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Готові списки джерел за темами / Ptk2b

Добірка наукової літератури з теми "Ptk2b"

Автор: Grafiati

Опубліковано: 15 червня 2024

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Статті в журналах з теми "Ptk2b":

1

Pallarès, Victor, Montserrat Hoyos, M. Chillón, Eva Barragán, M. Prieto Conde, Marta Llop, Aïda Falgàs, et al. "Focal Adhesion Genes Refine the Intermediate-Risk Cytogenetic Classification of Acute Myeloid Leukemia." Cancers 10, no. 11 (November 13, 2018): 436. http://dx.doi.org/10.3390/cancers10110436.

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In recent years, several attempts have been made to identify novel prognostic markers in patients with intermediate-risk acute myeloid leukemia (IR-AML), to implement risk-adapted strategies. The non-receptor tyrosine kinases are proteins involved in regulation of cell growth, adhesion, migration and apoptosis. They associate with metastatic dissemination in solid tumors and poor prognosis. However, their role in haematological malignancies has been scarcely studied. We hypothesized that PTK2/FAK, PTK2B/PYK2, LYN or SRC could be new prognostic markers in IR-AML. We assessed PTK2, PTK2B, LYN and SRC gene expression in a cohort of 324 patients, adults up to the age of 70, classified in the IR-AML cytogenetic group. Univariate and multivariate analyses showed that PTK2B, LYN and PTK2 gene expression are independent prognostic factors in IR-AML patients. PTK2B and LYN identify a patient subgroup with good prognosis within the cohort with non-favorable FLT3/NPM1 combined mutations. In contrast, PTK2 identifies a patient subgroup with poor prognosis within the worst prognosis cohort who display non-favorable FLT3/NPM1 combined mutations and underexpression of PTK2B or LYN. The combined use of these markers can refine the highly heterogeneous intermediate-risk subgroup of AML patients, and allow the development of risk-adapted post-remission chemotherapy protocols to improve their response to treatment.

2

Porter, Tyrel, Miguel Mayol del Valle, and Lilia Kucheryavykh. "Ethnicity-Based Variations in Focal Adhesion Kinase Signaling in Glioblastoma Gene Expression: A Study of the Puerto Rican Hispanic Population." International Journal of Molecular Sciences 25, no. 9 (May 1, 2024): 4947. http://dx.doi.org/10.3390/ijms25094947.

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Glioblastoma (GBM), an aggressive form of brain cancer, has a higher incidence in non-Hispanics when compared to the US Hispanic population. Using data from RT-PCR analysis of 21 GBM tissue from Hispanic patients in Puerto Rico, we identified significant correlations in the gene expression of focal adhesion kinase and proline-rich tyrosine kinase (PTK2 and PTK2B) with NGFR (nerve growth factor receptor), PDGFRB (platelet-derived growth factor receptor B), EGFR (epithelial growth factor receptor), and CXCR1 (C-X-C motif chemokine receptor 1). This study further explores these correlations found in gene expression while accounting for sex and ethnicity. Statistically significant (p < 0.05) correlations with an r value > ±0.7 were subsequently contrasted with mRNA expression data acquired from cBioPortal for 323 GBM specimens. Significant correlations in Puerto Rican male patients were found between PTK2 and PTK2B, NGFR, PDGFRB, EGFR, and CXCR1, which did not arise in non-Hispanic male patient data. The data for Puerto Rican female patients showed correlations in PTK2 with PTK2B, NGFR, PDGFRB, and EGFR, all of which did not appear in the data for non-Hispanic female patients. The data acquired from cBioPortal for non-Puerto Rican Hispanic patients supported the correlations found in the Puerto Rican population for both sexes. Our findings reveal distinct correlations in gene expression patterns, particularly involving PTK2, PTK2B, NGFR, PDGFRB, and EGFR among Puerto Rican Hispanic patients when compared to non-Hispanic counterparts.

3

Chen, Cui, Zhen Tao, Ya Li, Jie Li, and Yang Xu. "MicroRNA214 expression inhibits HCC cell proliferation through PTK2b/ Pyk2." Cellular and Molecular Biology 68, no. 1 (May 22, 2022): 20–25. http://dx.doi.org/10.14715/cmb/2022.68.1.4.

