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1
Kesselring, J. "Das Internationale Komitee vom Roten Kreuz." Nervenheilkunde 35, no. 06 (2016): 378–84. http://dx.doi.org/10.1055/s-0037-1616400.
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ZusammenfassungDas Internationale Komitee vom Roten Kreuz (IKRK) war Initiant der gesamten Rotkreuzbewegung und wurde 1863 in Genf gegründet. Heute ist es weltweit im Einsatz mit über 15 000 Mitarbeitern weltweit vor allem in bewaffneten Konflikten und als Hüter des Humanitären Völkerechtes. Seine Tätigkeit ist eine praktische Anwendung des Gedankengutes der Resilienz, d. h. der aufrichtenden Kräfte, die in verschiedenen Dimensionen so wichtig sind.
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Harroff-Tavel, Marion. "Strategie der Humanitären Aktion des IKRK gegenüber Konflikten des 21. Jahrhunderts." Schweizerisches Jahrbuch für Entwicklungspolitik, no. 18 (January 1, 1999): 51–61. http://dx.doi.org/10.4000/sjep.632.
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Khagoory, Fatima, and Ali Rahim. "Estimation of Coda Q Wave Attenuation Factors for Northern Iraq." Iraqi Geological Journal 56, no. 1A (2023): 149–60. http://dx.doi.org/10.46717/igj.56.1a.11ms-2023-1-23.
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The coda wave decay method was used to estimate the quality factor from the coda wave amplitude decay rate for the broadband seismic stations in northern Iraq using a single back-scattering model. The study aims to calculate the attenuation factor to comprehend the details of the structure of the earth's crust in the study area. The study was conducted using data from the Mesopotamian Network and the Iraqi Meteorological Organization and Seismology from 2007 to 2021. The selected earthquakes have magnitudes ranging from 4 to 6.1 ML and epicentral distances of less than < 100 km. Seventy seven earthquakes were recorded by three stations (SLY1, DHK1, and IKRK). These earthquakes were analyzed at eight center frequencies (1, 2, 3.5, 6, 8, 10, 12, and 16 Hz) and a 30-sec length window by using the Seisan package. The Qc values are computed by the frequency-dependent relationship QC= Q0 f α, where Q0 is QC at 1 Hz and α denotes the degree of frequency dependence. The attenuation relationship of station SLY1 is obtained as QC =88 f 1.02, QC = 90 f 0.97 in the DHK1 station, and QC = 91 f 1.04 in the IKRK station. The comparison of these three stations indicates that attenuation is highest in Sulaymaniyah, followed by Duhok, and then Kirkuk.
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GUHATHAKURTA, PULAK, AJIT TYAGI, and B. MUKHOPADHYAY. "Climatology at any point : A neural network solution." MAUSAM 64, no. 2 (2021): 231–50. http://dx.doi.org/10.54302/mausam.v64i2.682.
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lHkh mi;ksxdrkZvksa] ;kstuk cukus okyksa] vkink izca/ku dkfeZdksa] i;ZVu vkfn }kjk rkieku] vf/kdre rkieku] U;wure rkieku] ok;qeaMyh; nkc] o"kkZ vkfn tSls ekSle izkpyksa dh tyok;q foKku ij lwpukvksa dh mUur tkudkjh dh vR;kf/kd ek¡x jgh gSA fdlh LFkku fo'ks"k esa os/k’kkyk ds vHkko vkSj dHkh&dHkh nh?kZ vof/k ds igys ds vk¡dM+ksa dh vuqiyC/krk ds dkj.k ekSle foKku leqnk; ml LFkku fo’ks"k ds fy, visf{kr lwpukvksa dks miyC/k ugha djk ikrk gSA bl 'kks/k i= esa LFkkfud varosZ’ku ds {ks= esa U;wjy usVodZ ds rqyukRed u, vuqiz;ksx crk, x, gSaA iwjs ckjg eghuksa ds vf/kdre vkSj U;wure nksuksa rkiekuksa ds fy, U;wjy usVodZ varosZ’ku fun’kZ fodflr fd, x, gSaA ;g ekWMy ml LFkku fo’ks"k ij lkekU; vf/kdre vkSj U;wure rkiekuksa dks rS;kj djus ds fy, lwpukvksa ds :i esa v{kka’k] ns’kkUrj vkSj mUu;u tSlh HkkSxksfyd lwpukvksa dk mi;ksx djrk gSA varosZ’ku ds fy, LFkkfud ekWMyksa ds fu"iknuksa dh rqyuk vU; lkekU;r% iz;qDr i)fr ds lkFk dh xbZ gSA
 Advance knowledge of information on climatology of meteorological parameters like temperature, maximum temperature, minimum temperature, atmospheric pressure, rainfall etc are of great demands from all the users, planners, disaster managements personals, tourism etc. The information is required at the place concerned but this cannot be fulfilled by the meteorological community due to absent of observatory at that place and also some time absent of past data of long period. The present paper has described a comparatively new application of the neural network in the field of spatial interpolation. Neural network interpolation models are developed for both maximum and minimum temperatures for all the twelve months. The model utilizes geographical information like latitude, longitude and elevation as inputs to generate normal maximum and minimum temperatures at a place. The performances of the models are compared with the other commonly used method for spatial interpolation.
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RAO, Y. V. RAMA, H. R. HATWAR, and GEETA AGNIHOTRI. "Tropical cyclones prediction by numerical models in India Meteorological Department." MAUSAM 57, no. 1 (2021): 47–60. http://dx.doi.org/10.54302/mausam.v57i1.454.
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lkj & bl 'kks/k&Ik= esa Hkkjr ekSle foKku foHkkx ¼Hkk- ekS- fo- fo-½ esa viukbZ xbZ pØokr izfr:fir djus dh dfYir rduhdksa ij ppkZ dh xbZ gSA vDrwcj 1999 esa mM+hlk esa vk, egkpØokr ds izkjfEHkd {ks=ksa esa dkYifud Hkzfeyrk dk mi;ksx djds] pØokr ds fof’k"V ekWMy] Doklh ySaxjfx;u ekWMy ¼D;w- ,y- ,e-½ ls 72 ?kaVs ds iwokZuqeku vkSj Hkkjr ekSle foKku foHkkx ds lhfer {ks= fun’kZ ¼,y- ,- ,e-½ ls 36 ?kaVs ds iwokZuqeku izfr:fir fd, x,A bl 'kks/k esa] 26 ls 28 vDrwcj rd dh izkjafHkd fLFkfr;ksa ds vk/kkj ij D;w- ,y- ,e- ls pØokr ds ekxZ ds iwokZuqeku dh vkSlr =qfV;k¡ 24 ?kaVs ds fy, 21 fd-eh-] 48 ?kaVs ds fy, 91 fd-eh- vkSj 72 ?kaVs ds fy, 179 fd-eh- jghA 1998&2004 rd ds fiNys lkr o"kksZa ds nkSjku D;w- ,y- ,e- ls pØokr ds ekxZ ds iwokZuqeku dh =qfV;ksa ds vk¡dM+ksa ij Hkh blesa ppkZ dh xbZ gSA blds vykok] ,y- ,- ,e- ls fd, x, iwokZuqeku ij izkjafHkd fLFkfr;ksa ds izHkko dh Hkh tk¡p dh xbZA fofHkUu izkjafHkd fLFkfr;ksa ls rS;kj fd, x, vkSlr ¼lesfdr½ iwokZuqeku ls 24 ?kaVs ds iwokZuqeku esa 123 fd-eh- vkSj 36 ?kaVs ds iwokZuqeku esa 81 fd-eh- dh =qfV;k¡ ikbZ xbZ] tks ,dek= iwokZuqeku dh rqyuk esa de jghA bu iz;ksxksa ls ;g irk pyk fd dkYifud Hkzfeyrk okys D;w- ,y- ,e- ekWMy ls pØokr ds ekxZ dk lVhd iwokZuqeku izkIr fd;k tk ldrk gS tks vHkh rd la[;kRed ekWMyksa ls miyC/k gks ikrk FkkA
 In the present paper, the cyclone bogusing techniques followed in India Meteorological Department (IMD) were discussed. Using the idealized vortex in the initial fields for Orissa super cyclone October 1999, the specialized cyclone model, Quasi-Lagrangian Model (QLM) 72 hours track forecast and also 36 hours forecast with IMD limited area model (LAM) were simulated. In this case, the QLM average track forecast errors based on 26-28 October initial conditions were 21 km for 24 hours, 91 km for 48 hours and 179 km for 72 hours. Also the QLM track forecast error statistics during the last 7 years 1998-2004 are discussed. In addition, the impact of initial conditions on the LAM forecast was examined. It was observed that the mean (ensemble) forecast generated from different initial conditions was shown track error of 123 km in 24 hours and 81 km in 36 hours forecast which is less than individual forecast. These experiments have established that the QLM model, with idealized vortex, provides track forecast within an accuracy level that was currently available from numerical models.
