Relevant bibliographies by topics / Protein kinasa

Contents

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

Academic literature on the topic 'Protein kinasa'

Author: Grafiati
Published: 4 June 2021
Last updated: 1 February 2022

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources on the topic 'Protein kinasa.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Journal articles on the topic "Protein kinasa"

1

Mattei, Jean Camille, Corinne Bouvier-Labit, Doriane Barets, Nicolas Macagno, Mathieu Chocry, Frédéric Chibon, Philippe Morando, et al. "Pan Aurora Kinase Inhibitor: A Promising Targeted-Therapy in Dedifferentiated Liposarcomas With Differential Efficiency Depending on Sarcoma Molecular Profile." Cancers 12, no. 3 (March 3, 2020): 583. http://dx.doi.org/10.3390/cancers12030583.

Full text
Abstract:
Soft tissue sarcoma (STS) are rare and aggressive tumours. Their classification includes numerous histological subtypes of frequent poor prognosis. Liposarcomas (LPS) are the most frequent type among them, and the aggressiveness and deep localization of dedifferentiated LPS are linked to high levels of recurrence. Current treatments available today lead to five-year overall survival has remained stuck around 60–70% for the past three decades. Here, we highlight a correlation between Aurora kinasa A (AURKA) and AURKB mRNA overexpression and a low metastasis-free survival. AURKA and AURKB expression analysis at genomic and protein level on a 9-STS cell lines panel highlighted STS heterogeneity, especially in LPS subtype. AURKA and AURKB inhibition by RNAi and drug targeting with AMG 900, a pan Aurora Kinase inhibitor, in four LPS cell lines reduces cell survival and clonogenic proliferation, inducing apoptosis and polyploidy. When combined with doxorubicin, the standard treatment in STS, aurora kinases inhibitor can be considered as an enhancer of standard treatment or as an independent drug. Kinome analysis suggested its effect was linked to the inhibition of the MAP-kinase pathway, with differential drug resistance profiles depending on molecular characteristics of the tumor. Aurora Kinase inhibition by AMG 900 could be a promising therapy in STS.
APA, Harvard, Vancouver, ISO, and other styles
2

Pang, Kam-Lee, Wei-Li Thong, and Siew-Eng How. "Cinnamomum Iners as Mitogen-Activated Protein Kinase Kinase (MKK1) Inhibitor." International Journal of Engineering and Technology 1, no. 4 (2009): 310–13. http://dx.doi.org/10.7763/ijet.2009.v1.61.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Guda, B. B., V. V. Pushkarev, O. V. Zhuravel, A. Ye Kovalenko, V. M. Pushkarev, Y. M. Taraschenko, and M. D. Tronko. "Protein kinase Akt activity in human thyroid tumors." Ukrainian Biochemical Journal 88, no. 5 (October 31, 2016): 90–95. http://dx.doi.org/10.15407/ubj88.05.090.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Kim, Young-Sook. "A Protein Kinase-A Inhibitor, KT5720, Suppressed Cytopathic Effect Caused by Vesicular Stomatitis Virus." Journal of Life Science 17, no. 10 (October 30, 2007): 1361–67. http://dx.doi.org/10.5352/jls.2007.17.10.1361.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Stolworthy, Tiffany S., and Margaret E. Black. "The mouse guanylate kinase double mutant E72Q/D103N is a functional adenylate kinase." Protein Engineering, Design and Selection 14, no. 11 (November 2001): 903–9. http://dx.doi.org/10.1093/protein/14.11.903.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Moon, Il-Soo, and Dae-Hyun Seog. "Protein Kinase (PKC)-ε Interacts with the Serotonin Transporter (SERT) C-Terminal Region." Journal of Life Science 20, no. 10 (October 30, 2010): 1451–57. http://dx.doi.org/10.5352/jls.2010.20.10.1451.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Edwards, Amelia S., and John D. Scott. "A-kinase anchoring proteins: protein kinase A and beyond." Current Opinion in Cell Biology 12, no. 2 (April 2000): 217–21. http://dx.doi.org/10.1016/s0955-0674(99)00085-x.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Vallespí, Teresa, Mildred Borrego, Doulous Colomé, Ana Jaen, Maria Rozman, and Isabel Massagué. "Quantitative Polymerase Chain Reaction (qPCR) at Diagnosis and Follow-Up of Patients with Chronic Myeloid Leukemia in Treatment with Imatinib." Blood 104, no. 11 (November 16, 2004): 4688. http://dx.doi.org/10.1182/blood.v104.11.4688.4688.

