Relevant bibliographies by topics / X-chromosome inactivation

Academic literature on the topic 'X-chromosome inactivation'

Author: Grafiati
Published: 4 June 2021
Last updated: 25 May 2024

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

Select a source type:

Contents

Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources on the topic 'X-chromosome 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.

Journal articles on the topic "X-chromosome inactivation"

1

Cattanach, Bruce M., and Colin V. Beechey. "Autosomal and X-chromosome imprinting." Development 108, Supplement (April 1, 1990): 63–72. http://dx.doi.org/10.1242/dev.108.supplement.63.

Full text
Abstract:
Mouse genetic studies using Robertsonian and reciprocal translations have shown that certain autosomal regions of loci are subject to a parental germ line imprint, which renders maternal and paternal copies functionally inequivalent in the embryo or later stages of development. Duplication of maternal or paternal copies with corresponding paternal/maternal deficiencies in chromosomally balanced zygotes causes various effects. These range from early embryonic lethalities through to mid-fetal and neonatal lethalities, and in some instances viable young with phenotypic effects are obtained. Eight to nine chromosomal regions that give such imprinting effects have been identified. Six to seven of these regions are located in only three chromosomes (2, 7 and 17). The two other regions are located in chromosomes 6 and 11. Maternal and paternal disomies for each of four other chromosomes (1, 5, 9 and 14) have been recovered with different frequencies, but the possibility that this may be due to imprinting has yet to be supported by follow-up studies on regions of the chromosomes concerned. No clear evidence of genetic-background modifications of the imprinting process have been observed in these mouse genetic experiments. The mammalian X chromosome is also subject to imprinting, as demonstrated by the non-random, paternal X-inactivation in female mouse extra-embryonic tissues and in the somatic cells of marsupial females. There is also the opposite bias towards inactivation of the maternal X in the somatic cells of female mice. On the basis that both X-chromosome inactivation and autosomal chromosome imprinting may be concerned with gene regulation, it is suggested that evidence from X-chromosome inactivation studies may help to elucidate factors underlying the imprinting of autosomes. The relevant aspects of X-inactivation are summarized.
APA, Harvard, Vancouver, ISO, and other styles
2

Sado, Takashi, and Takehisa Sakaguchi. "Species-specific differences in X chromosome inactivation in mammals." REPRODUCTION 146, no. 4 (October 2013): R131—R139. http://dx.doi.org/10.1530/rep-13-0173.

Full text
Abstract:
In female mammals, the dosage difference in X-linked genes between XX females and XY males is compensated for by inactivating one of the two X chromosomes during early development. Since the discovery of the X inactive-specific transcript (XIST) gene in humans and its subsequent isolation of the mouse homolog, Xist, in the early 1990s, the molecular basis of X chromosome inactivation (X-inactivation) has been more fully elucidated using genetically manipulated mouse embryos and embryonic stem cells. Studies on X-inactivation in other mammals, although limited when compared with those in the mice, have revealed that, while their inactive X chromosome shares many features with those in the mice, there are marked differences in not only some epigenetic modifications of the inactive X chromosome but also when and how X-inactivation is initiated during early embryonic development. Such differences raise the issue about what extent of the molecular basis of X-inactivation in the mice is commonly shared among others. Recognizing similarities and differences in X-inactivation among mammals may provide further insight into our understanding of not only the evolutionary but also the molecular aspects for the mechanism of X-inactivation. Here, we reviewed species-specific differences in X-inactivation and discussed what these differences may reveal.
APA, Harvard, Vancouver, ISO, and other styles
3

Rastan, Sohaila, and Elizabeth J. Robertson. "X-chromosome deletions in embryo-derived (EK) cell lines associated with lack of X-chromosome inactivation." Development 90, no. 1 (December 1, 1985): 379–88. http://dx.doi.org/10.1242/dev.90.1.379.

