Добірка наукової літератури з теми "PRKCδ"
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Статті в журналах з теми "PRKCδ"
Arenas, Ailan F., Gladys E. Salcedo, and Jorge E. Gomez-Marin. "R Script Approach to Infer Toxoplasma Infection Mechanisms From Microarrays and Domain-Domain Protein Interactions." Bioinformatics and Biology Insights 11 (January 1, 2017): 117793221774725. http://dx.doi.org/10.1177/1177932217747256.
Повний текст джерелаTweedell, Rebecca, Le Qi, Zhaoli Sun, and Rhoel Dinglasan. "Kupffer Cells Survive Plasmodium berghei Sporozoite Exposure and Respond with a Rapid Cytokine Release." Pathogens 7, no. 4 (November 24, 2018): 91. http://dx.doi.org/10.3390/pathogens7040091.
Повний текст джерелаRicchiuti, Vincent, Christine G. Lian, Eveline M. Oestreicher, Loc Tran, James R. Stone, Tham Yao, Ellen W. Seely, Gordon H. Williams, and Gail K. Adler. "Estradiol increases angiotensin II type 1 receptor in hearts of ovariectomized rats." Journal of Endocrinology 200, no. 1 (October 17, 2008): 75–84. http://dx.doi.org/10.1677/joe-08-0199.
Повний текст джерелаLiu, Fangzhou, Yuanbai Li, Meng Li, Jing Wang, Yiying Zhang, Yu Du, and Yang Yang. "Study on Mechanism of Iridoid Glycosides Derivatives from Fructus Gardeniae in Jiangxi Province by Network Pharmacology." Evidence-Based Complementary and Alternative Medicine 2020 (June 27, 2020): 1–12. http://dx.doi.org/10.1155/2020/4062813.
Повний текст джерелаWang, Hao-Fan, Jian Jiang, Jia-Shun Wu, Mei Zhang, Xin Pang, Li Dai, Ya-Ling Tang, and Xin-Hua Liang. "Hypermethylation of PRKCZ Regulated by E6 Inhibits Invasion and EMT via Cdc42 in HPV-Related Head and Neck Squamous Cell Carcinoma." Cancers 14, no. 17 (August 27, 2022): 4151. http://dx.doi.org/10.3390/cancers14174151.
Повний текст джерелаYang, Qi-En, Manabu Ozawa, Kun Zhang, Sally E. Johnson, and Alan D. Ealy. "The requirement for protein kinase C delta (PRKCD) during preimplantation bovine embryo development." Reproduction, Fertility and Development 28, no. 4 (2016): 482. http://dx.doi.org/10.1071/rd14160.
Повний текст джерелаParzefall, Thomas, Julia Schnoell, Laura Monschein, Elisabeth Foki, David Tianxiang Liu, Alexandra Frohne, Stefan Grasl, et al. "PRKCA Overexpression Is Frequent in Young Oral Tongue Squamous Cell Carcinoma Patients and Is Associated with Poor Prognosis." Cancers 13, no. 9 (April 25, 2021): 2082. http://dx.doi.org/10.3390/cancers13092082.
Повний текст джерелаRotman, T., N. Etkovitz, A. Spiegel, S. Rubinstein та H. Breitbart. "Protein kinase A and protein kinase Cα/PPP1CC2 play opposing roles in the regulation of phosphatidylinositol 3-kinase activation in bovine sperm". REPRODUCTION 140, № 1 (липень 2010): 43–56. http://dx.doi.org/10.1530/rep-09-0314.
Повний текст джерелаOndee, Thunnicha, Thiranut Jaroonwitchawan, Trairak Pisitkun, Joseph Gillen, Aleksandra Nita-Lazar, Asada Leelahavanichkul та Poorichaya Somparn. "Decreased Protein Kinase C-β Type II Associated with the Prominent Endotoxin Exhaustion in the Macrophage of FcGRIIb−/− Lupus Prone Mice is Revealed by Phosphoproteomic Analysis". International Journal of Molecular Sciences 20, № 6 (18 березня 2019): 1354. http://dx.doi.org/10.3390/ijms20061354.