Full text
Abstract:
Abstract Imatinib, a selective inhibitor of tyrosin-kinasa BCR/ABL fusion protein, produces high response rates in patients with chronic myeloid leukemia (CML) in the chronic phase. The behavior of the levels of the BCR/ABL transcript by qPCR technique was studied in 24 patients (13M/11F; median age: 49.6 years, range: 23–73), diagnosed of CML in chronic phase, before and after the treatment with imatinib (at the 0, 3, 7, 11 and 15 months). Eight patients had previously received interferon alpha or busulphan and 16 hidroxiurea. The amplification of BCR/ABL with the qPCR technique, according to protocol BIOMED-2, was carried out in samples of bone marrow (n = 23) and peripheral blood (n = 48). Results were calculated in relation to a control gene of the glucuronidasa (GUS) and expressed in logarithmic scale (log10). Median time from the diagnosis was of 28 months and median treatment time with imatinib was 14 months. The median reduction of BCR/ABL transcripts was 1,98 log after three months and decreased further (2,71 log) during follow-up. Both of them were significative when compare with base line levels (P <0.001). The reduction was greater in patients who received a dose ³ 400 mg/day (n=16) than those with 300 mg/day (n=8). Three patients reached a major molecular response (ratio BCR-ABL/GUS <0.005) up to 15 months of treatment. In conclusion: the determination of the BCR/ABL transcripts by qPCR contributes with valuable information about the effect of imatinib in patients with CML. The logarithmic reduction is higher in the beginning of the treatment and doses ³ 400 mg/day are associated with a greater reduction of the tumoral load. Figure Figure
APA, Harvard, Vancouver, ISO, and other styles
9

Protopopov, M. V., O. V. Ostrynska, and D. H. Ivanchenko. "Developing of protein kinase CK2 inhibitors based on purine-2,6-diones derivatives." Ukrainian Biochemical Journal 89, no. 5 (October 25, 2017): 32–39. http://dx.doi.org/10.15407/ubj89.05.032.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Tougard, Pierre, Thanh Hung Le, Philippe Minard, Michel Desmadril, Jeannine M. Yon, Thierry Bizebard, Gérard Lebras, and Christian Dumas. "Structural and functional properties of mutant Arg203Pro from yeast phosphoglycerate kinase, as a model of phosphoglycerate kinase-Uppsala." "Protein Engineering, Design and Selection" 9, no. 2 (1996): 181–87. http://dx.doi.org/10.1093/protein/9.2.181.

Full text
APA, Harvard, Vancouver, ISO, and other styles
More sources

Dissertations / Theses on the topic "Protein kinasa"

1

Almela, Rojo Pilar. "Implicación de diferentes cascadas de señalización intracelular en los cambios adaptativos observados durante la dependencia de morfina." Doctoral thesis, Universidad de Murcia, 2008. http://hdl.handle.net/10803/10799.

Full text
Abstract:
El objetivo general de este trabajo ha sido estudiar la posible implicación de diferentes cascadas de proteín kinasas en las modificaciones cardiacas que se producen tras la administración de naloxona a ratas dependientes de morfina. Los datos obtenidos indican que durante la abstinencia a morfina se produce un aumento del turnover de NA, de la actividad TH y de su fosforilación en serina 40 y 31, lo que sugiere la puesta en marcha de mecanismos post-transcripcionales. Por otra parte, la vía de la PKA estaría implicada en el incremento del turnover de NA, en el aumento de TH total y en la fosforilación y activación de TH en serina 40 durante dicho síndrome. Por último, la vía de la PKC sería una de las vías implicadas en la expresión de c-fos, así como la de las ERK, que estaría también implicada en la activación de TH en serina 31.
The main aim of this work was to study the posible involvement of different protein kinases in the cardiac adaptive changes induced during morphine withdrawal. Our results show an increase of NA turnover, TH activity and TH phosphorylation at serine 31 and 40, suggesting starting post-trascriptional mechanisms. On the other hand, PKA transduction system could be implicated in the enhanced NA turnover, in the total TH increase and in the phosphorylation and activation of TH at serine 40 during this syndrome. Finally, PKC pathway would be involved in c-Fos expression as well as ERK system which would also be responsible for TH phosphorylation at serine 31.
APA, Harvard, Vancouver, ISO, and other styles
2

Gatesman, Ammer Amanda. "PKCalpha direct cSrc activation and podosome formation through the adaptor protein AFAP-110." Morgantown, W. Va. : [West Virginia University Libraries], 2004. https://etd.wvu.edu/etd/controller.jsp?moduleName=documentdata&jsp%5FetdId=3762.

