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Relevant bibliographies by topics / Identification of novel genes

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Academic literature on the topic 'Identification of novel genes'

Author: Grafiati

Published: 4 June 2021

Last updated: 9 February 2022

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Journal articles on the topic "Identification of novel genes"

1

Qi, Peng-Fei, Yu-Ming Wei, Qing Chen, Thérèse Ouellet, Jia Ai, Guo-Yue Chen, Wei Li, and You-Liang Zheng. "Identification of novel α-gliadin genes." Genome 54, no. 3 (March 2011): 244–52. http://dx.doi.org/10.1139/g10-114.

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Ten novel α-gliadin genes (Gli-ta, Gli-turg1, Gli-turg2, Gli-turg3, Gli-turg4, Gli-turg5, Gli-turg6, Gli-cs1, Gli-cs2, and Gli-cs3) with unique characteristics were isolated from wheat ( Triticum aestivum L.), among which Gli-cs1, Gli-cs2, Gli-cs3, and Gli-turg6 were pseudogenes. Gli-cs3 and nine other sequences were much larger and smaller, respectively, than the typical α-gliadins. This variation was caused by insertion or deletion of the unique domain I and a polyglutamine region, possibly the result of illegitimate recombination. Consequently, Gli-cs3 contained 10 cysteine residues, whereas there were 2 cysteine residues only in the other nine sequences. Gli-ta/Gli-ta-like α-gliadin genes are normally expressed during the development of seeds. SDS–PAGE analysis showed that in-vitro-expressed Gli-ta could form intermolecular disulphide bonds and could be chain extenders. A protein band similar in size to Gli-ta has been observed in seed extracts, and mass spectrometry results confirm that the band contains small molecular mass α-gliadins, which is a characteristic of the novel α-gliadins. Mass spectrometry results also indicated that the two cysteine residues of Gli-ta/Gli-ta-like proteins participated in the formation of intermolecular disulphide bonds in vivo.

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Koti, Madhuri, Galina Kataeva, and Azad K. Kaushik. "Identification of novel bovine DH genes." Veterinary Immunology and Immunopathology 128, no. 1-3 (March 2009): 211. http://dx.doi.org/10.1016/j.vetimm.2008.10.006.

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Zhao, Liang, Faisal Al Owaidi, Diwakar R. Pattabiraman, Emily Verrier, Anna Tsykin, Gregory J. Goodall, Paul Leo, and Thomas J. Gonda. "Identification of Novel MYB Target Genes." Blood 112, no. 11 (November 16, 2008): 3580. http://dx.doi.org/10.1182/blood.v112.11.3580.3580.

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Abstract The MYB oncogene encodes a transcription factor, Myb, which is essential for normal haemopoiesis and also for the proliferation of most acute leukaemias (reviewed in ref. 1). While a number of Myb target genes have been reported previously, these do not completely account for key elements of MYB’s activity, including its pro-leukaemic and differentiation-suppressing functions. We hypothesised that this reflects the fact that previous screens may have not been sufficiently comprehensive and/or employed the most appropriate cell systems. Thus we have embarked upon a program to identify and validate Myb targets critical for these functions. Here we report results from extensive expression profiling studies using a conditionally myb-transformed myeloid cell line, ERMYB (2). We have used ~44,000-element Illumina Beadchips in conjunction with a kinetic profiling strategy that selects candidates based on rapid, statistically-significant and consistent responses to both activation and inactivation of Myb. This has resulted in the identification of a substantial number of candidate Myb-activated and -repressed genes (381 and 502, respectively). In addition, we have used this cell system to identify candidate Myb-regulated microRNAs. Inspection of the list of candidate Myb-activated genes revealed several previously-described Myb targets including myc, bcl2, gstm1 and mpo, providing additional confidence in our approach. Our focus to date has been on novel candidates that may mediate myb’s ability to enhance proliferation, suppress differentiation and possibly suppress apoptosis. Q-RT-PCR was used as an initial validation step for a number of such targets; to date 13/14 genes identified by array screening have been confirmed by this method in ERMYB cells. A second approach to validation is to confirm correlation with Myb over-expression in a second cell system (FDB-1) (3). As in primary cells, enforced Myb expression can suppress differentiation and promote proliferation of these cells in the presence of GM-CSF (4). Amongst the Myb-activated genes are gfi1 and nucleostemin/gnl3, which are involved in stem-cell functions, cellular proliferation and in the case of gfi1, lineage-specific functions. Strikingly, candidate Myb-repressed genes include several important positive regulators of haemopoietic differentiation and/or negative regulators of proliferation, namely gata3, sfpi1/pu.1, cebpb, junb, klf’s-3,-6 -13 and btg1. Most of these genes have evolutionarily conserved internal or proximal candidate Myb binding sites. Our progress in validating these by chromatin immunoprecipitation will be presented. Finally, we have identified a number of microRNAs that are potentially regulated by Myb. These include members of the miR-17–92 cluster and mir-146b, which appear to be activated and repressed by Myb, respectively. These have been validated by Q-PCR for both the mature miR and the precursor pri-miR transcript. Interestingly, the mir-17–92 cluster has been strongly implicated in oncogenesis and cell cycle regulation (5), while miR-146a/b may have tumour suppressor activity.

