Log in

Relevant bibliographies by topics / ATRX

Contents

Journal articles

Academic literature on the topic 'ATRX'

Author: Grafiati

Published: 4 June 2021

Last updated: 4 March 2023

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

Select a source type:

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

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 "ATRX"

1

Pask, Andrew J., Kim Huynh, and Marilyn B. Renfree. "ATRX and ATRY in the Mammalian Gonad." Biology of Reproduction 78, Suppl_1 (2008): 306. http://dx.doi.org/10.1093/biolreprod/78.s1.306a.

Full text

APA, Harvard, Vancouver, ISO, and other styles

2

Ratnakumar, Kajan, and Emily Bernstein. "ATRX." Epigenetics 8, no. 1 (2013): 3–9. http://dx.doi.org/10.4161/epi.23271.

Full text

APA, Harvard, Vancouver, ISO, and other styles

3

Chami, Rose, Paula Marrano, Chinachote Teerapakpinyo, et al. "Immunohistochemistry for ATRX Can Miss ATRX Mutations." American Journal of Surgical Pathology 43, no. 9 (2019): 1203–11. http://dx.doi.org/10.1097/pas.0000000000001322.

Full text

APA, Harvard, Vancouver, ISO, and other styles

4

Irvin, David, Hannah Roberts, Vladislav Sharin, et al. "CSIG-09. ATRX DEFICIENCY IN GLIOMA IMPACTS TRANSCRIPTIONAL PROFILES AND THE IMMUNE MICROENVIRONMENT IN VIVO." Neuro-Oncology 22, Supplement_2 (2020): ii29. http://dx.doi.org/10.1093/neuonc/noaa215.121.

Full text

Abstract:

Abstract Current treatment for diffuse astrocytoma fails to address its underlying molecular mechanisms leading to inevitable disease progression and eventual patient death. Genomic studies have implicated ATRX alterations as critical to low grade glioma biology. Our lab has previously shown in vitro that ATRX influences glioma motility, cellular differentiation state, and epigenetic programming, however, the influence of ATRX alterations in vivo remains unclear. Here, we leveraged an RCAS/tva mouse tumor model to probe the role of ATRX deficiency in glioma. Atrx deficient murine tumors exhibi

APA, Harvard, Vancouver, ISO, and other styles

5

Attieh, Youmna, Yue Wei, Hui Yang, et al. "Low Frequency of Molecular Alterations of H3.3-Atrx-Daxx Chromatin Remodeling Component Genes in Myelodysplastic Syndromes (MDS)." Blood 120, no. 21 (2012): 3844. http://dx.doi.org/10.1182/blood.v120.21.3844.3844.

Full text

Abstract:

Abstract Abstract 3844 Novel sequencing technologies have allowed identification of a group of highly recurrent genetic mutations in myelodysplastic syndromes (MDS). Of importance, it has been noticed that a majority of these mutated genes in MDS encode important components of epigenetic regulation, including both DNA methylation and histone modifications. This phenomenon highlights the importance of epigenetic mechanisms in the pathogenesis of MDS. Recently, highly recurrent somatic mutations in the Histone H3.3-ATRX-DAXX chromatin remodeling pathway have been documented in pediatric glioblas

APA, Harvard, Vancouver, ISO, and other styles

6

Danussi, Carla, Anand Singh, Pavan Pinnamaneni, et al. "GENE-34. THERAPEUTICALLY TARGETING EPIGENOMIC AND TRANSCRIPTIONAL DYSFUNCTION IN ATRX-DEFICIENT GLIOMA." Neuro-Oncology 21, Supplement_6 (2019): vi104—vi105. http://dx.doi.org/10.1093/neuonc/noz175.436.

Full text

Abstract:

Abstract Diffusely infiltrating gliomas feature loss-of-function mutations in the chromatin remodeler gene ATRX as defining molecular alterations delineating major adult and pediatric disease subtypes. We recently reported that Atrx deficiency drives glioma-relevant phenotypes, such as increased motility and astrocytic differentiation profiles, by directly modulating epigenomic landscapes and the corresponding transcriptional profiles in glioma cells of origin. In particular, Atrx deficiency was associated with disruptions in H3.3 histone content at key genetic loci. To further understand the

APA, Harvard, Vancouver, ISO, and other styles

7

Shen, Chen, David Picketts, and Oren Becher. "DIPG-68. ALPHA-THALASSEMIA X-LINKED MENTAL RETARDATION PROTEIN (ATRX) LOSS-OF-FUNCTION IN A MOUSE MODEL OF DIFFUSE INTRINSIC PONTINE GLIOMA." Neuro-Oncology 22, Supplement_3 (2020): iii300. http://dx.doi.org/10.1093/neuonc/noaa222.111.