Full text
Abstract:
Thesis (Ph. D.)--West Virginia University, 2004
Title from document title page. Document formatted into pages; contains vii, 350 p. : ill. (some col.). Vita. Includes abstract. Includes bibliographical references (p. 322-346).
APA, Harvard, Vancouver, ISO, and other styles
3

Nguyen, Giang Huong. "A functional analysis of the human LPA₁G protein coupled receptor." Thesis, Available online, Georgia Institute of Technology, 2004:, 2004. http://etd.gatech.edu/theses/available/etd-06072004-131304/unrestricted/nguyen%5Fgiang%5Fh%5F200405%5Fms.pdf.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Cherezova, Lidia Nikolayevna. "Determining the effects of phosphorylation on AFAP-110 function." Morgantown, W. Va. : [West Virginia University Libraries], 2002. http://etd.wvu.edu/templates/showETD.cfm?recnum=2492.

Full text
Abstract:
Thesis (M.S.)--West Virginia University, 2002.
Title from document title page. Document formatted into pages; contains v, 105 p. : ill. (some col.). Vita. Includes abstract. Includes bibliographical references.
APA, Harvard, Vancouver, ISO, and other styles
5

Baisden, Joseph M. "AFAP-110 is a cSrc activator." Morgantown, W. Va. : [West Virginia University Libraries], 2003. http://etd.wvu.edu/templates/showETD.cfm?recnum=2766.

Full text
Abstract:
Thesis (Ph. D.)--West Virginia University, 2003.
Title from document title page. Document formatted into pages; contains v, 149 p. : ill. (some col.). Vita. Includes abstract. Includes bibliographical references.
APA, Harvard, Vancouver, ISO, and other styles
6

Walker, Valerie Glynis. "Pl3-kinase mediates cSrc activation and podosome formation through the adaptor protein, AFAP-110, in response to PKC[alpha] activation." Morgantown, W. Va. : [West Virginia University Libraries], 2007. https://eidr.wvu.edu/etd/documentdata.eTD?documentid=5191.

Full text
Abstract:
Thesis (Ph. D.)--West Virginia University, 2007.
Title from document title page. Document formatted into pages; contains viii, 306 p. : ill. (some col.). Vita. Includes abstract. Includes bibliographical references.
APA, Harvard, Vancouver, ISO, and other styles
7

Goodman, Alan Gabriel. "P58IPK, the cellular eIF2alpha kinase inhibitor, promotes viral mRNA translation and limits host death during influenza virus infection /." Thesis, Connect to this title online; UW restricted, 2007. http://hdl.handle.net/1773/8082.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Koscky, Paier Carlos Roberto 1983. "Padronização da expressão heterologa e de modelo de ensaio de atividade para a proteina quinase humana S6K." [s.n.], 2009. http://repositorio.unicamp.br/jspui/handle/REPOSIP/314787.