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Mirams, Michiko, Babatunde A. Ayodele, Liliana Tatarczuch, Frances M. Henson, Charles N. Pagel, and Eleanor J. Mackie. "Identification of novel osteochondrosis- Associated genes." Journal of Orthopaedic Research 34, no. 3 (September 8, 2015): 404–11. http://dx.doi.org/10.1002/jor.23033.

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Liu, Anna Chang, Junmeng Yang, Tina Yuan, and Yongsheng Bai. "Computational Identification of Novel Missense Variants in Coding Regions of Genes Associated with Intellectual Disability." International Journal of Bioscience, Biochemistry and Bioinformatics 11, no. 2 (April 2021): 22–33. http://dx.doi.org/10.17706/ijbbb.2021.11.2.22-33.

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6

Savory, Joanne G. A., Caitlin Edey, Bradley Hess, Alan J. Mears, and David Lohnes. "Identification of novel retinoic acid target genes." Developmental Biology 395, no. 2 (November 2014): 199–208. http://dx.doi.org/10.1016/j.ydbio.2014.09.013.

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7

Lafrenière, Ronald G., and Guy A. Rouleau. "Identification of Novel Genes Involved in Migraine." Headache: The Journal of Head and Face Pain 52 (October 2012): 107–10. http://dx.doi.org/10.1111/j.1526-4610.2012.02237.x.

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8

Hofsli, E., T. E. Wheeler, M. Langaas, A. Lægreid, and L. Thommesen. "Identification of novel neuroendocrine-specific tumour genes." British Journal of Cancer 99, no. 8 (September 30, 2008): 1330–39. http://dx.doi.org/10.1038/sj.bjc.6604565.

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Östlund, Gabriel, Mats Lindskog, and Erik L. L. Sonnhammer. "Network-based Identification of Novel Cancer Genes." Molecular & Cellular Proteomics 9, no. 4 (December 3, 2009): 648–55. http://dx.doi.org/10.1074/mcp.m900227-mcp200.

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Knowles, Margaret A. "Identification of novel bladder tumour suppressor genes." Electrophoresis 20, no. 2 (February 1, 1999): 269–79. http://dx.doi.org/10.1002/(sici)1522-2683(19990201)20:2<269::aid-elps269>3.0.co;2-7.

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Dissertations / Theses on the topic "Identification of novel genes"

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Travis, Kristina. "Identification of Novel Developmental Genes in Streptomyces Coelicolor." Otterbein University Distinction Theses / OhioLINK, 2005. http://rave.ohiolink.edu/etdc/view?acc_num=otbndist16204640123321.

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Kotian, Shweta. "Identification of Novel Genes in BRCA1-Regulated Pathways." The Ohio State University, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=osu1366341897.

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Archacki, Stephen R. "MOLECULAR IDENTIFICATION OF NOVEL GENES ASSOCIATED WITH ATHEROSCLEROSIS." Cleveland State University / OhioLINK, 2011. http://rave.ohiolink.edu/etdc/view?acc_num=csu1310652996.

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Hu, Xiao Ping. "Identification and characterisation of novel cellulolytic genes using metagenomics." Thesis, University of the Western Cape, 2010. http://etd.uwc.ac.za/index.php?module=etd&action=viewtitle&id=gen8Srv25Nme4_9293_1308049102.