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Fahma, Nabilatul, and Trianingsih Eni Lestari. "PENERAPAN ANALISIS DISKRIMINAN LINIER ROBUST DALAM PENGKLASIFIKASIAN INDEKS KEPEDULIAN TERHADAP ISU KEPENDUDUKAN (IKIK)." Jurnal Kajian Matematika dan Aplikasinya (JKMA) 3, no. 1 (2022): 30. http://dx.doi.org/10.17977/um055v3i12022p30-36.
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Abstract Robust linear discriminant analysis is used to classify data that contains outlier by replacing classical parameters in linear discriminant analysis with robust parameters. This study aims to classify the Index of Concern for Population Issues (IKIK) of 34 provinces in 2020 into two categories namely target fulfilled IKIK and target not fulfilled IKIK using robust linear discriminant analysis. The independen variabels used are quantity dimensions (X_1), quality dimensions (X_2), mobility dimensions (X_3), and environment dimensions (X_4). The results obtained are 17 provinces were categorized as target fulfilled IKIK, 17 provinces as target not fulfilled IKIK. There are 2 robust discriminant functions formed, each for target fulfilled and target not fulfilled IKIK. The accuracy of the robust linear discriminant functions formed is 97,06%, the APER value of the discriminant functions is 2,94% and the PressQ value = 30,11 is greater than the value of (Chi_(3,0.05)^2) = 7.81. This shows that the discriminant functions can classify observations accurately.Keywords: classification, Index of Concern for Population Issues, robust discriminant analysis
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Liaudanskaitė, Deimantė, and Lina Stungienė. "The effect of classic facial massage with caviar extract on mature female facial skin." Applied Scientific Research 2, no. 2 (2023): 204–14. http://dx.doi.org/10.56131/tmt.2023.2.2.173.
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The article analyzes the effect of classic facial massage with caviar extract on mature female skin. The criteria for evaluating the condition of the skin are presented: the degree of wrinkles, the length, width, depth of wrinkles, keratin level, skin elasticity, turgor, tone. The charts show the most significant changes depending on the procedures performed. Keywords: cosmetic massage, mature skin, caviar extract.
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Kamal, Abdol Moghset Bani, and Wahabuddin Ra’ees. "Iran’s Aid Diplomacy in Afghanistan: The Role of Imam Khomeini Relief Committee." Contemporary Review of the Middle East 5, no. 4 (2018): 308–26. http://dx.doi.org/10.1177/2347798918795369.
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This study aims at examining the Islamic Republic of Iran’s “aid diplomacy” officially referred to as “support diplomacy” and focuses on the Imam Khomeini Relief Committee (IKRC), a charity organization which is functioning as the main vehicle. The IKRC is highly active in many poor countries and this study focuses on the activities, strategies, and achievements of the IKRC in Afghanistan. The study among others finds that Iran is using rigorous aid diplomacy to penetrate into the downtrodden layers of Afghan society. The foundational principles of the IKRC suggest that this institution is functioning in the direction of Ayatollah Khomeini’s doctrine of “Exporting the Revolution.” In line with this, the IKRC is tasked to nurture Afghan sympathizers for the Islamic Republic of Iran to enhance this country’s soft power in Afghanistan and the relief efforts are heavily influenced by its official ideology that is based on Shia belief system.
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Huynh, Q. Khai, Nandini Kishore, Sumathy Mathialagan, Ann M. Donnelly та Catherine S. Tripp. "Kinetic Mechanisms of IκB-related Kinases (IKK) Inducible IKK and TBK-1 Differ from IKK-1/IKK-2 Heterodimer". Journal of Biological Chemistry 277, № 15 (2002): 12550–58. http://dx.doi.org/10.1074/jbc.m111526200.
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Liu, Fei, Yifeng Xia, Aaron S. Parker, and Inder M. Verma. "IKK biology." Immunological Reviews 246, no. 1 (2012): 239–53. http://dx.doi.org/10.1111/j.1600-065x.2012.01107.x.
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Field, N. "KSHV vFLIP binds to IKK- to activate IKK." Journal of Cell Science 116, no. 18 (2003): 3721–28. http://dx.doi.org/10.1242/jcs.00691.
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Hehner, Steffen P., Thomas G. Hofmann, Alexej Ushmorov та ін. "Mixed-Lineage Kinase 3 Delivers CD3/CD28-Derived Signals into the IκB Kinase Complex". Molecular and Cellular Biology 20, № 7 (2000): 2556–68. http://dx.doi.org/10.1128/mcb.20.7.2556-2568.2000.
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ABSTRACT The phosphorylation of IκB by the multiprotein IκB kinase complex (IKC) precedes the activation of transcription factor NF-κB, a key regulator of the inflammatory response. Here we identified the mixed-lineage group kinase 3 (MLK3) as an activator of NF-κB. Expression of the wild-type form of this mitogen-activated protein kinase kinase kinase (MAPKKK) induced nuclear immigration, DNA binding, and transcriptional activity of NF-κB. MLK3 directly phosphorylated and thus activated IκB kinase alpha (IKKα) and IKKβ, revealing its function as an IκB kinase kinase (IKKK). MLK3 cooperated with the other two IKKKs, MEKK1 and NF-κB-inducing kinase, in the induction of IKK activity. MLK3 bound to components of the IKC in vivo. This protein-protein interaction was dependent on the central leucine zipper region of MLK3. A kinase-deficient version of MLK3 strongly impaired NF-κB-dependent transcription induced by T-cell costimulation but not in response to tumor necrosis factor alpha or interleukin-1. Accordingly, endogenous MLK3 was phosphorylated and activated by T-cell costimulation but not by treatment of cells with tumor necrosis factor alpha or interleukin-1. A dominant negative version of MLK3 inhibited NF-κB- and CD28RE/AP-dependent transcription elicited by the Rho family GTPases Rac and Cdc42, thereby providing a novel link between these GTPases and the IKC.
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Láng, Eszter, and Gergely Makláry. "Sziámi ikrek, avagy kölcsönös egymásrautaltság: az EU – USA transzatlanti kapcsolatok gazdasági dimenziói." Competitio 3, no. 3 (2004): 83–100. http://dx.doi.org/10.21845/comp/2004/3/5.
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Sihombing, Pardomuan Robinson, Widdia Angraini, Busminoloan Busminoloan, and Usep Nugraha. "Faktor Yang Mempengaruhi Kualitas dan Indeks Pembangunan Ketenagakerjaan di Indonesia di Masa Pandemi 2020." Khatulistiwa: Jurnal Pendidikan dan Sosial Humaniora 2, no. 3 (2022): 52–60. http://dx.doi.org/10.55606/khatulistiwa.v2i3.384.
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Penelitian ini bertujuan mengetahui pengaruh Indeks Kompensasi Tenaga Kerja (IKTK), Indeks Pembangunan Manusia (IPM), Indeks Pembangunan Ekonomi Insklusif (IPEI) terhadap Indeks Pembangunan Ketenagakerjaan (IPK) melalui Indeks Kualitas Pekerjaan (IKP). Data yang digunakan berasal dari Badan Pusat Statistik, Bappenas dan Kemenaker menggunakan data 34 Provinsi Tahun 2020. Model yang digunakan adalah model SEM PLS dengan bantuan software SmartPLS 3.8. Hasil yang didapat IKTK, IPM, IPEI berpengaruh langsung terhadap IKP. Di sisi lain IKTK, IPM, IPEI berpengaruh tidak langsung terhadap IPK melalui IKP. Diperlukan kebijakan-kebijakan yang tepat sasaran dalam meningkatkan kualitas dan pembangunan ketenagakerjaan di Indonesia.