Full text
Abstract:
Orientador: Nilson Ivo Tonin Zanchin
Dissertação (mestrado) - Universidade Estadual de Campinas, Instituto de Biologia
Made available in DSpace on 2018-08-14T12:40:52Z (GMT). No. of bitstreams: 1 KosckyPaier_CarlosRoberto_M.pdf: 3760581 bytes, checksum: 99331529324819b59a4360d60efd9b9a (MD5) Previous issue date: 2009
Resumo: A quinase de 70 kDa da proteína ribossomal S6, isoforma 1 (S6K1), é uma fosfoproteína implicada na regulação de genes relacionados ao controle da tradução em mamíferos e possui uma forma nuclear (a1) e uma citoplasmática (a2). A fosforilação do seu principal alvo, a proteína RPS6, tem sido comumente associada ao recrutamento seletivo dos 5'-TOP (5' tract of oligopyrimidine) mRNAs pela maquinaria de tradução, embora haja estudos contrariando esta hipótese. Devido às funções de seus demais alvos, S6K1 tem sido implicada na sobrevivência celular e em diversos outros processos, como crescimento, câncer e resistência à insulina. S6K1 é ativada por um mecanismo que envolve fosforilação seqüencial através da ativação das vias mTORC1 (complexo 1 do alvo da rapamicina em mamíferos) e PI3K (fosfoinositol-3 quinase). Como uma quinase da família AGC, S6K1 deve ser fosforilada por mTORC1 no resíduo Thr389 do domínio hidrofóbico e, em seguida, por PDPK1 (proteína quinase 1 dependente de fosfoinositol) no resíduo Thr229 da alça T do domínio catalítico. Estes eventos ocorrem somente após a fosforilação em diversos sítios do domínio auto-inibitório carboxiterminal, por mTORC1. O objetivo deste trabalho foi desenvolver um ensaio modelo para análise da função da S6K1 in vitro e utilizá-lo como ferramenta na elucidação do papel de proteínas adaptadoras da via de mTOR em interações com a S6K1. Para isso foi necessário produzir as proteínas recombinantes para ensaios de interação e para realização de um ensaio de atividade para a S6K1. Foram testados vários sistemas de expressão para Escherichia coli para produção das construções GST-S6K1a1-His6, GST-S6K1a2-His6 e GST-S6K1a2T389E?CT (forma a2 de S6K1 com a substituição T389E e o carboxiterminal truncado), GST-PDPK1 e GST-CDPDPK1 (domínio catalítico de PDPK1 fusionado a GST). A expressão das formas truncadas de S6K1 e PDPK1 foi mais eficiente em E. coli. Embora o rendimento tenha ficado muito aquém do esperado, foi suficiente para os ensaios de interação in vitro. Também foi feita a expressão em E. coli da região C-terminal da proteína RPS6, que é o substrato da S6K1, em fusão com a proteína D do fago ?. Posteriormente, foram montados sistemas de expressão das construções His6-S6K1a2T389E?CT e His6-CDPDPK1 em células de inseto, a partir de vetor de baculovírus. Constatou-se que essas construções são expressas na forma de fosfoproteínas em células de inseto. Ensaios de GST pull-down com GST-S6K1a2-His6 e GST-S6K1a2T389E?CT contra as duas isoformas da subunidade catalítica da PP2AC, His6-PP2ACa(maior) e His6-PP2ACa(menor), revelaram que His6-PP2ACa(maior) não interage com GST-S6K1a2-His6, embora interaja fortemente com GST-S6K1a2T389E?CT. Já a construção His6-PP2ACa(menor) interage fracamente com as construções GST-S6K1a2-His6 e GST-S6K1a2T389E?CT. Tomados em conjunto, os resultados sugerem que a presença do C-terminal não fosforilado de S6K1a2 impede a interação com PP2ACa(maior). PP2ACa(menor) comporta-se de forma completamente diferente da isoforma maior, pois a interação entre PP2ACa(menor) e S6K1a2 parece ser independente do carboxiterminal da quinase, visto que as quantidades de S6K1a2T389E?CT e de S6K1a2 inteira que interagem com PP2ACa(menor) são semelhantes. Esses resultados necessitam ainda serem confirmados in vivo. Outros experimentos de GST pull-down confirmaram que as construções de S6K1 não interagem com a4, embora interajam com TIPRL1. Se confirmado in vivo, esse resultado compõe um novo quadro na regulação coordenada entre mTOR1 e PP2A, do qual TIPRL1 parece participar. As construções genéticas e os sistemas de expressão gerados neste trabalho possibilitaram a obtenção dos reagentes necessários para analisar o mecanismo de regulação da quinase S6K1, mediado por proteínas regulatórias. Permitem também desenvolver uma série de experimentos, como busca de inibidores específicos para a S6K1, que dependem da reconstituição de ensaios de atividade in vitro com a S6K1 ativada. Contudo, o ensaio de atividade realizado não apresentou resultados satisfatórios e precisa ser desenvolvido.
Abstract: The 70kDa ribosomal S6 protein kinase 1 (S6K1) is a phosphoprotein involved in the regulation of genes related to translational control in mammals. S6K1 shows distinct nuclear (a1) and cytoplasmic (a2) forms. Phosphorylation of the S6K1 best characterized target, the protein of the small ribosomal subunit (RPS6), has been generally associated to the selective recruitment of the 5'-TOP mRNAs (5' tract of oligopyrimidine) by the translational machinery, although there is still some controversy on this issue. Due to the function of its targets, S6K1 has been implicated in several cellular processes including cell growth, cancer and insulin resistance. S6K1 is activated by a mechanism of sequential phosphorylation following activation of the mTORC1 (mammalian target of rapamycin complex 1) and PI3K (phosphoinositide-3-kinase) pathways. As a kinase of the AGC family, S6K1 activation requires mTORC1 phosphorylation of residue Thr389 of the hydrophobic domain followed by PDPK1 (phosphoinositide dependent protein kinase 1) phosphorylation of residue Thr229 at the T loop of the catalytic domain. These take place only after phosphorylation by mTORC1 of several residues of the autoinhibitory C-terminal domain. The objective of this work was to develop an assay to analyze the function of S6K1 in vitro and use it as a tool in the discovering of the functions of regulators proteins of the mTOR cascade in interactions with S6K1. For these purposes, expression systems were constructed to produce the various recombinant proteins to be used in the interaction and activity assays. Several genetic constructions were tested in Escherichia coli for the production of GST-S6K1a1-His6, GST-S6K1a2-His6 and GST-S6K1a2T389E?CT (a2 form of S6K1 with the T389E substitution and truncated carboxiterminus), GST-PDPK1 and GST-CDPDPK1 (GST fusion protein of the catalytic domain of PDPK1). The truncated forms were expressed more efficiently in E. coli. Although the yield in E. coli was lower than expected, it was sufficient to perform interaction assays. The C-terminal domain of RPS6, a substrate for S6K1, was successfully expressed in E. coli as a fusion protein with the phage ? protein D. Subsequently, expression systems for production of His6-S6K1a2T389E?CT and His6-CDPDPK1 in insect cells were constructed using baculovirus vectors. It was found that these constructs are expressed in the form of phosphoproteins in insect cells. GST pull-down assays using GST-S6K1a2-His6 e GST-S6K1a2T389E?CT to test interaction with the PP2AC isoforms His6-PP2ACa(major) and His6-PP2ACa(minor) revealed that His6-PP2ACa(major) does not interact with GST-S6K1a2-His6, although it interacts strongly with GST-S6K1a2T389E?CT. On the other hand, His6-PP2ACa(minor) interacts weakly with both GST- S6K1a2-His6 and GST-S6K1a2T389E?CT. This finding suggests that the unphosphorylated C-terminal of S6K1a2 inhibits interaction with PP2ACa(major). His6-PP2ACa(minor) behaves differently form His6-PP2ACa(major). Its interaction with S6K1a2 seems to be independent of the C-terminal since the amounts of S6K1a2T389E?CT and S6K1a2 that interact with His6-PP2ACa(minor) are similar. Future work in vivo is required to confirm these results. GST pull-down assays confirmed that a4 does not interact with the constructions of S6K1, while TIPRL1 interacts with them. If confirmed in vivo, these results provides a new perspective for the coordinated regulation between mTOR1 and PP2A, which apparently involves also TIPRL1. The genetic constructions and expression systems established in this work allow the production of the reagents required to study the mechanism of S6K1 regulation mediated by adaptor proteins. They will also allow the development of experiments such as screening for specific S6K1 inhibitors, which depend on reconstitution of S6K1 activity assays using activated S6K1. Nevertheless, the activity assay performed did not yield satisfactory outcomes and must be improved.
Mestrado
Bioquimica
Mestre em Biologia Funcional e Molecular
APA, Harvard, Vancouver, ISO, and other styles
9

