Journal articles on the topic 'Gene frequency'

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1

Robbins, G. "GENE FREQUENCY FOR THALASSAEMIA." Lancet 325, no. 8428 (March 1985): 579. http://dx.doi.org/10.1016/s0140-6736(85)91235-8.

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2

Maheshri, Narendra. "Gene Expression: Dialing Up the Frequency." Current Biology 18, no. 24 (December 2008): R1136—R1139. http://dx.doi.org/10.1016/j.cub.2008.10.032.

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3

Caballero-Franco, C., and S. Kissler. "The autoimmunity-associated gene RGS1 affects the frequency of T follicular helper cells." Genes & Immunity 17, no. 4 (March 31, 2016): 228–38. http://dx.doi.org/10.1038/gene.2016.16.

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4

Takahama, Kazutaka, Masayoshi Matsuoka, Kazuhiro Nagahama, and Takahira Ogawa. "High-Frequency Gene Replacement in Cyanobacteria Using a Heterologous rps12 Gene." Plant and Cell Physiology 45, no. 3 (March 15, 2004): 333–39. http://dx.doi.org/10.1093/pcp/pch041.

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5

Durinovic-Belló, I., R. P. Wu, V. H. Gersuk, S. Sanda, H. G. Shilling, and G. T. Nepom. "Insulin gene VNTR genotype associates with frequency and phenotype of the autoimmune response to proinsulin." Genes & Immunity 11, no. 2 (January 7, 2010): 188–93. http://dx.doi.org/10.1038/gene.2009.108.

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6

Frankowiack, M., R.-M. Kovanen, G. A. Repasky, C. K. Lim, C. Song, N. L. Pedersen, and L. Hammarström. "The higher frequency of IgA deficiency among Swedish twins is not explained by HLA haplotypes." Genes & Immunity 16, no. 3 (January 8, 2015): 199–205. http://dx.doi.org/10.1038/gene.2014.78.

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7

Lewis, R. M., B. Grundy, and L. A. Kuehn. "Predicting population gene frequency from sample data." Animal Science 78, no. 1 (February 2004): 03–11. http://dx.doi.org/10.1017/s1357729800053789.

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AbstractWith an increase in the number of candidate genes for important traits in livestock, effective strategies for incorporating such genes into selection programmes are increasingly important. Those strategies in part depend on the frequency of a favoured allele in a population. Since comprehensive genotyping of a population is seldom possible, we investigate the consequences of sampling strategies on the reliability of the gene frequency estimate for a bi-allelic locus. Even within a subpopulation or line, often only a proportion of individuals will be genotype tested. However, through segregation analysis, probable genotypes can be assigned to individuals that themselves were not tested, using known genotypes on relatives and a starting (presumed) gene frequency. The value of these probable genotypes in estimation of gene frequency was considered. A subpopulation or line was stochastically simulated and sampled at random, over a cluster of years or by favouring a particular genotype. Line was simulated (replicated) 1000 times. The reliability of gene frequency estimates depended on the sampling strategy used. With random sampling, even when a small proportion of a line was genotyped (0·10), the gene frequency of the population was well estimated from the across-line mean. When information on probable genotypes on untested individuals was combined with known genotypes, the between-line variance in gene frequency was estimated well; including probable genotypes overcame problems of statistical sampling. When the sampling strategy favoured a particular genotype, unsurprisingly the estimate of gene frequency was biased towards the allele favoured. In using probable genotypes the bias was lessened but the estimate of gene frequency still reflected the sampling strategy rather than the true population frequency. When sampling was confined to a few clustered years, the estimation of gene frequency was biased for those generations preceding the sampling event, particularly when the presumed starting gene frequency differed from the true population gene frequency. The potential risks of basing inferences about a population from a potentially biased sample are discussed.
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8

Kiemeney, L., D. Timothy Bishop, DouglasF Easton, and Nicholas Hayward. "Frequency of familial melanoma and MLM2 gene." Lancet 345, no. 8949 (March 1995): 581–82. http://dx.doi.org/10.1016/s0140-6736(95)90489-1.