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MicroRNAs (miRNAs/miRs) are crucial regulatory molecules that act as the most significantly downregulated microRNAs in hepatocellular carcinoma (HCC). PTK2b/Pyk2 is a non-receptor protein tyrosine kinase, which plays an important role in the development and metastasis of cancer. In this study, we explored the expression level and functional relationship between MicroRNA-214 (miR-214) and PTK2b/ Pyk2 in liver cancer cells. For this purpose, we analyzed the expression of miR-214 and PTK2b/Pyk2 in 38 cases of HCC and paired non-neoplastic tissue specimens using real-time PCR. MTT, cell cycle and construct recombinant plasmids analysis were used to explore the effects of miR-214 and PTK2b/Pyk2 on liver cancer cell proliferation. Results showed that the expression level of mir-214 in liver cancer tissues and liver cancer cell lines was significantly lower than that in normal tissues and cells, while the expression of PTK2b/Pyk2 was significantly increased. The overexpression of mir-214 or inhibition PTK2b/Pyk2 inhibited the proliferation of HCC cells. This research showed that mir-214 has an inhibitory effect on liver cancer through the expression of PTK2b/Pyk2.

4

Luo, Jinping, Lynda K. McGinnis, Carol Carlton, Hilary E. Beggs, and William H. Kinsey. "PTK2b function during fertilization of the mouse oocyte." Biochemical and Biophysical Research Communications 450, no. 3 (August 2014): 1212–17. http://dx.doi.org/10.1016/j.bbrc.2014.03.083.

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5

N'Songo, Aurelie, Minerva M. Carrasquillo, Xue Wang, Jeremy D. Burgess, Thuy Nguyen, Yan W. Asmann, Daniel J. Serie, et al. "African American exome sequencing identifies potential risk variants at Alzheimer disease loci." Neurology Genetics 3, no. 2 (April 2017): e141. http://dx.doi.org/10.1212/nxg.0000000000000141.

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Objective:In African Americans, we sought to systematically identify coding Alzheimer disease (AD) risk variants at the previously reported AD genome-wide association study (GWAS) loci genes.Methods:We identified coding variants within genes at the 20 published AD GWAS loci by whole-exome sequencing of 238 African American participants, validated these in 300 additional participants, and tested their association with AD risk in the combined cohort of 538 and with memory endophenotypes in 319 participants.Results:Two ABCA7 missense variants (rs3764647 and rs3752239) demonstrated significant association with AD risk. Variants in MS4A6A, PTK2B, and ZCWPW1 showed significant gene-based association. In addition, coding variants in ZCWPW1 (rs6465770) and NME8 (rs10250905 and rs62001869) showed association with memory endophenotypes.Conclusions:Our findings support a role for ABCA7 missense variants in conferring AD risk in African Americans, highlight allelic heterogeneity at this locus, suggest the presence of AD-risk variants in MS4A6A, PTK2B, and ZCWPW1, nominate additional variants that may modulate cognition, and importantly provide a thorough screen of coding variants at AD GWAS loci that can guide future studies in this population.

6

Giralt, Albert, Benoit de Pins, Carmen Cifuentes-Díaz, Laura López-Molina, Amel Thamila Farah, Marion Tible, Vincent Deramecourt, et al. "PTK2B/Pyk2 overexpression improves a mouse model of Alzheimer's disease." Experimental Neurology 307 (September 2018): 62–73. http://dx.doi.org/10.1016/j.expneurol.2018.05.020.

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7

Ni, Bin, Jared S. Farrar, Shanshan Chen, Joseph C. Lownik, and Francesco S. Celi. "A novel role for PTK2B in cultured beige adipocyte differentiation." Biochemical and Biophysical Research Communications 501, no. 4 (July 2018): 851–57. http://dx.doi.org/10.1016/j.bbrc.2018.05.021.

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8

Chu, Weiwei, Lili Guan, Dihua Huang, Yuezhong Ren, and Yan Zhou. "Lovastatin exerts protective effects on endothelial cells via upregulation of PTK2B." Experimental and Therapeutic Medicine 12, no. 3 (July 26, 2016): 1741–49. http://dx.doi.org/10.3892/etm.2016.3547.

