Log in

Relevant bibliographies by topics / Genetic inactivation / Journal articles

To see the other types of publications on this topic, follow the link: Genetic inactivation.

Journal articles on the topic 'Genetic inactivation'

Author: Grafiati

Published: 4 June 2021

Last updated: 18 February 2022

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the top 50 journal articles for your research on the topic 'Genetic inactivation.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Browse journal articles on a wide variety of disciplines and organise your bibliography correctly.

1

Lyon, MF. "X-chromosome inactivation and human genetic disease." Acta Paediatrica 91 (January 2, 2007): 107–12. http://dx.doi.org/10.1111/j.1651-2227.2002.tb03120.x.

Full text

APA, Harvard, Vancouver, ISO, and other styles

2

Wang, Jian, Robert Yu, and Sanjay Shete. "X-Chromosome Genetic Association Test Accounting for X-Inactivation, Skewed X-Inactivation, and Escape from X-Inactivation." Genetic Epidemiology 38, no. 6 (2014): 483–93. http://dx.doi.org/10.1002/gepi.21814.

Full text

APA, Harvard, Vancouver, ISO, and other styles

3

Anderson, Richard J. E., and Hamish G. Spencer. "Population Models of Genomic Imprinting. I. Differential Viability in the Sexes and the Analogy With Genetic Dominance." Genetics 153, no. 4 (1999): 1949–58. http://dx.doi.org/10.1093/genetics/153.4.1949.

Full text

Abstract:

Abstract Many single-locus, two-allele selection models of genomic imprinting have been shown to reduce formally to one-locus Mendelian models with a modified parameter for genetic dominance. One exception is the model where selection at the imprinted locus affects the sexes differently. We present two models of maternal inactivation with differential viability in the sexes, one with complete inactivation, and the other with a partial penetrance for inactivation. We show that, provided dominance relations at the imprintable locus are the same in both sexes, a globally stable polymorphism exist

APA, Harvard, Vancouver, ISO, and other styles

4

Migeon, Barbara R. "X-chromosome inactivation: molecular mechanisms and genetic consequences." Trends in Genetics 10, no. 7 (1994): 230–35. http://dx.doi.org/10.1016/0168-9525(94)90169-4.

Full text

APA, Harvard, Vancouver, ISO, and other styles

5

Wert, Katherine J., Susanne F. Koch, Gabriel Velez, et al. "CAPN5 genetic inactivation phenotype supports therapeutic inhibition trials." Human Mutation 40, no. 12 (2019): 2377–92. http://dx.doi.org/10.1002/humu.23894.

Full text

APA, Harvard, Vancouver, ISO, and other styles

6

Karlsson, Åsa, Sylvie Giuriato, Flora Tang, Jingly Fung-Weier, Göran Levan, and Dean W. Felsher. "Genomically complex lymphomas undergo sustained tumor regression upon MYC inactivation unless they acquire novel chromosomal translocations." Blood 101, no. 7 (2003): 2797–803. http://dx.doi.org/10.1182/blood-2002-10-3091.

Full text

Abstract:

The targeted inactivation of oncogenes may be a specific and effective treatment for cancer. However, because human cancers are the consequence of multiple genetic changes, the inactivation of one oncogene may not be sufficient to cause sustained tumor regression. Moreover, cancers are genomically unstable and may readily compensate for the inactivation of a single oncogene. Here we confirm by spectral karyotypic analysis that MYC-induced hematopoietic tumors are highly genetically complex and genomically unstable. Nevertheless, the inactivation of MYC alone was found to be sufficient to induc

APA, Harvard, Vancouver, ISO, and other styles

7

Marshall, Catherine H., Eddie L. Imada, Zhuojun Tang, Luigi Marchionni, and Emmanuel S. Antonarakis. "CDK12 inactivation across solid tumors: an actionable genetic subtype." Oncoscience 6, no. 5-6 (2019): 312–16. http://dx.doi.org/10.18632/oncoscience.481.

Full text

APA, Harvard, Vancouver, ISO, and other styles

8

Lee, Jeannie T., and Rudolf Jaenisch. "The (epi)genetic control of mammalian X-chromosome inactivation." Current Opinion in Genetics & Development 7, no. 2 (1997): 274–80. http://dx.doi.org/10.1016/s0959-437x(97)80138-4.