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9

Thomas, Alun. "Accelerated Gene Counting for Haplotype Frequency Estimation." Annals of Human Genetics 67, no. 6 (November 2003): 608–12. http://dx.doi.org/10.1046/j.1529-8817.2003.00054.x.

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10

Dickinson, Paul, Wendy L. Kimber, Fiona M. Kilanowski, Barbara J. Stevenson, David J. Porteous, and Julia R. Dorin. "High frequency gene targeting using insertional vectors." Human Molecular Genetics 2, no. 8 (1993): 1299–302. http://dx.doi.org/10.1093/hmg/2.8.1299.

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11

Majumder, Partha P. "Principal axis analysis of gene frequency data." American Journal of Physical Anthropology 76, no. 3 (July 1988): 313–20. http://dx.doi.org/10.1002/ajpa.1330760305.

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12

Shaked, H., C. Melamed-Bessudo, and A. A. Levy. "High-frequency gene targeting in Arabidopsis plants expressing the yeast RAD54 gene." Proceedings of the National Academy of Sciences 102, no. 34 (August 10, 2005): 12265–69. http://dx.doi.org/10.1073/pnas.0502601102.

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13

Ali, Nadir, Bashir Ahmed, Humaira Akram, Junaid Akhtar, Ross Williams, and Ron Dixon. "HFE GENE MUTATIONS." Professional Medical Journal 25, no. 01 (January 8, 2018): 129–34. http://dx.doi.org/10.29309/tpmj/18.4462.

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14

Olson, Jane M. "Robust Estimation of Gene Frequency and Association Parameters." Biometrics 50, no. 3 (September 1994): 665. http://dx.doi.org/10.2307/2532781.

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15

Rubin, L. A., V. Peltekova, N. Janicic, C. C. Liew, D. Hwang, J. Evrovski, G. N. Hendy, and D. E. C. Cole. "Calcium sensing receptor gene: Analysis of polymorphism frequency." Scandinavian Journal of Clinical and Laboratory Investigation 57 (1997): 122–25. http://dx.doi.org/10.3109/00365519709168318.

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16

Vitalis, Renaud, Mathieu Gautier, Kevin J. Dawson, and Mark A. Beaumont. "Detecting and Measuring Selection from Gene Frequency Data." Genetics 196, no. 3 (December 20, 2013): 799–817. http://dx.doi.org/10.1534/genetics.113.152991.

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17

Novak, Sebastian, and Richard Kollár. "Spatial Gene Frequency Waves Under Genotype-Dependent Dispersal." Genetics 205, no. 1 (November 4, 2016): 367–74. http://dx.doi.org/10.1534/genetics.116.193946.

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18

Tan, Cheemeng, Faisal Reza, and Lingchong You. "Noise-Limited Frequency Signal Transmission in Gene Circuits." Biophysical Journal 93, no. 11 (December 2007): 3753–61. http://dx.doi.org/10.1529/biophysj.107.110403.

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19

Mary, C., F. Faraut, M. Deniau, J. Dereure, K. Aoun, S. Ranque, and R. Piarroux. "Frequency of Drug Resistance Gene Amplification in ClinicalLeishmaniaStrains." International Journal of Microbiology 2010 (2010): 1–8. http://dx.doi.org/10.1155/2010/819060.

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Experimental studies aboutLeishmaniaresistance to metal and antifolates have pointed out that gene amplification is one of the main mechanisms of drug detoxification. Amplified genes code for adenosine triphosphate-dependent transporters (multidrug resistance and P-glycoproteins P), enzymes involved in trypanothione pathway, particularly gamma glutamyl cysteine synthase, and others involved in folates metabolism, such as dihydrofolate reductase and pterine reductase. The aim of this study was to detect and quantify the amplification of these genes in clinical strains of visceral leishmaniasis agents:Leishmania infantum, L. donovani, andL. archibaldi. Relative quantification experiments by means of real-time polymerase chain reaction showed that multidrug resistance gene amplification is the more frequent event. For P-glycoproteins P and dihydrofolate reductase genes, level of amplification was comparable to the level observed after in vitro selection of resistant clones. Gene amplification is therefore a common phenomenon in wild strains concurring toLeishmaniagenomic plasticity. This finding, which corroborates results of experimental studies, supports a better understanding of metal resistance selection and spreading in endemic areas.
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20

Carney, Ellen F. "Frequency of podocyte-related gene mutations in FSGS." Nature Reviews Nephrology 10, no. 4 (February 25, 2014): 184. http://dx.doi.org/10.1038/nrneph.2014.29.