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9

Piaggio, Francesca, Veronica Tozzo, Cinzia Bernardi, Michela Croce, Roberto Puzone, Silvia Viaggi, Serena Patrone, et al. "Secondary Somatic Mutations in G-Protein-Related Pathways and Mutation Signatures in Uveal Melanoma." Cancers 11, no. 11 (October 30, 2019): 1688. http://dx.doi.org/10.3390/cancers11111688.

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Background: Uveal melanoma (UM), a rare cancer of the eye, is characterized by initiating mutations in the genes G-protein subunit alpha Q (GNAQ), G-protein subunit alpha 11 (GNA11), cysteinyl leukotriene receptor 2 (CYSLTR2), and phospholipase C beta 4 (PLCB4) and by metastasis-promoting mutations in the genes splicing factor 3B1 (SF3B1), serine and arginine rich splicing factor 2 (SRSF2), and BRCA1-associated protein 1 (BAP1). Here, we tested the hypothesis that additional mutations, though occurring in only a few cases (“secondary drivers”), might influence tumor development. Methods: We analyzed all the 4125 mutations detected in exome sequencing datasets, comprising a total of 139 Ums, and tested the enrichment of secondary drivers in Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways that also contained the initiating mutations. We searched for additional mutations in the putative secondary driver gene protein tyrosine kinase 2 beta (PTK2B) and we developed new mutational signatures that explain the mutational pattern observed in UM. Results: Secondary drivers were significantly enriched in KEGG pathways that also contained GNAQ and GNA11, such as the calcium-signaling pathway. Many of the secondary drivers were known cancer driver genes and were strongly associated with metastasis and survival. We identified additional mutations in PTK2B. Sparse dictionary learning allowed for the identification of mutational signatures specific for UM. Conclusions: A considerable part of rare mutations that occur in addition to known driver mutations are likely to affect tumor development and progression.

10

Liu, Zhen, Kai-Min Hao, Hao-Yu Wang, and Wen-Xiu Qi. "Histone deacetylase-6 modulates amyloid beta-induced cognitive dysfunction rats by regulating PTK2B." NeuroReport 31, no. 10 (May 21, 2020): 754–61. http://dx.doi.org/10.1097/wnr.0000000000001481.

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Більше джерел

Дисертації з теми "Ptk2b":

1

Melo, de Farias Ana Raquel. "Probing the Alzheimer’s disease risk gene PTK2B using human-derived induced neurons." Electronic Thesis or Diss., Université de Lille (2022-....), 2023. http://www.theses.fr/2023ULILS062.