Full text
Abstract:
The predictions of a model for the initiation of X-chromosome inactivation based on a single inactivation centre were tested in a cytogenetic study using six different embryo-derived (EK) stem cell lines, each with a different-sized deletion of the distal part of one of the X-chromosomes. Metaphase chromosomes were prepared by the Kanda method from each cell line in the undifferentiated state and after induction of differentiation, and cytogenetic evidence sought for a dark-staining inactive X-chromosome. The results confirm the predictions of the model in that when the inactivation centre is deleted from one of the X-chromosomes neither X present in a diploid cell can be inactivated, and in addition considerably further localize the position of the inactivation centre on the X-chromosome.
APA, Harvard, Vancouver, ISO, and other styles
4

Migeon, Barbara R. "X chromosome inactivation." Genome 31, no. 1 (January 1, 1989): 464. http://dx.doi.org/10.1139/g89-083.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Lyon, Mary F. "X-chromosome inactivation." Current Biology 9, no. 7 (April 1999): R235—R237. http://dx.doi.org/10.1016/s0960-9822(99)80151-1.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Malcore, Rebecca M., and Sundeep Kalantry. "A Comparative Analysis of Mouse Imprinted and Random X-Chromosome Inactivation." Epigenomes 8, no. 1 (February 10, 2024): 8. http://dx.doi.org/10.3390/epigenomes8010008.

Full text
Abstract:
The mammalian sexes are distinguished by the X and Y chromosomes. Whereas males harbor one X and one Y chromosome, females harbor two X chromosomes. To equalize X-linked gene expression between the sexes, therian mammals have evolved X-chromosome inactivation as a dosage compensation mechanism. During X-inactivation, most genes on one of the two X chromosomes in females are transcriptionally silenced, thus equalizing X-linked gene expression between the sexes. Two forms of X-inactivation characterize eutherian mammals, imprinted and random. Imprinted X-inactivation is defined by the exclusive inactivation of the paternal X chromosome in all cells, whereas random X-inactivation results in the silencing of genes on either the paternal or maternal X chromosome in individual cells. Both forms of X-inactivation have been studied intensively in the mouse model system, which undergoes both imprinted and random X-inactivation early in embryonic development. Stable imprinted and random X-inactivation requires the induction of the Xist long non-coding RNA. Following its induction, Xist RNA recruits proteins and complexes that silence genes on the inactive-X. In this review, we present a current understanding of the mechanisms of Xist RNA induction, and, separately, the establishment and maintenance of gene silencing on the inactive-X by Xist RNA during imprinted and random X-inactivation.
APA, Harvard, Vancouver, ISO, and other styles
7

Lyon, M. F. "X Chromosome Inactivation and Imprinting." Acta geneticae medicae et gemellologiae: twin research 45, no. 1-2 (April 1996): 85. http://dx.doi.org/10.1017/s0001566000001148.

Full text
Abstract:
In contrast to the random inactivation of either maternal or paternal X-chromosome in the somatic cells of eutherian mammals, in marsupials the paternal X-chromosome is preferentially inactivated in all cells. Similar exclusively paternal X-inactivation occurs in two extraembryonic cell lineages of mice and rats. Thus, genetic imprinting is an important feature of X-inactivation. In embryonic development the initiation of X-inactivation is thought to occur through the X-inactivation centre, located on the X-Chromosome, and thus imprinting probably acts through this centre. A candidate gene for a role in the inactivation centre is Xist (X inactive specific transcript) which is expressed only from the inactive X-Chromosome. The expression of Xist in the mouse embryo is appropriate for it to be a cause rather than a consequence of inactivation. It appears before inactivation, and only the paternal allele is expressed in the extraembryonic lineages. In the germ cells also changes in X-chromosome activity are accompanied by changes in Xist expression. Studies of methylation of the Xist gene have shown that in male tissues where Xist is not active it is fully methylated, whereas in the female the allele on the active X-chromosome only is methylated. In male germ cells, where Xist is expressed, it is demethylated and the demethylation persists in mature spermatozoa. Thus a methylation difference in germ cells could possibly be the imprint. In androgenotes, with paternally derived chromosomes, Xist is expressed at the 4-cell stage, whereas in gynogenotes and parthenogenotes expression does not appear until the blastocyst stage. Thus, Xist expression shows imprinting. When expression appears in parthenogenotes it is random, suggesting that the imprint has been lost. The Xist gene has no open reading frame and is thought to act through mRNA but its function is unknown.
APA, Harvard, Vancouver, ISO, and other styles
8

Shevchenko, Alexander I., Elena V. Dementyeva, Irina S. Zakharova, and Suren M. Zakian. "Diverse developmental strategies of X chromosome dosage compensation in eutherian mammals." International Journal of Developmental Biology 63, no. 3-4-5 (2019): 223–33. http://dx.doi.org/10.1387/ijdb.180376as.

