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Artykuły w czasopismach na temat „Interacteur”

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Data publikacji: 22 czerwca 2024

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1

Rowe, Robert, Mark Coniglio i Morton Subotnick. "Interactor 4.0.8". Leonardo Music Journal 2, nr 1 (1992): 122. http://dx.doi.org/10.2307/1513229.

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2

Godenzzi, Juan Carlos. "Significar e interactuar". Allpanchis 25, nr 42 (25.09.2020): 53–79. http://dx.doi.org/10.36901/allpanchis.v25i42.770.

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3

Andonova, Veneta, Antonio Ladrón de Guevara i Eric Brousseau. "Internet interacted: 1991‐2003". Management Research: Journal of the Iberoamerican Academy of Management 9, nr 3 (15.11.2011): 192–206. http://dx.doi.org/10.1108/1536-541111181903.

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4

Diwnale, Tanvi, Shreyas Done, Pornima Dokhale, Disha Borale, Yash Divate i Shardul Dixit. "GestureFlow: Intutive Multimedia Interactor". International Journal of Membrane Science and Technology 10, nr 2 (18.08.2023): 4288–95. http://dx.doi.org/10.15379/ijmst.v10i2.3406.

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Gesture Flow: Intutive Multimedia Control is a project aimed at revolutionizing the way users interact with digital media. Leveraging cutting-edge technologies and innovative design principles, this project introduces a media player that incorporates intuitive interactions and augments the user's senses. By merging the physical and digital realms, the Intutive Multimedia Interactor Media Player provides an immersive and seamless media experience. The key objective of this project is to enhance user engagement and convenience while consuming digital media content. The Intutive Multimedia Interactor Media Player utilizes advanced gesture recognition through image processing techniques to enable users to control media playback and access content effortlessly. Users can, pause, play, forward, rewind, adjust volume, and perform other playback functions using specific hand gestures.
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5

Liu, Songling, Richard T. Premont i Don C. Rockey. "G-protein-coupled Receptor Kinase Interactor-1 (GIT1) Is a New Endothelial Nitric-oxide Synthase (eNOS) Interactor with Functional Effects on Vascular Homeostasis". Journal of Biological Chemistry 287, nr 15 (31.01.2012): 12309–20. http://dx.doi.org/10.1074/jbc.m111.320465.

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Endothelial cell nitric-oxide (NO) synthase (eNOS), the enzyme responsible for synthesis of NO in the vasculature, undergoes extensive post-translational modifications that modulate its activity. Here we have identified a novel eNOS interactor, G-protein-coupled receptor (GPCR) kinase interactor-1 (GIT1), which plays an unexpected role in GPCR stimulated NO signaling. GIT1 interacted with eNOS in the endothelial cell cytoplasm, and this robust association was associated with stimulatory eNOS phosphorylation (Ser1177), enzyme activation, and NO synthesis. GIT1 knockdown had the opposite effect. Additionally, GIT1 expression was reduced in sinusoidal endothelial cells after liver injury, consistent with previously described endothelial dysfunction in this disease. Re-expression of GIT1 after liver injury rescued the endothelial phenotype. These data emphasize the role of GPCR signaling partners in eNOS function and have fundamental implications for vascular disorders involving dysregulated eNOS.
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6

McFarland, K. N., M. N. Huizenga, S. B. Darnell, G. R. Sangrey, O. Berezovska, J. H. J. Cha, T. F. Outeiro i G. Sadri-Vakili. "MeCP2: a novel Huntingtin interactor". Human Molecular Genetics 23, nr 4 (8.10.2013): 1036–44. http://dx.doi.org/10.1093/hmg/ddt499.

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7

Subotnick, Morton, i Mark Coniglio. "An interactive performance software (Interactor)". Journal of the Acoustical Society of America 88, S1 (listopad 1990): S72. http://dx.doi.org/10.1121/1.2029129.

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8

黃家彥, 黃家彥, 林佑樺 Chia-Yen Huang, 郭昱廷 Yu-Hua Lin, 汪雅雲 Yu-Ting Kuo, 柯智群 Ya-Yun Wang, 詹景全 Chih-Chun Ke i 林盈宏 Chying-Chyuan Chan. "TBC1D21結合蛋白RAB5C參與於精子型態生成". 輔仁醫學期刊 21, nr 1 (marzec 2023): 015–25. http://dx.doi.org/10.53106/181020932023032101002.

