Literatura académica sobre el tema "ALS inhibitor resistance"
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Artículos de revistas sobre el tema "ALS inhibitor resistance"
Beckie, Hugh J., Suzanne I. Warwick y Connie A. Sauder. "Basis for Herbicide Resistance in Canadian Populations of Wild Oat (Avena fatua)". Weed Science 60, n.º 1 (marzo de 2012): 10–18. http://dx.doi.org/10.1614/ws-d-11-00110.1.
Texto completoEberlein, Charlotte V., Mary J. Guttieri, Philip H. Berger, John K. Fellman, Carol A. Mallory-Smith, Donn C. Thill, Roger J. Baerg y William R. Belknap. "Physiological consequences of mutation for ALS-inhibitor resistance". Weed Science 47, n.º 4 (agosto de 1999): 383–92. http://dx.doi.org/10.1017/s0043174500091967.
Texto completoGuo, Jiaqi, Chance W. Riggins, Nicholas E. Hausman, Aaron G. Hager, Dean E. Riechers, Adam S. Davis y Patrick J. Tranel. "Nontarget-Site Resistance to ALS Inhibitors in Waterhemp (Amaranthus tuberculatus)". Weed Science 63, n.º 2 (junio de 2015): 399–407. http://dx.doi.org/10.1614/ws-d-14-00139.1.
Texto completoBeckie, Hugh J., Linda M. Hall, Scott Meers, James J. Laslo y F. Craig Stevenson. "Management Practices Influencing Herbicide Resistance in Wild Oat". Weed Technology 18, n.º 3 (septiembre de 2004): 853–59. http://dx.doi.org/10.1614/wt-03-124r.
Texto completoVaranasi, Vijay K., Jason K. Norsworthy, Chad Brabham y Robert C. Scott. "Characterization of Acetolactate Synthase (ALS)-Inhibitor Resistance in Pennsylvania smartweed (Persicaria pensylvanica)". Weed Science 66, n.º 6 (21 de septiembre de 2018): 710–14. http://dx.doi.org/10.1017/wsc.2018.44.
Texto completoBeckie, H. J., L. M. Hall, F. J. Tardif y G. Séguin-Swartz. "Acetolactate synthase inhibitor-resistant stinkweed (Thlaspi arvense L.) in Alberta". Canadian Journal of Plant Science 87, n.º 4 (1 de octubre de 2007): 965–72. http://dx.doi.org/10.4141/cjps06019.
Texto completoTranel, Patrick J., Chenxi Wu y Ahmed Sadeque. "Target-Site Resistances to ALS and PPO Inhibitors Are Linked in Waterhemp (Amaranthus tuberculatus)". Weed Science 65, n.º 1 (13 de diciembre de 2016): 4–8. http://dx.doi.org/10.1614/ws-d-16-00090.1.
Texto completoBeckie, Hugh J. y Xavier Reboud. "Selecting for Weed Resistance: Herbicide Rotation and Mixture". Weed Technology 23, n.º 3 (septiembre de 2009): 363–70. http://dx.doi.org/10.1614/wt-09-008.1.
Texto completoTseng, Te-Ming, Swati Shrestha, James D. McCurdy, Erin Wilson y Gourav Sharma. "Target-site Mutation and Fitness Cost of Acetolactate Synthase Inhibitor-resistant Annual Bluegrass". HortScience 54, n.º 4 (abril de 2019): 701–5. http://dx.doi.org/10.21273/hortsci13512-18.
Texto completoMolin, William T., Vijay K. Nandula, Alice A. Wright y Jason A. Bond. "Transfer and Expression of ALS Inhibitor Resistance from Palmer Amaranth (Amaranthus palmeri) to anA. spinosus×A. palmeriHybrid". Weed Science 64, n.º 2 (junio de 2016): 240–47. http://dx.doi.org/10.1614/ws-d-15-00172.1.
Texto completoTesis sobre el tema "ALS inhibitor resistance"
Iwakami, Satoshi. "Molecular mechanism of resistance in a multiple-herbicide resistant Echinochloa phyllopogon". Kyoto University, 2013. http://hdl.handle.net/2433/180368.