Toker, I. Alex. "Purification and characterisation of protein kinase C inhibitor proteins." Thesis, University College London (University of London), 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.277909.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Chan, Ka-wai, and 陳嘉威. "Characterization of a physiological 62-kDa protein substrate for ganglioside-stimulated protein kinase in central nervous systemmyelin." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2004. http://hub.hku.hk/bib/B30595575.

Full text
APA, Harvard, Vancouver, ISO, and other styles
More sources

Books on the topic "Protein kinasa"

1

Hardie, D. G. Protein kinase factsbook. London: Academic Press, 1995.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
2

Protein kinase technologies. New York: Humana Press, 2012.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
3

Pinna, Lorenzo A., ed. Protein Kinase CK2. Oxford, UK: John Wiley & Sons, Inc., 2013. http://dx.doi.org/10.1002/9781118482490.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Mukai, Hideyuki, ed. Protein Kinase Technologies. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-61779-824-5.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Reith, Alastair D. Protein Kinase Protocols. New Jersey: Humana Press, 2000. http://dx.doi.org/10.1385/1592590594.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Xavier, Gabriela Da Silva. Protein kinases. Rijeka: InTech, 2012.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
7

name, No. Protein kinase C protocols. Totowa, NJ: Humana Press, 2003.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
8

Edwards, Cassie. Protein kinase c protocols. [Place of publication not identified]: Humana, 2010.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
9

Cordero, Mario D., and Benoit Viollet, eds. AMP-activated Protein Kinase. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-43589-3.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Newton, Alexandra C. Protein Kinase C Protocols. New Jersey: Humana Press, 2003. http://dx.doi.org/10.1385/1592593976.