Повний текст джерелаQian, Yiguan, Yang Li, Luwei Xu, Ke Chen, Ning Liu, Xiaobing Yang, Qian Lv, et al. "Tumor Cell-Derived Exosomal circ-PRKCI Promotes Proliferation of Renal Cell Carcinoma via Regulating miR-545-3p/CCND1 Axis." Cancers 15, no. 1 (December 25, 2022): 123. http://dx.doi.org/10.3390/cancers15010123.
Повний текст джерелаДисертації з теми "PRKCδ"
Bisso, Andrea. "New microRNAS regulating the P53 signaling pathway." Doctoral thesis, Università degli studi di Trieste, 2010. http://hdl.handle.net/10077/3594.
Повний текст джерелаA vast body of evidence from clinical and basic research studies has demonstrated that the p53 pathway acts as an essential barrier in preventing cancer onset and development. ------------------------ A vast body of evidence from clinical and basic research studies has demonstrated that the p53 pathway acts as an essential barrier in preventing cancer onset and development. p53 receives and integrates a wide variety of cytotoxic and genotoxic stress signals from upstream sensors translating them into different cellular outcomes, ranging from apoptosis, cell cycle arrest, se-nescence, DNA repair or other tumor-suppressive responses. p53 exerts its role mainly at the transcriptional level and its timely activation/inactivation in response to stress depends on a complex repertoire of post-translational modifications and interactions with proteins. The crucial role of the p53 pathway in tumor suppression is highlighted by the fact that almost all tumors select for its functional inactivation, either by directly mutating the p53 gene or by altering the expression and functions of key p53 regulators and effectors. Therefore, identification of cellular factors that modulate this pathway and that could be altered in cancer cells, thus allowing to eva-de p53 control, is crucial for understanding cancer development and for designing novel effecti-ve therapeutic approaches. In this context, the aberrant expression or function of microRNAs (miRNAs) might be highly relevant. microRNAs are small non coding RNAs that finely regulate gene expression by binding the 3’UTR of their target mRNAs, thus altering their translation, stability and localization. It has been shown that several miRNAs modulate critical cellular processes deregulated in cancer, ac-ting either as oncogenes or tumor suppressors. On this basis, the aim of this thesis has been the identification and characterization of novel miRNAs able to modulate p53 functions by altering either upstream regulators (i.e. stress-activated kinases) or cofactors of p53. With this purpose we initially selected a panel of twenty-one candidate oncogenic miRNAs from the literature. First, we tested these miRNAs in a functional screening for their ability to modula-te p53-dependent functions in response to cisplatin (apoptosis) and nutlin-3 (cell cycle arrest). Second, miRNAs were also screened for their ability to impair p53 transcriptional activity through a reporter-based assay. We identified five candidate miRNAs from the first approach, and three from the second. miR-26a was identified through both approaches, suggesting that it might repersent a critical modulator of p53 functions. We demonstrated that miR-26a overe-xpression is able to dampen p53 transcriptional activity towards several p53 target promoters (Bax, Pig3 and p21). Moreover, we have shown that miR-26a strongly reduces p53-dependent apoptosis upon DNA damage in different cell lines, to a similar extent as obtained by RNAi-mediated p53 knock-down. At the molecular level, we observed that miR-26a impairs p53 activation by targeting multiple stress-activated kinases that phosphorylate p53, such as ATM, HIPK2 and PKCδ. Accordingly, miR-26a reduces p53 phosphorylation on Ser15 and Ser46 upon DNA damage. As a consequen-ce, miR-26a overexpression allows cells to proliferate in the presence of oncogenic stress, bypassing the induction of senescence (OIS) driven by RASV12 oncogene similar to what obtai-ned by knockdown of either p53 or its activationg kinase ATM. Considering our data and the reports describing miR-26a overexpression in several tumors (e.g. glioblastomas), we speculate that aberrant expression of miR-26a might represent an oncogenic process by preventing activation of the p53 pathway and thus relieving a primary barrier against transformation. For all these reasons, the perspective to block miR-26a expression/functions could represent a new important way to tackle tumors.