Texto completo0048
新制・課程博士
博士(農学)
甲第17830号
農博第2015号
新制||農||1016(附属図書館)
学位論文||H25||N4787(農学部図書室)
30645
京都大学大学院農学研究科農学専攻
(主査)教授 稲村 達也, 教授 冨永 達, 教授 奥本 裕
学位規則第4条第1項該当
Friesen, Lincoln Jacob Shane. "Identification of the mechanisms of wild radish herbicide resistance to PSII inhibitors, auxinics, and AHAS inhibitors". University of Western Australia. School of Plant Biology, 2008. http://theses.library.uwa.edu.au/adt-WU2008.0106.
Texto completoFerguson, Gabrielle Mary. "ALS-inhibitor resistance in populations of Amaranthus powellii S. Wats. and Amaranthus retroflexus L". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape2/PQDD_0023/MQ51062.pdf.
Texto completoWeerasooriya, Dilooshi Kumari. "Genetic analysis of interveinal chlorosis and reduced seedling vigor as related to agronomic performance in sorghum resistant to ALS inhibitor herbicides". Diss., Kansas State University, 2016. http://hdl.handle.net/2097/32896.
Texto completoDepartment of Agronomy
Tesfaye T. Tesso
The lack of effective post-emergence weed control options is often highlighted as one of the major factors behind dwindling acreage under sorghum (Sorghum bicolor (L.) Moench) in the United States. The discovery of herbicide resistance sources in wild sorghum population and subsequent efforts to incorporate them into cultivated sorghum was received with much optimism to change weed management practices in sorghum. As the development of the technology advances, especially of the Acetolactate synthase (ALS) resistance, concerns over the temporary interveinal chlorosis and reduced seedling vigor in some of the resistant families became heightened. This thesis research is designed to shed light on the genetic basis of seedling chlorosis and assess its impacts on yield potential. The study has three parts; the first part is focused on identifying the genetic causes and plant mechanisms associated with the chlorotic phenotype. ALS herbicide resistant sister-lines expressing normal and chlorotic phenotypes were analyzed via RNA sequencing at four time points during seedling growth. The study identified several variants of genes coding chloroplast precursors and those that cause epigenetic modifications. Once confirmed, genetic markers can be developed to track these gene variants in the breeding population and eliminate segregates genetically prone to chlorosis/yellowing. The second part of the study focuses on assessing the effect of ALS resistance associated chlorosis on agronomic and nutritional parameters of sorghum inbred lines. A set of ALS resistant lines expressing different levels of the chlorotic phenotype were evaluated in replicated field trials and laboratory methods. Results showed that interveinal chlorosis delays flowering but does not have negative effect on yield and nutritional parameters with and without herbicide treatment. The last part addresses whether there is any yield drag that may be associated with herbicide resistance traits and foliar interveinal chlorosis. For this, we synthesized a large set (182) of hybrids from ALS resistant, ACCase resistant and regular (susceptible) seed and pollinator parents. The hybrids were then evaluated in three sets at multiple locations during the 2014 and 2015 crop seasons along with commercial checks. The results revealed that resistance to both herbicides do not cause any drag to grain yield. The traits also do not have any negative impact on grain and nutritional quality of resistant hybrids.
Castel, Morales Pau. "Molecular mechanisms of resistance to PI3K inhibitors". Doctoral thesis, Universitat de Barcelona, 2016. http://hdl.handle.net/10803/396640.