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21

Cai, Long, Chiraj K. Dalal, and Michael B. Elowitz. "Frequency-modulated nuclear localization bursts coordinate gene regulation." Nature 455, no. 7212 (September 2008): 485–90. http://dx.doi.org/10.1038/nature07292.

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22

Holsinger, Kent E. "Forecasting Gene Frequency. N. J. T. Lo Cascio." Quarterly Review of Biology 66, no. 2 (June 1991): 242. http://dx.doi.org/10.1086/417232.

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23

WILLISON, KEITH R. "Sex and frequency of gene conversions in meiosis." Nature 313, no. 6003 (February 1985): 604. http://dx.doi.org/10.1038/313604a0.

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24

Spreafico, M., M. Karimi, S. Zeinali, P. M. Mannucci, and F. Peyvandi. "Allele Frequency of CYP2C9 Gene Polymorphisms in Iran." Thrombosis and Haemostasis 88, no. 11 (2002): 874–75. http://dx.doi.org/10.1055/s-0037-1613318.

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25

Newmark, Judith A., Frank Sacher, Gwilym S. Jones, and Carol M. Warner. "Ped gene deletion polymorphism frequency in wild mice." Journal of Experimental Zoology 293, no. 2 (June 28, 2002): 179–85. http://dx.doi.org/10.1002/jez.10117.

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26

Rubin, L. A., V. Peltekova, N. Janicic, C. C. Liew, D. Hwang, J. Evrovski, G. N. Hendy, and D. E. C. Cole. "Calcium sensing receptor gene: Analysis of polymorphism frequency." Scandinavian Journal of Clinical and Laboratory Investigation 57, sup227 (January 1997): 122–25. http://dx.doi.org/10.1080/00365519709168318.

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27

Jeong, Mi-Jeong, Chang-Ki Shim, Jin-Ohk Lee, Hawk-Bin Kwon, Yang-Han Kim, Seong-Kon Lee, Myeong-Ok Byun, and Soo-Chul Park. "Plant gene responses to frequency-specific sound signals." Molecular Breeding 21, no. 2 (July 28, 2007): 217–26. http://dx.doi.org/10.1007/s11032-007-9122-x.

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28

Broux, B., N. Hellings, K. Venken, J.-L. Rummens, K. Hensen, B. Van Wijmeersch, and P. Stinissen. "Haplotype 4 of the multiple sclerosis-associated interleukin-7 receptor alpha gene influences the frequency of recent thymic emigrants." Genes & Immunity 11, no. 4 (January 14, 2010): 326–33. http://dx.doi.org/10.1038/gene.2009.106.

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29

CHAKRABORTY, Supriyo. "Gene Frequency and Heritability of Rh Blood Group Gene in 44 Human Populations." Notulae Scientia Biologicae 2, no. 3 (September 27, 2010): 16–19. http://dx.doi.org/10.15835/nsb234756.

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30

Murti, J. R., M. Bumbulis, and J. C. Schimenti. "High-frequency germ line gene conversion in transgenic mice." Molecular and Cellular Biology 12, no. 6 (June 1992): 2545–52. http://dx.doi.org/10.1128/mcb.12.6.2545.

