Gotowe bibliografie tematyczne / SAPK

Gotowa bibliografia na temat „SAPK”

Autor: Grafiati
Data publikacji: 4 czerwca 2021
Data aktualizacji: 20 lutego 2023

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Artykuły w czasopismach na temat "SAPK"

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Schaller, Martin, Matthias Bein, Hans C. Korting, Stefan Baur, Gerald Hamm, Michel Monod, Sabine Beinhauer i Bernhard Hube. "The Secreted Aspartyl Proteinases Sap1 and Sap2 Cause Tissue Damage in an In Vitro Model of Vaginal Candidiasis Based on Reconstituted Human Vaginal Epithelium". Infection and Immunity 71, nr 6 (czerwiec 2003): 3227–34. http://dx.doi.org/10.1128/iai.71.6.3227-3234.2003.

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ABSTRACT Secreted aspartyl proteinases (Saps) contribute to the ability of Candida albicans to cause mucosal and disseminated infections. A model of vaginal candidiasis based on reconstituted human vaginal epithelium (RHVE) was used to study the expression and role of these C. albicans proteinases during infection and tissue damage of vaginal epithelium. Colonization of the RHVE by C. albicans SC5314 did not cause any visible epithelial damage 6 h after inoculation, although expression of SAP2, SAP9, and SAP10 was detected by reverse transcriptase PCR. However, significant epithelial damage was observed after 12 h, concomitant with the additional expression of SAP1, SAP4, and SAP5. Additional transcripts of SAP6 and SAP7 were detected at a later stage of the artificial infection (24 h). Similar SAP expression profiles were observed in three samples isolated from human patients with vaginal candidiasis. In experimental infection, secretion of antigens Sap1 to Sap6 by C. albicans was confirmed at the ultrastructural level by using polyclonal antisera raised against Sap1 to Sap6. Addition of the aspartyl proteinase inhibitors pepstatin A and the human immunodeficiency virus proteinase inhibitors ritonavir and amprenavir strongly reduced the tissue damage of the vaginal epithelia by C. albicans cells. Furthermore, SAP null mutants lacking either SAP1 or SAP2 had a drastically reduced potential to cause tissue damage even though SAP3, SAP4, and SAP7 were up-regulated in these mutants. In contrast the vaginopathic potential of mutants lacking SAP3 or SAP4 to SAP6 was not reduced compared to wild-type cells. These data provide further evidence for a crucial role of Sap1 and Sap2 in C. albicans vaginal infections.
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Felk, Angelika, Marianne Kretschmar, Antje Albrecht, Martin Schaller, Sabine Beinhauer, Thomas Nichterlein, Dominique Sanglard, Hans C. Korting, Wilhelm Schäfer i Bernhard Hube. "Candida albicans Hyphal Formation and the Expression of the Efg1-Regulated Proteinases Sap4 to Sap6 Are Required for the Invasion of Parenchymal Organs". Infection and Immunity 70, nr 7 (lipiec 2002): 3689–700. http://dx.doi.org/10.1128/iai.70.7.3689-3700.2002.

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ABSTRACT The ability to change between yeast and hyphal cells (dimorphism) is known to be a virulence property of the human pathogen Candida albicans. The pathogenesis of disseminated candidosis involves adhesion and penetration of hyphal cells from a colonized mucosal site to internal organs. Parenchymal organs, such as the liver and pancreas, are invaded by C. albicans wild-type hyphal cells between 4 and 24 h after intraperitoneal (i.p.) infection of mice. In contrast, a hypha-deficient mutant lacking the transcription factor Efg1 was not able to invade or damage these organs. To investigate whether this was due to the inability to undergo the dimorphic transition or due to the lack of hypha-associated factors, we investigated the role of secreted aspartic proteinases during tissue invasion and their association with the different morphologies of C. albicans. Wild-type cells expressed a distinct pattern of SAP genes during i.p. infections. Within the first 72 h after infection, SAP1, SAP2, SAP4, SAP5, SAP6, and SAP9 were the most commonly expressed proteinase genes. Sap1 to Sap3 antigens were found on yeast and hyphal cells, while Sap4 to Sap6 antigens were predominantly found on hyphal cells in close contact with host cells, in particular, eosinophilic leukocytes. Mutants lacking EFG1 had either noticeably reduced or higher expressed levels of SAP4 to SAP6 transcripts in vitro depending on the culture conditions. During infection, efg1 mutants had a strongly reduced ability to produce hyphae, which was associated with reduced levels of SAP4 to SAP6 transcripts. Mutants lacking SAP1 to SAP3 had invasive properties indistinguishable from those of wild-type cells. In contrast, a triple mutant lacking SAP4 to SAP6 showed strongly reduced invasiveness but still produced hyphal cells. When the tissue damage of liver and pancreas caused by single sap4, sap5, and sap6 and double sap4 and -6, sap5 and -6, and sap4 and -5 double mutants was compared to the damage caused by wild-type cells, all mutants which lacked functional SAP6 showed significantly reduced tissue damage. These data demonstrate that strains which produce hyphal cells but lack hypha-associated proteinases, particularly that encoded by SAP6, are less invasive. In addition, it can be concluded that the reduced virulence of hypha-deficient mutants is not only due to the inability to form hyphae but also due to modified expression of the SAP genes normally associated with the hyphal morphology.
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Tomida, Taichiro, Mutsuhiro Takekawa, Pauline O'Grady i Haruo Saito. "Stimulus-Specific Distinctions in Spatial and Temporal Dynamics of Stress-Activated Protein Kinase Kinase Kinases Revealed by a Fluorescence Resonance Energy Transfer Biosensor". Molecular and Cellular Biology 29, nr 22 (8.09.2009): 6117–27. http://dx.doi.org/10.1128/mcb.00571-09.