Texto completoEl desenvolupament de noves tècniques de seqüenciació massiva ha fomentat l’estudi d’un gran nombre de mostres de diversos tipus tumorals. Els resultats d’aquests estudis genòmics exhaustius ha revelat els gens que es troben mutats en major prevalença, contribuint a una millor comprensió dels processos de patogènesis, classificació molecular i estratègies terapèutiques per a aquesta malaltia. PIK3CA, el gen que codifica per a la isoforma PI3Kα, es troba entre els gens mes freqüentment mutats en el carcinoma de mama, cap i coll, colorectal, pulmó, entre d’altres. Les mutacions activadores a PIK3CA promouen la hiperactivació de la via de senyalització de PI3K/AKT, donant lloc a un increment en la proliferació, la supervivència, i el metabolisme de les cèl·lules tumorals. Els esforços actuals es centren en el desenvolupament d’inhibidors de l’enzim PI3K com a una possible teràpia efectiva en tumors que presenten mutacions a PIK3CA. Tot i que els assajos clínics inicials son prometedors, l’emergència de resistència a aquestes teràpies és una clara limitació. En aquesta tesis doctoral s’han explorat els possibles mecanismes de resistència per intentar entendre com els tumors evolucionen enfront d’aquest fàrmacs, poder definir les subpoblacions de pacients que respondran als inhibidors de PI3K i proporcionar noves combinacions farmacològiques per combatre el fenomen de la resistència. Hem demostrat que la pèrdua del supressor tumoral PTEN juga un paper important en la resistència als inhibidors de PI3Kα, tant en models preclínics com en pacients, mitjançant la reactivació de la via de PI3K/AKT que és resultat d’un increment en la dependència de la isoforma PI3Kβ. El nostre treball també ha evidenciat la noció d’evolució tumoral i ha demostrat el concepte d’evolució convergent fenotípica en resposta a la pressió terapèutica. També s’ha demostrat que la resistència intrínseca als inhibidors de PI3Kα es pot donar com a resultat d’una inhibició incompleta del complex 1 de mTOR (mTORC1), un efector clau de la via de PI3K/AKT. Cèl·lules resistents a inhibidors de PI3Kα es van poder sensibilitzar amb el bloqueig genètic o farmacològic de PDK1, una quinasa constitutivament activa. Experiments addicionals van poder demostrar que l’efector molecular de PDK1 era la quinasa SGK1, la qual promou la supervivència cel·lular a través de la fosforilació de proteïnes clau com FOXO3 i TSC2. El fenotip resistent es va poder revertir mitjançant la inhibició farmacològica d’aquesta proteïna, una aproximació terapèutica que ha revelat un rol interessant en la biologia tumoral. Els models murins modificats genèticament representen una eina segura per a l’estudi de la etiologia, biologia i progressió de malalties humanes, així com per explorar noves aproximacions terapèutiques. Com a resultat d’un descobriment imprevist, també hem pogut revelar el rol de les mutacions de PIK3CA en la formació de malformacions venoses, una aberració del desenvolupament normal de les venes que actualment no tenen un tractament específic. El nostre model animal de malformació venosa recapitula les característiques histopatològigues de la malaltia i proporciona una plataforma experimental única per a l’estudi de noves teràpies. En aquests models animals, els inhibidors de PI3Kα han demostrat ser efectius en la reducció de la morbiditat de les malformacions venoses.
Recondo, Gonzalo. "Resistance Mechanisms to ALK Tyrosine Kinase Inhibitors (TKIs) in NSCLC". Thesis, Université Paris-Saclay (ComUE), 2019. http://www.theses.fr/2019SACLS248/document.