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La maladie d'Alzheimer (MA) est le principal type de démence et représente un défi majeur pour la santé publique mondiale. Elle se caractérise par un déclin progressif de la cognition, de la mémoire et des fonctions comportementales et touche plus de 55 millions de personnes dans le monde. Au niveau moléculaire, la MA se définit par la présence d'enchevêtrements neurofibrillaires agrégés dans les neurones et par l'accumulation de plaques d'amyloïde-β (Aβ) dans le cerveau. Ces caractéristiques pathologiques sont associées à des altérations de l'activité neuronale, à la perte de synapses, à la gliose et à la neuroinflammation, conduisant à une neurodégénérescence irréversible. L'étiologie et la physiopathologie de la MA impliquent une interaction complexe entre des facteurs génétiques et environnementaux. Les études d'association à l'échelle du génome ont permis d'identifier plusieurs loci porteurs de polymorphismes de nucléotides simples (SNP) associés au risque de maladie d'Alzheimer. Parmi ces loci, celui qui héberge la Protéine Tyrosine Kinase 2β (PTK2B) est mis en évidence dans le présent travail. Ce gène code pour une protéine tyrosine kinase qui est impliquée dans la régulation des canaux ioniques induite par le calcium et dans l'activation de nombreuses voies de signalisation, telles que la MAP kinase. Des variations génétiques non synonymes dans le locus PTK2B ont été associées à un risque accru de maladie d'Alzheimer et on pense qu'elles régulent l'expression de PTK2B. Cependant, les rôles physiologiques et physiopathologiques de la PTK2B ne sont pas entièrement compris. Dans le cerveau humain, l'expression de la PTK2B est principalement observée dans les neurones glutamatergiques. Au cours de la progression de la maladie d'Alzheimer, son expression diminue et peut contribuer aux dysfonctionnements neuronaux observés, tels que l'augmentation de l'excitabilité électrique et les altérations synaptiques. Par conséquent, la compréhension du rôle de la PTK2B dans les neurones humains peut contribuer à révéler les mécanismes des dysfonctionnements neuronaux dans la MA. Dans cette optique, les objectifs de cette thèse sont de découvrir les processus cellulaires et les voies moléculaires régulés par la PTK2B dans les neurones humains. Pour ce faire, nous avons utilisé des cellules souches pluripotentes induites humaines (hiPSC) isogéniques pour générer des neurones exprimant différents niveaux de PTK2B. Ensuite, nous avons utilisé des tests fonctionnels et moléculaires pour étudier les conséquences de l'altération de l'expression de la PTK2B dans un contexte physiologique et dans un contexte similaire à celui de la MA. Nous montrons qu'une réduction de l'expression de PTK2B entraîne une augmentation de la phosphorylation de TAU à divers épitopes associés à la pathologie de la MA, ce qui suggère un rôle central de PTK2B dans la régulation de l'agrégation de TAU. En utilisant la transcriptomique à noyau unique, nous montrons également que l'expression réduite de la PTK2B entraîne des altérations transcriptionnelles spécifiques liées à l'activité électrique neuronale et à la transmission synaptique, principalement dans les neurones glutamatergiques. Les expériences d'imagerie calcique indiquent que la réduction de l'expression de PTK2B contribue à augmenter la fréquence des pointes de calcium sans affecter la synchronisation, ce qui indique une activité électrique neuronale élevée. En outre, les résultats des enregistrements électrophysiologiques effectués à partir de réseaux multi-électrodes (MEA) montrent une activité électrique accrue et des schémas d'éclatement perturbés dans les neurones mutants PTK2B. Dans l'ensemble, ces travaux mettent en lumière l'implication de PTK2B dans les processus cellulaires liés à la maladie d'Alzheimer, en donnant un aperçu des mécanismes moléculaires et des altérations fonctionnelles associés à la dysrégulation de PTK2B dans les cellules neuronales humaines dérivées des iPSCs
Alzheimer's disease (AD) is the main type of dementia and poses a significant global public health challenge. It is characterized by a progressive decline in cognition, memory, and behavioral functions and affects more than 55 million people worldwide. At the molecular level, AD is defined by the presence of aggregated neurofibrillary tangles within neurons and the accumulation of amyloid-β (Aβ) plaques in the brain. These pathological features are associated with alterations in neuronal activity, synapse loss, gliosis, and neuroinflammation, leading to irreversible neurodegeneration. AD etiology and pathophysiology involves a complex interplay between genetic and environmental factors. Genome-Wide Association Studies have identified several loci carrying single nucleotide polymorphisms (SNPs) associated with AD risk. Among these loci, the one harboring the Protein Tyrosine Kinase 2β (PTK2B) is highlighted in the present work. This gene encodes a protein tyrosine kinase that is involved in calcium-induced regulation of ion channels and activation of numerous signaling pathways, such as MAP kinase. Non-synonimous genetic variations in the PTK2B locus have been associated with an increased risk of AD and are thought to regulate PTK2B expression. However, both the physiological and pathophysiological roles of PTK2B are not fully understood. In the human brain, PTK2B expression is mainly observed in glutamatergic neurons. Its expression declines during AD progression and may contribute to neuronal dysfunctions observed in the disease, such as increased electrical excitability and synaptic alterations. Therefore, understanding the role of PTK2B in human neurons may contribute to reveal the mechanisms of neuronal dysfunctions in AD. Considering that, the aims of this thesis are to uncover the cellular processes and molecular pathways regulated by PTK2B in human neurons. To that, we took advantage of isogenic human induced-pluripotent stem cells (hiPSCs) to generate neurons expressing different levels of PTK2B. Next, we employed functional and molecular assays to probe the consequences of altered PTK2B expression both in a physiological and in an AD-like context. We show that reduced PTK2B expression leads to increased TAU phosphorylation at various epitopes associated with AD pathology, suggesting a central role of PTK2B in regulating TAU aggregation. Using single-cell transcriptomics, we also show that reduced PTK2B expression leads to specific transcriptional alterations related to neuronal electrical activity and synaptic transmission mainly in glutamatergic neurons. Calcium imaging experiments indicate that PTK2B downregulation contributes to increased calcium spikes frequency without affecting synchronization, indicating an elevated neuronal electrical activity. Additionally, results from electrophysiological recordings from multi-electrode array (MEA) show increased electrical activity and disrupted bursting patterns in PTK2B mutant neurons. Overall, this work sheds light on the involvement of PTK2B in AD-related cellular processes, providing insights into the molecular mechanisms and functional alterations associated with PTK2B dysregulation in human iPSC-derived neural cells