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Metagenomics has been successfully used to discover novel enzymes from uncultured microorganisms in the environment. In this study, metagenomic DNA from a Malawian hot spring soil sample was used to construct a fosmid library. This metagenomic library comprised of more than 10000 clones with an average insert size of 30 kb, representing more than 3.0 x 108 bp of metagenomic DNA (equivalent to approximately 100 bacterial genomes). The library was screened for cellulase activity using a Congo red plate assay to detect zones of carboxymethylcellulose hydrolysis. This yielded 15 positive fosmid clones, of which five were further characterised for activity and thermostability using the 3, 5-dinitrosalicylic assay. Two of the five fosmids (XP008C2 and XP026G5) were selected for DNA pyrosequencing. The full sequence of the XP008C2 (29800bp) fosmid insert is presented in this study and genes thereon were chosen for further study.

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Bennetts, Jennifer. "The identification and characterisation of novel genes in development /." [St. Lucia, Qld.], 2006. http://www.library.uq.edu.au/pdfserve.php?image=thesisabs/absthe19375.pdf.

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Looser, Jens. "Identification of two novel CVC domain-containing homeobox genes." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1995. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/MQ45845.pdf.

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Haviland, Rachel. "Identification of Novel STAT3 Target Genes Associated with Oncogenesis." Scholar Commons, 2011. http://scholarcommons.usf.edu/etd/3729.

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Cytokine and growth factor signaling pathways involving STAT3 are frequently constitutively activated in many human primary tumors, and are known for the transcriptional role they play in controlling cell growth and cell cycle progression. However, the extent of STAT3's reach on transcriptional control of the genome as a whole remains an important question. We predicted that this persistent STAT3 signaling affects a wide variety of cellular functions, many of which still remain to be characterized. We took a broad approach to identify novel STAT3 regulated genes by examining changes in the genome-wide gene expression profile by microarray, using cells expressing constitutively-activated STAT3. Using computational analysis, we were able to define the gene expression profiles of cells containing activated STAT3 and identify candidate target genes with a wide range of biological functions. Among these genes we identified Necdin, a negative growth regulator, as a novel STAT3 target gene, whose expression is down-regulated at the mRNA and protein levels when STAT3 is constitutively active. This repression is STAT3 dependent, since inhibition of STAT3 using siRNA restores Necdin expression. A STAT3 DNA-binding site was identified in the Necdin promoter and both EMSA and chromatin immunoprecipitation confirm binding of STAT3 to this region. Necdin expression has previously been shown to be down-regulated in a melanoma and a drug-resistant ovarian cancer cell line. Further analysis of Necdin expression demonstrated repression in a STAT3-dependent manner in human melanoma, prostate and breast cancer cell lines. These results suggest that STAT3 coordinates expression of genes involved in multiple metabolic and biosynthetic pathways, integrating signals that lead to global transcriptional changes and oncogenesis. STAT3 may exert its oncogenic effect by up-regulating transcription of genes involved in promoting growth and proliferation, but also by down-regulating expression of negative regulators of the same cellular processes, such as Necdin.

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Chu, Youngmin. "Identification of Novel Genes Involved in Female Mating Choice." Case Western Reserve University School of Graduate Studies / OhioLINK, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=case1364923180.

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9

Vyas, Aditi. "Identification of Novel Stat92E Target Genes in Drosophila Hematopoiesis." Ohio University / OhioLINK, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=ohiou1450868635.

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Gregorio-King, Claudia C., and mikewood@deakin edu au. "The Identification of novel genes differentially expressed in Haemopoietic progenitor cells." Deakin University. School of Health Sciences, 2001. http://tux.lib.deakin.edu.au./adt-VDU/public/adt-VDU20051111.113037.