Texto completoThe molecular study and classification of lung adenocarcinomas has led to the development of selective targeted therapies aiming to improve disease control and survival in patients. The anaplastic lymphoma kinase (ALK) is a tyrosine kinase receptor from the insulin tyrosine kinase receptor family, with a physiologic role in neural development. Gene rearrangements involving the ALK kinase domain occur in ~3-6% of patients with lung adenocarcinoma. The fusion protein dimerizes leading to transactivation of the ALK kinase domain in a ligand-independent and constitutive manner. Lorlatinib is a third generation ALK inhibitor with high potency and selectivity for this kinase in vitro and in vivo, and elevated penetrance in the central nervous system. Lorlatinib can overcome resistance mediated by over 16 secondary kinase domain mutations occurring in 13 residues upon progression to first - and second - generation ALK TKI. In addition, treatment with lorlatinib is effective for patients who have been previously treated with a first and a second generation or a second generation ALK TKI upfront and is currently approved for this indication. The full spectrum of biological mechanisms driving lorlatinib resistance in patients remains to be elucidated. It has been recently reported that the sequential acquisition of two or more mutations in the kinase domain, also referred as compound mutations, is responsible for disease progression in about 35% of patients treated with lorlatinib, mainly by impairing its binding to the ALK kinase domain. However, the effect of these compound mutations on the sensitivity to the repertoire of ALK inhibitors can vary, and other resistance mechanisms occurring in most patients are unknown. My PhD thesis aimed at exploring resistance to lorlatinib in patients with ALK-rearranged lung cancer through spatial and temporal tumor biopsies and development of patient-derived models. Within the institutional MATCH-R study (NCT02517892), we performed high-throughput whole exome, RNA and targeted next-generation sequencing, together with plasma sequencing to identify putative genomic and bypass mechanisms of resistance. We developed patient-derived cell lines and characterized novel mechanisms of resistance and personalized treatment strategies in vitro and in vivo. We characterized three mechanisms of resistance in four patients with paired biopsies. We studied the induction of epithelial-mesenchymal transition (EMT) by SRC activation in a patient-derived cell line exposed to lorlatinib. Mesenchymal cells were sensitive to combined SRC and ALK co-inhibition, showing that even in the presence of an aggressive and challenging phenotype, combination strategies can overcome ALK resistance. We identified two novel ALK kinase domain compound mutations, F1174L/G1202R, C1156Y/G1269A, occurring in two patients treated with lorlatinib. We developed Ba/F3 cell models harboring single and compound mutations to study the differential effect of these mutations on lorlatinib resistance. Finally, we characterized a novel mechanism of resistance caused by NF2 loss of function at the time of lorlatinib progression through the development of patients derived PDX and cell lines, and in vitro validation of NF2 knock-out with CRISPR/CAS9 gene editing. Downstream activation of mTOR was found to drive lorlatinib resistance by NF2 loss of function and was overcome by providing treatment with mTOR inhibitors.This study shows that mechanisms of resistance to lorlatinib are more diverse and complex than anticipated. Our findings also emphasize how longitudinal studies of tumor dynamics allow deciphering TKI resistance and identifying reversing strategies
Miller, David James. "Phosphinic acids as inhibitors of D-Ala-D-Ala adding enzyme". Thesis, University of Southampton, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.242865.
Texto completoLee, Liam Changwoo. "Functional identification of molecular oncotargets associated with the resistance to ALK inhibition in neuroblastoma via genome-wide CRISPR-Cas9 screens". Thesis, University of Cambridge, 2017. https://www.repository.cam.ac.uk/handle/1810/267921.
Texto completoRandhawa, Ranjeet Singh. "Characterization and Management of Acetolactate Synthase Inhibiting Herbicide Resistant Mouse-Ear Cress (Arabidopsis thaliana) in Winter Wheat". Thesis, Virginia Tech, 2017. http://hdl.handle.net/10919/79370.
Texto completoMaster of Science in Life Sciences
Llibre, Codina Josep Maria. "Clinical impact of HIV-1 resistance against nonnucleoside analogue reverse transcriptase Inhibitors. Impacte clínic de la resistència del VIH-1 als inhibidors de la transcriptassa inversa no anàlegs de nucleòsids". Doctoral thesis, Universitat Autònoma de Barcelona, 2015. http://hdl.handle.net/10803/322789.