2

Schmachtenberg, Anna-Juliane. "Differentielle Expression des Tyrosin-Kinoms bei akuter lymphatischer Leukämie des erwachsenen Alters." Doctoral thesis, Humboldt-Universität zu Berlin, 2018. http://dx.doi.org/10.18452/19369.

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Tyrosinkinasen (TK) sind Schlüsselregulatoren der zellulären Signaltransduktion und beeinflussen Zellzyklus, Zellüberleben, Apoptose, Proliferation und Differenzierung. Die Dysregulation der TK-Aktivität trägt zur Entwicklung von Leukämie und anderen malignen Erkrankungen bei. So sind 25% der akuten lymphatischen Leukämien bei Erwachsenen (ALL) durch die BCR-ABL1-Translokation bedingt. Trotz intensiver Therapie beträgt das 5-Jahres-Überleben von erwachsenen Patienten mit ALL nur etwa 50 %. Als Alternative zu herkömmlichen Chemotherapeutika bietet der Einsatz von spezifisch wirkenden TK-Inhibitoren einen individualisierten Therapieansatz mit idealerweise weniger Nebenwirkungen und einem dadurch verbesserten Outcome. Um mögliche neue therapeutische Ziele zu identifizieren, wurde eine systematische Untersuchung der Expressionsveränderungen des gesamten Tyrosinkinoms durchgeführt. Eine Vielzahl verschiedener Tyrosinkinasen zeigte starke Veränderungen im Expressionsprofil von ALL-Zellen. Ein Teil dieser Expressionsänderungen kam durch das veränderten Methylierungsprofil der ALL-Zellen zustande. EPHA7 und PTK2 sind potentielle Marker für B-Linien ALL und NTRK3, ERBB4 und ZAP70 für T-Linien ALL. Die interindividuell variierende Expression der Tyrosinkinasen EPHA3, EPHB3, KIT, ZAP70 und PDGFRB könnte eine genauere Risikoeinstufung ermöglichen. Insbesondere sind die Tyrosinkinasen ABL1, DDR1, EPHA7, FGFR1, ERBB4, FLT1, FLT3, FLT4, LCK, LTK, PTK2, PTK2B, PTK7, SRC, TEC und TYK2 vielversprechende therapeutische Ziele, die im hämatopoetischen System die Proliferation fördern und / oder die Apoptose hemmen. Eine proliferationsfördernde Wirkung von überexprimiertem FLT4 konnte erstmals gezeigt werden. Die Vielfalt der Veränderungen in der Tyrosinkinase-Expression scheint eine wichtige Rolle bei der Entwicklung von ALL zu spielen und TK könnte vielversprechende neue therapeutische Ziele sein.
Tyrosine kinases (TK) are key regulators of cellular signal transduction and affect cell cycle, cell survival, apoptosis, proliferation and differentiation. Dysregulation of TK activity contributes to the development of leukemia and other malignancies. So are 25 % of adult acute lymphoblastic leukemias (ALL) driven by the BCR-ABL1 translocation. Despite intensive therapy, the 5-year overall survival of adult patients with ALL is about 50 %. In contrast to conventional chemotherapeutic agents, the use of specific-acting TK-inhibitors offers an individualized therapeutic approach with less side-effects and a better outcome. To identify possible new therapeutic targets, a systematic survey of expression changes of the entire tyrosine kinome was carried out. A variety of different tyrosine kinases showed great changes in the expression profile of ALL-cells. Part of these expression changes can be attributed to a changed methylation profile in adult ALL. EPHA7 and PTK2 are potential markers for B-line ALL and the NTRK3, ERBB4 and ZAP70 for T-lines ALL. The interindividual varying expression of the tyrosine kinases EPHA3, EPHB3, KIT, ZAP70 and PDGFRB presumably allows a more precise risk classification. In particular, the tyrosine kinases ABL1, DDR1, EPHA7, FGFR1, ERBB4, FLT1, FLT3, FLT4, LCK, LTK, PTK2, PTK2B, PTK7, SRC, TEC and TYK2 are promising therapeutic targets, which promotes proliferation and/or inhibits apoptosis in the hematopoietic system. A proliferation promoting effect of overexpressed FLT4 could be shown for the first time. The variety of changes in the tyrosine kinase expression seems to play an important role in the development of ALL and TK could be promising new therapeutic targets.