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Gene conversion is the nonreciprocal transfer of genetic information between two related genes or DNA sequences. It can influence the evolution of gene families, having the capacity to generate both diversity and homogeneity. The potential evolutionary significance of this process is directly related to its frequency in the germ line. While measurement of meiotic inter- and intrachromosomal gene conversion frequency is routine in fungal systems, it has hitherto been impractical in mammals. We have designed a system for identifying and quantitating germ line gene conversion in mice by analyzing transgenic male gametes for a contrived recombination event. Spermatids which undergo the designed intrachromosomal gene conversion produce functional beta-galactosidase (encoded by the lacZ gene), which is visualized by histochemical staining. We observed a high incidence of lacZ-positive spermatids (approximately 2%), which were produced by a combination of meiotic and mitotic conversion events. These results demonstrate that gene conversion in mice is an active recombinational process leading to nonparental gametic haplotypes. This high frequency of intrachromosomal gene conversion seems incompatible with the evolutionary divergence of newly duplicated genes. Hence, a process may exist to uncouple gene pairs from frequent conversion-mediated homogenization.
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31

Murti, J. R., M. Bumbulis, and J. C. Schimenti. "High-frequency germ line gene conversion in transgenic mice." Molecular and Cellular Biology 12, no. 6 (June 1992): 2545–52. http://dx.doi.org/10.1128/mcb.12.6.2545-2552.1992.

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Gene conversion is the nonreciprocal transfer of genetic information between two related genes or DNA sequences. It can influence the evolution of gene families, having the capacity to generate both diversity and homogeneity. The potential evolutionary significance of this process is directly related to its frequency in the germ line. While measurement of meiotic inter- and intrachromosomal gene conversion frequency is routine in fungal systems, it has hitherto been impractical in mammals. We have designed a system for identifying and quantitating germ line gene conversion in mice by analyzing transgenic male gametes for a contrived recombination event. Spermatids which undergo the designed intrachromosomal gene conversion produce functional beta-galactosidase (encoded by the lacZ gene), which is visualized by histochemical staining. We observed a high incidence of lacZ-positive spermatids (approximately 2%), which were produced by a combination of meiotic and mitotic conversion events. These results demonstrate that gene conversion in mice is an active recombinational process leading to nonparental gametic haplotypes. This high frequency of intrachromosomal gene conversion seems incompatible with the evolutionary divergence of newly duplicated genes. Hence, a process may exist to uncouple gene pairs from frequent conversion-mediated homogenization.
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32

Shi, Jiancheng, Chusheng Huang, Tao Dong, and Xiuzhi Zhang. "High-frequency and low-frequency effects on vibrational resonance in a synthetic gene network." Physical Biology 7, no. 3 (September 1, 2010): 036006. http://dx.doi.org/10.1088/1478-3975/7/3/036006.

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33

Kenzhebayeva, S., G. Doktyrbay, N. Omirbekova, F. Sarsu, D. Tashenev, and A. Aibekova. "Frequency of vernalization requirement associated dominant VRN-A1 gene and earliness related Esp-A1 candidate genes in advanced wheat mutant lines and effect of allele on flowering time." International Journal of Biology and Chemistry 9, no. 1 (2016): 24–30. http://dx.doi.org/10.26577/2218-7979-2016-9-1-24-30.

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34

Li, Na, Tammy M. Joska, Catherine E. Ruesch, Samuel J. Coster, and William J. Belden. "The frequency natural antisense transcript first promotes, then represses, frequency gene expression via facultative heterochromatin." Proceedings of the National Academy of Sciences 112, no. 14 (March 23, 2015): 4357–62. http://dx.doi.org/10.1073/pnas.1406130112.

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The circadian clock is controlled by a network of interconnected feedback loops that require histone modifications and chromatin remodeling. Long noncoding natural antisense transcripts (NATs) originate from Period in mammals and frequency (frq) in Neurospora. To understand the role of NATs in the clock, we put the frq antisense transcript qrf (frq spelled backwards) under the control of an inducible promoter. Replacing the endogenous qrf promoter altered heterochromatin formation and DNA methylation at frq. In addition, constitutive, low-level induction of qrf caused a dramatic effect on the endogenous rhythm and elevated circadian output. Surprisingly, even though qrf is needed for heterochromatic silencing, induction of qrf initially promoted frq gene expression by creating a more permissible local chromatin environment. The observation that antisense expression can initially promote sense gene expression before silencing via heterochromatin formation at convergent loci is also found when a NAT to hygromycin resistance gene is driven off the endogenous vivid (vvd) promoter in the Δvvd strain. Facultative heterochromatin silencing at frq functions in a parallel pathway to previously characterized VVD-dependent silencing and is needed to establish the appropriate circadian phase. Thus, repression via dicer-independent siRNA-mediated facultative heterochromatin is largely independent of, and occurs alongside, other feedback processes.
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35