Texto completoNon-nucleoside reverse transcriptase inhibitors (NNRTIs) are popular components of antiretroviral therapy due to their efficacy and simplicity. Resistance is caused only by specific mutations at drug-resistance positions. Despite its proven efficacy, the clinical use of first-generation NNRTIs (nevirapine and efavirenz) has been limited by side effects and low barrier to resistance. To overcome these limitations, a second-generation of NNRTIs has been developed including etravirine and rilpivirine, both recently approved. Rilpivirine also depicts a low barrier to resistance development. Like nevirapine and efavirenz, complete drug resistance can arise with only one or two resistance-associated mutations (RAMs). In addition, there is a considerable degree of class cross-resistance among all NNRTIs, nearly complete between nevirapine and efavirenz, and more limited from first to second generation NNRTIs. Therefore, the knowledge of RAMs selected by first-generation NNRTIs that have a potential to impact both rilpivirine or etravirine in subsequent treatments is of paramount importance. Genotypic scores are now fully developed for all these drugs, therefore allowing resistance analyses in clinical samples and offering a unique opportunity to investigate the clinical impact of HIV-1 resistance on treatment response both in initial, salvage or simplification treatment. In this PhD thesis, we discuss the relevance of RAMs on treatment response; we pinpoint the patterns of RAMs selected at virologic failure (VF) with specific NNRTIs, and the consequent risk of failure to salvage or simplification with NNRTIs. The first chapter evaluates the effectiveness of etravirine in salvage regimens in VF recruited at four acute-care University hospitals in Barcelona. These regimens were generally well tolerated and achieved rates of virological suppression that exceed those observed in etravirine’s pivotal clinical trials, probably due to the inclusion of a higher number of active drugs in the regimens. We identified baseline CD4+ T cell count >200 cells/mm3 and use of raltegravir and darunavir as factors associated with lower treatment failure rates using a multivariate analysis. We found no relationship between prior interruption or VF with nevirapine or efavirenz and response to etravirine. The second chapter assesses the RAMs selected in subjects failing NNRTI-based treatments (with nevirapine, efavirenz or etravirine) at 22 clinics in Spain and the potential impact on rilpivirine’s activity. Rilpivirine resistance was recognized in 20% of these patients, more commonly following etravirine or nevirapine failures than efavirenz. The most prevalent rilpivirine RAMs in subjects failing other NNRTIs were Y181C, K101E/P, H221Y and E138A/G/K. E138K/M184I, the most frequently selected combination in initial treatment with rilpivirine, was absent in this treatment-experienced population. L100I and V108I were significantly more frequent in efavirenz failures. Conversely, Y181C/I, V106A, H221Y and F227L were more prevalent in nevirapine ones. Finally, the third chapter estimates the effectiveness of a nevirapine-based switch regimen in subjects with suppressed viremia, combined with tenofovir and emtricitabine (or lamivudine). The analysis has been done in our clinic in Barcelona. No unexpected RAMs or patterns of RAMs were selected in treatment failures to this regimen. At week 48, nearly 90% of the subjects had HIV-1 RNA <50 copies/mL, VF was uncommon, and 25 (7.4%) subjects discontinued the treatment due to toxicity. Factors independently associated with VF in multivariate analysis were intravenous drug use, time with undetectable viral load before the switch, number of prior NRTIs or NNRTIs, and previous nevirapine or efavirenz unscheduled interruptions. Reinitiation of nevirapine plus tenofovir plus emtricitabine (or lamivudine) should be discouraged in subjects experiencing unplanned treatment interruptions, even with an undetectable plasma viral load at the time of treatment withdrawal. Unexpectedly, we found a significantly higher rate of VF with lamivudine instead of emtricitabine with this regimen, with a significantly higher selection of M184V as well. Our findings suggest caution against substituting emtricitabine for lamivudine, at least in nevirapine- and tenofovir-based regimens.
Libros sobre el tema "ALS inhibitor resistance"
Gilbert, Paul y Jennifer S. Mascaro. Compassion Fears, Blocks and Resistances. Editado por Emma M. Seppälä, Emiliana Simon-Thomas, Stephanie L. Brown, Monica C. Worline, C. Daryl Cameron y James R. Doty. Oxford University Press, 2017. http://dx.doi.org/10.1093/oxfordhb/9780190464684.013.29.
Texto completoTobon, Amalia Londono y Hanna E. Stevens. Adolescents with SSRI-Resistant Depression. Editado por Ish P. Bhalla, Rajesh R. Tampi, Vinod H. Srihari y Michael E. Hochman. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190625085.003.0008.
Texto completoWong, Han Hsi, Basma Greef y Tim Eisen. Treatment of metastatic renal cancer. Editado por James W. F. Catto. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199659579.003.0089.