3

LI, PETRI Giovanna. "SYNTHESIS AND BIOLOGICAL EVALUATION OF NEW IMIDAZO[2,1-b][1,3,4]THIADIAZOLE DERIVATIVES AS ANTICANCER AND ANTIBIOFILM AGENTS, AND PRECLINICAL INVESTIGATION OF ANTI-LDH-A COMPOUNDS AGAINST MALIGNANT MESOTHELIOMA." Doctoral thesis, Università degli Studi di Palermo, 2020. http://hdl.handle.net/10447/395253.

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Частини книг з теми "Ptk2b":

1

Beck, T., A. Danneberg, and V. Friedberg. "Wertigkeit histomorphologischer Befunde für die Ergebnisse operativer Therapie des Zervixkarzinom im Stadium pT2b." In Gynäkologie und Geburtshilfe 1988, 560–61. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-74784-7_282.

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2

Vernetti, Lawrence A., A. Jay Gandolfi, and Raymond B. Nagle. "Selective Alteration of Cytokeratin Intermediate Filament by Cyclosporine A is a Lethal Toxicity in PTK2 Cell Cultures." In Advances in Experimental Medicine and Biology, 847–51. Boston, MA: Springer New York, 1991. http://dx.doi.org/10.1007/978-1-4684-5877-0_119.

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3

"PTK2." In Encyclopedia of Signaling Molecules, 4286. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_103157.

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4

Safer, Daniel, and Vivianne T. Nachmias. "Thymosin β4." In Guidebook to the Cytoskeletal and Motor Proteins, 149–51. Oxford University PressOxford, 1999. http://dx.doi.org/10.1093/oso/9780198599579.003.0049.

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Abstract There is good agreement that increasing T,β4 by microinjection or by transient transfection leads to disassembly of stress fibre bundles in NRK, PtK2, and CV1 cells (see Fig. 1 for a living PtK2 cell), and micro-injection at high concentrations also leads to disappearance of submembranous F-actin and relaxation of the cytokinetic furrow,15 This is what would be expected if the added β4 thymosin were acting in vivo to further sequester G-actin.

5

Frederick, K. "Irrigation efficiency, a key issue." In Water Crisis, 105–18. Taylor & Francis, 2006. http://dx.doi.org/10.1201/9781439834275.pt2b.

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6

"Conclusion to Part II." In XML Databases and the Semantic Web, 171. CRC Press, 2002. http://dx.doi.org/10.1201/9781420000023.pt2b.

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7

"Some problems in the use of language in economics." In Economics of Legal Relationships, 165–74. Routledge, 2007. http://dx.doi.org/10.4324/9780203964675.pt2b.

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8

Carvalho, D., J. Paschoalin Filho, and P. Albuquerque. "Behavior of continuous flight auger piles subjected to uplift load tests in unsaturated diabasic soil." In Deep Foundations on Bored and Auger Piles - BAP V, 197–204. CRC Press, 2008. http://dx.doi.org/10.1201/9780203882870.pt2b.