Full text
Abstract:
In eutherian mammals, dosage compensation arose to balance X-linked gene expression between sexes and relatively to autosomal gene expression in the evolution of sex chromosomes. Dosage compensation occurs in early mammalian development and comprises X chromosome upregulation and inactivation that are tightly coordinated epigenetic processes. Despite a uniform principle of dosage compensation, mechanisms of X chromosome inactivation and upregulation demonstrate a significant variability depending on sex, developmental stage, cell type, individual, and mammalian species. The review focuses on relationships between X chromosome inactivation and upregulation in mammalian early development.
APA, Harvard, Vancouver, ISO, and other styles
9

Tukiainen, Taru, Alexandra-Chloé Villani, Angela Yen, Manuel A. Rivas, Jamie L. Marshall, Rahul Satija, Matt Aguirre, et al. "Landscape of X chromosome inactivation across human tissues." Nature 550, no. 7675 (October 12, 2017): 244–48. http://dx.doi.org/10.1038/nature24265.

Full text
Abstract:
Abstract X chromosome inactivation (XCI) silences transcription from one of the two X chromosomes in female mammalian cells to balance expression dosage between XX females and XY males. XCI is, however, incomplete in humans: up to one-third of X-chromosomal genes are expressed from both the active and inactive X chromosomes (Xa and Xi, respectively) in female cells, with the degree of ‘escape’ from inactivation varying between genes and individuals1,2. The extent to which XCI is shared between cells and tissues remains poorly characterized3,4, as does the degree to which incomplete XCI manifests as detectable sex differences in gene expression5 and phenotypic traits6. Here we describe a systematic survey of XCI, integrating over 5,500 transcriptomes from 449 individuals spanning 29 tissues from GTEx (v6p release) and 940 single-cell transcriptomes, combined with genomic sequence data. We show that XCI at 683 X-chromosomal genes is generally uniform across human tissues, but identify examples of heterogeneity between tissues, individuals and cells. We show that incomplete XCI affects at least 23% of X-chromosomal genes, identify seven genes that escape XCI with support from multiple lines of evidence and demonstrate that escape from XCI results in sex biases in gene expression, establishing incomplete XCI as a mechanism that is likely to introduce phenotypic diversity6,7. Overall, this updated catalogue of XCI across human tissues helps to increase our understanding of the extent and impact of the incompleteness in the maintenance of XCI.
APA, Harvard, Vancouver, ISO, and other styles
10

Zlotorynski, Eytan. "X-chromosome inactivation unravelled." Nature Reviews Molecular Cell Biology 16, no. 6 (May 8, 2015): 325. http://dx.doi.org/10.1038/nrm3998.

Full text
APA, Harvard, Vancouver, ISO, and other styles
More sources

Dissertations / Theses on the topic "X-chromosome inactivation"

1

Norris, Dominic Paul. "X chromosome inactivation in the mouse." Thesis, Open University, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.282142.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Benjamin, Don. "Molecular studies of human X chromosome inactivation." Thesis, University of Oxford, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.318784.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Paterno, Gary David. "X chromosome inactivation in mouse embryonal carcinoma cells." Thesis, University of Ottawa (Canada), 1985. http://hdl.handle.net/10393/4629.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Metello, de Napoles Mariana. "Epigenetic modifications during X-chromosome inactivation and reactivation." Thesis, Imperial College London, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.422058.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Ager, Miranda. "Mechanisms of X chromosome inactivation : a transgenic approach." Thesis, University of Oxford, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.342240.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

林德深 and Tak-sum Lam. "A biochemical study of mammalian x chromosome inactivation." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1987. http://hub.hku.hk/bib/B31981306.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Dossin, François. "Mechanistic dissection of SPEN functionduring X chromosome inactivation." Thesis, Université Paris sciences et lettres, 2021. http://www.theses.fr/2021UPSLS042.