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Koppe, Reisinger, Wehr, et al. "An NF-kappaB- and IKK-Independent Function of NEMO Prevents Hepatocarcinogenesis by Suppressing Compensatory Liver Regeneration." Cancers 11, no. 7 (2019): 999. http://dx.doi.org/10.3390/cancers11070999.
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The IκBKinase (IKK) complex represents a central signaling nexus in the TNF-dependent activation of the pro-inflammatory NF-κB pathway. However, recent studies suggested that the distinct IKK subunits (IKK, IKK, and NEMO) might withhold additional NF-κB-independent functions in inflammation and cancer. Here, we generated mice lacking all three IKK subunits in liver parenchymal cells (LPC) (IKK//NEMOLPC-KO) and compared their phenotype with mice lacking both catalytic subunits (IKK/LPC-KO), allowing to functionally dissect putative I-κB-Kinase-independent functions of the regulatory subunit NEMO. We show that the additional deletion of NEMO rescues IKK/LPC-KO mice from lethal cholestasis and biliary ductopenia by triggering LPC apoptosis and inducing a strong compensatory proliferation of LPC including cholangiocytes. Beyond this beneficial effect, we show that increased hepatocyte cell-death and compensatory proliferation inhibit the activation of LPC-necroptosis but trigger spontaneous hepatocarcinogenesis in IKK//NEMOLPC-KO mice. Collectively, our data show that free NEMO molecules unbound to the catalytic IKK subunits control LPC programmed cell death pathways and proliferation, cholestasis and hepatocarcinogenesis independently of an IKK-related function. These findings support the idea of different functional levels at which NEMO controls inflammation and cancer in the liver.
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Hacker, H., and M. Karin. "Regulation and Function of IKK and IKK-Related Kinases." Science's STKE 2006, no. 357 (2006): re13. http://dx.doi.org/10.1126/stke.3572006re13.
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Ayu Arwati, I. Gusti, Euis Nina Saparina, and Nur Endah Retno Wuryandari. "OVERCOMING OBSTACLES IN THE DEVELOPMENT OF IKRT / UMK THROUGH APPLICATION OF APPROPRIATE TECHNOLOGY." Dinasti International Journal of Digital Business Management 1, no. 3 (2020): 386–93. http://dx.doi.org/10.31933/dijdbm.v1i3.242.
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The SME sector that has an important role in the Indonesian industry is the small and home industry (IKRT) or micro and small businesses (MSME). In everyday life, washing clothes and washing the house is an activity that is usually done by everyone, especially by the home industry. IKRT (UMK) Suradita RW 09 Suradita Indah Complex, is IKRT (UMK) in the Suradita sub-district, which produces green cleaning products guided by Universitas Mercu Buana lecturers who have been operating for one year. IKRT (UMK) was established to increase the knowledge of housewives who live in RW 09, where production is marketed in the surrounding area as well. In addition there is no good management governance, also a good marketing strategy. Based on the above, the objectives of community service are (1) using appropriate technology in the green cleaner production process, (2) improving the quality of green cleaner product formulations, (3) implementing good governance management and marketing strategies to be more effective and efficient and has sustainable competitiveness. The results of this community service are (1) appropriate technology that can be used in the production process. (2) Improving the quality of green cleaner product formulations and (3) governance management and marketing strategies. And can avoid Suradita IKRT which is more effective and efficient and has sustainable competitiveness.
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Aupperle, Karlfried R., Brydon L. Bennett, David L. Boyle, Paul-Peter Tak, Anthony M. Manning та Gary S. Firestein. "NF-κB Regulation by IκB Kinase in Primary Fibroblast-Like Synoviocytes". Journal of Immunology 163, № 1 (1999): 427–33. http://dx.doi.org/10.4049/jimmunol.163.1.427.
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Abstract NF-κB is a key regulator of inflammatory gene transcription and is activated in the rheumatoid arthritis (RA) synovium. In resting cells, NF-κB is retained as an inactive cytoplasmic complex by its inhibitor, IκB. Phosphorylation of IκB targets it for proteolytic degradation, thereby releasing NF-κB for nuclear translocation. Recently, two related IκB kinases (IKK-1 and IKK-2) were identified in immortalized cell lines that regulate NF-κB activation by initiating IκB degradation. To determine whether IKK regulates NF-κB in primary cells isolated from a site of human disease, we characterized IKK in cultured fibroblast-like synoviocytes (FLS) isolated from synovium of patients with RA or osteoarthritis. Immunoreactive IKK protein was found to be abundant in both RA and osteoarthritis FLS by Western blot analysis. Northern blot analysis showed that IKK-1 and IKK-2 genes were constitutively expressed in all FLS lines. IKK function in FLS extracts was determined by measuring phosphorylation of recombinant IκB in vitro. IKK activity in both RA and osteoarthritis FLS was strongly induced by TNF-α and IL-1 in a concentration-dependent manner. Activity was significantly increased within 10 min of stimulation and declined to near basal levels within 80 min. Activation of IKK in FLS was accompanied by phosphorylation and degradation of endogenous IκBα as determined by Western blot analysis. Concomitant activation and nuclear translocation of NF-κB was documented by EMSA and immunohistochemistry. Transfection with a dominant negative IKK-2 mutant prevented TNF-α-mediated NF-κB nuclear translocation, whereas a dominant negative IKK-1 mutant had no effect. This is the first demonstration that IKK-2 is a pivotal regulator of NF-κB in primary human cells.
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Lee, Frank S., Robert T. Peters, Luan C. Dang та Tom Maniatis. "MEKK1 activates both IκB kinase α and IκB kinase β". Proceedings of the National Academy of Sciences 95, № 16 (1998): 9319–24. http://dx.doi.org/10.1073/pnas.95.16.9319.
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A critical step in the signal-induced activation of the transcription factor NF-κB is the site-specific phosphorylation of its inhibitor, IκB, that targets the latter for degradation by the ubiquitin–proteasome pathway. We have previously shown that mitogen-activated protein kinase/ERK kinase kinase 1 (MEKK1) can induce both this site-specific phosphorylation of IκBα at Ser-32 and Ser-36 in vivo and the activity of a high molecular weight IκB kinase complex in vitro. Subsequently, others have identified two proteins, IκB kinase α (IKK-α) and IκB kinase β (IKK-β), that are present in a tumor necrosis factor α-inducible, high molecular weight IκB kinase complex. These kinases are believed to directly phosphorylate IκB based on the examination of the kinase activities of IKK immunoprecipitates, but more rigorous proof of this has yet to be demonstrated. We show herein that recombinant IKK-α and IKK-β can, in fact, directly phosphorylate IκBα at Ser-32 and Ser-36, as well as homologous residues in IκBβ in vitro, and thus are bona fide IκB kinases. We also show that MEKK1 can induce the activation of both IKK-α and IKK-β in vivo. Finally, we show that IKK-α is present in the MEKK1-inducible, high molecular weight IκB kinase complex and treatment of this complex with MEKK1 induces phosphorylation of IKK-α in vitro. We conclude that IKK-α and IKK-β can mediate the NF-κB-inducing activity of MEKK1.
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Akbar, Yuma, Iim Muhaemin Abdul Azis, Aulia Farhani, and Reda Hayati Nufus. "Rancang Bangun Sistem Informasi Kas pada Ikatan Remaja Pesantren Akmaliah Berbasis Web." AJAD : Jurnal Pengabdian kepada Masyarakat 4, no. 1 (2024): 148–55. http://dx.doi.org/10.59431/ajad.v4i1.288.
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Ikatan Remaja Pondok Pesantren Akmaliah (IKRA) is a management organization within the Akmaliah Islamic Boarding School. Akmaliah Islamic Boarding School is a place for teaching or studying Islamic teachings. Based on information from one of the administrators of the IKRA organization, there are problems with the management system and cash contributions at this organization called IKRA. In the previous cash system, recording of outgoing and incoming funds was still done manually and information about the recording was still done manually, namely through the WhatsApp Group social media application. This research aims to develop a Web-based cash information system for the Akmaliah Islamic Boarding School Youth Association Organization. The development of this system was carried out using the PHP programming language with the database management used being MySQL. The results of developing this system produce a cash management website that can be managed by every IKRA member online via the website which includes managing and recording outgoing and incoming funds, thereby increasing efficiency and transparency in managing the organization's cash.
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Zhang, Shetuan. "Isolation and characterization of IKr in cardiac myocytes by Cs+ permeation." American Journal of Physiology-Heart and Circulatory Physiology 290, no. 3 (2006): H1038—H1049. http://dx.doi.org/10.1152/ajpheart.00679.2005.