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Roovers, G., I. Rocabado, and M. Huygens. "Future flood risks and comprehensive flood management." In Water and Urban Development Paradigms, 251–56. CRC Press, 2008. http://dx.doi.org/10.1201/9780203884102.pt2b.

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"Conclusion to Part II." In Managing and Mining Multimedia Databases, 139. CRC Press, 2001. http://dx.doi.org/10.1201/9781420042559.pt2b.

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Тези доповідей конференцій з теми "Ptk2b":

1

Ono, Matthew D., Daryl Preece, Michelle L. Duquette, and Michael W. Berns. "Mitotic Tethers Connect Sister Chromosomes During Anaphase A in PtK2 Cells." In Optical Trapping Applications. Washington, D.C.: OSA, 2017. http://dx.doi.org/10.1364/ota.2017.otm4e.4.

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2

Skinner, Heath D., Uma Giri, John S. Yordy, Michael D. Story, Jing Wang, Lauren A. Byers, Michelle D. Williams, et al. "Abstract 3441: Proteomic profiling identifies PTK2/FAK as a targetable marker of radioresistance in head and neck cancer." In 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.am2015-3441.

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Gomard, Guillaume, Donie Yidenekachew, Radwanul Hasan Siddique, Ruben Huenig, Hendrik Hoelscher, Karsten Bittkau, Valérie Depauw, et al. "Controlling disorder for improved light management in solar cells." In Optical Nanostructures and Advanced Materials for Photovoltaics. Washington, D.C.: OSA, 2015. http://dx.doi.org/10.1364/pv.2015.pth2b.1.

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Isabella, O., R. Vismara, A. Ingenito, and M. Zeman. "Decoupled front/back dielectric textures for flat ultrathin c-Si solar cells." In Optical Nanostructures and Advanced Materials for Photovoltaics. Washington, D.C.: OSA, 2015. http://dx.doi.org/10.1364/pv.2015.pth2b.2.

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Abass, Aimi, and Carsten Rockstuhl. "Analytical Model of Guided Modes in Structures with Rough Surfaces." In Optical Nanostructures and Advanced Materials for Photovoltaics. Washington, D.C.: OSA, 2015. http://dx.doi.org/10.1364/pv.2015.pth2b.3.

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Ding, H., L. Lalouat, B. Gonzalez-Acevedo, A. Harouri, R. Orobtchouk, V. Depauw, E. Drouard, and C. Seassal. "Pseudo-disordered design assists mono-crystalline Si thin film solar cells." In Optical Nanostructures and Advanced Materials for Photovoltaics. Washington, D.C.: OSA, 2015. http://dx.doi.org/10.1364/pv.2015.pth2b.4.

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Schumann, M. F., A. Abass, S. Wiesendanger, C. Rockstuhl, and M. Wegener. "Cloaking of Contact Fingers on Solar Cells Enabled by Transformation Optics." In Optical Nanostructures and Advanced Materials for Photovoltaics. Washington, D.C.: OSA, 2015. http://dx.doi.org/10.1364/pv.2015.ptu2b.3.

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Li, Juntao, Kezheng Li, Christian Schuster, Rongbin Su, Xuehua Wang, Ben-Hur V. Borges, Thomas F. Krauss, and Emiliano R. Martins. "Fourier analysis and Spatial resolution of light trapping nanostructures." In Optical Nanostructures and Advanced Materials for Photovoltaics. Washington, D.C.: OSA, 2015. http://dx.doi.org/10.1364/pv.2015.pth2b.5.

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Krč, Janez, and Marko Topič. "Nanostructures for light trapping in photovoltaic devices – approaches and challenges." In Optical Nanostructures and Advanced Materials for Photovoltaics. Washington, D.C.: OSA, 2015. http://dx.doi.org/10.1364/pv.2015.ptu2b.1.

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Mellor, A., N. P. Hylton, F. Shirley, T. Thomas, K. H. Lee, Y. Al-Saleh, A. Braun, et al. "Nanostructured Solar Cells: Surface Textures and Quantum Dots." In Optical Nanostructures and Advanced Materials for Photovoltaics. Washington, D.C.: OSA, 2015. http://dx.doi.org/10.1364/pv.2015.ptu2b.2.

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