Full text
Abstract:
Chez les mammifères placentaires femelles, la transcription d’un des deux chromosomes X est inactivée (ICX) au cours du développement embryonnaire. Cette inactivation est permise par Xist, un ARN non-codant qui recouvre le chromosome X à partir duquel il est exprimé, induisant ensuite l’extinction transcriptionnelle de tout ce chromosome. Les mécanismes moléculaires par lesquels Xist permet une telle répression des gènes liés à l’X demeurent globalement incompris. En 2015, la protéine SPEN a été identifiée comme interagissant directement avec l’ARN de Xist, mais sa fonction précise ainsi que son mécanisme d’action au cours de l’ICX restaient à découvrir.Au cours de mon travail de thèse, j’ai utilisé la technique du dégron inductible à l’auxine, une approche de type perte de function, permettant de dégrader SPEN à façon dans des cellules souches embryonnaires de souris (CSES) en cours d’ICX. Grâce à cette technique, je démontre que SPEN est absolument necessaire pour la repression transcriptionnelle de tout le chromosome X pendant l’ICX. Aussi, en ayant recours à des embryons de souris Spen KO, je montre que SPEN is tout autant essentiel pour l’inactivation du chromosome X paternel au cours de l’ICX soumise à empreinte. En revanche, la perte de SPEN dans des cellules différenciées, où l’ICX est déjà établie, révèle que SPEN n’est plus requis ni pour maintenir les gènes éteints, ni pour préserver l’organisation tridimensionnelle du chromosome X inactif.Par des approches de microscopie en cellules vivantes, je rapporte ensuite que SPEN est colocalisé avec l’ARN de Xist immédiatement après l’expression de ce dernier, suggérant que SPEN peut initier la répression transcriptionnelle très tôt pendand l’ICX. La caractérisation des sites de liaisons de SPEN à la chromatine révèle que SPEN est recruté uniquement au niveau des promoteurs et des enhancers des gènes actifs. Aussi, la magnitude du recrutement de SPEN aux promoteurs liés à l’X prédit la rapidité avec laquelle les gènes sont inactivés au cours de l’ICX. Enfin, une fois les genes inactivés, SPEN se dissocie de la chromatine, ce qui indique qu’une activité transcriptionnelle est requise pour l’association de SPEN à la chromatine.Par complémentation fonctionnelle, le domaine SPOC est identifié comme l’effecteur principal de l’activité répressive de SPEN pendant l’ICX, et le recrutement « forcé » de SPOC sur l’ARN de Xist suffit à entraîner l’inactivation des gènes à l’échelle du chromosome entier. L’identification de l’interactome protéique de SPOC par spectrométrie de masse révèle que SPOC interagit avec de nombreux complexes impliqués dans la répression transcriptionnelle : NCoR/SMRT (désacétylation des histones), NuRD (remodelage de la chromatine et désacétylation des histones) et la machinerie de méthylation m6A des ARN, ainsi qu’avec la machinerie de transcription (Pol2).En utilisant des approches de biophysique et de biologie structurale, je montre que SPOC interagit directement et spécifiquement avec le domaine C-terminal (CTD) de Pol2, seulement quand ce dernier est phosphorylé sur la Sérine 5. Ces résultats suggèrent que SPEN peut réprimer la transcription directement en interférant avec les évènements transcriptionnels dépendant de Pol2-CTD Ser5P.Ainsi, mon travail de these souligne l’essentialité de SPEN pour éteindre la transcription à l’échelle du chromosome X entier au cours de l’ICX, aussi bien in vitro que in vivo. Immédiatement après l’expression de Xist, SPEN est recruté aux promoteurs et enhancers de gènes actifs, réprime la transcription, puis se dissocie de la chromatin une fois les gènes éteints. Grâce à ses domaines RRMs et SPOC, SPEN joue un rôle d’intégrateur, asociant Xist à des désacétylases des histones, des remodeleurs de la chromatine, mais surtout, à la machinerie de transcription