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<p>背景與目的: 不孕是重要的公眾健康議題，造成不孕的因素其中一半與男性相關。其中造成男性不孕的一項重要病因是畸型精子症。在先前的研究中，我們以cDNA微晶片比較造精功能正常與異常的睪丸組織中各別基因的表現量。其中發現一個與不孕相關Rab GTPase激活蛋白，名為TBC1D21蛋白。TBC1D21特異的表現於減數分裂後期精細胞中。而於Tbc1d21基因剔除小鼠模式中發現嚴重精子尾部的中節區域損壞。進一步我們以蛋白質質體學方法鑑定出與TBC1D21結合蛋白。於本研究中我們聚焦於其中一個TBC1D21結合蛋白RAB5C。研究方法與結果: RAB5C蛋白表現於小鼠睪丸組織切片中的精子細胞的頂體與尾部。於成熟精子中，RAB5C蛋白濃縮於頭部頂體與散落於尾部中節區域。其中有趣的是精子經過頂體反應後，於頂體的RAB5C蛋白量明顯下降消失。最後我們利用共同免疫染色法確認RAB5C與TBC1D21共同散落於成熟精子尾部中節區域。結論:基於以上結果，我們發現TBC1D21 交互作用蛋白RAB5C參與於精子頭部頂體與尾部中節的形成。</p> <p>&nbsp;</p><p>Background and purpose: Infertility is a critical public health issue, and half of its causes are related to male factors. Teratozoospermia is one of major cause of male infertility. In our previous studies, we identified the TBC1 domain family member 21 (TBC1D21) gene, a Rab GTPase-activating protein (GAP), as a sterility-related gene in cDNA microarray compared to normal and spermatogenic testicular tissues. TBC1D21 is specifically expressed in post-meiotic male germ cells. Furthermore, the loss of Tbc1d21 allele in mice results in severe defects in the midpiece of the sperm&rsquo;s tail. Additionally, TBC1D21 interactors were selected using proteomic assays. Herein, we focused on RAB5C, which is a TBC1D21 interactor. Methods and Results: RAB5C was localized in the acrosomal region and elongating tail in spermatids of murine testicular sections. In a mature sperm cell, RAB5C signals were concentrated in the acrosome and were scattered around the midpiece. Interestingly, RAB5C pro-tein levels decreased in the acrosome after triggering acrosomal reaction. Finally, we confirmed that the interspersed RAB5C signals were co-localized with TBC1D21 within the midpieces of the mature sperm cells. Conclusion: Based on these results, we suggest RAB5C, a TBC1D21 interactor, was involved in acrosomal and midpiece formation.</p> <p>&nbsp;</p>
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9

Weihl, Conrad C. "Another VCP interactor: NF is enough". Journal of Clinical Investigation 121, nr 12 (1.12.2011): 4627–30. http://dx.doi.org/10.1172/jci61126.

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10

Ferro, Anabela, Ana Luísa Carvalho, Andreia Teixeira-Castro, Carla Almeida, Ricardo J. Tomé, Luísa Cortes, Ana-João Rodrigues i in. "NEDD8: A new ataxin-3 interactor". Biochimica et Biophysica Acta (BBA) - Molecular Cell Research 1773, nr 11 (listopad 2007): 1619–27. http://dx.doi.org/10.1016/j.bbamcr.2007.07.012.

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11

Lafay, J. F., P. Zagalak i H. A. Herrera. "Reduced form of the interactor matrix". IEEE Transactions on Automatic Control 37, nr 11 (1992): 1778–82. http://dx.doi.org/10.1109/9.173150.

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12

Dion, J. M., L. Dugard i J. Carrillo. "Interactor and multivariable adaptive model matching". IEEE Transactions on Automatic Control 33, nr 4 (kwiecień 1988): 399–401. http://dx.doi.org/10.1109/9.192200.

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13

Bittanti, S., P. Colaneri i M. Mongiovi. "Singular filtering via spectral interactor matrix". IEEE Transactions on Automatic Control 40, nr 8 (1995): 1492–97. http://dx.doi.org/10.1109/9.402250.

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14

Watanabe, Tomio, Masashi Okubo, Mutsuhiro Nakashige i Ryusei Danbara. "InterActor: Speech-Driven Embodied Interactive Actor". International Journal of Human-Computer Interaction 17, nr 1 (marzec 2004): 43–60. http://dx.doi.org/10.1207/s15327590ijhc1701_4.

