Relevant bibliographies by topics / CHD1 gene

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Academic literature on the topic 'CHD1 gene'

Author: Grafiati
Published: 4 June 2021
Last updated: 12 June 2025

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Journal articles on the topic "CHD1 gene"

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Davitkov, Dajana, Milos Vucicevic, Uros Glavinic, et al. "Potential of Inter- and Intra-Species Variability of CHD1 Gene in Birds as a Forensic Tool." Acta Veterinaria 71, no. 2 (2021): 147–57. http://dx.doi.org/10.2478/acve-2021-0013.

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Abstract Nowadays, illegal trafficking and smuggling of animals are among the greatest threats to many avian species. Most commonly smuggled birds belong to parrots, song birds, raptor species and owls. All of these species are protected by national and international legislations. In order to prevent and reduce wildlife trafficking, DNA methods have become an important forensic tool in species and sex identification. In this study, CHD1R/CHD1F primer pair was used to amplify a part of the CHD1 gene from 65 birds that belong to 43 species. For 36 species this is the first time that the length of CHD1 amplicons was measured for the purpose of species determination. The results were visualized using capillary electrophoresis and enabled simultaneous determination of sex and species. Based on the number of amplicons (two in females, one in males) sex was successfully determined in all species, even in cases where gel electrophoresis failed to give results. Moreover, the species was successfully determined in most bird species based on the species-specific sizes of CHD1 amplicon. The method used in this study is of great importance for veterinary forensic medicine and the prevention of wildlife smuggling. Still, further work is necessary to confirm the effectiveness of the method in all bird species.
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Rodgers, Melissa J., David J. Banks, Kenneth A. Bradley, and John AT Young. "CHD1 and CHD2 are positive regulators of HIV-1 gene expression." Virology Journal 11, no. 1 (2014): 180. http://dx.doi.org/10.1186/1743-422x-11-180.

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Pilarowski, Genay O., Hilary J. Vernon, Carolyn D. Applegate, et al. "Missense variants in the chromatin remodeler CHD1 are associated with neurodevelopmental disability." Journal of Medical Genetics 55, no. 8 (2017): 561–66. http://dx.doi.org/10.1136/jmedgenet-2017-104759.

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BackgroundThe list of Mendelian disorders of the epigenetic machinery has expanded rapidly during the last 5 years. A few missense variants in the chromatin remodeler CHD1 have been found in several large-scale sequencing efforts focused on uncovering the genetic aetiology of autism.ObjectivesTo explore whether variants in CHD1 are associated with a human phenotype.MethodsWe used GeneMatcher to identify other physicians caring for patients with variants in CHD1. We also explored the epigenetic consequences of one of these variants in cultured fibroblasts.ResultsHere we describe six CHD1 heterozygous missense variants in a cohort of patients with autism, speech apraxia, developmental delay and facial dysmorphic features. Importantly, three of these variants occurred de novo. We also report on a subject with a de novo deletion covering a large fraction of the CHD1 gene without any obvious neurological phenotype. Finally, we demonstrate increased levels of the closed chromatin modification H3K27me3 in fibroblasts from a subject carrying a de novo variant in CHD1.ConclusionsOur results suggest that variants in CHD1 can lead to diverse phenotypic outcomes; however, the neurodevelopmental phenotype appears to be limited to patients with missense variants, which is compatible with a dominant negative mechanism of disease.
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Stokes, D. G., and R. P. Perry. "DNA-binding and chromatin localization properties of CHD1." Molecular and Cellular Biology 15, no. 5 (1995): 2745–53. http://dx.doi.org/10.1128/mcb.15.5.2745.