Texto completoMukherji, Deborah, Aurelius Omlin, Carmel Pezaro y Johann De Bono. Novel therapies and emerging strategies for the treatment of patients with castration-resistant prostate cancer. Editado por James W. F. Catto. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199659579.003.0069.
Texto completoEwald, Paul W. Evolutionary control of infectious disease in low-income countries. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780198789833.003.0009.
Texto completoBarnard, Matthew y Nicola Jones. Intensive care management after cardiothoracic surgery. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0368.
Texto completoMacdougall, Iain C. Erythropoiesis-stimulating agents in chronic kidney disease. Editado por David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0124.
Texto completoWhitworth, Caroline y Stewart Fleming. Malignant hypertension. Editado por Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0216.
Texto completoCapítulos de libros sobre el tema "ALS inhibitor resistance"
Eberlein, C. V., M. J. Guttieri, C. A. Mallory-Smith y D. C. Thill. "Effects of Mutation for ALS-Inhibitor Resistance on ALS Activity in Resistant and Susceptible Near-Isonuclear Lactuca Lines". En Weed and Crop Resistance to Herbicides, 191–97. Dordrecht: Springer Netherlands, 1997. http://dx.doi.org/10.1007/978-94-011-5538-0_21.
Texto completoSimionato, Francesca, Carmine Carbone, Giampaolo Tortora y Davide Melisi. "Resistance to ALK Inhibitors". En Resistance to Targeted Anti-Cancer Therapeutics, 147–63. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-46091-8_5.
Texto completoShibaike, Hiroyuki, Akira Uchino y Kazuyuki Itoh. "Molecular Characterization of Resistance to Acetolactate Synthase Inhibitors inLindernia micrantha: Origin and Expansion of Resistant Biotypes". En ACS Symposium Series, 244–54. Washington, DC: American Chemical Society, 2005. http://dx.doi.org/10.1021/bk-2005-0899.ch021.
Texto completoMüllner, H., P. Eckes y G. Donn. "Engineering Crop Resistance to the Naturally Occurring Glutamine Synthetase Inhibitor Phosphinothricin". En ACS Symposium Series, 38–47. Washington, DC: American Chemical Society, 1993. http://dx.doi.org/10.1021/bk-1993-0524.ch003.
Texto completoShaner, D. L. y I. Heap. "Herbicide Resistance in North America: The Case for Resistance to ALS Inhibitors in the United States". En ACS Symposium Series, 161–67. Washington, DC: American Chemical Society, 2001. http://dx.doi.org/10.1021/bk-2002-0808.ch010.
Texto completoMancini, Maicol y Yosef Yarden. "Resistance of Lung Cancer to Kinase Inhibitors Specific to EGFR or ALK". En Resistance to Targeted Anti-Cancer Therapeutics, 29–49. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67932-7_2.
Texto completoIshikawa, Toshihisa, Yutaka Inoue, Yoji Ikegami, Takahiro Fujishiro, Tomohiro Osaki, Yoshinaga Kajimoto, Shin-Ichi Miyatake y Toshihiko Kuroiwa. "A New Strategy of ALA-Photodynamic Cancer Therapy: Inhibition of ABC Transporter ABCG2". En Resistance to Targeted Anti-Cancer Therapeutics, 89–104. Cham: Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-09801-2_4.
Texto completoOhta, Hiroki, Noburo Kyomura, Yoji Takahashi y Philip S. Magee. "Inhibition of Susceptible and Resistant Green Rice Leafhopper Acetylcholinesterase byN-Methylcarbamate and Oxadiazolone Insecticides". En ACS Symposium Series, 136–46. Washington, DC: American Chemical Society, 1989. http://dx.doi.org/10.1021/bk-1989-0413.ch009.
Texto completoMitsuya, Hiroaki y Arun K. Ghosh. "Development of HIV-1 Protease Inhibitors, Antiretroviral Resistance, and Current Challenges of HIV/AIDS Management". En Aspartic Acid Proteases as Therapeutic Targets, 245–62. Weinheim, Germany: Wiley-VCH Verlag GmbH & Co. KGaA, 2011. http://dx.doi.org/10.1002/9783527630943.ch9.