Full text

APA, Harvard, Vancouver, ISO, and other styles

9

Dewey, Frederick E., Viktoria Gusarova, Richard L. Dunbar, et al. "Genetic and Pharmacologic Inactivation of ANGPTL3 and Cardiovascular Disease." New England Journal of Medicine 377, no. 3 (2017): 211–21. http://dx.doi.org/10.1056/nejmoa1612790.

Full text

APA, Harvard, Vancouver, ISO, and other styles

10

Handel, M. A., C. Park, and M. Kot. "Genetic control of sex-chromosome inactivation during male meiosis." Cytogenetic and Genome Research 66, no. 2 (1994): 83–88. http://dx.doi.org/10.1159/000133672.

Full text

APA, Harvard, Vancouver, ISO, and other styles

11

Kim, Jin Woo, Yu Cheng, Wennuan Liu, et al. "Genetic and epigenetic inactivation ofLPLgene in human prostate cancer." International Journal of Cancer 124, no. 3 (2009): 734–38. http://dx.doi.org/10.1002/ijc.23972.

Full text

APA, Harvard, Vancouver, ISO, and other styles

12

Moore, Tom, Laurence D. Hurst, and Wolf Reik. "Genetic conflict and evolution of mammalian X-chromosome inactivation." Developmental Genetics 17, no. 3 (1995): 206–11. http://dx.doi.org/10.1002/dvg.1020170305.

Full text

APA, Harvard, Vancouver, ISO, and other styles

13

Casimiro, Isabel, Prameladevi Chinnasamy, and Nicholas E. S. Sibinga. "Genetic inactivation of the allograft inflammatory factor-1 locus." genesis 51, no. 10 (2013): 734–40. http://dx.doi.org/10.1002/dvg.22424.

Full text

APA, Harvard, Vancouver, ISO, and other styles

14

Viloria, Cristina G., Alvaro J. Obaya, Angela Moncada-Pazos, et al. "Genetic Inactivation of ADAMTS15 Metalloprotease in Human Colorectal Cancer." Cancer Research 69, no. 11 (2009): 4926–34. http://dx.doi.org/10.1158/0008-5472.can-08-4155.

Full text

APA, Harvard, Vancouver, ISO, and other styles

15

Robertson, Donald S. "GENETIC STUDIES ON THE LOSS OF Mu MUTATOR ACTIVITY IN MAIZE." Genetics 113, no. 3 (1986): 765–73. http://dx.doi.org/10.1093/genetics/113.3.765.

Full text

Abstract:

ABSTRACT Mutator activity of the Mu mutator system of maize can be lost by either outcrossing or inbreeding Mu stocks. The nature of these two kinds of Mu-loss phenomena was analyzed by testing the results of crossing Mu-loss stocks by active Mu lines. Outcross-Mu-loss stocks are capable of supporting Mu activity if crossed by an active mutator line. Inbred-Mu-loss stocks, however, inactivate the active Mu system contributed by a Mu line. Also, inbred-Mu-loss lines do not regain Mu activity after at least three generations of outcrossing to non-Mu stocks. These results suggest that, once the M

APA, Harvard, Vancouver, ISO, and other styles

16

Donat, M., A. Louis, K. Kreskowski, et al. "X-autosome and X-Y translocations in female carriers: X-chromosome inactivation easily detectable by 5-ethynyl-2-deoxyuridine (EdU)." Balkan Journal of Medical Genetics 20, no. 1 (2017): 87–90. http://dx.doi.org/10.1515/bjmg-2017-0012.

Full text

Abstract:

Abstract Here we report one new case each of an X-autosome translocation (maternally derived), and an X-Y-chromosome translocation. Besides characterizing the involved breakpoints and/or imbalances in detail by molecular cyto-genetics, also skewed X-chromosome inactivation was determined on single cell level using 5-ethynyl-2-deoxyuridine (EdU). Thus, we confirmed that the recently suggested EdU approach can be simply adapted for routine diagnostic use. The latter is important, as only by knowing the real pattern of the skewed X-chromosome inactivation, correct interpretation of obtained resul

APA, Harvard, Vancouver, ISO, and other styles

17

Deol, M. S., Gillian M. Truslove, and Anne McLaren. "Genetic activity at the albino locus in Cattanach's insertion in the mouse." Development 96, no. 1 (1986): 295–302. http://dx.doi.org/10.1242/dev.96.1.295.