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15

Yabuki, Soichi, i Fumio Mizutani. "Electrochemical measurement of phenothiazine-interacted DNA". Bioelectrochemistry 63, nr 1-2 (czerwiec 2004): 253–55. http://dx.doi.org/10.1016/j.bioelechem.2003.10.022.

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16

Nakajima, Hideaki, Toshiki Tamura, Miyuki Ito, Fumi Shibata, Kana Kuroda, Yumi Fukuchi, Naohide Watanabe, Toshio Kitamura, Yasuo Ikeda i Makoto Handa. "SHD1 is a novel cytokine-inducible, negative feedback regulator of STAT5-dependent transcription". Blood 113, nr 5 (29.01.2009): 1027–36. http://dx.doi.org/10.1182/blood-2008-01-133405.

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Abstract STAT5 is a critical mediator of a variety of cytokine signaling whose transcriptional activity is regulated by associating with various proteins. During a search for STAT5-interacting proteins, we identified SHD1, a mammalian homologue of yeast gene Sac3, as a potential interacter. SHD1 was localized in the nucleus, and induced by cytokines that activate STAT5, such as erythropoietin, interleukin-2 (IL-2), or IL-3. SHD1 interacted specifically with STAT5A and STAT5B, and interestingly, it specifically repressed STAT5-dependent transcription in vitro without affecting the stability or phosphorylation of STAT5 protein. Gene disruption study revealed that T, B, or bone marrow cells from mice lacking SHD1 were hyperresponsive to T-cell–receptor engagement, or stimulation with various STAT5-activating cytokines. These results suggest that SHD1 is a novel cytokine-inducible negative feedback regulator of STAT5.
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17

Das, Supratik. "Integrase Interactor 1 in Health and Disease". Current Protein & Peptide Science 16, nr 6 (2.07.2015): 478–90. http://dx.doi.org/10.2174/1389203716666150316115156.

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18

KATOH, Hisao, i Yasuyuki FUNAHASHI. "New Method to Derive Generalized Interactor Matrices". Transactions of the Society of Instrument and Control Engineers 33, nr 1 (1997): 63–65. http://dx.doi.org/10.9746/sicetr1965.33.63.

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19

KASE, Wataru. "A Derivation of Lower Triangular Interactor Matrix". Transactions of the Society of Instrument and Control Engineers 39, nr 12 (2003): 1156–58. http://dx.doi.org/10.9746/sicetr1965.39.1156.

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20

Guerra, E. S., i C. R. Carvalho. "Entanglement swapping: entangling atoms that never interacted". Journal of Modern Optics 53, nr 7 (10.05.2006): 865–82. http://dx.doi.org/10.1080/09500340500352790.

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21

Mezzanotte, M., i F. Paternó. "Including time in the notion of interactor". ACM SIGCHI Bulletin 28, nr 2 (kwiecień 1996): 57–61. http://dx.doi.org/10.1145/226650.226672.

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22

Sugimoto, Kenji. "Interactor Extraction for Strictly Proper Transfer Matrices". IFAC Proceedings Volumes 31, nr 18 (lipiec 1998): 185–90. http://dx.doi.org/10.1016/s1474-6670(17)41989-6.

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23

Duden, Rainer. "Enter a novel COP I interactor: DSL1". Trends in Cell Biology 12, nr 2 (luty 2002): 61. http://dx.doi.org/10.1016/s0962-8924(01)02236-x.

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24

Steinestel, K., F. Gläsle, S. Brüderlein, J. Steinestel, C. Pröpper i P. Möller. "Abelson interactor 1 (Abi1) im kolorektalen Karzinom". Der Pathologe 34, S2 (listopad 2013): 189–94. http://dx.doi.org/10.1007/s00292-013-1810-1.

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25

Chua, D. K. H., i G. M. Li. "RISim: Resource-Interacted Simulation Modeling in Construction". Journal of Construction Engineering and Management 128, nr 3 (czerwiec 2002): 195–202. http://dx.doi.org/10.1061/(asce)0733-9364(2002)128:3(195).

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26

Watanabe, T., M. Okubo, H. Ogawa i R. Danbara. "2A1-K10 Embodied Commnication Support: InterRobot/InterActor". Proceedings of JSME annual Conference on Robotics and Mechatronics (Robomec) 2001 (2001): 49. http://dx.doi.org/10.1299/jsmermd.2001.49_8.

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27

Diop, S. "On System Structure Theory and Nonlinear Interactor". IFAC Proceedings Volumes 28, nr 14 (czerwiec 1995): 329–33. http://dx.doi.org/10.1016/s1474-6670(17)46852-2.