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ABSTRACT The stress-activated protein kinases (SAPKs), namely, p38 and JNK, are members of the mitogen-activated protein kinase family and are important determinants of cell fate when cells are exposed to environmental stresses such as UV and osmostress. SAPKs are activated by SAPK kinases (SAP2Ks), which are in turn activated by various SAP2K kinases (SAP3Ks). Because conventional methods, such as immunoblotting using phospho-specific antibodies, measure the average activity of SAP3Ks in a cell population, the intracellular dynamics of SAP3K activity are largely unknown. Here, we developed a reporter of SAP3K activity toward the MKK6 SAP2K, based on fluorescence resonance energy transfer, that can uncover the dynamic behavior of SAP3K activation in cells. Using this reporter, we demonstrated that SAP3K activation occurs either synchronously or asynchronously among a cell population and in different cellular compartments in single cells, depending on the type of stress applied. In particular, SAP3Ks are activated by epidermal growth factor and osmostress on the plasma membrane, by anisomycin and UV in the cytoplasm, and by etoposide in the nucleus. These observations revealed previously unknown heterogeneity in SAPK responses and supplied answers to the question of the cellular location in which various stresses induce stimulus-specific SAPK responses.
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Naglik, Julian R., George Newport, Theodore C. White, Lynette L. Fernandes-Naglik, John S. Greenspan, Deborah Greenspan, Simon P. Sweet, Stephen J. Challacombe i Nina Agabian. "In Vivo Analysis of Secreted Aspartyl Proteinase Expression in Human Oral Candidiasis". Infection and Immunity 67, nr 5 (1.05.1999): 2482–90. http://dx.doi.org/10.1128/iai.67.5.2482-2490.1999.

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ABSTRACT Secreted aspartyl proteinases are putative virulence factors inCandida infections. Candida albicans possesses at least nine members of a SAP gene family, all of which have been sequenced. Although the expression of the SAPgenes has been extensively characterized under laboratory growth conditions, no studies have analyzed in detail the in vivo expression of these proteinases in human oral colonization and infection. We have developed a reliable and sensitive procedure to detect C. albicans mRNA from whole saliva of patients with oral C. albicans infection and those with asymptomaticCandida carriage. The reverse transcription-PCR protocol was used to determine which of the SAP1 to SAP7genes are expressed by C. albicans during colonization and infection of the oral cavity. SAP2 and the SAP4to SAP6 subfamily were the predominant proteinase genes expressed in the oral cavities of both Candida carriers and patients with oral candidiasis; SAP4, SAP5, orSAP6 mRNA was detected in all subjects. SAP1and SAP3 transcripts were observed only in patients with oral candidiasis. SAP7 mRNA expression, which has never been demonstrated under laboratory conditions, was detected in several of the patient samples. All seven SAP genes were simultaneously expressed in some patients with oral candidiasis. This is the first detailed study showing that the SAP gene family is expressed by C. albicans during colonization and infection in humans and that C. albicans infection is associated with the differential expression of individualSAP genes which may be involved in the pathogenesis of oral candidiasis.
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Cambien, Béatrice, Manuel Pomeranz, Marie-Ange Millet, Bernard Rossi i Annie Schmid-Alliana. "Signal transduction involved in MCP-1–mediated monocytic transendothelial migration". Blood 97, nr 2 (15.01.2001): 359–66. http://dx.doi.org/10.1182/blood.v97.2.359.

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Abstract Monocyte chemoattractant protein-1 (MCP-1) is a major chemoattractant for monocytes and T lymphocytes. The MonoMac6 cell line was used to examine MCP-1 receptor-mediated signal transduction events in relation to MCP-1–mediated monocytic transendothelial migration. MCP-1 stimulates, with distinct time courses, extracellular signal-related kinases (ERK1 and ERK2) and stress-activated protein kinases (SAPK1/JNK1 and SAPK2/p38). SAPK1/JNK1 activation was blocked by piceatannol, indicating that it is regulated by Syk kinase, whereas SAPK2/p38 activation was inhibited by PP2, revealing an upstream regulation by Src-like kinases. In contrast, ERK activation was insensitive to PP2 and piceatannol. Pertussis toxin, a blocker of Go/Gi proteins, abrogated MCP-1–induced ERK activation, but was without any effect on SAPK1/JNK1 and SAPK2/p38 activation. These results underscore the major implication of Go/Gi proteins and nonreceptor tyrosine kinases in the early MCP-1 signaling. Furthermore, MCP-1–mediated chemotaxis and transendothelial migration were significantly diminished by a high concentration of SB202190, a broad SAPK inhibitor, or by SB203580, a specific inhibitor of SAPK2/p38, and abolished by pertussis toxin treatment. Altogether, these data suggest that coordinated action of distinct signal pathways is required to produce a full response to MCP-1 in terms of monocytic locomotion.
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ADAM, Dieter, Andrea RUFF, Astrid STRELOW, Katja WIEGMANN i Martin KRÖNKE. "Induction of stress-activated protein kinases/c-Jun N-terminal kinases by the p55 tumour necrosis factor receptor does not require sphingomyelinases". Biochemical Journal 333, nr 2 (15.07.1998): 343–50. http://dx.doi.org/10.1042/bj3330343.

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Ceramide has been implicated in the activation of stress-activated protein kinases/c-Jun N-terminal kinases (SAPK/JNK). Binding of tumour necrosis factor (TNF) to its 55 kDa receptor (TR55) leads to the generation of ceramide through activation of either acid or neutral sphingomyelinase (A/N-SMase) as well as to potent activation of SAPK/JNK. We have examined a putative role of both N- and A-SMase in the TR55-dependent activation of SAPK/JNK. The analysis of TR55 deletion mutants expressed in 70Z/3 pre-B cells revealed that activation of SAPK/JNK occurs independently of N-SMase. Although both SAPK/JNK and A-SMase are activated by the death domain of TR55, pharmacological prevention of the TR55-dependent activation of A-SMase, or proteolytic degradation of A-SMase in 70Z/3 cells, did not impair SAPK/JNK activation, indicating that SAPK/JNK are not secondary to A-SMase. In addition, proteolytic degradation of A-SMase also did not affect SAPK/JNK activation by ultraviolet (UV-C) irradiation, arguing against a general role of A-SMase in stress-mediated responses. Furthermore, fibroblasts from Niemann–Pick A patients deficient in A-SMase did not show altered activation of SAPK/JNK in response to either TNF or UV-C. These results suggest that TR55 can activate SAPK/JNK without direct participation of sphingomyelinases or ceramide.
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Fritz, Gerhard, i Bernd Kaina. "Late Activation of Stress Kinases (SAPK/JNK) by Genotoxins Requires the DNA Repair Proteins DNA-PKcs and CSB". Molecular Biology of the Cell 17, nr 2 (luty 2006): 851–61. http://dx.doi.org/10.1091/mbc.e05-07-0606.