Full text

Abstract:

Cattanach's insertion (Is(In7;X)1Ct or XCt) includes the normal allele at the albino locus (c+), which is subject to inactivation of the X chromosome carrying it, so that XCtX; c c mice have albino and pigmented patches. The X-autosome translocation T(X;16)16H or XT16H leads to preferential inactivation of the other X chromosome in female cells, so that XCtXT16H; c c mice are almost entirely white. However, they grow darker with age, as if reversal of inactivation of the c+ allele were taking place in increasing numbers of melanocytes. To test whether this is dependent only on age or whether i

APA, Harvard, Vancouver, ISO, and other styles

18

Ishikawa, Yasunobu, Sorin Fedeles, Arnaud Marlier, et al. "Spliced XBP1 Rescues Renal Interstitial Inflammation Due to Loss of Sec63 in Collecting Ducts." Journal of the American Society of Nephrology 30, no. 3 (2019): 443–59. http://dx.doi.org/10.1681/asn.2018060614.

Full text

Abstract:

BackgroundSEC63 encodes a resident protein in the endoplasmic reticulum membrane that, when mutated, causes human autosomal dominant polycystic liver disease. Selective inactivation of Sec63 in all distal nephron segments in embryonic mouse kidney results in polycystin-1–mediated polycystic kidney disease (PKD). It also activates the Ire1α-Xbp1 branch of the unfolded protein response, producing Xbp1s, the active transcription factor promoting expression of specific genes to alleviate endoplasmic reticulum stress. Simultaneous inactivation of Xbp1 and Sec63 worsens PKD in this model.MethodsWe e

APA, Harvard, Vancouver, ISO, and other styles

19

Kaemmerer, Elke, Paula Kuhn, Ursula Schneider, et al. "Intestinal genetic inactivation of caspase-8 diminishes migration of enterocytes." World Journal of Gastroenterology 21, no. 15 (2015): 4499–508. http://dx.doi.org/10.3748/wjg.v21.i15.4499.

Full text

APA, Harvard, Vancouver, ISO, and other styles

20

Pisanti, Simona, Paola Picardi, Lucia Prota, et al. "Genetic and pharmacologic inactivation of cannabinoid CB1 receptor inhibits angiogenesis." Blood 117, no. 20 (2011): 5541–50. http://dx.doi.org/10.1182/blood-2010-09-307355.

Full text

Abstract:

Abstract In this study we investigated the role of CB1 receptor signaling in angiogenesis and the therapeutic exploitation of CB1 inactivation as an antiangiogenic strategy. We started from the observation that CB1 receptor expression is induced during angiogenesis and that the endocannabinoid anandamide stimulated bFGF-induced angiogenesis in the nanomolar physiologic range. To define the functional involvement of CB1 receptor signaling during angiogenesis, 2 different strategies have been carried out: siRNA-mediated knockdown and pharmacologic antagonism of CB1 receptors. CB1 receptors inact

APA, Harvard, Vancouver, ISO, and other styles

21

Strathdee, Gordon. "Epigenetic versus genetic alterations in the inactivation of E-cadherin." Seminars in Cancer Biology 12, no. 5 (2002): 373–79. http://dx.doi.org/10.1016/s1044-579x(02)00057-3.

Full text

APA, Harvard, Vancouver, ISO, and other styles

22

Calaway, John D., Alan B. Lenarcic, John P. Didion, et al. "Genetic Architecture of Skewed X Inactivation in the Laboratory Mouse." PLoS Genetics 9, no. 10 (2013): e1003853. http://dx.doi.org/10.1371/journal.pgen.1003853.

Full text

APA, Harvard, Vancouver, ISO, and other styles

23

Lavalou, Perrine, Helene Eckert, Louise Damy, et al. "Strategies for genetic inactivation of long noncoding RNAs in zebrafish." RNA 25, no. 8 (2019): 897–904. http://dx.doi.org/10.1261/rna.069484.118.