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28

WANG, Wei, Ting LI i Hongwei GE. "Interacted grid tagging for sentiment word extraction". Journal of Measurement Science and Instrumentation 14, nr 3 (2023): 369–78. http://dx.doi.org/10.62756/jmsi.1674-8042.2023042.

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KASE, Wataru, i Katsutoshi TAMURA. "A Design of G-Interactor for Multivariable MRACS". Transactions of the Society of Instrument and Control Engineers 24, nr 10 (1988): 1048–55. http://dx.doi.org/10.9746/sicetr1965.24.1048.

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Marcinkowski, Michał, Tomaš Pilžys, Damian Garbicz, Jan Piwowarski, Kaja Przygońska, Maria Winiewska-Szajewska, Karolina Ferenc, Oleksandr Skorobogatov, Jarosław Poznański i Elżbieta Grzesiuk. "Calmodulin as Ca2+-Dependent Interactor of FTO Dioxygenase". International Journal of Molecular Sciences 22, nr 19 (8.10.2021): 10869. http://dx.doi.org/10.3390/ijms221910869.

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FTO is an N6-methyladenosine demethylase removing methyl groups from nucleic acids. Several studies indicate the creation of FTO complexes with other proteins. Here, we looked for regulatory proteins recognizing parts of the FTO dioxygenase region. In the Calmodulin (CaM) Target Database, we found the FTO C-domain potentially binding CaM, and we proved this finding experimentally. The interaction was Ca2+-dependent but independent on FTO phosphorylation. We found that FTO–CaM interaction essentially influences calcium-binding loops in CaM, indicating the presence of two peptide populations—exchanging as CaM alone and differently, suggesting that only one part of CaM interacts with FTO, and the other one reminds free. The modeling of FTO–CaM interaction showed its stable structure when the half of the CaM molecule saturated with Ca2+ interacts with the FTO C-domain, whereas the other part is disconnected. The presented data indicate calmodulin as a new FTO interactor and support engagement of the FTO protein in calcium signaling pathways.
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31

Serizawa, K., i H. Higuchi. "Fragmentation of actin filaments interacted with myosin molecules". Seibutsu Butsuri 41, supplement (2001): S187. http://dx.doi.org/10.2142/biophys.41.s187_1.

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KASE, Wataru, i Makoto TERANISHI. "A Calculation of Invariant Zeros Using Interactor Matrix". Transactions of the Society of Instrument and Control Engineers 35, nr 7 (1999): 964–66. http://dx.doi.org/10.9746/sicetr1965.35.964.

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33

Sharma, Sugandha, Priyanka Giri, Gohar Taj i Anil Kumar. "WRKY Transcription Factor- the Interactor of MAPK Cascade". International Journal of Agriculture, Environment and Biotechnology 6, nr 3 (2013): 341. http://dx.doi.org/10.5958/j.2230-732x.6.3.001.

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34

Cabello, Adán. "Maximum quantum nonlocality between systems that never interacted". Physics Letters A 377, nr 1-2 (grudzień 2012): 64–68. http://dx.doi.org/10.1016/j.physleta.2012.11.015.

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35

Yeh, Chung-Hsin, Ya-Yun Wan, Ying-Yu Wu, Han-Sun Chiang i Ying-Hung Lin. "Identification of mgcrapgap-interacted substrates during mammalian spmiogenesis". Urological Science 27, nr 2 (czerwiec 2016): S72—S73. http://dx.doi.org/10.1016/j.urols.2016.05.273.

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Zhang, Zhihong, Yiyang Tian, Lu Bai, Jianbing Xiahou i Edwin Hancock. "High-order covariate interacted Lasso for feature selection". Pattern Recognition Letters 87 (luty 2017): 139–46. http://dx.doi.org/10.1016/j.patrec.2016.08.005.

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37

Markopoulos, Panos, Jon Rowson i Peter Johnson. "Composition and synthesis with a formal interactor model". Interacting with Computers 9, nr 2 (listopad 1997): 197–223. http://dx.doi.org/10.1016/s0953-5438(97)00011-8.

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38

Pan, Jian-Wei, Dik Bouwmeester, Harald Weinfurter i Anton Zeilinger. "Experimental Entanglement Swapping: Entangling Photons That Never Interacted". Physical Review Letters 80, nr 18 (4.05.1998): 3891–94. http://dx.doi.org/10.1103/physrevlett.80.3891.