XXI Ciclo
1981
Foulquier, Elodie. "Du métabolisme carboné à la morphogenèse : Rôle interprété par YvcK, protéine de Bacillus subtilis." Thesis, Aix-Marseille 2, 2011. http://www.theses.fr/2011AIX22077.
Повний текст джерелаThe YvcK protein is a bacterial conserved protein of unknown function. It is essential in Staphylococcus aureus but not essential in both Bacillus subtilis and Escherichia coli. In B. subtilis, inactivation of the yvcK gene seriously affects growth and morphology on neoglucogenic carbon sources. The defects observed in a yvcK mutant can be offset by the addition of high concentrations of magnesium or by inactivation of genes involved in metabolism. This suggests that, when grown on some carbon sources, yvcK mutants display alterations in their cell wall probably due to a disorder in this metabolism. The phenotype associated with the absence of YvcK is similar to that observed with strains mutated in genes involved in peptidoglycan synthesis or encoding proteins of the cytoskeleton. The major component of cytoskeleton, MreB, an actin-like protein, together with other proteins, forms a helical structure at the cell membrane that participates in the organization and positioning of the enzymes of peptidoglycan synthesis and maturation. We showed that YvcK is organized as a helical like pattern localized near the inner surface of the membrane, independently of the presence of MreB. Surprisingly and despite that these two proteins do not harbour any similarity of sequence or structure, an overproduction of YvcK restored a normal morphology in an mreB mutant strain and vice versa. Furthermore, as already observed for the mreB mutant, in a yvcK mutant strain, the penicillin-binding protein PBP1 is delocalized and deletion of its gene restores growth of a yvcK mutant on gluconate medium. All these results suggest that YvcK is not only involved in the synthesis of cell wall from gluconeogenic carbon sources but also plays a role in cell morphogenesis. In addition, we have shown that similarily to its Mycobacterium tuberculosis homolog, YvcK is phosphorylated in vitro. We have characterized the phosphorylation of YvcK by the protein kinase PrkC and we identified the Thr 304 as the single phosphorylation site. Furthermore, this phosphorylation appears to play an important role in the complementation of the mreB mutant and repositioning of PBP1
Paraboschi, E. M. "ROLE OF THE PRKCA GENE AND OF MICRORNAS IN THE SUSCEPTIBILITY TO MULTIPLE SCLEROSIS." Doctoral thesis, Università degli Studi di Milano, 2012. http://hdl.handle.net/2434/168392.
Повний текст джерелаCibrian-Uhalte, Elena. "Function of the alpha1B1 subunit of Na +, K + ATPase during zebrafish heart development." Doctoral thesis, Humboldt-Universität zu Berlin, Mathematisch-Naturwissenschaftliche Fakultät I, 2008. http://dx.doi.org/10.18452/15818.
Повний текст джерелаThe zebrafish heart and mind (had) mutation which disrupts the alpha1B1 subunit of Na+,K+ ATPase causes heart tube elongation defects and other developmental abnormalities that are reminiscent of several epithelial cell polarity mutants including nagie oko (nok) and heart and soul (has). In this work, I investigated the function and regulatory mechanisms of Had/Na+,K+ ATPase during zebrafish cardiac morphogenesis, as well as its´ possible interactions with Has/Prkci and Nok/Mpp5. In this study, I demonstrate genetic interactions between had and nok in maintaining Zonula occludens-1 (ZO-1) positive junction belts within myocardial cells during heart development. My results strongly suggest that the interaction between Nok/Mpp5 and Had/Na+,K+ ATPase in the maintenance of myocardial ZO-1 junction belts requires the Na pump function and that the correct ionic balance contributes to the maintenance of myocardial integrity. My results show phosphorylation of the N-terminal intracellular tail of Had/Na+,K+ ATPase by PKCs. PKCs have previously been implicated in the regulation of the Na pump function via phosphorylation of N-terminal residues. Therefore, my results raise the possibility that this mechanism is conserved in the zebrafish embryo. The analysis of the subcellular distribution of a phosphorylation-deficient form of Had/Na+,K+ ATPase suggests that, during heart tube elongation, Had/Na+,K+ ATPase activity is regulated at the membrane via phosphorylation at an amino-terminal site. Previous studies suggest that heart morphogenesis is driven via direct phosphorylation of Has/Prkci targets. Therefore, identification of Has/Prkci phosphorylation targets would contribute to better understand cardiac morphogenesis. For this purpose, a chemical genetic approach was designed to identify Has/Prcki direct phosphorylation targets.