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Although genotoxic agents are powerful inducers of stress kinases (SAPK/JNK), the contribution of DNA damage itself to this response is unknown. Therefore, SAPK/JNK activation of cells harboring specific defects in DNA damage-recognition mechanisms was studied. Dual phosphorylation of SAPK/JNK by the genotoxin methyl methanesulfonate (MMS) occurred in two waves. The early response (≤2 h after exposure) was similar in cells knockout for ATM, PARP, p53, and CSB or defective in DNA-PKcs compared with wild-type cells. The late response however (≥4 h), was drastically reduced in DNA-PKcs and Cockayne's syndrome B (CSB)-deficient cells. Similar results were obtained with human cells lacking DNA-PKcs and CSB. Activation of SAPK/JNK by MMS was not affected upon inhibition of base excision repair (BER), indicating base damage itself does not signal to SAPK/JNK. Because SAPK/JNK activation was attenuated in nongrowing cells, DNA replication-dependent processing of lesions, involving DNA-PKcs and CSB, appears to be required. DNA-PKcs coprecipitates with SEK1/MKK4 and SAPK/JNK, supporting a role of DNA-PKcs in SAPK/JNK activation. In this process, Rho GTPases are involved since inhibition of Rho impairs MMS-induced signaling to SAPK/JNK. The data show that sensing of DNA damage by DNA-PKcs and CSB causes a delayed SEK1/MKK4-mediated dual phosphorylation of SAPK/JNK.
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Wu, Qihan. "Dual Specificity Phosphotase 18, Interacting with SAPK, Dephosphorylates SAPK and Inhibits SAPK/JNK Signal Pathway in vivo". Frontiers in Bioscience 11, nr 1 (2006): 2714. http://dx.doi.org/10.2741/2001.

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Chen, Guofeng, Baoqiang Liu, Jiajun Chen, Hongyu Liu, Beiping Tan, Xiaohui Dong, Qihui Yang, Shuyan Chi, Shuang Zhang i Min Yao. "Supplementing Sulfate-Based Alginate Polysaccharide Improves Pacific White Shrimp (Litopenaeus vannamei) Fed Fishmeal Replacement with Cottonseed Protein Concentrate: Effects on Growth, Intestinal Health, and Disease Resistance". Aquaculture Nutrition 2022 (8.02.2022): 1–21. http://dx.doi.org/10.1155/2022/7132362.

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Sulfate-based alginate polysaccharide (SAP) is a novelty marine prebiotic. To investigate the beneficial effects of SAP in Pacific white shrimp (Litopenaeus vannamei) fed low-fishmeal diets, six diets (whole fishmeal group: FM; fishmeal replacement with cottonseed protein concentrate and SAP supplementary groups: SAP0, SAP1, SAP2, SAP3, and SAP4) were formulated and fed shrimp for 56 days. The results showed that SAP2 and SAP3 groups reached the best weight gain and specific growth rate ( P < 0.05 ). In serum, the activities of lysozyme and acid phosphatase showed the trend of firstly increased and then decreased ( P < 0.05 ). In the gut, the highest activities of trypsin, lipase, and amylase were found in SAP2 and SAP3 groups ( P < 0.05 ); the histological indexes gradually improved with SAP levels increased ( P < 0.05 ); sequencing of microbiota revealed that the composition and structure of microbiota have been improved, especially in the decreasing abundance of Vibrio, Pseudoalteromonas, and Candidatus Bacilloplasma at genus level. Besides, transcriptomics revealed a degree of similarity in differential gene expression patterns in shrimp; the comparison of RNA-Seq and qRT-PCR verified that SAP improved antioxidant and immunity in shrimp. The challenge revealed that SAP strengthened the resistance against Vibrio parahaemolyticus. Totally, the supplementary SAP to low-fishmeal diets improved growth, intestinal health, and disease resistance in shrimp. Based on the polynomial curve analysis of specific growth rate among SAPs groups, the optimum SAP supplementary level was 1.91%.
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Yoshida, Kiyotsugu, Ralph Weichselbaum, Surender Kharbanda i Donald Kufe. "Role for Lyn Tyrosine Kinase as a Regulator of Stress-Activated Protein Kinase Activity in Response to DNA Damage". Molecular and Cellular Biology 20, nr 15 (1.08.2000): 5370–80. http://dx.doi.org/10.1128/mcb.20.15.5370-5380.2000.

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ABSTRACT The cellular response to DNA damage includes activation of the nuclear Lyn protein tyrosine kinase. Using cells deficient in Lyn expression, the present studies demonstrate that Lyn is required in part for induction of the stress-activated protein kinase (SAPK) in the response to 1-β-d-arabinofuranosylcytosine (ara-C) and other genotoxic agents. By contrast, exposure of Lyn-deficient cells to ara-C, ionizing radiation, or cisplatin had no effect on activation of extracellular signal-regulated protein kinase or p38 mitogen-activated protein kinase. Similar findings were obtained in cells stably expressing a kinase-inactive, dominant-negative Lyn(K-R) mutant. Coexpression studies demonstrate that Lyn, but not Lyn(K-R), induces SAPK activity. In addition, the results demonstrate that Lyn activates SAPK by an MKK7-dependent, SEK1-independent mechanism. As MEKK1 functions upstream to MKK7 and SAPK, the finding that a dominant-negative MEKK1(K-M) mutant blocks Lyn-induced SAPK activity supports involvement of the MEKK1→MKK7 pathway. The results also demonstrate that inhibition of Lyn-induced SAPK activity abrogates the apoptotic response of cells to genotoxic stress. These findings indicate that activation of SAPK by DNA damage is mediated in part by Lyn and that the Lyn→MEKK1→MKK7→SAPK pathway is functional in the induction of apoptosis by genotoxic agents.
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Rozprawy doktorskie na temat "SAPK"

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Girardin, Stephen. "Régulation de la voie de signalisation intracellulaire JNK/SAPK". Université Louis Pasteur (Strasbourg) (1971-2008), 2001. http://www.theses.fr/2001STR13179.

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Carbonell, Núñez Caterina 1987. "Regulation of alternative splicing by the p38 SAPK in response to stress". Doctoral thesis, Universitat Pompeu Fabra, 2016. http://hdl.handle.net/10803/664502.