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39

Gaillard, M. K. "HISTORY OF PHYSICS:Complex Facets of a Strong Interactor". Science 286, nr 5440 (22.10.1999): 687. http://dx.doi.org/10.1126/science.286.5440.687.

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40

Sambrook, Joseph, i David W. Russell. "Two-hybrid Systems Stage 2: Selecting an Interactor". Cold Spring Harbor Protocols 2006, nr 1 (czerwiec 2006): pdb.prot3888. http://dx.doi.org/10.1101/pdb.prot3888.

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41

Saboury, Ali Akbar, Soghra Bagheri, Ghasem Ataie, Masoud Amanlou, Ali Akbar Moosavi-Movahedi, Gholam Hossein Hakimelahi, Gloria Cristalli i Saeid Namaki. "Binding Properties of Adenosine Deaminase Interacted with Theophylline". CHEMICAL & PHARMACEUTICAL BULLETIN 52, nr 10 (2004): 1179–82. http://dx.doi.org/10.1248/cpb.52.1179.

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42

Johnson, Craig M., Daniel R. Perez, Roy French, William C. Merrick i Ruben O. Donis. "The NS5A protein of bovine viral diarrhoea virus interacts with the α subunit of translation elongation factor-1". Journal of General Virology 82, nr 12 (1.12.2001): 2935–43. http://dx.doi.org/10.1099/0022-1317-82-12-2935.

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A cellular protein that interacts with the NS5A polypeptide of bovine viral diarrhoea virus (BVDV) was identified in a yeast two-hybrid screen. The NS5A interactor was identified as the α subunit of bovine translation elongation factor 1A (eEF1A). Cell-free binding studies were performed with chimeric NS5A fused to glutathione S-transferase (GST–NS5A) expressed in bacteria. GST–NS5A bound specifically to both in vitro-translated and mammalian cell-expressed eEF1A. Moreover, purified eEF1A bound specifically to GST–NS5A attached to a solid phase. Conservation of this interaction was then analysed using a set of NS5A proteins derived from divergent BVDV strains encompassing known biotypes and genotypes. NS5A from all BVDV strains tested so far interacted with eEF1A. The conserved association of eEF1A with virus molecules involved in genome replication and the postulated role of pestivirus and hepacivirus NS5A in replication indicate that this interaction may play a role in the replication of BVDV.
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43

Phee, Hyewon, Ivan Dzhagalov, Marianne Mollenauer, Yana Wang, Darrell Irvine, Ellen Robey i Arthur Weiss. "Regulation of thymocyte positive selection and motility by GIT2 (113.9)". Journal of Immunology 186, nr 1_Supplement (1.04.2011): 113.9. http://dx.doi.org/10.4049/jimmunol.186.supp.113.9.

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Abstract Thymocytes are highly motile cells that migrate under the influence of chemokines in distinct thymic compartments as they mature. The motility of thymocytes is tightly regulated; however, the molecular mechanisms that control thymocyte motility are not well understood. Herein, we report that G protein-coupled receptor kinase-interactor 2 (GIT2) is required for efficient positive selection. Interestingly, GIT2-/- double positive (DP) thymocytes display increased Rac activation, actin polymerization and migration towards SDF-1 and CCL25 in vitro. Using two-photon laser scanning microscopy, we found that scanning activity of GIT2-/- thymocytes is severely compromised in the thymic cortex. Moreover, the GIT2-/- thymocytes accumulated at discrete small regions throughout the cortex including areas adjacent to SDF-1 positive blood vessels and interacted with them extensively. The impaired scanning activity of GIT2-/- thymocytes was accompanied by impaired positive selection in TCR transgenic GIT2-/- mice, suggesting GIT2 plays a key role in controlling chemokine-mediated motility of DP thymocytes and ultimately regulates positive selection.
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44

Frachon, Nadia, Sylvie Demaretz, Elie Seaayfan, Lydia Chelbi, Dalal Bakhos-Douaihy i Kamel Laghmani. "AUP1 Regulates the Endoplasmic Reticulum-Associated Degradation and Polyubiquitination of NKCC2". Cells 13, nr 5 (24.02.2024): 389. http://dx.doi.org/10.3390/cells13050389.