Cuenot, Elodie. "Rôle des Sérine/Thréonine kinases PrkC et CD2148 dans la physiologie du pathogène Clostridium difficile." Thesis, Sorbonne Paris Cité, 2018. http://www.theses.fr/2018USPCC286.
Повний текст джерелаClostridium difficile (CD) is the leading cause of intestinal nosocomial post-antibiotic infections in adults. Exposure to certain antibiotics including cephalosporins induces dysbiosis promoting CD infection. Resistance of CD to these antibiotics is a major concern while resistance mechanisms remain poorly characterized. CD produces two toxins that cause epithelial cell damage and inflammation while additional factors associated to cell surface participate in the colonization process. During infection, CD also encounters several stresses in the gut such as secondary bile salts that are toxic for vegetative cells, antibiotics, antimicrobial peptides released by the host, reactive oxygen and nitrogen species produced during inflammation. Pathogen survival depends on its capacity to rapidly adapt to the host environment. Protein phosphorylation is a reversible post-translational modification employed for signal transduction and regulation. Bacterial Ser/Thr kinases (STKs) regulate numerous physiological processes. In response to specific stimuli, STKs phosphorylate substrates on Ser or Thr residues to trigger the appropriate cellular response. Nothing is known about the role of the two STKs of CD, PrkC and CD2148, in the physiology of this enteropathogen. To investigate their function, we constructed ∆prkC and ∆CD2148 mutants. Cells of the ∆prkC mutant had an increased size and abnormal septa. The ∆prkC mutant also had a reduced motility and formed more biofilms. PrkC inactivation increased sensitivity to antimicrobial compounds that CD may encounter in the gut during infection such as deoxycholate, cephalosporins, cationic antimicrobial peptides and lysozyme. This increased susceptibility was not associated to differences in the structure of peptidoglycan. By contrast, we showed that the ∆prkC mutant released more polysaccharide II (PSII) in the supernatant suggesting a decreased deposition of this glycopolymer to the cell surface in this mutant. Our results also revealed that the ∆prkC mutant had a delay in gut implantation in a hamster model. Finally, we observed that the mutant ∆CD2148 formed chains of cells and sporulated more rapidly than the wild-type strain. Accordingly, key sporulation genes were up-regulated in this mutant. Work is now in progress to detect proteins phosphorylated in vivo using phosphoproteomic approaches and to identify substrates of PrkC and CD2148
Yao, Sheng. "SiRNA inhibition of PRKC-σ-vb expression abrogates the aggressive phenotype of human prostate cancer cells". Thesis, University of Liverpool, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.510949.
Повний текст джерелаMadec, Edwige. "Analyse moléculaire d'une protéine-kinase, PrkC, et d'une phosphatase, PrpC, impliquées dans deux processus de développement chez Bacillus subtilis." Paris 11, 2002. http://www.theses.fr/2002PA112283.