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Cells have the ability to respond and adapt to environmental changes through activation of stress-activated protein kinases (SAPKs). Activation of the p38 SAPK is critical to elicit the early gene expression program required for cell adaptation to stress. Alternative splicing (AS) is a crucial mechanism for gene regulation that has been shown to be modulated in response to a wide range of extracellular stimuli. However, the mechanisms behind AS regulation and the functional consequences of differential isoform expression in stress conditions remain largely unknown. In this study, we identified novel associations between p38 and the splicing machinery, providing mechanisms by which p38 regulates AS. Furthermore, characterization of protein isoforms produced by p38-dependent AS give an insight into the biological relevance of this regulation in adaptation to environmental stresses. Altogether, the results of this thesis highlight a role for SAPK signaling pathways in adaptation to environmental changes through AS modulation.
Les cèl·lules tenen l'habilitat de detectar i respondre a les fluctuacions en el seu entorn a través de l'activació de les proteïnes quinasa activades per estrès (SAPKs). L'activació de la SAPK p38 és essencial per activar el programa d'expressió gènica necessari perquè les cèl·lules s’adaptin als estímuls extracel·lulars. El processament alternatiu del pre-ARNm és un mecanisme de regulació gènica crucial que es regula en resposta a diferents canvis en l'ambient. No obstant, els mecanismes moleculars pels quals es regula, així com la funció de les diferents isoformes de les proteïnes que s'expressen en resposta a estrès no es coneixen. En conjunt, els resultats presentats en aquesta tesis proporcionen una nova visió dels mecanismes pels quals p38 modula el processament alternatiu del pre-ARNm en resposta a estrès i posen en evidència la importància d'aquest mecanisme per l'adaptació de la cèl·lula a canvis en l'ambient extracel·lular.
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Bellini, Angela. "Rôle des voies de réponse au stress dans le maintien de la stabilité génomique chez la levure Schizosaccharomyces pombe". Thesis, Paris 11, 2012. http://www.theses.fr/2012PA11T048/document.

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Le génome est sans cesse menacé dans sa structure par des stress génotoxiques d’origine endogène (stress oxydant, blocage de la réplication…) ou exogène (irradiations, produits chimiques, métaux lourds…). La voie de réponse aux dommages de l’ADN coordonne un réseau d’événements en cascades qui incluent les points de surveillance du cycle cellulaire, la réplication/réparation/recombinaison de l’ADN et la mort cellulaire programmée. Ces voies collaborent pour assurer la transmission fidèle du génome et empêcher la prolifération des cellules qui aurait accumulé des altérations génétiques. En général, des défauts dans une de ces voies entraînent un changement de sensibilité aux agents génotoxiques, une instabilité génétique et une prédisposition au cancer. La recombinaison homologue (RH) est une voie essentielle pour la réparation de l’ADN ; elle joue un rôle fondamental dans le maintien de la stabilité du génome. Le stress oxydant, résultant d’une augmentation de la concentration intracellulaire de ERO, est une des causes majeures de dommages aux lipides, aux protéines et à l’ADN et pour cela, il représente un défi pour la survie cellulaire et pour la stabilité du génome. Les ERO apparaissent physiologiquement lors de la respiration cellulaire ou résultent d’un stress environnemental, comme l’exposition aux radiations UV ou agents chimiques oxydants. Elles contribuent à certains processus comme la croissance cellulaire, l’activité et au repliement des protéines, la sénescence et la mort cellulaire programmée. Il est important de souligner qu’un état redox altéré est souvent associé à un fonctionnement anormal des cellules, comme il est observé pour les cellules cancéreuses et les cellules sénescentes. L’objectif de ce projet a été d’analyser l’interface entre les voies DDR et SAPK (Stress activated protein kinase) évolutivement conservées et d’en étudier les conséquences sur la stabilité du génome en utilisant comme organisme modèle la levure à fission. Nos résultats montrent que la voie SAPK joue un rôle sur la RH en promouvant la phosphorylation de Rad52, une protéine impliquée dans différentes sous-voies de la RH. Nous avons aussi montré que Rad52 est phosphorylée sur différents acides aminés, parmi lesquels certains sont les cibles de kinases inconnues qui n’ont aucun lien avec la voie SAPK. Nous avons observé que Rad52 est phosphorylée soit après un stress oxydant, soit dans des cellules génétiquement sujettes à des perturbations de la RH. Nous avons identifié deux sites de phosphorylation de la protéine Rad52, dont un seul est dépendant de la voie SAPK. En étudiant la phosphorylation de Rad52 dans les cellules invalidées pour la voie SAPK ou mutées pour un des sites de phosphorylation de Rad52, nous avons pu montrer que la RH est modulée par la voie SAPK même en absence de insulte externe. Notre travail ouvre le chemin vers une nouvelle compréhension des mécanismes fondamentaux du maintien de l’intégrité du génome
Genomes are routinely submitted to injuries from either endogenous stress (oxidative stress, DNA replication block…) or from exogenous sources (radiations, chemicals, heavy metals…). The DNA damage response (DDR) coordinates a network of pathways including cell cycle checkpoints, DNA replication/repair/recombination, and programmed cell death, ensuring faithful genome transmission and preventing from the proliferation of cells bearing genetic alterations. Defect in one of these pathways generally results in altered sensitivity to genotoxins, genetic instability and cancer predisposition. Homologous recombination (HR) is an essential DNA repair pathway playing pivotal role to maintain genome stability.Oxidative stress, resulting from increased intracellular concentration of ROS, is one of the major causes of lipid, protein and DNA damage, and therefore a challenge for cell survival and genome stability. ROS are generated physiologically as by-products of cellular respiration, or as result of environmental stresses, such as exposure to solar UV radiations or to oxidant chemicals, and they actively participate in processes such as cellular growth, protein activity and folding, senescence and programmed cell death. It is noteworthy that an altered redox homeostasis is often associated to abnormally functioning cells, such as cancer and senescent cells. The aim of this project was to study the interface between two major evolutionarily conserved pathways, DDR and SAPK (Stress activated protein kinase) and the consequences on genome stability using fission yeast as a model organism. We report data showing that SAPK pathway impinges on HR by promoting phosphorylation of Rad52, a key protein involved in all sub-pathways of HR. We also revealed that Rad52 is phosphorylated at multiple different sites some of which are substrate for unidentified kinases unrelated to the SAPK pathway. Rad52 phosphorylation occurs either after oxidative stress or in cells genetically prone to HR perturbation. We identified two sites of phosphorylation, one of which is dependent on functional SAPK pathway. By studying Rad52 phosphorylation in cells mutated in the SAPK pathway or mutated at the Rad52 site of phosphorylation, we showed that HR is modulated by SAPK even in the absence of external insults. Our work pave the way to a novel understanding of fundamental mechanisms required for genome integrity maintenance
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Krestow, Julia Katherine Ellen. "Functional dissociation of SAPK and apoptosis in epithelial and endothelial cells, implications for anoikis". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape2/PQDD_0026/MQ50416.pdf.