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Inactivating mutations of kidney Na-K-2Cl cotransporter NKCC2 lead to antenatal Bartter syndrome (BS) type 1, a life-threatening salt-losing tubulopathy. We previously reported that this serious inherited renal disease is linked to the endoplasmic reticulum-associated degradation (ERAD) pathway. The purpose of this work is to characterize further the ERAD machinery of NKCC2. Here, we report the identification of ancient ubiquitous protein 1 (AUP1) as a novel interactor of NKCC2 ER-resident form in renal cells. AUP1 is also an interactor of the ER lectin OS9, a key player in the ERAD of NKCC2. Similar to OS9, AUP1 co-expression decreased the amount of total NKCC2 protein by enhancing the ER retention and associated protein degradation of the cotransporter. Blocking the ERAD pathway with the proteasome inhibitor MG132 or the α-mannosidase inhibitor kifunensine fully abolished the AUP1 effect on NKCC2. Importantly, AUP1 knock-down or inhibition by overexpressing its dominant negative form strikingly decreased NKCC2 polyubiquitination and increased the protein level of the cotransporter. Interestingly, AUP1 co-expression produced a more profound impact on NKCC2 folding mutants. Moreover, AUP1 also interacted with the related kidney cotransporter NCC and downregulated its expression, strongly indicating that AUP1 is a common regulator of sodium-dependent chloride cotransporters. In conclusion, our data reveal the presence of an AUP1-mediated pathway enhancing the polyubiquitination and ERAD of NKCC2. The characterization and selective regulation of specific ERAD constituents of NKCC2 and its pathogenic mutants could open new avenues in the therapeutic strategies for type 1 BS treatment.
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TAMURA, Katsutoshi, Wataru KASE i Osamu MUKOHYAMA. "A Comparison Study of Multivariable MRACS with Interactor Matrix". Transactions of the Society of Instrument and Control Engineers 24, nr 6 (1988): 650–52. http://dx.doi.org/10.9746/sicetr1965.24.650.

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ITATANI, Kiyoshi, Sayaka IKEGAMI, Takashi HAYASHITA, Ian J. DAVIES, Tomohiro UMEDA, Yoshiro MUSHA i Seiichiro KODA. "PREPARATION OF POROUS SPHERICAL HYDROXYAPATITE AGGLOMERATES INTERACTED WITH CYCLODEXTRIN". Phosphorus Research Bulletin 24 (2010): 54–61. http://dx.doi.org/10.3363/prb.24.54.

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Andreev, Andrey V., Vladimir A. Maksimenko, Alexander N. Pisarchik i Alexander E. Hramov. "Synchronization of interacted spiking neuronal networks with inhibitory coupling". Chaos, Solitons & Fractals 146 (maj 2021): 110812. http://dx.doi.org/10.1016/j.chaos.2021.110812.

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Pérez i López, Marta. "Un enfocament interactiu de la història de la física". Ciències: revista del professorat de ciències de Primària i Secundària, nr 11 (29.01.2009): 16. http://dx.doi.org/10.5565/rev/ciencies.219.

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Kase, Wataru. "A Simple Derivation of Interactor Matrix and its Applications". IEEJ Transactions on Electronics, Information and Systems 121, nr 4 (2001): 808–13. http://dx.doi.org/10.1541/ieejeiss1987.121.4_808.

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Ma, Xiaoyuan, Eléonore Verweij, Marco Siderius, Rob Leurs i Henry Vischer. "Identification of TSPAN4 as Novel Histamine H4 Receptor Interactor". Biomolecules 11, nr 8 (30.07.2021): 1127. http://dx.doi.org/10.3390/biom11081127.

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The histamine H4 receptor (H4R) is a G protein-coupled receptor that is predominantly expressed on immune cells and considered to be an important drug target for various inflammatory disorders. Like most GPCRs, the H4R activates G proteins and recruits -arrestins upon phosphorylation by GPCR kinases to induce cellular signaling in response to agonist stimulation. However, in the last decade, novel GPCR-interacting proteins have been identified that may regulate GPCR functioning. In this study, a split-ubiquitin membrane yeast two-hybrid assay was used to identify H4R interactors in a Jurkat T cell line cDNA library. Forty-three novel H4R interactors were identified, of which 17 have also been previously observed in MYTH screens to interact with other GPCR subtypes. The interaction of H4R with the tetraspanin TSPAN4 was confirmed in transfected cells using bioluminescence resonance energy transfer, bimolecular fluorescence complementation, and co-immunoprecipitation. Histamine stimulation reduced the interaction between H4R and TSPAN4, but TSPAN4 did not affect H4R-mediated G protein signaling. Nonetheless, the identification of novel GPCR interactors by MYTH is a starting point to further investigate the regulation of GPCR signaling.
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