Повний текст джерелаProtein phosphorylation on Ser/Thr/Tyr residues plays a vital role in many cellular processes. My studies in this Thesis concerned the characterization, for the first time of PrkC, a membrane linked protein kinase in Bacillus subtilis, belonging to the super-family of Hanks kinases, predominantly found in eukaryotes. PrkC was shown to be an integral membrane protein with the topology of some receptor kinases found in humans, with an external domain presumed sensor, a single transmembrane domain (TMD) and a highly conserved kinase domain. I have shown that PrkC forms dimers with both the extracellular domain and the TMD capable of promoting dimerization. In the presence of ATP, PrkC or its catalytic domain, PrkCc, autophosphorylates in vitro and phosphorylates MBP. In both cases, phosphorylation involves one or more Thr residues. In collaboration with Ole Jensen (Danemark), we were able to identify precisely eight phosphorylated residues in PrkC by mass spectrometry. These residues were localised to specific regions of a 3D structure of PrkCc modelled on known kinase structures. Four Thr were localised to the activation loop whereas three Thr are in the juxtamembrane region, and one Ser in a non conserved region. Site directed mutagenesis of these residues confirmed that autophosphorylation of Ser214 and the threonine residues in the activation loop is essential for kinase activity. In a complementary approach, PrpC, a protein phosphatase homologue of the human PP2C family was also characterized. The autophosphorylated form of PrkC was dephosphorylated by PrpC. PrkC and PrpC are encoded by adjacent genes which are co-transcribed. These results indicate that these enzymes form a functional protein kinase/phosphatase couple. Moreover, other studies showed that mutants deleted for prkC or prpC displayed reduced biofilm formation and sporulation frequencies. A better understanding of the role of PrkC and PrpC in the cell requires identification of targets/partners
Absalon, Cédric. "Identification des cibles du couple Prkc/Prpc et analyse du rôle de la GTPase associée CPGA chez Bacillus subtilis." Paris 11, 2007. http://www.theses.fr/2007PA112171.
Повний текст джерелаMy studies have concerned a signalling system of unknown function composed of a eukaryote-like sensor kinase, a phosphatase and a GTPase, encoded by a gene cluster, conserved in many Gram positive bacteria. We hypothesised that PrkC PrpC and CpgA constitute a single signalling pathway concerned cell wall biogenesis – the external PASTA domain of PrkC binds penicillin or peptidoglycan (PG). This was supported by my demonstration that CpgA is implicated in the biogenesis of PG. Thus, cells depleted for CpgA displayed bizarre shapes, non-uniform deposition of the cell wall and accumulation of late PG precursors. A major part of my work also involved identification of targets of PrkC and PrpC. First, the co-ordinated function of the 3 proteins was supported by demonstrating that CpgA is a substrate for PrkC and PrpC in vitro. The crystal structure of CpgA previously indicated a role as a translation factor. Thus we proposed that CpgA controls the synthesis of proteins, including morphogenic factors, or factors coupling the expansion of the PG layer with protein synthesis. This hypothesis is supported by my demonstration that EF-Tu is also a target for PrkC and PrpC. The third target of PrkC/PrpC identified was YezB, a protein of unknown function. YezB is apparently a component of the stressosome that is known to transduce signals, emanating from environmental stress or energy limitation, to activate the sigma B dependent general stress regulon. YezB could conceivably function as a transducer of inappropriate expansion of or damage to the peptidoglycan, via phosphorylation by PrkC
Landendinger, Melanie [Verfasser]. "Häufigkeit der Spinocerebellären Ataxie Typ 14 (SCA14) in einem Kollektiv von Ataxie-Patienten : Mutationsscreening des Proteinkinase C Gamma-Gens (PRKCG) / Melanie Landendinger." Gießen : Universitätsbibliothek, 2012. http://d-nb.info/106395441X/34.
Повний текст джерелаBaumann, Ursula [Verfasser], Florian [Akademischer Betreuer] [Gutachter] Bassermann, Bernhard [Gutachter] Küster, and Claus [Gutachter] Belka. "The role of the ubiquitin-proteasome system in the pathology and treatment of B-cell lymphoma : Characterization of the PRKCD-FBXO25-HAX1 axis in lymphomagenesis and treatment resistance of B-cell lymphoma / Ursula Baumann ; Gutachter: Bernhard Küster, Claus Belka, Florian Bassermann ; Betreuer: Florian Bassermann." München : Universitätsbibliothek der TU München, 2017. http://d-nb.info/1137010452/34.