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CHD1 is a novel DNA-binding protein that contains both a chromatin organization modifier (chromo) domain and a helicase/ATPase domain. We show here that CHD1 preferentially binds to relatively long A.T tracts in double-stranded DNA via minor-groove interactions. Several CHD1-binding sites were found in a well-characterized nuclear-matrix attachment region, which is located adjacent to the intronic enhancer of the kappa immunoglobulin gene. The DNA-binding activity of CHD1 was localized to a 229-amino-acid segment in the C-terminal portion of the protein, which contains sequence motifs that have previously been implicated in the minor-groove binding of other proteins. We also demonstrate that CHD1 is a constituent of bulk chromatin and that it can be extracted from nuclei with 0.6 M NaCl or with 2 mM EDTA after mild digestion with micrococcal nuclease. In contrast to another chromo-domain protein, HP1, CHD1 is not preferentially located in condensed centromeric heterochromatin, even though centromeric DNA is highly enriched in (A+T)-rich tracts. Most interestingly, CHD1 is released into the cytoplasm when cells enter mitosis and is reincorporated into chromatin during telophase-cytokinesis. These observations lend credence to the idea that CHD1, like other proteins with chromo or helicase/ATPase domains, plays an important role in the determination of chromatin architecture.
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Savitri, Diana, Irhamna Putri, Warih Pulung Nugrahani, Medania Purwaningrum, and Aris Haryanto. "Molecular bird sexing of sulphur‐crested cockatoo (Cacatua galerita) by poly." Indonesian Journal of Biotechnology 26, no. 1 (2021): 1. http://dx.doi.org/10.22146/ijbiotech.54611.

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Sex identification of endangered and protected birds in captivity is very important for conservation programs. Half of the world’s bird species are monomorphic, where male and female are difficult to distinguished morphologically, including cockatoos. Sex identification using molecular bird sexing is more accurate and applicable because it directly targets the sex chromosomes. The purpose of this study was to determine the sex of Sulphur‐crested cockatoo (Cacatua galerita) by detecting differences in the intron size of the chromodomain helicase DNA‐binding 1 (CHD1) gene on the Z and W chromosomes by polymerase chain reaction (PCR) method and to compare of plucked feathers and blood samples as DNA sources for molecular bird sexing. DNA was extracted from feather and blood samples from four C. galerita. Extracted DNA was amplified on the CHD1 gene by PCR method with P2, MP, and NP primers, which were visualized using agarose gel 1.5% under UV transilluminator with a wavelength of 280 nm. The resulting PCR product was detected at 392 bp for the CHD1 Z gene segment and 297 bp for CHD1 W gene segments, where males showed a single DNA band (ZZ) and females showed a double DNA band (ZW). Four C. galerita were 100% successfully determined, consisting of one female and three males. Electrophoresis results showed DNA bands from blood samples were thicker and brighter than DNA bands from feather samples.
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Tsang, Jimmy S. H., and Laiju Sam. "Cloning and Characterization of a Cryptic Haloacid Dehalogenase from Burkholderia cepacia MBA4." Journal of Bacteriology 181, no. 19 (1999): 6003–9. http://dx.doi.org/10.1128/jb.181.19.6003-6009.1999.

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ABSTRACT Burkholderia cepacia MBA4 has been shown to produce a single dehalogenase batch culture. Moreover, other cryptic dehalogenases were also detected when the cells were grown in continuous culture. In this paper, we report the cloning and characterization of one of the cryptic dehalogenases in MBA4. This cryptic haloacid dehalogenase, designated Chd1, was expressed constitutively in Escherichia coli. This recombinant Chd1 had a relative molecular weight of 58,000 and existed predominantly as a dimer. The subunits had a relative molecular weight of 27,000. Chd1 exhibited isomer specificity, being active towards thel-isomer of 2-monochloropropionic acid only. The structural gene, chd1, was isolated on a 1.7-kb PstI fragment. This fragment contains a functional promoter, because expression of chd1 in E. coli is orientation independent. The nucleotide sequence of this fragment was determined and characterized. An open reading frame of 840 bp encoding a putative peptide of 280 amino acids was identified. This corresponds closely with the size of the subunit. The nucleotide sequence of chd1 did not show any homology with those of other dehalogenase genes. Comparison of the predicted amino acid sequence, however, shows significant homology, ranging from 42 to 50%, with the amino acid sequences of many other dehalogenases. Chd1 is unusual in having a long leader sequence, a property of periplasmic enzymes.
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Kareddula, Aparna, Daniel J. Medina, Whitney Petrosky, et al. "The role of chromodomain helicase DNA binding protein 1 (CHD1) in promoting an invasive prostate cancer phenotype." Therapeutic Advances in Urology 13 (January 2021): 175628722110224. http://dx.doi.org/10.1177/17562872211022462.