Full text

APA, Harvard, Vancouver, ISO, and other styles

24

Muccioli, Giulio G., Angela Sia, Paul J. Muchowski, and Nephi Stella. "Genetic Manipulation of Palmitoylethanolamide Production and Inactivation in Saccharomyces cerevisiae." PLoS ONE 4, no. 6 (2009): e5942. http://dx.doi.org/10.1371/journal.pone.0005942.

Full text

APA, Harvard, Vancouver, ISO, and other styles

25

Chan, David W., Joyce M. F. Lee, Patrick C. Y. Chan, and Irene O. L. Ng. "Genetic and epigenetic inactivation ofT‐cadherinin human hepatocellular carcinoma cells." International Journal of Cancer 123, no. 5 (2008): 1043–52. http://dx.doi.org/10.1002/ijc.23634.

Full text

APA, Harvard, Vancouver, ISO, and other styles

26

Iijima, Hironobu, Yoshio Tomizawa, Yasuki Iwasaki, et al. "Genetic and epigenetic inactivation ofLTFgene at 3p21.3 in lung cancers." International Journal of Cancer 118, no. 4 (2005): 797–801. http://dx.doi.org/10.1002/ijc.21462.

Full text

APA, Harvard, Vancouver, ISO, and other styles

27

Cheng, Yu, Jin Woo Kim, Wennuan Liu, et al. "Genetic and epigenetic inactivation of TNFRSF10C in human prostate cancer." Prostate 69, no. 3 (2008): 327–35. http://dx.doi.org/10.1002/pros.20882.

Full text

APA, Harvard, Vancouver, ISO, and other styles

28

Wang, Jian, Rajesh Talluri, and Sanjay Shete. "Selection of X-chromosome Inactivation Model." Cancer Informatics 16 (January 1, 2017): 117693511774727. http://dx.doi.org/10.1177/1176935117747272.

Full text

Abstract:

To address the complexity of the X-chromosome inactivation (XCI) process, we previously developed a unified approach for the association test for X-chromosomal single-nucleotide polymorphisms (SNPs) and the disease of interest, accounting for different biological possibilities of XCI: random, skewed, and escaping XCI. In the original study, we focused on the SNP-disease association test but did not provide knowledge regarding the underlying XCI models. One can use the highest likelihood ratio (LLR) to select XCI models (max-LLR approach). However, that approach does not formally compare the LL

APA, Harvard, Vancouver, ISO, and other styles

29

Middleton, Jason K., Tonya F. Severson, Kartik Chandran, Anne Lynn Gillian, John Yin та Max L. Nibert. "Thermostability of Reovirus Disassembly Intermediates (ISVPs) Correlates with Genetic, Biochemical, and Thermodynamic Properties of Major Surface Protein μ1". Journal of Virology 76, № 3 (2002): 1051–61. http://dx.doi.org/10.1128/jvi.76.3.1051-1061.2002.

Full text

Abstract:

ABSTRACT Kinetic analyses of infectivity loss during thermal inactivation of reovirus particles revealed substantial differences between virions and infectious subvirion particles (ISVPs), as well as between the ISVPs of reoviruses type 1 Lang (T1L) and type 3 Dearing (T3D). The difference in thermal inactivation of T1L and T3D ISVPs was attributed to the major surface protein μ1 by genetic analyses with reassortant viruses and recoated cores. Irreversible conformational changes in ISVP-bound μ1 were shown to accompany thermal inactivation. The thermal inactivation of ISVPs approximated first-

APA, Harvard, Vancouver, ISO, and other styles

30

Rastan, S., and S. D. M. Brown. "The search for the mouse X-chromosome inactivation centre." Genetics Research 56, no. 2-3 (1990): 99–106. http://dx.doi.org/10.1017/s0016672300035163.