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Isolation of the rapidly activating delayed rectifier potassium current ( IKr) from other cardiac currents has been a difficult task for quantitative study of this current. The present study was designed to separate IKr using Cs+ in cardiac myocytes. Cs+ have been known to block a variety of K+ channels, including many of those involved in the cardiac action potential such as inward rectifier potassium current IK1 and the transient outward potassium current Ito. However, under isotonic Cs+ conditions (135 mM Cs+), a significant membrane current was recorded in isolated rabbit ventricular myocytes. This current displayed the voltage-dependent onset of and recovery from inactivation that are characteristic to IKr. Consistently, the current was selectively inhibited by the specific IKr blockers. The biophysical and pharmacological properties of the Cs+-carried human ether-a-go-go-related gene (hERG) current were very similar to those of the Cs+-carried IKr in ventricular myocytes. The primary sequence of the selectivity filter in hERG was in part responsible for the Cs+ permeability, which was lost when the sequence was changed from GFG to GYG, characteristic of other, Cs+-impermeable K+ channels. Thus the unique high Cs+ permeability in IKr channels provides an effective way to isolate IKr current. Although the biophysical and pharmacological properties of the Cs+-carried IKr are different from those of the K+-carried IKr, such an assay enables IKr current to be recorded at a level that is large enough and sufficiently robust to evaluate any IKr alterations in native tissues in response to physiological or pathological changes. It is particularly useful for exploring the role of reduction of IKr in arrhythmias associated with heart failure and long QT syndrome due to the reduced hERG channel membrane expression.
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Watanabe, Ryo, Ryoko Wakizono Azuma, Jun-ichi Suzuki та ін. "Inhibition of NF-κB activation by a novel IKK inhibitor reduces the severity of experimental autoimmune myocarditis via suppression of T-cell activation". American Journal of Physiology-Heart and Circulatory Physiology 305, № 12 (2013): H1761—H1771. http://dx.doi.org/10.1152/ajpheart.00159.2013.
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NF-κB, which is activated by the inhibitor of NF-κB kinase (IKK), is involved in the progression of inflammatory disease. However, the effect of IKK inhibition on the progression of myocarditis is unknown. We examined the effect of IKK inhibition on the progression of myocarditis. Lewis rats were immunized with porcine cardiac myosin to induce experimental autoimmune myocarditis (EAM). We administered the IKK inhibitor (IMD-0354; 15 mg·kg−1·day−1) or vehicle to EAM rats daily. Hearts were harvested 21 days after immunization. Although the untreated EAM group showed increased heart weight-to-body weight ratio, and severe myocardial damage, these changes were attenuated in the IKK inhibitor-treated group. Moreover, IKK inhibitor administration significantly reduced NF-κB activation and mRNA expression of IFN-γ, IL-2, and monocyte chemoattractant protein-1 in myocardium compared with vehicle administration. In vitro study showed that the IKK inhibitor treatment inhibited T-cell proliferation and Th1 cytokines production induced by myosin stimulation. The IKK inhibitor ameliorated EAM by suppressing inflammatory reactions via suppression of T-cell activation.
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Shinohara, Hisaaki, Tomoharu Yasuda, Yuichi Aiba та ін. "PKCβ regulates BCR-mediated IKK activation by facilitating the interaction between TAK1 and CARMA1". Journal of Experimental Medicine 202, № 10 (2005): 1423–31. http://dx.doi.org/10.1084/jem.20051591.
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The B cell antigen receptor (BCR)–mediated activation of IκB kinase (IKK) and nuclear factor–κB require protein kinase C (PKC)β; however, the mechanism by which PKCβ regulates IKK is unclear. Here, we demonstrate that another protein kinase, TGFβ-activated kinase (TAK)1, is essential for IKK activation in response to BCR stimulation. TAK1 interacts with the phosphorylated CARMA1 (also known as caspase recruitment domain [CARD]11, Bimp3) and this interaction is mediated by PKCβ. IKK is also recruited to the CARMA1–Bcl10–mucosal-associated lymphoid tissue 1 adaptor complex in a PKCβ-dependent manner. Hence, our data suggest that phosphorylation of CARMA1, mediated by PKCβ, brings two key protein kinases, TAK1 and IKK, into close proximity, thereby allowing TAK1 to phosphorylate IKK.
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Foley, J. F. "IKK Targets PI3K." Science Signaling 5, no. 218 (2012): ec100-ec100. http://dx.doi.org/10.1126/scisignal.2003101.
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Foley, J. F. "IKK Goes BAD." Science Signaling 6, no. 260 (2013): ec31-ec31. http://dx.doi.org/10.1126/scisignal.2004004.
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Bohn Stafleu van Loghum. "Onduidelijkheid over IKK." Management Kinderopvang 24, no. 1 (2018): 33. http://dx.doi.org/10.1007/s41190-018-0008-4.
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HL. "IKK gegen Einheitsbeitrag." Der Hausarzt 49, no. 15 (2012): 12. http://dx.doi.org/10.1007/s15200-012-0805-y.
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Gósy, Mária, and Márta Pregitzer. "Beszédészlelés és beszédmegértés ikreknél és nem ikreknél." Anyanyelv-pedagógia 12, no. 3 (2019): 5–17. http://dx.doi.org/10.21030/anyp.2019.3.1.
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A kutatási eredmények a genetikai tényező mellett a környezeti hatás meghatározó szerepét igazolják a nyelvelsajátításban. Az ikrek anyanyelvi jellemzőinek összevető vizsgálata nem ikergyermekekéivel információt nyújthat az eltérő környezeti hatás következményeiről. Kutatásunkban a beszédészlelés és a beszédmegértés két-két folyamatát elemeztük közel 400 gyermek (5–9 évesek) teszteléses vizsgálata alapján. Az eredmények szerint a beszédhang-differenciálásban jóformán nincs különbség az ikrek és a nem ikrek között, míg a szeriális észlelésben csak a 7 és a 8 évesek esetében nem volt jelentős eltérés kimutatható. A mondatmegértés csak az 5 évesek esetében mutatott különbséget az ikerlét függvényében. A szövegértésben az 5 évesek kivételével az összes vizsgált életkorban a nem ikergyermekek szignifikánsan jobban teljesítettek az ikreknél. Eredményeink felhívják a figyelmet a beszédfeldolgozási nehézségekre és a fejlesztés mielőbbi megkezdésére.
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Nemoto, Shino, Joseph A. DiDonato та Anning Lin. "Coordinate Regulation of IκB Kinases by Mitogen-Activated Protein Kinase Kinase Kinase 1 and NF-κB-Inducing Kinase". Molecular and Cellular Biology 18, № 12 (1998): 7336–43. http://dx.doi.org/10.1128/mcb.18.12.7336.
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ABSTRACT IκB kinases (IKKα and IKKβ) are key components of the IKK complex that mediates activation of the transcription factor NF-κB in response to extracellular stimuli such as inflammatory cytokines, viral and bacterial infection, and UV irradiation. Although NF-κB-inducing kinase (NIK) interacts with and activates the IKKs, the upstream kinases for the IKKs still remain obscure. We identified mitogen-activated protein kinase kinase kinase 1 (MEKK1) as an immediate upstream kinase of the IKK complex. MEKK1 is activated by tumor necrosis factor alpha (TNF-α) and interleukin-1 and can potentiate the stimulatory effect of TNF-α on IKK and NF-κB activation. The dominant negative mutant of MEKK1, on the other hand, partially blocks activation of IKK by TNF-α. MEKK1 interacts with and stimulates the activities of both IKKα and IKKβ in transfected HeLa and COS-1 cells and directly phosphorylates the IKKs in vitro. Furthermore, MEKK1 appears to act in parallel to NIK, leading to synergistic activation of the IKK complex. The formation of the MEKK1-IKK complex versus the NIK-IKK complex may provide a molecular basis for regulation of the IKK complex by various extracellular signals.
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Antonia, Ricardo J., and Albert S. Baldwin. "IKK promotes cytokine-induced and cancer-associated AMPK activity and attenuates phenformin-induced cell death in LKB1-deficient cells." Science Signaling 11, no. 538 (2018): eaan5850. http://dx.doi.org/10.1126/scisignal.aan5850.