Texto completoXu, Feng, Benjamin D. Sherry y Timothy A. Blizzard. "Discovery and Chemical Development of Relebactam: A Potent β-Lactamase Inhibitor in Combination with Primaxin® for the Treatment of Serious and Antibiotic-Resistant Bacterial Infections". En ACS Symposium Series, 253–84. Washington, DC: American Chemical Society, 2020. http://dx.doi.org/10.1021/bk-2020-1369.ch008.
Texto completoActas de conferencias sobre el tema "ALS inhibitor resistance"
Nawaz, Muddasir, Sehrish Habib, Adnan Khan, Abdul Shakoor y Ramazan Kahraman. "Cellulose microfibers (CMFs) reinforced smart self-healing polymeric composite coatings for corrosion protection of steel". En Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2020. http://dx.doi.org/10.29117/quarfe.2020.0003.
Texto completoBaker, J. B., M. P. McGrogan, C. Simonsen, R. L. Gronke y B. W. Festoff. "STRUCTURE AND PROPERTIES OF PROTEASE NEXIN I". En XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644765.
Texto completoDardaei, Leila, Hui Qin Wang, Manrose Singh, Paul Fordjour, Satoshi Yoda, Grainne Kerr, Jinsheng Liang et al. "Abstract A145: SHP2 inhibition restores sensitivity to ALK inhibitors in resistant ALK-rearranged NSCLC". En Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics; October 26-30, 2017; Philadelphia, PA. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1535-7163.targ-17-a145.
Texto completoLiu, Jin-hua, Bin Gong, E. Jang, Wei-gang Ma, Ju-hua Wen y Yan-chun He. "Corrosion Inhibitor on Copper and Stainless Steel for Component Cooling Water System of NPP". En 2013 21st International Conference on Nuclear Engineering. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/icone21-16249.
Texto completoGriffith, T. M., D. H. Edwards, R. L. Davies, T. J. Harrison y K. L. Evans. "EDRF AND RESISTANCE VESSELS". En XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643721.
Texto completoCortelazzo, S., D. Castagna, M. Galli, T. Barbui y G. de Gaetano. "INCREASED RESPONSE TO ARACHIDONIC ACID AND U-46619 AND RESISTANCE TO INHIBITORY PR0STAGLANDING IN PATIENTS WITH CHRONIC MYELOPROLIFE RATIVE DISORDERS". En XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643381.
Texto completoKatayama, Ryohei, Noriko Yanagitani, Sumie Koike, Takuya Sakashita, Satoru Kitazono, Makoto Nishio, Yasushi Okuno, Jeffrey A. Engelman, Alice T. Shaw y Naoya Fujita. "Abstract 3590: Resistance mechanisms to ALK inhibitors". En Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-3590.
Texto completoKim, Soyeon, Tae Min Kim, Yong-Oon Ahn, Bhumsuk Keam, Se-Hoon Lee, Dae Seog Heo y Dong-Wan Kim. "Abstract 1842: Synergistic inhibition of ALK inhibitor-resistant lung cancer cells by dual-targetingEGFRandALKpathways". En Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-1842.
Texto completoZhai, Dayong, Wei Deng, Zhongdong Huang, Evan Rogers y J. Jean Cui. "Abstract 2132: The novel, rationally-designed, ALK/SRC inhibitor TPX-0005 overcomes multiple acquired resistance mechanisms to current ALK inhibitors". En Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-2132.
Texto completoAl-Jaber, Hend Sultan, Layla Jadea Al-Mansoori y Mohamed Aghar Elrayess. "The Role of GATA3 in Adipogenesis & Insulin Resistance". En Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2020. http://dx.doi.org/10.29117/quarfe.2020.0143.
Texto completoInformes sobre el tema "ALS inhibitor resistance"
Lance, Richard y Xin Guan. Variation in inhibitor effects on qPCR assays and implications for eDNA surveys. Engineer Research and Development Center (U.S.), agosto de 2021. http://dx.doi.org/10.21079/11681/41740.
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