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ICHIKAWA, KENJI, TAKANORI NAKAMURA, YUJI KUBOTA i MUTSUHIRO TAKEKAWA. "REGULATION OF STRESS-ACTIVATED MAP KINASE PATHWAYS DURING CELL FATE DECISIONS". Nagoya University School of Medicine, 2011. http://hdl.handle.net/2237/14910.

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Böhm, Markus. "Klonierung, Charakterisierung und Funktion der beiden SAPK-Mitglieder JNK und p38 MAPK des marinen Schwamms S. domuncula". [S.l. : s.n.], 2001. http://ArchiMeD.uni-mainz.de/pub/2002/0019/diss.pdf.

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Adrover, Nadal Miguel Angel. "Qualitative and quantitative study of the effect of osmotress on cell cycle of Saccharomyces cerevisiae". Doctoral thesis, Universitat Pompeu Fabra, 2009. http://hdl.handle.net/10803/7211.

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Control of cell cycle by Stress Activated Protein Kinases (SAPKs) is an essential aspect for adaptation to extracellular stimuli. In Saccharomyces cerevisiae, the activation of the Hog1 SAPK, results in a delayed transcription of the G1 cyclins CLN1,2 and the stabilization of the B-type cyclin inhibitor SIC1, therefore postponing entry into S phase. The results displayed here, show, by a combination of mathematical modelling and quantitative in vivo experiments, that, before Start, the control of G1-S transition is mainly exerted by inhibiting expression of cyclins, both G1 (CLN1,2) and S phase (CLB5,6) cyclins. On the other hand, after Start, it is the phosphorylation and stabilization of Sic1 by Hog1 that becomes imperative to prevent inadequate firing of replication before adaptation. Therefore, we found that there is a distinct temporal role for Sic1 and cyclins on the G1 regulation by a SAPK in response to stress. We have also found that Hog1 induces a G2 delay, by down-regulating CLB2 transcription and phosphorylating Hsl1 to promote Hsl7 delocalization and subsequent accumulation of Swe1, an inhibitor of Clb1,2-Cdc28, and thus postponing anaphase. Altogether, we demonstrate novel Systems Biology approaches are useful to better understand how an intracellular signalling pathway incises on cell cycle control, beyond a mechanistic description, as well as showing how a single MAPK modulates different cell cycle checkpoints to improve cell survival upon stress.
El control del cicle cel·lular per Proteïna Cinases Activades per Estrès (SAPKs) es un aspecte essencial per a l'adaptació als estímuls extracel·lulars. A Saccharomyces cerevisiae, l'activació de la SAPK Hog1, resulta en un retardament de la transcripció de les ciclines de G1 (CLN1,2) i l'estabilització del inhibidor de les ciclines del tipus B, SIC1, i per tant posposa l'entrada en fase S. Els resultats que aquí s'exposen, mostren, mitjançant la combinació de modelatge matemàtic i experiments quantitatius in vivo, que, abans d'Start, el control de la transició es duu a terme principalment inhibint l'expressió de les ciclines, tant les de G1 (CLN1,2) com les de la fase S (CLB5,6). Per altra banda, després d'Start, la fosforilació i estabilització de Sic1 per part de Hog1 esdevé un fet necessari per a prevenir la iniciació de la replicació abans d'adaptar-se. Per tant, hem descobert aquí que la regulació de Sic1 i les ciclines juguen un paper diferent segons el moment en que apareix l'estrès. Hem descrit també, que Hog1 produeix una parada a G2 a través de la inhibició de la transcripció de CLB2 i la fosforilació d'Hsl1, la qual promou la deslocalització d'Hsl7 i la subsegüent estabilització de Swe1, un inhibidor específic de Clb1,2-Cdc28, i d'aquesta manera es posposa l'entrada en Anafase. Tot plegat, demostra que l'ús d'aproximacions pròpies de la Biologia de Sistemes és útil per a entendre de quina forma una via de senyalització intracel·lular incideix sobre el control del cicle cel·lular, mes enllà de la pura descripció de la mecànica del sistema. D'aquesta forma, proposem que una sola MAPK modula distints punts de control del cicle cel·lular per millorar la probabilitat de supervivència en front de l'estrès osmòtic.
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Schroder, Wayne Ashley. "Cloning and Characterisation of the Human SinRIP Proteins". Thesis, Griffith University, 2003. http://hdl.handle.net/10072/366190.