Liu, Su-Ching, Ching-Tien Peng, Tsai-Hsiu Lin, Shiow-Jain Wang, Mu-Chin Shih, Ni Tien, Chao-Chin Chang, Jang-Jih Lu, and Chien-Yu Lin. "Molecular Lesion Frequency Of Hemoglobin Gene Disorders In Taiwan." Hemoglobin 35, no. 3 (May 20, 2011): 228–36. http://dx.doi.org/10.3109/03630269.2011.572524.

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36

Amandykova, М. D., К. Zh Dossybayev, A. M. Baibagysov, I. A. Litus, M. K. Iklasov, A. S. Мussayeva, B. O. Bekmanov, and N. Saitou. "CSN3 gene distribution frequency in camels of Almaty region." Experimental Biology 81, no. 4 (2019): 34–42. http://dx.doi.org/10.26577/eb-2019-4-b4.

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37

Finocchiaro, G., M. Tenan, B. M. Colombo, L. Cajola, G. Broggi, and B. Pollo. "Low frequency of NF1 gene mutations in malignant gliomas." European Journal of Cancer 29, no. 8 (January 1993): 1217–18. http://dx.doi.org/10.1016/s0959-8049(05)80329-6.

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38

Grundy, B., and R. M. Lewis. "Gene frequency estimation from a biased sample of individuals." Proceedings of the British Society of Animal Science 2001 (2001): 44. http://dx.doi.org/10.1017/s1752756200004269.

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With individual genes being identified that have an important effect on performance and fitness in livestock it is likely that such genes will be included in selection programmes. However, in order to devise sensible strategies to achieve this, knowledge of the frequency of the gene of interest is required. In practice, it is possible that estimates for gene frequency are based on genotype testing of only a subset of the population. The question then arises as to what conclusions can be drawn about the population gene frequency particularly in the likely scenario where the sample genotyped is not chosen at random. A procedure was developed by Van Arendonk et al. (1989) to have genotype information on as many individuals as possible given financial limits in the numbers genotyped. In this procedure the genotypes of individuals are predicted using pedigree information and the rules of Mendelian inheritance. What is less clear is the value of the additional information in predicting the population gene frequency. The objective of this study was to assess to consequence of sampling procedures on estimates of gene frequency when additional genotype information is or is not obtained by predicting genotypes on individuals themselves not tested.
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39

Feeney, Ann J., Peter Goebel, and Celia R. Espinoza. "Many levels of control of V gene rearrangement frequency." Immunological Reviews 200, no. 1 (August 2004): 44–56. http://dx.doi.org/10.1111/j.0105-2896.2004.00163.x.

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40

Cobo, A. M., J. J. Poza, A. Blanco, A. Lopez de Munain, A. Saenz, M. Azpitarte, J. Marchessi, and J. F. Marti Masso. "Frequency of myotonic dystrophy gene carriers in cataract patients." Journal of Medical Genetics 33, no. 3 (March 1, 1996): 221–23. http://dx.doi.org/10.1136/jmg.33.3.221.

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41

Simpson, M. L., C. D. Cox, and G. S. Sayler. "Frequency domain analysis of noise in autoregulated gene circuits." Proceedings of the National Academy of Sciences 100, no. 8 (April 1, 2003): 4551–56. http://dx.doi.org/10.1073/pnas.0736140100.