In female placental mammals, dosage compensation of X-linked gene expression is achieved early during development through transcriptional inactivation of one of the two X chromosomes (XCI). This process is dependent on Xist, a long non-coding RNA which coats and silences the X chromosome from which it is transcribed. The mechanisms through which Xist initiates transcriptional silencing during XCI remain however completely unknown. In 2015, several studies identified that the SPEN protein binds Xist RNA directly, and its implication in mediating gene silencing was reported. However, its precise function and mechanism(s) of action during XCI are unclear.During my PhD, I made use of a conditional loss of function approach, the auxin inducible degron, to acutely deplete SPEN in mouse embryonic stem cells (mESCs) undergoing XCI. Using this approach, I demonstrate that SPEN is absolutely necessary for chromosome-wide Xist-mediated gene silencing during initiation of XCI. Furthermore, using conditional Spen KO mouse embryos, I show that SPEN is also required for the transcriptional inactivation of the paternal X chromosome during imprinted X inactivation. Depleting SPEN in differentiated cells, in which XCI has been established, reveals that SPEN is neither required to maintain gene silencing nor to preserve the spatial organization of the inactive X chromosome.By combining fixed and live cell imaging of Xist and SPEN, I show that SPEN colocalizes with Xist RNA, and accumulates on the X chromosome, immediately upon Xist upregulation, suggesting that SPEN can initiate gene silencing very early on during XCI. Profiling SPEN chromatin binding sites reveals that SPEN is recruited to promoters and enhancers of active genes specifically. The magnitude of SPEN recruitment to X-linked promoters dictates the efficiency with which these genes will be silenced. Remarkably, SPEN disengages from chromatin after gene silencing, indicating that active transcription required for SPEN’s association with chromatin.Using a functional complementation approach, I identify the SPOC domain as the effector of SPEN’s gene silencing activity during XCI. Artificial tethering of SPOC to Xist RNA results in transcriptional repression along the entire X chromosome, demonstrating that SPOC contains all the sufficient potential to instruct gene silencing during XCI. I further characterize the protein interactors of SPOC using mass spectrometry and reveal that SPOC interacts with several protein complexes involved in repressing transcription, including the NCoR/SMRT (histone deacetylation), the NuRD (nucleosome remodeling/histone deacetylation) and the m6A writing (governing mRNA fate) complexes. Finally, several transcription initiation and elongation factors are found to interact with SPOC, as well as the RNA polymerase II (RNAPII) transcription machinery.I identify that SPOC interacts directly and specifically with the C-terminal domain (CTD) of RNAPII only when the latter is phosphorylated on Ser5, and determine the 3D structure of the SPOC/RNAPII-CTD Ser5-P complex at 1.8Å resolution. These results suggest that SPEN could directly repress transcription during XCI by interfering with RNAPII-CTD Ser5-P templated processes.Altogether, my PhD work reveals that SPEN is essential for chromosome-wide transcriptional silencing during XCI, both in mESCs and in vivo. Following Xist upregulation, SPEN is immediately recruited to active gene promoters and enhancers, silences transcription, and subsequently disengages from chromatin. Through its RRMs and SPOC domains, SPEN acts as a molecular integrator, bridging Xist with histone deacetylases, nucleosome remodelers, RNA methyltransferases and most importantly, the transcription machinery
APA, Harvard, Vancouver, ISO, and other styles
8