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This thesis describes the cloning and characterisation of a novel human gene and its protein products, which have been designated SAPK- and Ras-interacting protein (SinRIP). SinRIP shares identity with JC310, a partial human cDNA that was previously identified a candidate Ras-inhibitor (Colicelli et al., 1991, Proc Natl Acad Sci USA 88, p. 2913). In this study, it was shown that SinRIP is a member of an orthologous family of proteins that is conserved from yeast to mammals and contains proteins involved in Ras- and SAPK-mediated signalling pathways. Comparison of this family of proteins showed that human SinRIP contains a potential Ras-binding domain (RBD; residues 279-354), a PH-like domain (PHL; 376-487), and a highly conserved novel region designated the CRIM (134-265). Several other potential targeting sites, such as nuclear localisation signals and target sites for kinases, were identified within the SinRIP sequence. The human SinRIP gene is unusually large (>280 kbp) and is located on chromosome 9 at 9q34. SinRIP mRNA was detected in a wide variety of tissue-types and cell lines by RT-PCR, and the SinRIP sequences in the EST database were derived from an diverse array of tissues, suggesting a widespread or ubiquitous expression. Northern blot analysis revealed the highest levels in skeletal muscle and heart tissue. However, the steady-state levels of SinRIP mRNA vary greatly from cell to cell, and SinRIP expression is likely to be regulated at multiple post-transcriptional levels. It was shown that SinRIP mRNA is likely to be translated inefficiently by the normal cap-scanning mechanism, due to the presence of a GC-rich and structured 5’-UTR, which also contains upstream ORFs. Alternative polyadenylation signals in the SinRIP 3’-UTR can be used, resulting in the expression of short and long SinRIP mRNA isoforms. Several potential A/T-rich regulatory elements were also identified in SinRIP mRNA, which may target specific SinRIP mRNA isoforms for rapid degradation. Importantly, it was shown that SinRIP mRNA is alternatively spliced, resulting in the production of distinct SinRIP protein isoforms. Three isoforms, SinRIP2-4, were definitively identified by RT-PCR and full-length cloning. The SinRIP isoforms contain deletions in conserved regions, and are likely to have biochemical characteristics that are different to full-length SinRIP1. SinRIP2 is C-terminally truncated and lacks the PHL domain and part of the RBD, and relatively high levels of SinRIP2 expression arelikely to occur in kidneys. The RBD is disrupted in SinRIP3, but all other domains are intact, and RT-PCR analyses suggest that SinRIP3 is present in some cells at levels comparable to SinRIP1. A rabbit polyclonal antiserum against SinRIP was generated and detected endogenous SinRIP proteins. Using the anti-SinRIP antibody in immunoblots, multiple SinRIP isoforms were observed in most cell types. SinRIP1 and another endogenous SinRIP protein, likely to be SinRIP3, were detected in most cell lines, and appear to be are the major SinRIP proteins expressed in most cells. The subcellular localisation of both recombinant and endogenous SinRIP proteins was investigated by immunofluorescence assays and biochemical fractionation. Recombinant SinRIP1 protein was found in the cytoplasm and associated with the plasma membrane. In contrast, the SinRIP2 protein was predominantly nuclear, with only low-level cytoplasmic staining observed. The endogenous SinRIP proteins, likely to comprise these and other SinRIP isoforms, were found in both the nucleus and cytoplasm. SinRIP1 interacted with GTP-bound (active) Ras, but not GDP-bound (inactive) Ras, in an in vitro assay, and also co-localised with activated H- and K-Ras in cells. The binding profile observed is typical of Ras-effectors, and SinRIP did not inhibit signalling by the Ras proteins, suggesting that it is not likely to be a Ras-inhibitor. It was also shown that SinRIP1 and SinRIP2 both interact and colocalise with c-Jun NH2- terminal kinase (JNK). Both SinRIP proteins were able to recruit JNK to their respective sub-cellular compartments. These interactions suggest an adaptor role for SinRIP in the Ras and/or JNK pathways. In addition, Sam68 was isolated as a SinRIP-binding protein in a yeast two-hybrid screen. Sam68 was shown to colocalise with SinRIP2 and endogenous SinRIP proteins, but not SinRIP1. Further colocalisation studies showed that endogenous SinRIP proteins localise in nuclear structures that may be associated with pre-mRNA splicing. Likely functions for SinRIP, as indicated by experimental results and studies of the orthologues of SinRIP in other species, are discussed.
Thesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Biomolecular and Biomedical Sciences
Faculty of Science
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Helbig, Lars [Verfasser]. "Aktivierung von c-Jun-N-terminalen Kinasen (SAPK,JNK) als Teil der späten Cisplatin abhängigen DNA-Schadensantwort / Lars Helbig". Mainz : Universitätsbibliothek Mainz, 2013. http://d-nb.info/1034965247/34.

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Wang, Shu-Zong. "Cloning and characterization of SAPK interacting protein 1 (SIN1), a type 1 IFN receptor subunit 2 (IFNAR2)-interacting protein /". Free to MU Campus, others may purchase, 2004. http://wwwlib.umi.com/cr/mo/fullcit?p3137761.

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Książki na temat "SAPK"

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Hawkes, Ken. Sark. Vale, Guernsey: Guernsey Press, 1992.

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John, Kinsella. Sack. Fremantle, W.A: Fremantle Press, 2014.

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Mattingley, Christobel. Sack. London: Puffin Books, 1993.

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Sapo. Corvallis, Ore: Ecopress, 1996.

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Remphry, Martin. Sark folklore. Sark: Gateway Publishing Ltd, 2003.

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Mustaffa, Faisal. Sapu Malaysia. Petaling Jaya, Selangor: Orange Dove, 2010.

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Reese, Bob. Sack lunch. Chicago: Childrens Press, 1992.

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ill, Sandoval Gerardo 1974, i Fuentes Benny ill, red. Sack attack! Mankato, Minn: Stone Arch Books, 2012.

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Lalji. Sapt Suran. Ranchi: Sindhi-Smriti, 2005.

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McLeese, Don. Jonas Salk. Vero Beach, Fla: Rourke Pub., 2006.

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Części książek na temat "SAPK"

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Chadee, Deborah N., i John M. Kyriakis. "Activation of SAPK/JNKs In Vitro". W MAP Kinase Signaling Protocols, 59–73. Totowa, NJ: Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60761-795-2_3.

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Nishina, Hiroshi, Tomomi Watanabe, Kentaro Nakagawa, Shinya Ohata, Satoshi Asaka i Toshiaki Katada. "SAPK/JNK Signaling Participates in Embryonic Hepatoblast Proliferation via a Pathway Different from NF-κB-Induced Anti-Apoptosis". W Stem Cell and Liver Regeneration, 1–14. Tokyo: Springer Japan, 2004. http://dx.doi.org/10.1007/978-4-431-53971-1_1.

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Zhang, Jinling, Yinghua Lu, Lin Wang, Hongxin Zhang, Bo Zhang, Yeqiu Wang, Kai Wu i Stefan Wolfl. "Uncentered (Absolute) Correlation Clustering Method Fit for Establishing Theoretical SAPK/JNK Signaling Pathway in Human Soft Tissue Sarcoma Samples". W Intelligent Data Engineering and Automated Learning – IDEAL 2006, 1329–36. Berlin, Heidelberg: Springer Berlin Heidelberg, 2006. http://dx.doi.org/10.1007/11875581_158.

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Montoya, Richard. "Sapo". W Reclaiming Greek Drama for Diverse Audiences, 277–325. London ; New York : Routledge, 2020.: Routledge, 2020. http://dx.doi.org/10.4324/9780429470448-14.