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42

Laaser, Ingeborg, Fabian J. Theis, Martin Hrabé de Angelis, Hans-Jochem Kolb, and Jerzy Adamski. "Huge Splicing Frequency in Human Y Chromosomal UTY Gene." OMICS: A Journal of Integrative Biology 15, no. 3 (March 2011): 141–54. http://dx.doi.org/10.1089/omi.2010.0107.

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43

Wilkinson, Emma. "High frequency of gene mutations in metastatic prostate cancer." Lancet Oncology 17, no. 8 (August 2016): e326. http://dx.doi.org/10.1016/s1470-2045(16)30316-3.

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44

Chiang, Sarah, Rola Ali, Nataliya Melnyk, Jessica N. McAlpine, David G. Huntsman, C. Blake Gilks, Cheng-Han Lee, and Esther Oliva. "Frequency of Known Gene Rearrangements in Endometrial Stromal Tumors." American Journal of Surgical Pathology 35, no. 9 (September 2011): 1364–72. http://dx.doi.org/10.1097/pas.0b013e3182262743.

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45

Ritland, K. "Estimation of gene frequency and heterozygosity from pooled samples." Molecular Ecology Notes 2, no. 3 (September 2002): 370–72. http://dx.doi.org/10.1046/j.1471-8286.2002.00182.x.

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46

Cox, Chris D., James M. McCollum, Derek W. Austin, Michael S. Allen, Roy D. Dar, and Michael L. Simpson. "Frequency domain analysis of noise in simple gene circuits." Chaos: An Interdisciplinary Journal of Nonlinear Science 16, no. 2 (June 2006): 026102. http://dx.doi.org/10.1063/1.2204354.

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47

Hosoi, Gaku, Junichi Hara, Takayuki Okamura, Yuko Osugi, Shigehiko Ishihara, Masahiro Fukuzawa, Akira Okada, Shintaro Okada, and Akio Tawa. "Low frequency of the p53 gene mutations in neuroblastoma." Cancer 73, no. 12 (June 15, 1994): 3087–93. http://dx.doi.org/10.1002/1097-0142(19940615)73:12<3087::aid-cncr2820731230>3.0.co;2-9.

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48

Esteve, Asunción, Ghyslaine Martel-Planche, Bakary S. Sylla, Monica Hollstein, Pierre Hainaut, and Ruggero Montesano. "Low frequency ofp16/CDKN2 gene mutations in esophageal carcinomas." International Journal of Cancer 66, no. 3 (May 3, 1996): 301–4. http://dx.doi.org/10.1002/(sici)1097-0215(19960503)66:3<301::aid-ijc5>3.0.co;2-2.

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49

Oh, Myoung-Don, Sung Soon Kim, Eun Young Kim, Sunhee Lee, Namjoong Kim, Keun Yong Park, Uiseok Kim, et al. "The frequency of mutation in CCR5 gene among Koreans." International Journal of STD & AIDS 11, no. 4 (April 1, 2000): 266–67. http://dx.doi.org/10.1258/0956462001915688.

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To better understand a role of the Delta32 allele of the CCR5 gene in HIV-1 transmission and disease progression, we determined the CCR5 genotypes within several groups of Koreans. Amplification of DNA from each subject was achieved with polymerase chain reaction, using the CCR5 specific primer pair, which flanks the 32 bp deletion. The 1.2 kb coding sequences of CCR5 were examined to see the possible effects of CCR5 polymorphism. All of the 339 healthy, HIV-uninfected individuals had no mutation in the CCR5 gene. All of the 115 HIV-1-infected patients including 11 long-term non-progressors (LTNPs) and 18 discordant spouses were also wild homozygotes. No variation in the 1.2 kb CCR5 coding sequence was found in 5 LTNPs and 5 discordant spouses. In conclusion, the 32 bp deletion mutant is rarely present in Koreans. Our data suggest that factors other than the CCR5 coding sequences may also play a role in the resistance to HIV infection.
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50

Barbujani, Guido. "Detecting and comparing the direction of gene-frequency gradients." Journal of Genetics 67, no. 2 (August 1988): 129–40. http://dx.doi.org/10.1007/bf02927793.

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