Full text

Abstract:

Abstract Diffuse Intrinsic Potine Glioma (DIPG) is a rare pediatric brain tumor for which no cure or efficacious therapies exist. Previous discoveries have revealed that, DIPG harbors distinct genetic alterations, when compared with adult high-grade glioma (HGG) or even with non-DIPG pediatric HGGs. ATRX alteration is found in 9% of clinical cases of DIPG, and significantly overlaps with H3.3K27M mutation and p53 loss, the two most common genetic changes in DIPG, found in 80% and 77% clinical cases, respectively. Here we developed genetically engineered mouse model of brainstem glioma using th

APA, Harvard, Vancouver, ISO, and other styles

8

Becker, Aline P., Erica Hlavin Bell, Jessica Fleming, et al. "Comprehensive assessment of ATRX mutation, protein expression, and alternative lengthening of telomeres (ALT) phenotype in grade II and III gliomas." Journal of Clinical Oncology 35, no. 15_suppl (2017): 2064. http://dx.doi.org/10.1200/jco.2017.35.15_suppl.2064.

Full text

Abstract:

2064 Background: ATRX mutations are key molecular markers for classification of gliomas. We aimed to evaluate ATRXmutations and protein expression and the ALT phenotype as potential biomarkers for grade II and III gliomas. Methods: Retrospective analysis of 156 adult gliomas, with long-term follow up. Gene sequencing ( IDH1/2 and ATRX), Oncoscan array (1p19q co-deletion), FISH assays (1p19q co-deletion and ALT phenotype) and immunohistochemistry (IDH1 R132H and ATRX) were performed and the results were correlated with OS and PFS. Results: Twenty-six out of 94 samples (27.7%) had ATRX mutations

APA, Harvard, Vancouver, ISO, and other styles

9

Ritchie, Kieran, Claudia Seah, Jana Moulin, Christian Isaac, Frederick Dick, and Nathalie G. Bérubé. "Loss of ATRX leads to chromosome cohesion and congression defects." Journal of Cell Biology 180, no. 2 (2008): 315–24. http://dx.doi.org/10.1083/jcb.200706083.

Full text

Abstract:

αThalassemia/mental retardation X linked (ATRX) is a switch/sucrose nonfermenting-type ATPase localized at pericentromeric heterochromatin in mouse and human cells. Human ATRX mutations give rise to mental retardation syndromes characterized by developmental delay, facial dysmorphisms, cognitive deficits, and microcephaly and the loss of ATRX in the mouse brain leads to reduced cortical size. We find that ATRX is required for normal mitotic progression in human cultured cells and in neuroprogenitors. Using live cell imaging, we show that the transition from prometaphase to metaphase is prolong

APA, Harvard, Vancouver, ISO, and other styles

10

Yuan, Ming, Karlyne Reilly, Christine Pratilas, Christopher Heaphy, and Fausto Rodriguez. "NFB-01. FUNCTIONAL CHARACTERIZATION OF ATRX LOSS IN NF1-ASSOCIATED GLIOMA AND MPNST." Neuro-Oncology 22, Supplement_3 (2020): iii417—iii418. http://dx.doi.org/10.1093/neuonc/noaa222.605.

Full text

Abstract:

Abstract To identify the biologic relevance of ATRX loss in NF1-associated gliomagenesis, we studied the effects of Atrx loss using four previously characterized Nf1+/-Trp53+/- murine glioma lines. Lines 130G#3 and 158D#8 (corresponding to grade IV and III gliomas, respectively) displayed preserved ATRX protein expression compared to NIH-3T3 cells. We studied the effects of Atrx knockdown in these two lines in the presence and absence of the TERT inhibitor, BIRBR1532. Using a telomere-specific FISH assay, we identified increased signal intensity after Atrx knockdown, only in the presence of th

APA, Harvard, Vancouver, ISO, and other styles

More sources

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!