Повний текст джерелаЧастини книг з теми "PRKCδ"
Newton, Alexandra C. "Protein Kinase C (Prkc)." In Encyclopedia of Signaling Molecules, 4216–22. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_101822.
Повний текст джерелаNewton, Alexandra C. "Protein Kinase C (Prkc)." In Encyclopedia of Signaling Molecules, 1–6. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4614-6438-9_101822-1.
Повний текст джерелаAhmed, Tahseen, Tuneer Ranjan Mallick, Michael A. Walter, and Moulinath Acharya. "Role of PRKC Apoptosis WT1 Regulator in Ocular Development and Diseases." In Tumor Suppressor Par-4, 255–67. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-80558-6_16.
Повний текст джерелаТези доповідей конференцій з теми "PRKCδ"
Forno, E., Q. Yan, E. Herrera-Luis, M. Pino-Yanes, R. Rios, Y. Y. Han, S. Oh, et al. "PRKCH and Severe Asthma Exacerbations in Latino Children." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a7478.
Повний текст джерелаGoudarzi, Atta, N. Gokgoz, M. Gill, J. S. Wunder, and I. L. Andrulis. "Abstract 4917: PRKCE and other genetic networks in osteosarcoma metastasis." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-4917.
Повний текст джерелаJoseph, S. K., S. Krlshnamurthi, Y. Patel, and V. V. Kakkar. "1,2-DIOCTANOYLGLYCERIOL (diC8) BUT NOT 1-OLEOYL 2-ACETYLGLYCEROL (OAG) INHIBITS AGONIST-INDUCED PLATELET RESPONSES." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644506.
Повний текст джерелаKrishnamurthi, S., S. K. Joseph, and V. V. Kakkar. "EFFECT OF PROTEIN KINASE C (PrkC) ACTIVATORS ON AGONIST-INDUCED ARACHIDONATE RELEASE IN HUMAN PLATELETS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644508.
Повний текст джерелаRehmani, Hina. "Abstract 4856: Suppression of PRKCI gene-amplified ovarian cancer using aptamer-delivered siRNA." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-4856.
Повний текст джерелаRehmani, Hina. "Abstract 4856: Suppression of PRKCI gene-amplified ovarian cancer using aptamer-delivered siRNA." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-4856.
Повний текст джерелаTsang, Tsun Yee, Gayatry Mohapatra, Hiroaki Itamochi, Samuel C. Mok, and Michael J. Birrer. "Abstract 1102: Integrated genomic analysis of clear-cell ovarian cancer identifies PRKCI as a therapeutic target." 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.am2015-1102.
Повний текст джерелаGalanter, Joshua M., Marc Via, Celeste Eng, Kenny Beckman, Jose Rodriguez-Santana, William Rodríguez-Cintrón, Alfonso Torres-Palacios, Rocio Chapela, Pedro Avila, and Esteban Gonzalez-Burchard. "Polymorphisms In The PRKCA Gene Are Weakly Associated With Asthma But Not BMI In Latino Americans." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a1323.
Повний текст джерелаIrie, Hanna Yoko, Jessica H. Byerly, and Elisa R. Port. "Abstract P3-06-14: Inhibition of PRKCQ enhances chemosensitivity of triple negative breast cancer by regulating EMT and Bim." In Abstracts: 2019 San Antonio Breast Cancer Symposium; December 10-14, 2019; San Antonio, Texas. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.sabcs19-p3-06-14.
Повний текст джерелаIrie, HY, and J. Byerly. "Abstract P2-06-07: PRKCQ regulates taxol sensitivity of triple negative breast cancer cells via IL-6/Stat3 signaling." In Abstracts: Thirty-Eighth Annual CTRC-AACR San Antonio Breast Cancer Symposium; December 8-12, 2015; San Antonio, TX. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.sabcs15-p2-06-07.
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