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The 5′ AMP-activated protein kinase (AMPK) is an energy sensor that is activated upon phosphorylation of Thr172 in its activation loop by the kinase LKB1, CAMKK2, or TAK1. TAK1-dependent AMPK phosphorylation of Thr172 is less well characterized than phosphorylation of this site by LKB1 or CAMKK2. An important target of TAK1 is IκB kinase (IKK), which controls the activation of the transcription factor NF-κB. We tested the hypothesis that IKK acted downstream of TAK1 to activate AMPK by phosphorylating Thr172. IKK was required for the phosphorylation of Thr172 in AMPK in response to treatment with the inflammatory cytokine IL-1β or TNF-α or upon TAK1 overexpression. In addition, IKK regulated basal AMPK Thr172 phosphorylation in several cancer cell types independently of TAK1, indicating that other modes of IKK activation could stimulate AMPK. We found that IKK directly phosphorylated AMPK at Thr172 independently of the tumor suppressor LKB1 or energy stress. Accordingly, in LKB1-deficient cells, IKK inhibition reduced AMPK Thr172 phosphorylation in response to the mitochondrial inhibitor phenformin. This response led to enhanced apoptosis and suggests that IKK inhibition in combination with phenformin could be used clinically to treat patients with LKB1-deficient cancers.
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Hua, Fei, David C. Johns, and Robert F. Gilmour. "Suppression of electrical alternans by overexpression of HERG in canine ventricular myocytes." American Journal of Physiology-Heart and Circulatory Physiology 286, no. 6 (2004): H2342—H2351. http://dx.doi.org/10.1152/ajpheart.00793.2003.
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Suppression of electrical alternans may be antiarrhythmic. Our previous computer simulations have suggested that increasing the rapid component of the delayed rectifier K+ current ( IKr) suppresses alternans. To test this hypothesis, IKr in isolated canine ventricular myocytes was increased by infection with an adenovirus containing the gene for the pore-forming domain of IKr [human ether-a-go-go gene (HERG)]. With the use of the perforated or whole cell patch-clamp technique, action potentials recorded at different pacing cycle lengths (CLs) were applied to the myocytes as the command waveforms. HERG infection markedly increased peak IKr during the action potential (from 0.54 ± 0.03 pA/pF in control to 3.60 ± 0.81 pA/pF). Rate-dependent alterations of peak IKr were similar for freshly isolated myocytes and HERG-infected myocytes. In both cell types, IKr increased when CL decreased from 1,000 to 500 ms and then decreased progressively as CL decreased further. During alternans at CL = 170 ms, peak IKr was larger for the short than for the long action potential for both groups, but the difference in peak IKr was larger for HERG-infected myocytes. The voltage at which peak IKr occurred was significantly less negative in HERG-infected myocytes, in association with shifts of the steady-state voltage-dependent activation and inactivation curves to less negative potentials. Pacing at short CL induced stable alternans in freshly isolated myocytes and in cultured myocytes without HERG infection, but not in HERG-infected myocytes. These data support the idea that increasing IKr may be a viable approach to suppressing electrical alternans.
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Zhu, Haijuan, Jinbao Wang та Lihua Huang. "Dexmedetomidine relieves inflammatory response in rats with acute spinal cord injury through IKK/NF-κB signaling pathway". Tropical Journal of Pharmaceutical Research 21, № 3 (2022): 543–48. http://dx.doi.org/10.4314/tjpr.v21i3.13.
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Purpose: To examine the effect of dexmedetomidine (DEX) on inflammatory response in spinal cord damage, and involvement of IKK/NF-κB signaling pathway in the process.Methods: Sixty healthy male Wistar rats were selected and randomly divided into sham, control, IKK inhibition, and DEX groups. Rat hind limb motor function in each group at 1, 24 and 48 h after surgery was determined using Basso Beattie Bresnahan (BBB) method, while Western blot assay was used to evaluate the protein expression levels of IL-1β, IKK and NF-κB in spinal cord tissue.Results: In DEX rat group, neuromotor function at 24 and 48 h, and protein expression level of IL-1β in spinal cord tissue significantly decreased, relative to IKK inhibition group (p < 0.05). There were higher protein expressions of IKK and NF-κB in IKK inhibition and DEX groups than in sham rats, but were lower than the corresponding values for model group (p < 0.05). However, these proteins were significantly downregulated in DEX group, relative to the IKK inhibition rats (p < 0.05).Conclusion: DEX mitigates inflammatory response in rats with acute spinal cord injury via IKK/NF-κB signaling pathway. This provides some ideas for research and development of other drugs for the treatment of acute spinal cord injury.
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Devin, Anne, Yong Lin, Shoji Yamaoka, Zhiwei Li, Michael Karin та Zheng-gang Liu. "The α and β Subunits of IκB Kinase (IKK) Mediate TRAF2-Dependent IKK Recruitment to Tumor Necrosis Factor (TNF) Receptor 1 in Response to TNF". Molecular and Cellular Biology 21, № 12 (2001): 3986–94. http://dx.doi.org/10.1128/mcb.21.12.3986-3994.2001.
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ABSTRACT The activation of IκB kinase (IKK) is a key step in the nuclear translocation of the transcription factor NF-κB. IKK is a complex composed of three subunits: IKKα, IKKβ, and IKKγ (also called NEMO). In response to the proinflammatory cytokine tumor necrosis factor (TNF), IKK is activated after being recruited to the TNF receptor 1 (TNF-R1) complex via TNF receptor-associated factor 2 (TRAF2). We found that the IKKα and IKKβ catalytic subunits are required for IKK-TRAF2 interaction. This interaction occurs through the leucine zipper motif common to IKKα, IKKβ, and the RING finger domain of TRAF2, and either IKKα or IKKβ alone is sufficient for the recruitment of IKK to TNF-R1. Importantly, IKKγ is not essential for TNF-induced IKK recruitment to TNF-R1, as this occurs efficiently in IKKγ-deficient cells. Using TRAF2−/− cells, we demonstrated that the TNF-induced interaction between IKKγ and the death domain kinase RIP is TRAF2 dependent and that one possible function of this interaction is to stabilize the IKK complex when it interacts with TRAF2.
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Purcell, Nicole H., Chenfei Yu, Daoyao He та ін. "Activation of NF-κB by hepatitis B virus X protein through an IκB kinase-independent mechanism". American Journal of Physiology-Gastrointestinal and Liver Physiology 280, № 4 (2001): G669—G677. http://dx.doi.org/10.1152/ajpgi.2001.280.4.g669.
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pX, the hepatitis B virus-encoded transcription coactivator, is involved in viral infection in vivo. pX stimulates the activity of several transcription factors including nuclear factor-κB (NF-κB), but the mechanism of activation is poorly understood. The IκB kinase complex (IKK) mediates activation of NF-κB in response to various extracellular stimuli, including inflammatory cytokines like tumor necrosis factor and interleukin 1, human T cell lymphoma virus 1 Tax protein, and tumor promoters like phorbol esters. It is not known whether IKK also mediates activation of NF-κB by pX. Here we report that IKK was not essential for activation of NF-κB by pX. Expression of pX resulted in the degradation of IκBα in the absence of its phosphorylation at Ser32and Ser36residues. Although pX stimulated the activity of cotransfected IKK-β when it was overexpressed, it failed to activate endogenous IKK. Furthermore, expression of pX stimulated NF-κB nuclear translocation and transcriptional activity in IKK-γ-null fibroblast 5R cells. Our data indicate that pX stimulates NF-κB activity through a mechanism that is dependent on IκBα degradation but not on IKK activation.
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Trushin, Sergey A., Kevin N. Pennington, Eva M. Carmona та ін. "Protein Kinase Cα (PKCα) Acts Upstream of PKCθ To Activate IκB Kinase and NF-κB in T Lymphocytes". Molecular and Cellular Biology 23, № 19 (2003): 7068–81. http://dx.doi.org/10.1128/mcb.23.19.7068-7081.2003.