Full text

Abstract:

SummaryThe phenomenon of X-chromosome inactivation in female mammals, whereby one of the two X chromosome present in each cell of the female embryo is inactivated early in development, was first described by Mary Lyon in 1961. Nearly 30 years later, the mechanism of X-chromosome inactivation remains unknown. Strong evidence has accumulated over the years, however, for the involvement of a major switch or inactivation centre on the mouse X chromosome. Identification of the inactivation centre at the molecular level would be an important step in understanding the mechanism of X-inactivation. In

APA, Harvard, Vancouver, ISO, and other styles

31

Patil, Ajinkya, Mark Manzano, and Eva Gottwein. "Genome-wide CRISPR screens reveal genetic mediators of cereblon modulator toxicity in primary effusion lymphoma." Blood Advances 3, no. 14 (2019): 2105–17. http://dx.doi.org/10.1182/bloodadvances.2019031732.

Full text

Abstract:

Abstract Genome-wide CRISPR/Cas9 screens represent a powerful approach to studying mechanisms of drug action and resistance. Cereblon modulating agents (CMs) have recently emerged as candidates for therapeutic intervention in primary effusion lymphoma (PEL), a highly aggressive cancer caused by Kaposi’s sarcoma-associated herpesvirus. CMs bind to cereblon (CRBN), the substrate receptor of the cullin-RING type E3 ubiquitin ligase CRL4CRBN, and thereby trigger the acquisition and proteasomal degradation of neosubstrates. Downstream mechanisms of CM toxicity are incompletely understood, however.

APA, Harvard, Vancouver, ISO, and other styles

32

Eid, Rita, Marie-Véronique Demattei, Harikleia Episkopou, et al. "Genetic Inactivation ofATRXLeads to a Decrease in the Amount of Telomeric Cohesin and Level of Telomere Transcription in Human Glioma Cells." Molecular and Cellular Biology 35, no. 16 (2015): 2818–30. http://dx.doi.org/10.1128/mcb.01317-14.

Full text

Abstract:

Mutations in ATRX (alphathalassemia/mentalretardation syndromeX-linked), a chromatin-remodeling protein, are associated with the telomerase-independent ALT (alternative lengthening of telomeres) pathway of telomere maintenance in several types of cancer, including human gliomas. In telomerase-positive glioma cells, we found by immunofluorescence that ATRX localized not far from the chromosome ends but not exactly at the telomere termini. Chromatin immunoprecipitation (ChIP) experiments confirmed a subtelomeric localization for ATRX, yet short hairpin RNA (shRNA)-mediated genetic inactivation o

APA, Harvard, Vancouver, ISO, and other styles

33

Han, Dongxiao, Meiling Hao, Lianqiang Qu, and Wei Xu. "A novel model for the X-chromosome inactivation association on survival data." Statistical Methods in Medical Research 29, no. 5 (2019): 1305–14. http://dx.doi.org/10.1177/0962280219859037.

Full text

Abstract:

The X-linked genetic association is overlooked in most of the genetic studies because of the complexity of X-chromosome inactivation process. In fact, the biological process of the gene at the same locus can vary across different subjects. Besides, the skewness of X-chromosome inactivation is inherently subject-specific (even tissue-specific within subjects) and cannot be accurately represented by a population-level parameter. To tackle this issue, a new model is proposed to incorporate the X-linked genetic association into right-censored survival data. The novel model can present that the X-l

APA, Harvard, Vancouver, ISO, and other styles

34

Heyman, M., O. Rasool, L. Borgonovo Brandter, et al. "Prognostic importance of p15INK4B and p16INK4 gene inactivation in childhood acute lymphocytic leukemia." Journal of Clinical Oncology 14, no. 5 (1996): 1512–20. http://dx.doi.org/10.1200/jco.1996.14.5.1512.

Full text

Abstract:

PURPOSE The present study explores the prognostic importance of p16INK4/p15INK4B gene inactivation in childhood acute lymphocytic leukemia (ALL). MATERIALS AND METHODS Cells from 79 pediatric ALL patients were investigated for inactivation of the p15INK4B and p16INK4 genes or loss of heterozygosity (LOH) for chromosome 9p markers by use of Southern hybridization, restriction fragment length polymorphism (RFLP) analysis, microsatellite analysis as well as single-strand conformation polymorphism (SSCP) analysis, and nucleotide sequencing of the p15INK4B and p16INK4 genes. Genetic data were corre

APA, Harvard, Vancouver, ISO, and other styles

35

Kucsera, Judit, Ilona Pfeiffer, and Lajos Ferenczy. "A novel method for hybridization of Saccharomyces species without genetic markers." Canadian Journal of Microbiology 44, no. 10 (1998): 959–64. http://dx.doi.org/10.1139/w98-093.