Lam, Tak-sum. "A biochemical study of mammalian x chromosome inactivation." [Hong Kong : University of Hong Kong], 1987. http://sunzi.lib.hku.hk/hkuto/record.jsp?B12827186.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Forrester, Lesley Margaret. "Murine haematopoiesis : studies using X chromosome-inactivation mosaics." Thesis, University of Edinburgh, 1987. http://hdl.handle.net/1842/28042.

Full text
Abstract:
Blood erythrocytes and leukocytes were serially sampled over many months from female mice that were heterozygous at the X-chromosomal locusencoding the glycolytic enzyme phosphoglycerate kinase (PGK-1). PGK-1A andPGK-1B alloenzymes were identified and quantified electrophoretically. There was little variation in PGK-1 phenotype between serial samples from individual mice. This small amount of variation was discussed in terms of the number of clones participating in haematopoiesis and the contribution of technical factors. Similar studies were performed using radiation chimaeras, repopulated with either a high dose (107 cells) or a low dose (105 cells) of PGK-1AB bonemarrow. The variation in PGK-1 phenotype between serial samples taken fromthe animals repopulated with a high dose of bone marrow was comparable to that seen in normal animals. In contrast, the variation observed in the low- dose chimaeras was. relatively large. These animals were used to study the clonal organisation of the haematopoietic system. The development of B lymphocytes carrying the X-linked immunodeficiency mutation (xid) was studied in mice that were heterozygous at both the x[d and the Pgk-1 loci. An abnormallly large population of B lymphocytes, possessing an characteristic membrane phenotype, was observed in the peripheral blood of a group of experimental mice. This behaved as a transplantable neoplasia. Subsequently, similar populations were found in several aged (>2 years) CBA/Ca mice. A preliminary characterisation of these cells was carried out and their possible relevance to human chronic lymphocytic leukaemia (CLL) was discussed.
APA, Harvard, Vancouver, ISO, and other styles
10

Sprong, Amy Nicole. "X Chromosome Aneuploidy: A Look at the Effects of X Inactivation." Miami University Honors Theses / OhioLINK, 2008. http://rave.ohiolink.edu/etdc/view?acc_num=muhonors1209079846.

Full text
APA, Harvard, Vancouver, ISO, and other styles
More sources

Books on the topic "X-chromosome inactivation"

1

Sado, Takashi, ed. X-Chromosome Inactivation. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-8766-5.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Spotswood, Hugh Timothy. Histone modification and the epigenetics of X chromosome inactivation. Birmingham: University of Birminghm, 2002.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
3

Michalickova, Katerina. X-chromosome inactivation in females with deletions at Xq27-q28. Ottawa: National Library of Canada, 1996.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
4

Females are mosaics: X inactivation and sex differences in disease. New York, NY: Oxford University Press, 2006.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
5

Sado, Takashi. X-Chromosome Inactivation: Methods and Protocols. Springer New York, 2018.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
6

Sado, Takashi. X-Chromosome Inactivation: Methods and Protocols. Springer New York, 2019.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
7

Brown, Carolyn Janet *. Studies of human X chromosome inactivation. 1991.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
8

Migeon, Barbara. Females Are Mosaics: X Inactivation and Sex Differences in Disease. Oxford University Press, 2007.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
9

Migeon, Barbara. Females Are Mosaics: X Inactivation and Sex Differences in Disease. Oxford University Press, USA, 2007.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
10

Females Are Mosaics: X Inactivation and Sex Differences in Disease. Oxford University Press, Incorporated, 2013.

Find full text
APA, Harvard, Vancouver, ISO, and other styles

Book chapters on the topic "X-chromosome inactivation"

1

Gartler, S. M. "X Chromosome Inactivation." In Human Genetics, 192–95. Berlin, Heidelberg: Springer Berlin Heidelberg, 1987. http://dx.doi.org/10.1007/978-3-642-71635-5_22.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Lee, Jeannie T. "X-Chromosome Inactivation." In Development, 407–19. Berlin, Heidelberg: Springer Berlin Heidelberg, 1999. http://dx.doi.org/10.1007/978-3-642-59828-9_25.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Robinson, Wendy P., Allison M. Cotton, Maria S. Peñaherrera, Samantha B. Peeters, and Carolyn J. Brown. "X-Chromosome Inactivation." In Epigenetics and Complex Traits, 63–88. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-8078-5_3.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Brahmachari, Vani, and Shruti Jain. "X Chromosome Inactivation." In Encyclopedia of Systems Biology, 2363. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4419-9863-7_859.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Adams, Roger L. P., and Roy H. Burdon. "X-Chromosome Inactivation." In Molecular Biology of DNA Methylation, 163–69. New York, NY: Springer New York, 1985. http://dx.doi.org/10.1007/978-1-4612-5130-9_9.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Jaenisch, Rudolf, Caroline Beard, Jeannie Lee, York Marahrens, and Barbara Panning. "Mammalian X Chromosome Inactivation." In Novartis Foundation Symposia, 200–213. Chichester, UK: John Wiley & Sons, Ltd., 2007. http://dx.doi.org/10.1002/9780470515501.ch12.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Lyon, Mary F. "Imprinting and X-Chromosome Inactivation." In Results and Problems in Cell Differentiation, 73–90. Berlin, Heidelberg: Springer Berlin Heidelberg, 1999. http://dx.doi.org/10.1007/978-3-540-69111-2_4.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Schorderet, Daniel F., and Stanley M. Gartler. "Steroid Sulphatase Inactivation Patterns and X-chromosome Inactivation." In Trends in Chromosome Research, 110–18. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-662-10621-1_8.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Ma, Wenxiu, Giancarlo Bonora, Joel B. Berletch, Xinxian Deng, William S. Noble, and Christine M. Disteche. "X-Chromosome Inactivation and Escape from X Inactivation in Mouse." In Methods in Molecular Biology, 205–19. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-8766-5_15.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Singer-Sam, Judith, and Arthur D. Riggs. "X chromosome inactivation and DNA methylation." In DNA Methylation, 358–84. Basel: Birkhäuser Basel, 1993. http://dx.doi.org/10.1007/978-3-0348-9118-9_16.