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ABSTRACT NF-κB is an ubiquitous transcription factor that is a key in the regulation of the immune response and inflammation. T-cell receptor (TCR) cross-linking leads to NF-κB activation, an IκB kinase (IKK)-dependent process. However, the upstream kinases that regulate IKK activity following TCR activation remain to be fully characterized. Herein, we demonstrate using genetic analysis, pharmacological inhibition, and RNA interference (RNAi) that the conventional protein kinase C (PKC) isoform PKCα, but not PKCβ1, is required for the activation of the IKK complex following T-cell activation triggered by CD3/CD28 cross-linking. We find that in the presence of Ca2+ influx, the catalytically active PKCαA25E induces IKK activity and NF-κB-dependent transcription; which is abrogated following the mutations of two aspartates at positions 246 and 248, which are required for Ca2+ binding to PKCα and cell membrane recruitment. Kinetic studies reveal that an early phase (1 to 5 min) of IKK activation following TCR/CD28 cross-linking is PKCα dependent and that a later phase (5 to 25 min) of IKK activation is PKCθ dependent. Activation of IKK- and NF-κB-dependent transcription by PKCαA25E is abrogated by the PKCθ inhibitor rottlerin or the expression of the kinase-inactive form of PKCθ. Taken together, our results suggest that PKCα acts upstream of PKCθ to activate the IKK complex and NF-κB in T lymphocytes following TCR activation.
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Llona-Minguez, Sabin, Jessica Baiget та Simon P. Mackay. "Small-molecule inhibitors of IκB kinase (IKK) and IKK-related kinases". Pharmaceutical Patent Analyst 2, № 4 (2013): 481–98. http://dx.doi.org/10.4155/ppa.13.31.
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Lee, Dung-Fang, and Mien-Chie Hung. "Advances in Targeting IKK and IKK-Related Kinases for Cancer Therapy." Clinical Cancer Research 14, no. 18 (2008): 5656–62. http://dx.doi.org/10.1158/1078-0432.ccr-08-0123.
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Sanguinetti, M. C., and N. K. Jurkiewicz. "Two components of cardiac delayed rectifier K+ current. Differential sensitivity to block by class III antiarrhythmic agents." Journal of General Physiology 96, no. 1 (1990): 195–215. http://dx.doi.org/10.1085/jgp.96.1.195.
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An envelope of tails test was used to show that the delayed rectifier K+ current (IK) of guinea pig ventricular myocytes results from the activation of two outward K+ currents. One current was specifically blocked by the benzenesulfonamide antiarrhythmic agent, E-4031 (IC50 = 397 nM). The drug-sensitive current, "IKr" exhibits prominent rectification and activates very rapidly relative to the slowly activating drug-insensitive current, "IKs." IKs was characterized by a delayed onset of activation that occurs over a voltage range typical of the classically described cardiac IK. Fully activated IKs, measured as tail current after 7.5-s test pulses, was 11.4 times larger than the fully activated IKr. IKr was also blocked by d-sotalol (100 microM), a less potent benzenesulfonamide Class III antiarrhythmic agent. The activation curve of IKr had a steep slope (+7.5 mV) and a negative half-point (-21.5 mV) relative to the activation curve of IKs (slope = +12.7 mV, half-point = +15.7 mV). The reversal potential (Erev) of IKr (-93 mV) was similar to EK (-94 mV for [K+]o = 4 mM), whereas Erev of IKs was -77 mV. The time constants for activation and deactivation of IKr made up a bell-shaped function of membrane potential, peaking between -30 and -40 mV (170 ms). The slope conductance of the linear portion of the fully activated IKr-V relation was 22.5 S/F. Inward rectification of this relation occurred at potentials greater than -50 mV, resulting in a voltage-dependent decrease in peak IKr at test potentials greater than 0 mV. Peak IKr at 0 mV averaged 0.8 pA/pF (n = 21). Although the magnitude of IKr was small relative to fully activated IKs, the two currents were of similar magnitude when measured during a relatively short pulse protocol (225 ms) at membrane potentials (-20 to +20 mV) typical of the plateau phase of cardiac action potentials.
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Kearly, Alyssa, Kristina Ottens, Michael C. Battaglia, Anne B. Satterthwaite, and Lee Ann Garrett-Sinha. "B Cell Activation Results in IKK-Dependent, but Not c-Rel- or RelA-Dependent, Decreases in Transcription of the B Cell Tolerance-Inducing Gene Ets1." ImmunoHorizons 6, no. 11 (2022): 779–89. http://dx.doi.org/10.4049/immunohorizons.2100065.
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Abstract Ets1 is a key transcription factor in B cells that is required to prevent premature differentiation into Ab-secreting cells. Previously, we showed that BCR and TLR signaling downregulate Ets1 levels and that the kinases PI3K, Btk, IKK, and JNK are required for this process. PI3K is important in activating Btk by generating the membrane lipid phosphatidylinositol (3,4,5)-trisphosphate, to which Btk binds via its PH domain. Btk in turn is important in activating the IKK kinase pathway, which it does by activating phospholipase Cγ2→protein kinase Cβ signaling. In this study, we have further investigated the pathways regulating Ets1 in mouse B cells. Although IKK is well known for its role in activating the canonical NF-κB pathway, IKK-mediated downregulation of Ets1 does not require either RelA or c-Rel. We also examined the potential roles of two other IKK targets that are not part of the NF-κB signaling pathway, Foxo3a and mTORC2, in regulating Ets1. We find that loss of Foxo3a or inhibition of mTORC2 does not block BCR-induced Ets1 downregulation. Therefore, these two pathways are not key IKK targets, implicating other as yet undefined IKK targets to play a role in this process.
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Tsai, Julie, Rianna Zhang, Wei Qiu, Qiaozhu Su, Mark Naples та Khosrow Adeli. "Inflammatory NF-κB activation promotes hepatic apolipoprotein B100 secretion: evidence for a link between hepatic inflammation and lipoprotein production". American Journal of Physiology-Gastrointestinal and Liver Physiology 296, № 6 (2009): G1287—G1298. http://dx.doi.org/10.1152/ajpgi.90540.2008.
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Insulin-resistant states are commonly associated with chronic inflammation and hepatic overproduction of apolipoprotein B100 (apoB100), leading to hypertriglyceridemia and a metabolic dyslipidemic profile. Molecular mechanisms linking hepatic inflammatory cascades and the pathways of apoB100-lipoprotein production are, however, unknown. In the present study, we employed a diet-induced, insulin-resistant hamster model, as well as cell culture studies, to investigate the potential link between activation of hepatic inflammatory nuclear factor-κB (NF-κB) signaling cascade and the synthesis and secretion of apoB100-containing lipoproteins. Using an established insulin-resistant animal model, the fructose-fed hamster, we found that feeding fructose (previously shown to induce hepatic inflammation) for as little as 4 days reduced hepatic IκB (inhibitor of NF-κB) level, indicating activation of the inflammatory NF-κB cascade. Importantly, IKK (IκB kinase) inhibition was found to suppress apoB100 overproduction in fructose-fed hamster hepatocytes. As IKK, the upstream activator of NF-κB has been shown to inhibit insulin signaling, and insulin is a major regulator of apoB100, we modulated IKK activity in primary hamster hepatocytes and HepG2 cells and assessed the effects on hepatic apoB100 biosynthesis. Inhibition of the IKK-NF-κB pathway by BMS345541 and activation of the pathway by adenoviral-mediated IKK overexpression decreased and increased newly synthesized apoB100 levels, respectively. Pulse-chase and metabolic labeling experiments revealed that IKK activation regulates apoB100 levels at the levels of apoB100 biosynthesis and protein stability. Inhibition of the IKK-NF-κB pathway significantly enhanced proteasomal degradation of hepatic apoB100, while direct IKK activation led to reduced degradation and increased apoB100 mRNA translation. Together, our results reveal important links between modulation of the inflammatory IKK-NF-κB signaling cascade and hepatic synthesis and secretion of apoB100-containing lipoproteins. Hepatic inflammation may be an important underlying factor in hepatic apoB100 overproduction observed in insulin resistance.
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Zerzová, J., and S. Šebestová. "Příležitosti k rozvíjení interkulturní komunikační kompetence v kontextu řečových dovedností: IVŠV videostudie anglického jazyka." Pedagogická orientace 24, no. 3 (2014): 394–422. http://dx.doi.org/10.5817/pedor2014-3-394.