Full text

Abstract:

Protoplasts of Saccharomyces cerevisiae were inactivated by treatment with different concentrations of antifungal compounds for various periods. Of the 14 compounds tested, N-ethylmaleimide proved to be the most efficient. The inactivation effect was fully reproducible. The inactivated protoplasts could be reactivated and still function as fusion partners. They were fused with untreated protoplasts by polyethylene glycol treatment and produced viable hybrid cells. Nuclear and extrachromosomal genetic analysis and chromosome separation of the fusion products from fusion experiments involving in

APA, Harvard, Vancouver, ISO, and other styles

36

Giulino, Lisa B., Susan Mathew, Wayne Tam, et al. "TNFAIP3 (A20) Genetic Alterations In EBV Associated AIDS Related Lymphomas." Blood 116, no. 21 (2010): 802. http://dx.doi.org/10.1182/blood.v116.21.802.802.

Full text

Abstract:

Abstract Abstract 802 Introduction: AIDS related lymphomas (ARL) are a heterogeneous group of lymphoproliferative disorders that are frequently associated with Epstein Barr virus (EBV) infection. EBV expresses latent viral oncoproteins that constitutively activate the transcription factor NF-κB, a potent inducer of genes involved in B cell survival and proliferation (Keller SA et al, Blood 2006). Lymphomas that are not associated with EBV can also display increased NF-κB activity and recent reports have described mutations in regulators of NF-κB in subsets of B cell lymphomas. One of the frequ

APA, Harvard, Vancouver, ISO, and other styles

37

Vickers, Mark A., Ewan McLeod, Timothy D. Spector, and Ian J. Wilson. "Assessment of mechanism of acquired skewed X inactivation by analysis of twins." Blood 97, no. 5 (2001): 1274–81. http://dx.doi.org/10.1182/blood.v97.5.1274.

Full text

Abstract:

Skewed X-chromosome inactivation in peripheral blood granulocytes becomes more frequent with increasing age, affecting up to half of those over 75 years old. To investigate the mechanisms underlying this phenomenon, X-inactivation profiles in 33 monozygotic and 22 dizygotic elderly twin pairs were studied. Differential methylation-sensitive restriction enzyme cutting at a hypervariable locus in the human androgen receptor gene (HUMARA) was studied on purified granulocytes using T cells as controls. A large genetic effect on skewed granulocytic X inactivation was shown (P &lt; .05); heritab

APA, Harvard, Vancouver, ISO, and other styles

38

Cervera, Saint T., Carlos Rodríguez-Martín, Enrique Fernández-Tabanera, et al. "Therapeutic Potential of EWSR1–FLI1 Inactivation by CRISPR/Cas9 in Ewing Sarcoma." Cancers 13, no. 15 (2021): 3783. http://dx.doi.org/10.3390/cancers13153783.

Full text

Abstract:

Ewing sarcoma is an aggressive bone cancer affecting children and young adults. The main molecular hallmark of Ewing sarcoma are chromosomal translocations that produce chimeric oncogenic transcription factors, the most frequent of which is the aberrant transcription factor EWSR1–FLI1. Because this is the principal oncogenic driver of Ewing sarcoma, its inactivation should be the best therapeutic strategy to block tumor growth. In this study, we genetically inactivated EWSR1–FLI1 using CRISPR-Cas9 technology in order to cause permanent gene inactivation. We found that gene editing at the exon

APA, Harvard, Vancouver, ISO, and other styles

39

Satılmış, Uuml rguuml n., and Buzrul Sencer. "Use of genetic algorithms for high hydrostatic pressure inactivation of microorganisms." African Journal of Biotechnology 10, no. 65 (2011): 14543–51. http://dx.doi.org/10.5897/ajb11.1683.