Full text
APA, Harvard, Vancouver, ISO, and other styles
More sources

Book chapters on the topic "Protein kinasa"

1

Cuevas, Bruce D. "Mitogen-Activated Protein Kinase Kinase Kinases." In Encyclopedia of Cancer, 1–5. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-27841-9_7192-1.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Cuevas, Bruce D. "Mitogen-Activated Protein Kinase Kinase Kinases." In Encyclopedia of Cancer, 2872–76. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-662-46875-3_7192.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Chiosi, E., A. Spina, F. Valente, and G. Illiano. "Protein Kinase C and G Proteins." In Adenine Nucleotides in Cellular Energy Transfer and Signal Transduction, 257–68. Basel: Birkhäuser Basel, 1992. http://dx.doi.org/10.1007/978-3-0348-7315-4_23.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Defnet, Amy, Ramon Martinez, and Paul Shapiro. "Protein Kinase Interactions with Regulatory and Effector Proteins." In Next Generation Kinase Inhibitors, 61–80. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-48283-1_4.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Baker, Julien S., Fergal Grace, Lon Kilgore, David J. Smith, Stephen R. Norris, Andrew W. Gardner, Robert Ringseis, et al. "Protein Kinase." In Encyclopedia of Exercise Medicine in Health and Disease, 732. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-540-29807-6_2920.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Schomburg, Dietmar, and Dörte Stephan. "Protein kinase." In Enzyme Handbook 13, 763–70. Berlin, Heidelberg: Springer Berlin Heidelberg, 1997. http://dx.doi.org/10.1007/978-3-642-59176-1_148.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Ward, Tony Milford. "Protein Kinase." In Proteins and Tumour Markers May 1995, 1363. Dordrecht: Springer Netherlands, 1995. http://dx.doi.org/10.1007/978-94-011-0681-8_72.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Shiryaev, Alexey, Marijke Van Ghelue, and Ugo Moens. "Mitogen-Activated Protein Kinase-Activated Protein Kinases and Metastasis." In Signal Transduction in Cancer Metastasis, 41–76. Dordrecht: Springer Netherlands, 2010. http://dx.doi.org/10.1007/978-90-481-9522-0_4.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Kinoshita, Eiji, Emiko Kinoshita-Kikuta, and Tohru Koike. "Phos-tag Affinity Electrophoresis for Protein Kinase Profiling." In Protein Kinase Technologies, 13–34. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-61779-824-5_2.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Niefind, Karsten, and Roberto Battistutta. "Structural Bases of Protein Kinase CK2 Function and Inhibition." In Protein Kinase CK2, 1–75. Oxford, UK: John Wiley & Sons, Inc., 2013. http://dx.doi.org/10.1002/9781118482490.ch1.

Full text
APA, Harvard, Vancouver, ISO, and other styles

Conference papers on the topic "Protein kinasa"

1

Timmons, Sheila, and Jack Hawiger. "REGULATION OF PLATELET RECEPTORS FOR FIBRINOGEN AND VON WILLEBRAND FACTOR BY PROTEIN KINASE." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644674.

Full text
Abstract:
Positive and negative regulation of platelet receptors for adhesive proteins, fibrinogen (F) and von Willebrand Factor (vWF) determines whether binding of these ligands will or will not take place. We have shown previously that ADP stimulates and cyclic AMP inhibits binding of F and vWF to human platelets. Now we show that positive regulation of F and vWF binding to platelets via the glycoprotein 11b/1111a complex is dependent on platelet Protein Kinase C, a calcium- and phospholipid-dependent enzyme. A potent activator of Protein Kinase C, phorbol-12-myristoyl-13-acetate (PMA) induced saturable and specific binding of F and vWF which was inhibited by synthetic peptides, gamma chain .dodecapeptide (gamma 400-411) and RGDS. The phosphorylation of 47kDa protein (P47), a marker of Protein Kinase C activation in platelets, preceded binding of F and vWF induced with PMA as well as with ADP and thrombin. Sphingosine, an inhibitor of Protein Kinase C, blocked binding of F and vWF to platelets stimulated with PMA, ADP, and thrombin. Inhibition of binding was concentration-dependent and it was accompanied by inhibition of platelet aggregation. Thus, stimulation of Protein Kinase C is required for exposure of platelet receptors for adhesive proteins whereas inhibition of Protein Kinase C prevents receptorexposure. Protein Kinase C fulfills the role of an intraplatelet signal transducer, regulating receptors for adhesive proteins, and constitutes a target for pharmacologic modulation of the adhesive interactions of platelets.
APA, Harvard, Vancouver, ISO, and other styles
2

Chiang, T. M., R. J. H. Wojcikiewicz, A. H. Kang, and J. N. Fain. "PHOSPHORYLATION OF THE OUTER SURFACE OF PLATELETS ENHANCES THE EFFECTS OF COLLAGEN ON PLATELET AGGREGATION, ATP RELEASE, CALCIUM TRANSLOCATION AND PHOSPHOINOSITIDE HYDROLYSIS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644477.