Full text
APA, Harvard, Vancouver, ISO, and other styles

Conference papers on the topic "X-chromosome inactivation"

1

"X-chromosome Inactivation in American Mink iPSCs." In Bioinformatics of Genome Regulation and Structure/ Systems Biology. institute of cytology and genetics siberian branch of the russian academy of science, Novosibirsk State University, 2020. http://dx.doi.org/10.18699/bgrs/sb-2020-310.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Song, Yilin, Bryan M. McCauley, Melissa C. Larson, Sebastian M. Armasu, Kate Lawrenson, Ellen L. Goode, Nicholas B. Larson, and Stacey J. Winham. "Abstract 2452: Evidence of decreased X chromosome inactivation in primary ovarian tumors." 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.am2020-2452.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Castellini-Pérez, Olivia, Elena Povedano-Espejo, Guillermo Barturen, Abir Azri, Ruth Dominguez, Marta E. Alarcón-Riquelme, and Elena Carnero-Montoro. "O5 Exploring the impact of genome-wide DNA methylation alterations on chromosome X inactivation and female lupus." In 14th European Lupus Meeting, Bruges, Belgium, March 19–22, 2024. Lupus Foundation of America, 2024. http://dx.doi.org/10.1136/lupus-2024-el.15.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Ibeawuchi, Helen, Nicole Werner, and Les Keniston. "Role of X chromosome Inactivation Escapees andATMGene in Breast Neoplasia Severity and Survival." In ASPET 2024 Annual Meeting Abstract. American Society for Pharmacology and Experimental Therapeutics, 2024. http://dx.doi.org/10.1124/jpet.405.944050.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Winham, Stacey J., Nicholas B. Larson, Sebastian M. Armasu, Zachary C. Fogarty, Melissa C. Larson, Kimberly R. Kalli, Kate Lawrenson, Simon Gayther, Brooke L. Fridley, and Ellen L. Goode. "Abstract 2420: Integrative analyses of gene expression, DNA methylation, genotype and copy number alterations characterize X-chromosome inactivation in ovarian cancer." 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.am2017-2420.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Manié, E., T. Popova, A. Vincent-Salomon, T. Dubois, O. Delattre, X. Sastre-Garau, D. Stoppa-Lyonnet, and M.-H. Stern. "P3-06-03: Hypodiploidy, 1pter Loss and Inactive X Chromosome Retention Are Associated with BRCA1 Somatic or Germline Inactivation in Basal-Like Breast Carcinomas: Proposal for a New BRCAness Genomic Signature." In Abstracts: Thirty-Fourth Annual CTRC‐AACR San Antonio Breast Cancer Symposium‐‐ Dec 6‐10, 2011; San Antonio, TX. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/0008-5472.sabcs11-p3-06-03.

Full text
APA, Harvard, Vancouver, ISO, and other styles

Reports on the topic "X-chromosome inactivation"

1

Panning, Barbara. X Chromosome Inactivation and Breast Cancer: Epigenetic Alteration in Tumor Initiation and Progression. Fort Belvoir, VA: Defense Technical Information Center, September 2007. http://dx.doi.org/10.21236/ada474949.

Full text
APA, Harvard, Vancouver, ISO, and other styles
You might also be interested in the extended bibliographies on the topic 'X-chromosome inactivation' for particular source types:
Journal articles Dissertations / Theses
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!

To the bibliography