Full text

APA, Harvard, Vancouver, ISO, and other styles

40

Nakahara, Yukiko, Paul A. Northcott, Meihua Li, et al. "Genetic and Epigenetic Inactivation of Kruppel-like Factor 4 in Medulloblastoma." Neoplasia 12, no. 1 (2010): 20–27. http://dx.doi.org/10.1593/neo.91122.

Full text

APA, Harvard, Vancouver, ISO, and other styles

41

Chen, Wen Yong, and Stephen B. Baylin. "Inactivation of Tumor Suppressor Genes: Choice Between Genetic and Epigenetic Routes." Cell Cycle 4, no. 1 (2004): 10–12. http://dx.doi.org/10.4161/cc.4.1.1361.

Full text

APA, Harvard, Vancouver, ISO, and other styles

42

Lavalou, Perrine, Helene Eckert, Louise Damy, et al. "Corrigendum: Strategies for genetic inactivation of long noncoding RNAs in zebrafish." RNA 26, no. 4 (2020): 529. http://dx.doi.org/10.1261/rna.074989.120.

Full text

APA, Harvard, Vancouver, ISO, and other styles

43

Sato, Kazuyo, Shigeki Uehara, Masaki Hashiyada, et al. "Genetic significance of skewed X-chromosome inactivation in premature ovarian failure." American Journal of Medical Genetics 130A, no. 3 (2004): 240–44. http://dx.doi.org/10.1002/ajmg.a.30256.

Full text

APA, Harvard, Vancouver, ISO, and other styles

44

Godwin Christopher, J., A. G. Murugesan, and N. Sukumaran. "Genetic Inactivation of Stinging Catfish (Heteropneustes fossilis) Sperm with UV Irradiation." Journal of Applied Aquaculture 21, no. 2 (2009): 128–37. http://dx.doi.org/10.1080/10454430902892941.

Full text

APA, Harvard, Vancouver, ISO, and other styles

45

Leclercq, R., A. Brisson-Noel, J. Duval, and P. Courvalin. "Phenotypic expression and genetic heterogeneity of lincosamide inactivation in Staphylococcus spp." Antimicrobial Agents and Chemotherapy 31, no. 12 (1987): 1887–91. http://dx.doi.org/10.1128/aac.31.12.1887.

Full text

APA, Harvard, Vancouver, ISO, and other styles

46

Bushell, Kevin R., Yukyoung Kim, Fong Chun Chan, et al. "Genetic inactivation of TRAF3 in canine and human B-cell lymphoma." Blood 125, no. 6 (2015): 999–1005. http://dx.doi.org/10.1182/blood-2014-10-602714.

Full text

APA, Harvard, Vancouver, ISO, and other styles

47

Park, Seon, Amy Bernard, Kevin E. Bove, et al. "Inactivation of WT1 in nephrogenic rests, genetic precursors to Wilms' tumour." Nature Genetics 5, no. 4 (1993): 363–67. http://dx.doi.org/10.1038/ng1293-363.

Full text

APA, Harvard, Vancouver, ISO, and other styles

48

Kristiansen, Marianne, Gun P. S. Knudsen, Lise Bathum, et al. "Twin study of genetic and aging effects on X chromosome inactivation." European Journal of Human Genetics 13, no. 5 (2005): 599–606. http://dx.doi.org/10.1038/sj.ejhg.5201398.

Full text

APA, Harvard, Vancouver, ISO, and other styles

49

McGillicuddy, Lauren T., Jody A. Fromm, Pablo E. Hollstein, et al. "Proteasomal and Genetic Inactivation of the NF1 Tumor Suppressor in Gliomagenesis." Cancer Cell 16, no. 1 (2009): 44–54. http://dx.doi.org/10.1016/j.ccr.2009.05.009.

Full text

APA, Harvard, Vancouver, ISO, and other styles

50

Keer, J. T., R. M. J. Hamvas, N. Brockdorff, D. Page, S. Rastan, and S. D. M. Brown. "Genetic mapping in the region of the mouse X-inactivation center." Genomics 7, no. 4 (1990): 566–72. http://dx.doi.org/10.1016/0888-7543(90)90200-e.

Full text

APA, Harvard, Vancouver, ISO, and other styles

We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!