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Empirická studie je věnována problematice rozvíjení interkulturní komunikační kompetence (IKK) a její integraci s rozvíjením řečových dovedností ve výuce anglického jazyka (AJ) na 2. stupni ZŠ. V rámci hledání odpovědi na otázku, jakým způsobem a za jakých podmínek rozvíjení IKK ve výuce AJ probíhá, je cílem této studie nahlédnout do toho, v integraci s jakými řečovými dovednostmi je IKK rozvíjena a jaké je jejich zastoupení. Po úvodní části a vymezení teoretických východisek následuje část metodologická (kapitola 3) představující zkoumaný soubor (79 vyučovacích hodin AJ v 7. a 8. ročnících natočených u 25 učitelů na 2. stupni ZŠ ve třech krajích v rámci IVŠV videostudie anglického jazyka), způsob zpracování dat (způsob natáčení, transkripce, kódování), výzkumné otázky a kategoriální systémy (kategoriální systém IKK a kategoriální systém Řečové dovednosti), jež byly pro analýzu videozáznamů použity. Výsledky výzkumu naznačují, že mezi zastoupením řečových dovedností ve výuce a rozvíjením IKK existuje vztah, jenž se ve vzorku natočených hodin projevil vyšším zastoupením receptivních řečových dovedností a omezeným zastoupením produktivních řečových dovedností, vedoucím k rozvíjení IKK, jež se omezilo pouze na kognitivní úroveň, bez zastoupení zbývajících složek (konativní/behaviorální, afektivní).
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Park, Min-Young, Ji-hyun Moon, Ki-Sung Lee та ін. "FAF1 Suppresses IκB Kinase (IKK) Activation by Disrupting the IKK Complex Assembly". Journal of Biological Chemistry 282, № 38 (2007): 27572–77. http://dx.doi.org/10.1074/jbc.c700106200.
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This study presents a molecular inhibitory mechanism by Fas-associated factor 1 (FAF1) on IκB kinase (IKK) activation, where divergent NF-κB-activating stimuli converge. FAF1 interacts with IKKβ in response to proinflammatory stimuli (such as tumor necrosis factor-α, interleukin-1β, and lipopolysaccharide) and suppresses IKK activation. Interaction of the leucine-zipper domain of IKKβ with FAF1 affected the IKK heterocomplex (IKKα/β) and homocomplex (IKKα/α, IKKβ/β) formations and attenuated IKKγ recruitment to IKKβ. Overexpression of FAF1 reduced the level of IKKβ activity, whereas FAF1 depletion increased the activity. These results indicate that FAF1 inhibits IKK activation and its downstream signaling by interrupting the IKK complex assembly through physical interaction with IKKβ. Taken together, FAF1 robustly suppresses NF-κB activation through the inhibition of IKK activation in combination with previously reported cytoplasmic retention of NF-κB p65 (Park, M. Y., Jang, H. D., Lee, S. Y., Lee, K. J., and Kim, E. (2004) J. Biol. Chem. 279, 2544–2549). Such redundant suppression would prevent inadvertent activation of the NF-κB pathway.
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Muhammad Amar. "EFEKTIVITAS PELAYANAN TERHADAP PELANGGAN AIR BERSIH PDAM SPAM IKK KELURAHAN PASIR PUTIH KECAMATAN SINJAI BORONG." Jurnal Ilmu Administrasi Negara 19, no. 1 (2022): 165–76. http://dx.doi.org/10.59050/jian.v19i1.213.
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Penelitian ini bertujuan untuk untuk mengetahui bagaimana Pelayanan Terhadap Pelanggan Air Bersih Perusahaan Daerah Air Minum SPAM IKK Kelurahan Pasir Putih Kecamatan Sinjai Borong Kabupaten Sinjai ,untuk mengetahui prosedur pelayanan pelamggan air bersih, untuk mengetahui waktu penyelesaian pelayanan pelanggan air bersih mengetahui bagaimana Pelayanan Terhadap Pelanggan Air Bersih Perusahaan Daerah Air Minum SPAM IKK Kelurahan Pasir Putih Kecamatan Sinjai Borong Kabupaten Sinjai. Penelitian ini menggunakan deskriptif kualitatif, teknik pengumpulan data yaitu observasi, wawancara dan dokuemntasi dengan teknik analisis data yaitu reduksi data, penyajian data dan penarikan kesimpulan yang di proleh dari Kepala SPAM IKK Kecamatan Sinjai Borong, pegawai/Staf SPAM IKK Kecamatan Sinjai Borong, pelanggang Air Bersih Kecamatan Sinjai Borong, tokoh Masyarakat Kecamatan Sinjai Borong. Hasil penelitian tentang efektivitas pelayanan terhadap pelanggan air bersih perusahaan daerah air minum SPAM IKK Kelurahan pasir putih Kecamatan Sinjai Borong Kabupaten sinjai disimpulkan sebagai berikut : prosedur pelayanan SPAM IKK kecamatan sinjai borong terhadap pelanggan air bersih sudah cukup efektif hal ini dapat di lihat dari pelayanannya yang cepat, pemberian arahan kepadawarga untuk di mintai alamat
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Mercurio, Frank, Brion W. Murray, Andrej Shevchenko та ін. "IκB Kinase (IKK)-Associated Protein 1, a Common Component of the Heterogeneous IKK Complex". Molecular and Cellular Biology 19, № 2 (1999): 1526–38. http://dx.doi.org/10.1128/mcb.19.2.1526.
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ABSTRACT Activation of the transcription factor NF-κB is controlled by the sequential phosphorylation, ubiquitination, and degradation of its inhibitory subunit, IκB. We recently purified a large multiprotein complex, the IκB kinase (IKK) signalsome, which contains two regulated IκB kinases, IKK1 and IKK2, that can each phosphorylate IκBα and IκBβ. The IKK signalsome contains several additional proteins presumably required for the regulation of the NFκB signal transduction cascade in vivo. In this report, we demonstrate reconstitution of IκB kinase activity in vitro by using purified recombinant IKK1 and IKK2. Recombinant IKK1 or IKK2 forms homo- or heterodimers, suggesting the possibility that similar IKK complexes exist in vivo. Indeed, in HeLa cells we identified two distinct IKK complexes, one containing IKK1-IKK2 heterodimers and the other containing IKK2 homodimers, which display differing levels of activation following tumor necrosis factor alpha stimulation. To better elucidate the nature of the IKK signalsome, we set out to identify IKK-associated proteins. To this end, we purified and cloned a novel component common to both complexes, named IKK-associated protein 1 (IKKAP1). In vitro, IKKAP1 associated specifically with IKK2 but not IKK1. Functional analyses revealed that binding to IKK2 requires sequences contained within the N-terminal domain of IKKAP1. Mutant versions of IKKAP1, which either lack the N-terminal IKK2-binding domain or contain only the IKK2-binding domain, disrupt the NF-κB signal transduction pathway. IKKAP1 therefore appears to mediate an essential step of the NF-κB signal transduction cascade. Heterogeneity of IKK complexes in vivo may provide a mechanism for differential regulation of NF-κB activation.
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Rajamani, Sridharan, Corey L. Anderson, Carmen R. Valdivia, et al. "Specific serine proteases selectively damage KCNH2 (hERG1) potassium channels and IKr." American Journal of Physiology-Heart and Circulatory Physiology 290, no. 3 (2006): H1278—H1288. http://dx.doi.org/10.1152/ajpheart.00777.2005.
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KCNH2 ( hERG1) encodes the α-subunit proteins for the rapidly activating delayed rectifier K+ current ( IKr), a major K+ current for cardiac myocyte repolarization. In isolated myocytes IKr frequently is small in amplitude or absent, yet KCNH2 channels and IKr are targets for drug block or mutations to cause long QT syndrome. We hypothesized that KCNH2 channels and IKr are uniquely sensitive to enzymatic damage. To test this hypothesis, we studied heterologously expressed K+, Na+, and L-type Ca2+ channels, and in ventricular myoctyes IKr, slowly activating delayed rectifier K+ current ( IKs), and inward rectifier K+ current ( IK1), by using electrophysiological and biochemical methods. 1) Specific exogenous serine proteases (protease XIV, XXIV, or proteinase K) selectively degraded KCNH2 current ( IKCNH2) and its mature channel protein without damaging cell integrity and with minimal effects on the other channel currents; 2) immature KCNH2 channel protein remained intact; 3) smaller molecular mass KCNH2 degradation products appeared; 4) protease XXIV selectively abolished IKr; and 5) reculturing HEK-293 cells after protease exposure resulted in the gradual recovery of IKCNH2 and its mature channel protein over several hours. Thus the channel protein for IKCNH2 and IKr is uniquely sensitive to proteolysis. Analysis of the degradation products suggests selective proteolysis within the S5-pore extracellular linker, which is structurally unique among Kv channels. These data provide 1) a new mechanism to account for low IKr density in some isolated myocytes, 2) evidence that most complexly glycosylated KCNH2 channel protein is in the plasma membrane, and 3) new insight into the rate of biogenesis of KCNH2 channel protein within cells.