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Zeytinoglu, Arkan, i Manuela Hötzl. "Saak". W Geometry of Light, 124–25. Vienna: Springer Vienna, 2011. http://dx.doi.org/10.1007/978-3-7091-0539-9_15.

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Mahadevan, Malathi. "Joseph Sack". W Data Professionals at Work, 183–95. Berkeley, CA: Apress, 2018. http://dx.doi.org/10.1007/978-1-4842-3967-4_15.

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Korte, Hermann. "Sack, Gustav". W Kindlers Literatur Lexikon (KLL), 1. Stuttgart: J.B. Metzler, 2020. http://dx.doi.org/10.1007/978-3-476-05728-0_19104-1.

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Vermeulen, Jeroen. "Edward Sapir". W Handbook of Pragmatics, 1–16. Amsterdam: John Benjamins Publishing Company, 2000. http://dx.doi.org/10.1075/hop.4.sap1.

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Zwißler, Sonja. "SAP". W Xpert.press, 389–417. Berlin, Heidelberg: Springer Berlin Heidelberg, 2002. http://dx.doi.org/10.1007/978-3-642-45777-7_15.

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Kagermann, Henning, i Christopher Sorek. "SAP". W Deutsche Standards, 280–83. Wiesbaden: Gabler Verlag, 2005. http://dx.doi.org/10.1007/978-3-322-82497-4_67.

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Streszczenia konferencji na temat "SAPK"

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Andrade, Pamela V., Mariana T. Ruckert, Carlos Alberto O. Biagi Junior i Vanessa S. Silveira. "Abstract C51: Targeted inhibition of DUSP1 and DUSP6 suppresses pancreatic adenocarcinoma cells’ growth and glucose metabolism via SAPK/JNK pathway activation". W Abstracts: AACR Special Conference on Pancreatic Cancer: Advances in Science and Clinical Care; September 6-9, 2019; Boston, MA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.panca19-c51.

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Chancellor, Cody, i Mahmoud Elsharafi. "Swelling and Deswelling Kinetics of Superabsorbent Polymer". W ASME 2016 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2016. http://dx.doi.org/10.1115/imece2016-68042.

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In the oil industry, techniques that decrease unwanted water production have drawn large amounts of interest from many companies. During water injection operations, water is injected into the reservoir in order to extract oil remaining in the formation. Due to the heterogeneity in the reservoir formation, oil production will decline and water production will increase as the injected water sweeps the high permeability zones. In order to flush out the oil remaining in the low permeability zones, many treatments have been used. One such treatment involves the injection of a superabsorbent polymer (SAP) into the high permeability zones. The swelled polymer will decrease heterogeneity in the reservoir’s permeability, thus forcing injected water into the oil rich, unswept zones/areas of the formation. Proper application of an SAP can have a dramatic impact on both the production and lifespan of mature oil wells. Understanding the swelling and deswelling kinetics of the SAP is crucial to its application. The following work focused on the use of AT-O3S polymer, a Sodium salt of crosslinked polyacrylic acid purchased from Emerging Technologies®. The polymer had a particle size of 35 to 60 meshes, or 250 to 500 microns. The swelling and deswelling ratio of such a polymer is heavily influenced by salinity, temperature, and pH. In order to study the polymer’s kinetics, 1% (for swelling) or 0.1% (for deswelling) by solution weight of polymer was allowed to swell and deswell over time in various brines. These brines were made up of deionized water, 1% to 20% (by wt.) Sodium Chloride, and/or 1% to 10% (by wt.) Calcium Chloride. The effect of temperature on the final swelling ratio was afterwards tested. Understanding the reaction of SAPs to conditions similar to those found in an oil formation can help the oil industry to utilize this tool with greater efficiency.
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Otto, Tilman P. "SAPL". W the 2002 conference. New York, New York, USA: ACM Press, 2002. http://dx.doi.org/10.1145/602231.602250.

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Bhojwani, Praveen S., Jason D. Lee i Rabi N. Mahapatra. "SAPP". W the 2007 international symposium. New York, New York, USA: ACM Press, 2007. http://dx.doi.org/10.1145/1283780.1283852.

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Dreossi, Tommaso. "Sapo". W HSCC '17: 20th International Conference on Hybrid Systems: Computation and Control. New York, NY, USA: ACM, 2017. http://dx.doi.org/10.1145/3049797.3049824.

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Lidiyawati, Anna, Binti Khopsoh i Riska Faradila. "Kejadian Mastitis Subklinis Pada Induk Sapi Perah Laktasi di Desa Sumbersari Kecamatan Udanawu Kabupaten Blitar". W Kedaulatan Pangan Nasional Melalui Pengembangan Potensi Ternak Lokal di Era Kenormalan Baru. Animal Science : Polije Proceedings Series, 2020. http://dx.doi.org/10.25047/proc.anim.sci.2020.12.

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Penelitian ini bertujuan untuk mendeskripsikan jumlah induk sapi perah laktasi yang terindikasi mastitis subklinis di Desa Sumbersari Kecamatan Udanawu Kabupaten Blitar. Metode survei dan wawancara dilakukan terhadap 12 peternak sapi perah dengan kriteria responden adalah peternak sapi perah yang telah memelihara sapi perah selama 2 tahun. Jumlah sapi perah yang diperiksa menggunakan uji mastitis California (CMT) adalah 136 ekor dan dilakukan wawancara terhadap peternak tentang cara pencegahan yang sudah dilakukan dalam mengurangi kejadian mastitis subklinis. Data yang terkumpul kemudian dianalisa menggunakan Analisa deskriptif. Hasil penelitian menunjukkan 41,91% induk laktasi ternyata terindikasi mastitis subklinis. Sisanya 58,08 % induk laktasi dalam kondisi yang sehat tidak ditemukan mastitis klinis. Pencelupan antiseptik pasca pemerahan dilakukan kepada 20 induk sapi sebagai perlakuan sedangkan sisanya 116 ekor hanya dilakukan pembilasan. Belum ditemukan peternak sapi perah yang memberikan treatment pada masa kering dan cek mastitis secara berkala, peternak hanya berfokus pada penambahan pakan untuk induk sebagai persiapan sebelum melahirkan. Untuk mengurangi kejadian mastitis maka perlu adanya edukasi ditingkat peternak berkaitan dengan penanganan susu, teat dips, treatment masa kering dan tes mastitis secara berkala.
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Zahran, Ahmed H., Jason J. Quinlan, K. K. Ramakrishnan i Cormac J. Sreenan. "SAP". W MMSys'17: Multimedia Systems Conference 2017. New York, NY, USA: ACM, 2017. http://dx.doi.org/10.1145/3083187.3083199.

