvoir, VA: Defense Technical Information Center, April 2005. http://dx.doi.org/10.21236/ada436916.

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Zagozdzon, Radoslaw, and Hava Avraham. Effects of CSK Homologous Kinase Overexpression on HER2/Neu-Mediated Signal Transduction Pathways in Breast Cancer Cells. Fort Belvoir, VA: Defense Technical Information Center, April 2003. http://dx.doi.org/10.21236/ada416967.

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Zagozdzon, Radoslaw, and Hava Avraham. Effects of CSK Homologous Kinase Overexpression on HER2/Neu-Mediated Signal Transduction Pathways in Breast Cancer Cells. Fort Belvoir, VA: Defense Technical Information Center, April 2004. http://dx.doi.org/10.21236/ada425671.

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REED, A. V. Evaluation of CSB Cask Receipt Pressure. Office of Scientific and Technical Information (OSTI), August 1999. http://dx.doi.org/10.2172/797705.

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Trew, Sebastian, Daryl Higgins, Douglas Russell, Kerryann Walsh, and Maria Battaglia. Parent engagement and involvement in education for children and young people’s online, relationship, and sexual safety : A rapid evidence assessment and implications for child sexual abuse prevention education. Australian Catholic University, August 2021. http://dx.doi.org/10.24268/acu.8w9w4.

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[Excerpt] We recently conducted a rapid evidence review on educational programs that focus on child sexual abuse (CSA) prevention (Trew et al., 2021). In that review, we learned that child-focused CSA prevention education could be enhanced by looking at how to improve the parent engagement or involvement. We know from a previous review (Hunt & Walsh, 2011), that parents’ views about CSA prevention education are important. But further evidence is needed to develop concrete strategies for strengthening parent engagement in appropriate and effective ways. As identified in the above-mentioned review (Trew et al., 2021), prominent researchers in the CSA prevention field have noted that if prevention efforts are to be successful, it is imperative to include parents (Hunter, 2011; Mendelson & Letourneau, 2015; J. Rudolph & M.J. Zimmer-Gembeck, 2018; Wurtele & Kenny, 2012). This research focuses on two complementary aspects of parent engagement in CSA prevention: (i) parent participation in parent-focused CSA prevention (ii) parent participation in school-based or child-focused CSA prevention.
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Ye, Binglin, Shuling Li, Fengqi Sun, Youfu Fan, Weiguo Chen, and Xiangfu Wang. Effect of full-endoscopic cervical laminectomy and decompression versus anterior cervical decompression with fusion in the treatment of patients with cervical spondylotic myelopathy: A protocol for systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, August 2021. http://dx.doi.org/10.37766/inplasy2021.8.0034.

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Review question / Objective: This systematic review aims to comprehensively assess the efficacy and safety of full-endoscopic cervical laminectomy and decompression versus anterior cervical decompression with fusion in treating cervical spondylotic myelopathy (CSM) patients. Condition being studied: Cervical spondylotic myelopathy (CSM) is a degenerative disease associated with cervical cord compression, which has increased significant health-related social costs and derived disabilities. Anterior cervical discectomy and fusion (ACDF) is the "gold standard" for the treatment of CSM. However, the application of ACDF may cause some complications. Recently, full-endoscopic cervical laminectomy and decompression have shown potential therapeutic effects for CSM. However, no systematic review or meta-analysis has focused on the effects of full-endoscopic cervical laminectomy and decompression in the treatment of CSM. This systematic review aims to comprehensively assess the efficacy and safety of full-endoscopic cervical laminectomy and decompression versus anterior cervical decompression with fusion in treating CSM patients.
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Baich, M. A. CST/FRIT Settling, CST Particle Size Reduction and CST Loading. Office of Scientific and Technical Information (OSTI), August 2000. http://dx.doi.org/10.2172/761150.

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Pang, Xiaoying. CSR for drift. Office of Scientific and Technical Information (OSTI), August 2014. http://dx.doi.org/10.2172/1159042.

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