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The biochemical and molecular processes that maintain the stem cell pool, and govern the proliferation and differentiation of haemopoietic stem/progenitor cells (HSPCs) have been widely investigated but are incompletely understood. The purpose of this study was to identify and characterise novel genes that may play a part in regulating the mechanisms that control the proliferation, differentiation and self-renewal of human HSPCs. Reverse transcription differential display polymerase chain reaction (dd-PCR) was used to identify differences in gene expression between a HSPC population defined by expression of the CD34 phenotype, and the more mature CD34 depleted populations. A total of 6 differentially expressed complementary deoxyribonucleic acid (cDNA) sequences were identified. Four of these transcripts were homologous to well characterised genes, while two (band 1 and band 20) were homologous to unknown and uncharacterised partial gene sequences on the GenBank database and were thus chosen for further investigation. The partial cDNA sequences for band 1 and band 20 were designated ORP-3 and MERP-1 (respectively) due to homologies with other well-characterised gene families. Differential expression of the ORP-3 and MERP-1 genes was confirmed using Taqman™ real-time polymerase chain reaction (PCR) with 3 - 4-fold and 4-10 -fold higher levels in the CD34+ fractions of haemopoietic cells compared to CD34- populations respectively. Additionally, expression of both these genes was down regulated with proliferation and differentiation of CD34+ cells further confirming higher expression in a less differentiated subset of haemopoietic cells. The full coding sequences of ORP-3 and MERP-1 were elucidated using bioinformatics, rapid amplification of cDNA ends (RACE) and PCR amplification. The MERP-1 cDNA is 2600 nucleotides (nt) long, and localizes by bioinformatics to chromosome 7.. It consists of three exons and 2 introns spanning an entire length of 31.4 kilobases (kb). The MERP-1 open reading frame (ORF) codes for a putative 344 amino acid (aa) type II transmembrane protein with an extracellular C-terminal ependymin like-domain and an intracellular N-terminal sequence with significant homology to the cytoplasmic domains of members of the protocadherin family of transmembrane glycoproteins. Ependymins and protocadherins are well-characterised calcium-dependant cell adhesion glycoproteins. Although the function of MERP-1 remains to be elucidated, it is possible that MERP-1 like its homologues plays a role in calcium dependent cell adhesion. Differential expression of the MERP-1 gene in haemopoietic cells suggests a role in haemopoietic stem cell proliferation and differentiation, however, its broad tissue distribution implies that it may also play a role in many cell types. Characterization of the MERP-1 protein is required to elucidate these possible roles. The ORP-3 cDNA is 6631nt long, and localizes by bioinformatics to chromosome 7pl5-p21. It consists of 23 exons and 22 introns spanning an entire length of 183.5kb. The ORP-3 ORF codes for a putative 887aa protein which displays the consensus sequence for a highly conserved oxysterol-binding domain. Other well-characterised proteins expressing these domains have been demonstrated to bind oxysterols (OS) in a dose dependant fashion. OS are hydroxylated derivatives of cholesterol Their biological activities include inhibition of cholesterol biosynthesis and cell proliferation in a variety of cell types, including haemopoietic cells. Differential expression of the ORP-3 gene in haemopoietic cells suggests a possible role in the transduction of OS effects on haemopoietic cells, however, its broad tissue distribution implies that it may also play a role in many cell types. Further investigation of ORP-3 gene expression demonstrates a significant correlation with CD34+ sample purity, and 2-fold higher expression in a population of haemopoietic cells defined by the CD34+38- phenotype compared to more mature CD34+38+ cells. This finding, taken together with the previous observation of down-regulation of ORP-3 expression with proliferation and differentiation of CD34+ cells, indicates that ORP-3 expression may be higher in a less differentiated subset of cells with a higher proliferative capacity. This hypothesis is supported by the observation that expression of the ORP-3 gene is approximately 2-fold lower in differentiated HL60 promyelocytic cells compared to control, undifferentiated cells. ORP-3 expression in HL60 cells during normal culture conditions was also found to vary with expression positively correlated with cell number. This indicates a possible cell cycle effect on ORP-3 gene expression with levels highest when cell density, and therefore the percentage of cells in G(0)/G(1) phase of the cell cycle is highest. This observation also correlates with the observation of higher ORP-3 expression in CD34+38-cells, and in CD34+ and HL60 cells undergoing OS induced and camptothecin induced apoptosis that is preceded by cell cycle arrest at G(0)/G(1). Expression of the ORP-3 gene in CD34+ HSPCs from UCB was significantly decreased to approximately half the levels observed in control cells after 24 hours incubation in transforming growth factor beta-1 (TGFâl). As ≥90% of these cells are stimulated into cell cycle entry by TGFâl, this observation further supports the hypothesis that ORP-3 expression is highest when cells reside in the G(0)/G(1) phase of the cell cycle. Data obtained from investigation of ORP-3 gene expression in synchronised HL60 cells however does not support nor disprove this hypothesis. Culture of CD34+ enriched HSPCs and HL60 cells with 25-OHC significantly increased ORP-3 gene expression to approximately 1.5 times control levels. However, as 25-OHC treatment also increased the percentage of apoptotic cells in these experiments, it is not valid to make any conclusions regarding the regulation of ORP-3 gene expression by OS. Indeed, the observation that camptothecin induced apoptosis also increased ORP-3 gene expression in HL60 cells raises the possibility that up-regulation of ORP-3 gene expression is also associated with apoptosis, Taken together, expression of the ORP-3 gene appears to be regulated by differentiation and apoptosis of haemopoietic progenitors, and may also be positively associated with proliferative and G(0)/G(1) cell cycle status indicating a possible role in all of these processes. Given the important regulatory role of apoptosis in haemopoiesis and differential expression of the ORP-3 gene in haemopoietic progenitors, final investigations were conducted to examine the effects OS on human HSPCs. Granulocyte/macrophage colony forming units (CFU-GM) generated from human bone marrow (ABM) and umbilical cord blood (UCB) were grown in the presence of varying concentrations of three different OS - 7keto-cholesterol (7K-C), 7beta-hydroxycholesterol (7p-OHC) and 25-hydroxycholesterol (25-OHC). Similarly, the effect of OS on HL60 and CD34+ cells was investigated using annexin-V staining and flow cytometry to measure apoptosis. Reduction of nitroblue tetrazolium (NBT) was used to assess differentiative status of HL60 cells. CFU-GM from ABM and HL60 growth was inhibited by all three OS tested, with 25-OHC being the most potent. 25-OHC inhibited ≥50% of bone marrow CFU-GM and ≥95% of HL60 cell growth at a level of 1 ug/ml. Compared to UCB, CFU-GM derived from ABM were more sensitive to the effects of all OS tested. Only 25-OHC and 7(5-OHC significantly inhibited growth of UCB derived CFU-GM. OS treatment increased the number of annexin-V CD34+ cells and NBT positive HL60 cells indicating that OS inhibition of CFU-GM and HL60 cell growth can be attributed to induction of apoptosis and differentiation. From these studies, it can be concluded that dd-PCR is an excellent tool for the discovery of novel genes expressed in human HSPCs. Characterisation of the proteins encoded by the novel genes ORP-3 and MERP-1 may reveal a regulatory role for these genes in haemopoiesis. Finally, investigations into the effects of OS on haemopoietic progenitor cells has revealed that OS are a new class of inhibitors of HSPC proliferation of potential relevance in vivo and in vitro.