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Indra Digdoyono Notohamijoyo, MT, Setiadi. "INDEKS KUALITAS KEBIJAKAN SEBAGAI INSTRUMEN PENJAMIN MUTU KEBIJAKAN KETAHANAN DAGING SAPI DAN BERAS NASIONAL BERBASIS BUKTI." Jurnal Analis Kebijakan 4, no. 1 (2020): 41–56. http://dx.doi.org/10.37145/jak.v4i1.426.
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Mengacu kepada kebijakan publik berbasis bukti, Lembaga Administrasi Negara pada tahun2016 telah menerbitkan Indeks Kualitas Kebijakan (IKK). IKK adalah suatu instrumen penilaikualitas kebijakan publik sesuai harapan masyarakat. Harapan publik untuk ketahanan dagingsapi dan beras adalah mewujudkan Nawa Cita jilid II dalam penyediaan beras dan daging sapisecara mandiri guna memaksimalkan kesejahteraan petani.Tulisan ini akan menggunakan IKK dalam menilai dan merumuskan rekomendasiimplementasi kebijakan ketahanan beras dan daging sapi nasional sesuai harapan publik. Penilaian IKK difokuskan pada kualitas implementasi kebijakan dan evaluasi kebijakan.Penilaian implementasi kebijakan disorot dari dimensi perencanaan, kelembagaan, dankomunikasi. Penilaian evaluasi kebijakan dilihat dari efektifitas, efisiensi, dampak, dankeberlanjutan kebijakan.
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Sachse, F., K. Becker, T. J. Basel, D. Weiss, and C. Rudack. "IKK-2 inhibitor TPCA-1 represses nasal epithelial inflammation in vitro." Rhinology journal 49, no. 2 (2011): 168–73. http://dx.doi.org/10.4193/rhino10.099.
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BACKGROUND: Nasal polyposis (NP) is considered a subgroup within chronic rhinosinusitis. NP can be further subdivided into aspirin sensitive- and aspirin tolerant types (ASNP/ ATNP). Although the true etiology of NP has not been identified so far, it is agreed that NP represents an inflammatory disease of the nasal mucosa. Alterations of cellular kinase activities including that of IKK-2 might play a role in this inflammatory process. METHODS: Paraffin sections of ASNP, ATNP and controls were immunostained with Phospho-IkB-α antibody that detects the direct IKK-2 product (IkB-α. Intensity of epithelial staining was analysed semi-quantitatively by two independent observers. In cultured nasal polyp epithelial cells (NPECs) epithelial derived cytokines IL-8 and GRO α were induced by TNF-α or Staphylococcal supernatants and subsequently repressed by IKK-2 inhibitor TPCA-1. RESULTS: Significant Phospho-IkB-α staining was observed in the nasal epithelium of ASNP compared to ATNP and controls suggesting strong IKK-2 activation in patients with ASNP in vivo. In vitro, pro-inflammatory cytokines IL-8 and GRO-α in NPECs were significantly repressed by TPCA-1. CONCLUSION: IKK-2 activity is increased in the subgroup of ASNP. IL-8 and GRO-α responses were repressed by IKK-2 inhibitor TPCA-1 in vitro. IKK-2 inhibitors might represent a potential target for anti-inflammatory intervention in ASNP.
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Urrutia, Janire, Aintzane Alday, Mónica Gallego та ін. "Mechanisms of IhERG/IKr Modulation by α1-Adrenoceptors in HEK293 Cells and Cardiac Myocytes". Cellular Physiology and Biochemistry 40, № 6 (2016): 1261–73. http://dx.doi.org/10.1159/000453180.
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Background: The rapid delayed rectifier K+ current (IKr), carried by the hERG protein, is one of the main repolarising currents in the human heart and a reduction of this current increases the risk of ventricular fibrillation. α1-adrenoceptors (α1-AR) activation reduces IKr but, despite the clear relationship between an increase in the sympathetic tone and arrhythmias, the mechanisms underlying the α1-AR regulation of the hERG channel are controversial. Thus, we aimed to investigate the mechanisms by which α1-AR stimulation regulates IKr. Methods: α1-adrenoceptors, hERG channels, auxiliary subunits minK and MIRP1, the non PIP2-interacting mutant D-hERG (with a deletion of the 883-894 amino acids) in the C-terminal and the non PKC-phosphorylable mutant N-terminal truncated-hERG (NTK-hERG) were transfected in HEK293 cells. Cell membranes were extracted by centrifugation and the different proteins were visualized by Western blot. Potassium currents were recorded by the patch-clamp technique. IKr was recorded in isolated feline cardiac myocytes. Results: Activation of the α1-AR reduces the amplitude of IhERG and IKr through a positive shift in the activation half voltage, which reduces the channel availability at physiological membrane potentials. The intracellular pathway connecting the α1-AR to the hERG channel in HEK293 cells includes activation of the Gαq protein, PLC activation and PIP2 hydrolysis, activation of PKC and direct phosphorylation of the hERG channel N-terminal. The PKC-mediated IKr channel phosphorylation and subsequent IKr reduction after α1-AR stimulation was corroborated in feline cardiac myocytes. Conclusions: These findings clarify the link between sympathetic nervous system hyperactivity and IKr reduction, one of the best characterized causes of torsades de pointes and ventricular fibrillation.
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Bayon, Yolanda, Maria A. Ortiz, Francisco J. Lopez-Hernandez та ін. "Inhibition of IκB Kinase by a New Class of Retinoid-Related Anticancer Agents That Induce Apoptosis". Molecular and Cellular Biology 23, № 3 (2003): 1061–74. http://dx.doi.org/10.1128/mcb.23.3.1061-1074.2003.
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ABSTRACT The transcription factor NF-κB is overexpressed or constitutively activated in many cancer cells, where it induces expression of antiapoptotic genes correlating with resistance to anticancer therapies. Small molecules that inhibit the NF-κB signaling pathway could therefore be used to induce apoptosis in NF-κB-overexpressing tumors and potentially serve as anticancer agents. We found that retinoid antagonist MX781 inhibited the activation of NF-κB-dependent transcriptional activity in different tumor cell lines. MX781 was able to completely inhibit tumor necrosis factor alpha-mediated activation of IκB kinase (IKK), the upstream regulator of NF-κB. Inhibition of IKK activity resulted from direct binding of MX781 to the kinase, as demonstrated by in vitro inhibition studies. Two other molecules, MX3350-1 and CD2325, which are retinoic acid receptor gamma-selective agonists, were capable of inhibiting IKK in vitro, although they exerted variable inhibition of IKK and NF-κB activities in intact cells in a cell type-specific manner. However, N-(4-hydroxyphenyl)-retinamide, another apoptosis-inducing retinoid, and retinoic acid as well as other nonapoptotic retinoids did not inhibit IKK. Inhibition of IKK by the retinoid-related compounds and other small molecules correlated with reduced cell proliferation and increased apoptosis. Reduced cell viability was also observed after overexpression of an IKKβ kinase-dead mutant or the IκBα superrepressor. The induction of apoptosis by the retinoid-related molecules that inhibited IKK was dependent on caspase activity but independent of the retinoid receptors. Thus, the presence of an excess of retinoic acid or a retinoid antagonist did not prevent the inhibition of IKK activation by MX781 and CD2325, indicating a retinoid receptor-independent mechanism of action.
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Hu, Yinling. "A feedforward loop of NLRC5 (de)ubiquitination keeps IKK–NF-κB in check". Journal of Cell Biology 211, № 5 (2015): 941–43. http://dx.doi.org/10.1083/jcb.201511039.
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Many receptors signal via adaptors to the IKK–NF-κB axis, transducing extracellular cues to transcriptional regulation. In this issue, Meng et al. (2015. J. Cell Biol. http://dx.doi.org/10.1083/jcb.201505091) reveal that the IKK regulator NLRC5 shapes NF-κB activity through a feedforward loop of NLRC5 ubiquitination and deubiquitination, highlighting a new pathway modulating IKK–NF-κB activity.