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Huang, Scott C. H., Hao Zhu i Wensheng Zhang. "SAP". W the 3rd international conference. New York, New York, USA: ACM Press, 2006. http://dx.doi.org/10.1145/1185373.1185415.

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Triasih, Dyah, Erik Febrianto, Nurul Aqila Maulidya i Laily Tahajjudy. "Peran Serta Peternak Sapi Perah dalam Pengelolahan Biogas Menuju Daerah Zero Waste". W Kedaulatan Pangan Nasional Melalui Pengembangan Potensi Ternak Lokal di Era Kenormalan Baru. Animal Science : Polije Proceedings Series, 2020. http://dx.doi.org/10.25047/proc.anim.sci.2020.31.

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Penelitian ini bertujuan untuk mengetahui peran serta peternak dalam pengelolahan biogas menuju daerah zero waste desa Glagahagung, Kecamatan Purwoharjo, Kabupaten Banyuwangi, Jawa Timur. Penelitian ini dilaksanakan pada bulan Juni sampai dengan Agustus 2020, dengan mengambil sampel sekitar 35 responden dari peternak sapi perah sekaligus melakukan pendampingan tentang bagaimana cara pembuatan biogas dan pupuk yang berasal dari slurry biogas. Hasil penelitian ini menunjukkan bahwa peran peternak dalam pengelolaan limbah kotoran sapi cukup baik, hal ini dapat dilihat dari inisiatif yang sudah terbentuk, serta antusiasme peternak dalam mengolah limbah kotoran sapi menjadi biogas dan pupuk dari slurry dan keberhasilan peran masyarakat dalam mengelola limbah kotoran sapi secara komprehensif.
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Nafianda, Nezar, Mega Mila Panjuni, Hanung Pratiwi, Aan Awaludin, Dyah Laksito Rukmi i Theo Mahiseta Syahniar. "Kajian karakteristik peternak terhadap tingkat kebuntingan sapi potong di Kecamatan Nusawungu, Cilacap, Jawa Tengah". W The 2nd National Conference of Applied Animal Science (CAAS) 2021. Politeknik Negeri Jember, 2021. http://dx.doi.org/10.25047/animpro.2021.20.

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Penelitian ini bertujuan untuk mengevaluasi karakteristik peternak terhadap tingkat keberhasilan inseminasi buatan (IB) di Kecamatan Nusawungu, Kabupaten Cilacap, Jawa Tengah. Karakteristik peternak yang diamati antara lain usia, tingkat pendidikan, pekerjaan, pengalaman beternak, dan tingkat kemampuan peternak dalam mendeteksi birahi sapi. Koleksi data primer dilakukan dengan metode survei menggunakan kuisioner dan data sekunder melalui data rekording dari dinas peternakan terkait. Metode pengambilan sampel menggunakan random sampling. Data yang terkumpul ditabulasi, diolah, dan disajikan secara deskriptif. Hasil penelitian menunjukkan bahwa mayoritas peternak berusia 41-60 tahun (50%), tingkat pendidikan SMA/SMK (46%), pekerjaan sebagai petani (60%), dan pengalaman beternak sekitar 6-10 tahun (53%). Tingkat kemampuan peternak dalam mendeteksi birahi sapi sebesar 74% melalui tanda-tanda berupa sapi gelisah, bersuara, menaiki ternak lain, dan/atau keluar lendir bening dari vulva sapi. Hasil penelitian dapat disimpulkan bahwa karakteristik peternak dapat menjadi salah satu faktor yang mempengaruhi tingkat kebuntingan sapi potong rakyat di Kecamatan Nusawungu Kabupaten Cilacap.
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Raporty organizacyjne na temat "SAPK"

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Beck, Steve, i Joe Reynolds. Sensor Agent Processing Software (SAPS). Fort Belvoir, VA: Defense Technical Information Center, maj 2004. http://dx.doi.org/10.21236/ada423980.

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Respatiadi, Hizkia, i Hana Nabila. Reformasi Kebijakan Daging Sapi : Menghapus Pembatasan Perdagangan untuk Menurunkan Harga Daging Sapi di Indonesia. Jakarta, Indonesia: Center for Indonesian Policy Studies, 2017. http://dx.doi.org/10.35497/271871.

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Kramer, Mitchell. SAP NetWeaver Portal. Boston, MA: Patricia Seybold Group, kwiecień 2006. http://dx.doi.org/10.1571/pr4-20-06cc.

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Marshak, David. SAP Enterprise Portal. Boston, MA: Patricia Seybold Group, lipiec 2003. http://dx.doi.org/10.1571/pr7-11-03cc.

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Cline, Joseph I. Surface Absorption Polarization Sensors (SAPS), Final Technical Report, Laser Probing of Immobilized SAPS Actuators Component. Office of Scientific and Technical Information (OSTI), kwiecień 2010. http://dx.doi.org/10.2172/977056.

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Abstract book for SAPC ASM 2019. Chair John Campbell, Jose M. Valderas i Willie Hamilton. SAPC, lipiec 2019. http://dx.doi.org/10.37361/asm.2019.1.1.

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Richards, Suzanne. Abstract book for SAPC ASM 2021. Redaktorzy Richard Neal i Carolyn Chew-Graham. Society for Academic Primary Care, lipiec 2021. http://dx.doi.org/10.37361/asm.2021.1.1.

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Abstract book for SAPC ASM 2022. Chair Umesh Chauhan. Society for Academic Primary Care, sierpień 2022. http://dx.doi.org/10.37361/asm.2022.1.1.

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Boch, Patrick. Why SAP Security matters? Denmark: River Publishers, sierpień 2016. http://dx.doi.org/10.13052/popcas007.

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Marshak, David. SAP Enterprise Portal 6.0. Boston, MA: Patricia Seybold Group, grudzień 2003. http://dx.doi.org/10.1571/pr12-4-03cc.

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