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Books on the topic "Identification of novel genes"

1

Looser, Jens. Identification of two novel CVC domain-containing homeobox genes. Ottawa: National Library of Canada, 1995.

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Vanti, William B. Identification of a null mutation in a trace amine receptor gene and nine novel G-protein-coupled receptor genes. Ottawa: National Library of Canada, 2003.

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Tomlekova, N. B., M. I. Kozgar, and M. R. Wani, eds. Mutagenesis: exploring novel genes and pathways. The Netherlands: Wageningen Academic Publishers, 2014. http://dx.doi.org/10.3920/978-90-8686-787-5.

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To, Minh Dong. Identification of transcriptionally deregulated genes in breast cancer. Ottawa: National Library of Canada, 1998.

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King, Kathryn Elizabeth. Identification and analysis of genes expressed during chondrocyte differentiation. Manchester: University of Manchester, 1997.

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Finelli, Antonio. Identification of genes important to Pseudomonas aeruginosa biofilm formation. Ottawa: National Library of Canada, 2001.

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Buchanan, Edna. Legally dead: A novel. New York: Simon & Schuster, 2008.

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Lee, Dennis K. Characterization of novel G protein-coupled receptor genes and the novel ligand apelin. Ottawa: National Library of Canada, 1999.

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9

Philbin, Tom. Blink: A novel. New York: Jove Books, 1994.

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Philbin, Tom. Blink: A novel. New York: Jove Books, 1994.

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Book chapters on the topic "Identification of novel genes"

1

Burssens, S., L. De Veylder, M. Van Montagu, and D. Inzé. "Identification of Novel Cell Cycle Genes in Arabidopsis Thaliana." In Plant Biotechnology and In Vitro Biology in the 21st Century, 355–58. Dordrecht: Springer Netherlands, 1999. http://dx.doi.org/10.1007/978-94-011-4661-6_81.