Full text
Abstract:
We have recently isolated and purified from human plasma two isomeric forms of protein kinase, both of which can phosphorylate the outer surface proteins of human platelets. One of the proteins phosphorylated is the platelet collagen receptor. The phosphorylation of the outer surface proteins of human platelets increased their functional responsiveness to collagen. Collagen-stimulated platelet aggregation, release of ATP and calcium translocation were all enhanced by pretreatment with plasma protein kinase in the presence of ATP. The mechanism by which phosphorylated platelets become hypersensitive to collagen is not established. In the present study, we have used [3H]myo-inositol-labeled human platelets to investigate the possible role of phosphoinositide metabolism in mediating this hypersensitivity. Formation of inositol mono-, bis-, and trisphosphate in response to collagen was more pronounced in phosphorylated platelets than controls. these results indicate that enhanced phosphoinositide hydrolysis in phosphorylated platelets correlate with the increased functional responses to collagen.
APA, Harvard, Vancouver, ISO, and other styles
3

Gear, LR A., D. Freas, and J. D. Carty. "EARLY (< 5 SEC) PHOSPHORYLATIONS OF PLATELET PROTEINS FOLLOWING ACTIVATION BY ADP AND ADRENALIN, SEPARATELY AND IN COMBINATION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643640.

Full text
Abstract:
Understanding the earliest events (< 1 sec) in signal transduction of platelets is important, since there is evicenee that “shape change,” aggregation and secretion can all begin within this period. We have employed a guenched-flow approach to study these early events and found that thrombin can induce rapid phosphorylation of myosin light-chain kinase (20K) and a 47K protein (Blood, 67, 1738, 1986). To investigate the role of rapid phosphorylations in platelet activation, we have studied the influence of adrenalin and ADP during early (0.3 to 5 sec) stimulation. Aggregation in washed human platelets was assessed by following the loss of single particles and phosphorylation by analysing 32P-labeled proteins after gel electrophoresis. 15 µM adrenalin (without ADP) did not initiate significant aggregation or phosphorylation of myosin light chain (MLC). Phosphorylation of the 47K protein was increased by 20% at 5 sec. 0.5 µM ADP did not induce significant aggregation, but increased phosphorylation of MLC by 130% and the 47 protein by 20%. The combination of 0.5 µM ADP and 15 uM adrenalin induced significant aggregation by 0,3 sec (7.6%), which increased to 25.6% by 5 sec. Interestingly, MLC or 47K protein phosphorylation was not increased above control levels. However, the phosphorylation of four other proteins (77K, 102K, 140K and 185K), which previously had been very rapid (<1 sec) and reversible with 0.5 µM ADP alone, was now maintained, peaking at 3 sec. 10 µM ADP caused small sustained increases in phosphorylation of the same proteins. Adrenalin also caused rapid increases in the phosphorylation of 27K, 213 and 250K proteins. High levels of ADP (10 µM) only increased the 213 and 250K proteins; therefore the 27K protein appears adrenalin specific. Analysis of these early platelet phosphorylations will help understand how they are linked to initiation and maintenance of aggregation. Supported by NIH HL-27014.
APA, Harvard, Vancouver, ISO, and other styles
4

Zorina, A. A. "Protein kinases in cyanobacteria." In IX Congress of society physiologists of plants of Russia "Plant physiology is the basis for creating plants of the future". Kazan University Press, 2019. http://dx.doi.org/10.26907/978-5-00130-204-9-2019-182.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Nickkholgh, Bita, Sivanandane Sittadjody, Michael B. Rothberg, and KC Balaji. "Abstract LB-243: Protein kinase D1 induces cell cycle arrest independent from check point kinases." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-lb-243.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Hong, Chin-Yih, Shieh-Yueh Yang, Herng-Er Horng, Jen-Jie Chieh, and Hong-Chang Yang. "Universal Behavior for Characteristic Curve of Immunomagnetic Reduction Assay With Aid of Biofunctionalized Magnetic Nanoparticles." In ASME 2009 International Design Engineering Technical Conferences and Computers and Information in Engineering Conference. ASMEDC, 2009. http://dx.doi.org/10.1115/detc2009-86436.