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Sinnarasan, Vigneshwar Suriya Prakash, Dahrii Paul, Leimarembi Devi Naorem, Mathavan Muthaiyan, Dinakara Rao Ampasala, and Amouda Venkatesan. "Identification of Potential Key Genes Involved in Progression of Gastric Cancer Using Bioinformatics Analysis." In Novel therapeutic approaches for gastrointestinal malignancies, 101–14. Singapore: Springer Singapore, 2020. http://dx.doi.org/10.1007/978-981-15-5471-1_7.

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Schubert, Peter, Andreas Pries, Niels Krüger, and Alexander Steinbüchel. "Molecular analysis of the Alcaligenes eutrophus PHB-biosynthetic genes: identification of the NH2-terminus of PHB synthase and identification of the transcription start site of phbC." In Novel Biodegradable Microbial Polymers, 447–48. Dordrecht: Springer Netherlands, 1990. http://dx.doi.org/10.1007/978-94-009-2129-0_42.

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Frugier, F., S. Poirier, A. Kondorosi, and M. Crespi. "Identification of Novel Putative Regulatory Genes Induced During Nodule Development in Medicago." In Biological Nitrogen Fixation for the 21st Century, 341. Dordrecht: Springer Netherlands, 1998. http://dx.doi.org/10.1007/978-94-011-5159-7_199.

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Onouchi, Yoshihiro. "Identification of Novel Kawasaki Disease Susceptibility Genes by Genome-Wide Association Studies." In Kawasaki Disease, 23–29. Tokyo: Springer Japan, 2016. http://dx.doi.org/10.1007/978-4-431-56039-5_4.

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Sveric, Kruno, Moyra Mason, Till Roenneberg, and Martha Merrow. "Novel Strategies for the Identification of Clock Genes Neurospora With Insertional Mutagenesis." In Methods in Molecular Biology, 173–85. Totowa, NJ: Humana Press, 2007. http://dx.doi.org/10.1007/978-1-59745-257-1_12.

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Pandotra, Pankaj, Parshant Bakshi, Anil Kumar Singh, and Suphla Gupta. "Exploring Genetic Resources for Identification of Potential Novel Genes for Crop Improvement." In Rediscovery of Genetic and Genomic Resources for Future Food Security, 225–37. Singapore: Springer Singapore, 2020. http://dx.doi.org/10.1007/978-981-15-0156-2_7.

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Liew, C. C., D. M. Hwang, R. X. Wang, S. H. Ng, A. Dempsey, D. H. Y. Wen, H. Ma, et al. "Construction of a human heart cDNA library and identification of cardiovascular based genes (CVBest)." In Novel Methods in Molecular and Cellular Biochemistry of Muscle, 81–87. Boston, MA: Springer US, 1997. http://dx.doi.org/10.1007/978-1-4615-6353-2_8.

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Lehoux, Dario E., François Sanschagrin, Irena Kukavica-Ibrulj, Eric Potvin, and Roger C. Levesque. "Identification of Novel Pathogenicity Genes by PCR Signature-Tagged Mutagenesis and Related Technologies." In Genomics, Proteomics, and Clinical Bacteriology, 289–304. Totowa, NJ: Humana Press, 2004. http://dx.doi.org/10.1385/1-59259-763-7:289.

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Staudt, L. M., A. Dent, C. Ma, D. Allman, J. Powell, R. Maile, P. Scherle, and T. Behrens. "Rapid Identification of Novel Human Lymphoid-Restricted Genes by Automated DNA Sequencing of Subtracted cDNA Libraries." In Current Topics in Microbiology and Immunology, 155–61. Berlin, Heidelberg: Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-642-79275-5_19.

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Conference papers on the topic "Identification of novel genes"

1

Aga, H., N. Hallahan, W. Jonas, P. Gottmann, M. Jaehnert, H. Vogel, and A. Schürmann. "Identification of novel genes mediating β-cell failure." In Diabetes Kongress 2019 – 54. Jahrestagung der DDG. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1688106.

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Crona, Daniel James, Oscar Suzuki, O. Joseph Trask, Bethany Parks, Amber Frick, Timothy Wiltshire, and Federico Innocenti. "Abstract 5486: Identification of novel candidate genes associated with sorafenib cytotoxicity." 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.am2015-5486.

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Hu, Yunping, and Wesley Hsu. "Abstract 2021: Identification of novel brachyury target genes in lung cancer." In 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.am2016-2021.