Full text
Abstract:
By biofunctionalizing magnetic nanoparticles with bioprobes, magnetic nanoparticles are able to specifically label bio-molecules. With the association between magnetic nanoparticles and bio-molecules, the mixed-frequency AC magnetic susceptibility generated with the physical rotation of individual magnetic nanoparticles under external AC magnetic fields is reduced. This detection technology is so-called immunomagnetic reduction (IMR) assay. In the experiment, several kinds of proteins and small-molecule chemicals were detected via IMR. The characteristic curves, i.e. the reduction versus the concentration of protein/chemical, for these proteins or chemicals can be scaled to one universal curve.
APA, Harvard, Vancouver, ISO, and other styles
7

Mueller, Daniel, Frank Totzke, Thomas Weber, Marcel Pathe, Christoph Schaechtele, and Michael H. Kubbutat. "Abstract 2388: IC50 profiling against 320 protein kinases: Improving the accuracy of kinase inhibitor selectivity testing." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-2388.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Safaei, Javad, Jan Manuch, Arvind Gupta, Ladislav Stacho, and Steven Pelech. "Prediction of human protein kinase substrate specificities." In 2010 IEEE International Conference on Bioinformatics and Biomedicine (BIBM 2010). IEEE, 2010. http://dx.doi.org/10.1109/bibm.2010.5706573.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Gosal, Gurinder Pal Singh, Natarajan Kannan, and Krys J. Kochut. "ProKinO: A Framework for Protein Kinase Ontology." In 2011 IEEE International Conference on Bioinformatics and Biomedicine (BIBM). IEEE, 2011. http://dx.doi.org/10.1109/bibm.2011.125.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Rozinek, Sarah C., Robert J. Thomas, and Lorenzo Brancaleon. "Photoinduced structural changes to protein kinase A." In SPIE BiOS, edited by E. Duco Jansen, Robert J. Thomas, Gerald J. Wilmink, and Bennett L. Ibey. SPIE, 2014. http://dx.doi.org/10.1117/12.2038561.

Full text
APA, Harvard, Vancouver, ISO, and other styles

Reports on the topic "Protein kinasa"

1

Trewhella, J., G. A. Olah, D. A. Walsh, and R. D. Mitchell. Solution structure of the cAMP-dependent protein kinase. Office of Scientific and Technical Information (OSTI), December 1998. http://dx.doi.org/10.2172/560750.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Burma, Sandeep. Interaction of BRCA1 with the DNA-Dependent Protein Kinase. Fort Belvoir, VA: Defense Technical Information Center, September 2005. http://dx.doi.org/10.21236/ada486717.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Lannigan, Deborah A. The Protein Kinase RSK Family - Roles in Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, February 2005. http://dx.doi.org/10.21236/ada433888.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Lannigan, Deborah. The Protein Kinase RSK Family - Roles in Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, February 2006. http://dx.doi.org/10.21236/ada452371.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Burma, Sandeep. Interaction of BRCA1 With the DNA-Dependent Protein Kinase. Fort Belvoir, VA: Defense Technical Information Center, September 2004. http://dx.doi.org/10.21236/ada432142.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Heidenreich, Kim A. Protein Kinase Pathways That Regulate Neuronal Survival and Death. Fort Belvoir, VA: Defense Technical Information Center, August 2004. http://dx.doi.org/10.21236/ada429843.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Heidenreich, Kim A. Protein Kinase Pathways that Regulate Neuronal Survival and Death. Fort Belvoir, VA: Defense Technical Information Center, August 2003. http://dx.doi.org/10.21236/ada419485.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Yang, Dejun. Structure-Based Discovery of Novel Inhibitors of Protein Kinase. Fort Belvoir, VA: Defense Technical Information Center, September 2003. http://dx.doi.org/10.21236/ada424718.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Parker, Amanda P., Barbara S. Beckman, and Matthew Burow. Phosphatidylinositol 3-Kinase and Protein Kinase C as Molecular Determinants of Chemoresistance in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, July 2002. http://dx.doi.org/10.21236/ada409382.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Parker, Amanda, Barbara Beckman, and Matthew E. Burow. Phosphatidylinositol 3-Kinase and Protein Kinase C as Molecular Determinants of Chemoresistance in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, July 2004. http://dx.doi.org/10.21236/ada431891.

Full text
APA, Harvard, Vancouver, ISO, and other styles
You might also be interested in the extended bibliographies on the topic 'Protein kinasa' for particular source types:
Journal articles Dissertations / Theses Books
We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!

To the bibliography