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Van der Plaat, D. A., K. De Jong, J. M. Vonk, C. C. Van Diemen, C. M. Van Duijn, L. Lahousse, G. G. Brusselle, D. S. Postma, and H. M. Boezen. "Identification of novel genes related to airway obstruction in never-smokers." In Annual Congress 2015. European Respiratory Society, 2015. http://dx.doi.org/10.1183/13993003.congress-2015.oa1459.

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Abe, Masanobu, Satoshi Yamashita, Yoshiyuki Mori, Takahiro Abe, Hideto Saijo, Toshikazu Ushijima, and Tsuyoshi Takato. "Abstract 430: Identification of novel methylation-silenced genes in oral squamous cell carcinomas." In 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.am2014-430.

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Koyama, Takahiko, and Laxmi Parida. "Abstract 2771: Identification of novel genes associated with metastasis from TCGA transcriptomic data." 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.am2019-2771.

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Koyama, Takahiko, and Laxmi Parida. "Abstract 2771: Identification of novel genes associated with metastasis from TCGA transcriptomic data." 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.sabcs18-2771.

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Nunga, Lalchung, Ed Schwalbe, Fadhel Lafta, Deborah Tweddle, John Maris, Timothy Barrow, and Gordon Strathdee. "Abstract 1275: Identification of cancer-specific synthetic lethal genes as novel therapeutic targets." In Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-1275.

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Al-Watban, Abdullatif, Zi Hua Yang, Richard Everson, and Zheng Rong Yang. "A novel data mining approach for differential genes identification in small cancer expression data." In 2012 7th International Symposium on Health Informatics and Bioinformatics (HIBIT). IEEE, 2012. http://dx.doi.org/10.1109/hibit.2012.6209033.

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Kouyama, Yuta, Yushi Ogawa, Takaaki Masuda, Yukihiro Yoshikawa, Miwa Noda, Hiroaki Wakiyama, Kuniaki Sato, et al. "Abstract 1972: Identification of novel candidate driver genes of colorectal cancer on chromosome 7p." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-1972.

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Reports on the topic "Identification of novel genes"

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Gelman, Irwin H. Identification of Novel Breast Cancer Metastasis-Suppressor Genes. Fort Belvoir, VA: Defense Technical Information Center, August 2010. http://dx.doi.org/10.21236/ada540929.

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Qi, Chao. Identification of Novel Tumor Suppressor Genes for Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, March 2006. http://dx.doi.org/10.21236/ada453400.

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Petty, Elizabeth M. Identification of Novel Mitotic Checkpoint Genes in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, May 2002. http://dx.doi.org/10.21236/ada408761.

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Eaves, Connie, and Yun Zhao. Identification of Novel Genes and Candidate Targets in CML Stem Cells. Fort Belvoir, VA: Defense Technical Information Center, January 2009. http://dx.doi.org/10.21236/ada502095.

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Hengartner, Michael O. Identification and Characterization of Novel Nematode Cell Death Genes and Their Mammalian Homologs. Fort Belvoir, VA: Defense Technical Information Center, August 2000. http://dx.doi.org/10.21236/ada398562.

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Sternberg, Paul W. Identification of Novel Candidate Tumor Suppressor Genes Using C. elegans as a Model. Fort Belvoir, VA: Defense Technical Information Center, November 1996. http://dx.doi.org/10.21236/ada323557.

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Sternberg, Paul W. Identification of Novel Candidate Tumor Suppressor Genes Using C. elegans as a Model. Fort Belvoir, VA: Defense Technical Information Center, December 1997. http://dx.doi.org/10.21236/ada344938.

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Sternberg, Paul W. Identification of Novel Candidate Tumor Suppressor Genes Using C. elegans as a Model. Fort Belvoir, VA: Defense Technical Information Center, November 1999. http://dx.doi.org/10.21236/ada391240.

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Hengartner, Michael. Identification and Characterization of Novel Nematode Cell Death Genes and Their Mammalian Homologs. Fort Belvoir, VA: Defense Technical Information Center, July 1998. http://dx.doi.org/10.21236/ada360212.

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Belinsky, Steven. Critical Role for Aberrant CpG Island Methylation in the Evolution and Progression of Breast Cancer: Characterization of Known Genes and Identification of Novel Genes. Fort Belvoir, VA: Defense Technical Information Center, September 2001. http://dx.doi.org/10.21236/ada397409.

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