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Background: Prostate cancer (PCa) phenotypes vary from indolent to aggressive. Molecular subtyping may be useful in predicting aggressive cancers and directing therapy. One such subtype involving deletions of chromodomain helicase DNA binding protein 1 ( CHD1), a tumor suppressor gene, are found in 10–26% of PCa tumors. In this study, we evaluate the functional cellular effects that follow CHD1 deletion. Methods: CHD1 was knocked out (KO) in the non-tumorigenic, human papillomavirus 16 (HPV16)-immortalized prostate epithelial cell line, RWPE-1, using CRISPR/Cas9. In vitro assays such as T7 endonuclease assay, western blot, and sequencing were undertaken to characterize the CHD1 KO clones. Morphologic and functional assays for cell adhesion and viability were performed. To study expression of extracellular matrix (ECM) and adhesion molecules, a real-time (RT) profiler assay was performed using RWPE-1 parental, non-target cells (NT2) and CHD1 KO cells. Result: Compared to parental RWPE-1 and non-target cells (NT2), the CHD1 KO cells had a smaller, rounder morphology and were less adherent under routine culture conditions. Compared to parental cells, CHD1 KO cells showed a reduction in ECM and adhesion molecules as well as a greater proportion of viable suspension cells when cultured on standard tissue culture plates and on plates coated with laminin, fibronectin or collagen I. CHD1 KO cells showed a decrease in the expression of secreted protein acidic and rich in cysteine (SPARC), matrix metalloproteinase 2 (MMP2), integrin subunit alpha 2 (ITGA2), integrin subunit alpha 5 (ITGA5), integrin subunit alpha 6 (ITGA6), fibronectin (FN1), laminin subunit beta-3 precursor (LAMB3), collagen, tenascin and vitronectin as compared to parental and NT2 cells. Conclusion: These data suggest that in erythroblast transformation specific (ETS) fusion-negative, phosphatase and tensin homolog ( PTEN) wildtype PCa, deletion of CHD1 alters cell-cell and cell-matrix adhesion dynamics, suggesting an important role for CHD1 in the development and progression of PCa.
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Sinha, Arpan, Adriana De La Garza, Amit Verma, J. Kimble Frazer, and Teresa V. Bowman. "CHD1 - a Novel Epigenetic Regulator in Myeloid Malignancies with a Role in DNA Repair." Blood 132, Supplement 1 (2018): 2607. http://dx.doi.org/10.1182/blood-2018-99-114259.

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Abstract Myelodysplastic syndromes (MDS) and acute myeloid leukemias (AML) are clonal hematopoietic disorders resulting from genetic alterations in hematopoietic stem cells. These myeloid disorders are clinically heterogeneous and biologically complex. Despite major advances in understanding the genetic and molecular landscape of MDS/AML, along with the introduction of newer and targeted therapies, the cure rates in AML are still only about 60% in children, and much lower in adults. Exploiting the genetic tractability of the zebrafish (Danio rerio) vertebrate model, we are investigating the role of a novel epigenetic regulator, Chromodomain helicase DNA binding protein-1 (CHD1) in hematopoiesis and its misregulation leading to MDS and AML. CHD1 is located at chromosome 5q21, which lies within the most frequent breakpoints seen with the deletion of the long arm of chromosome 5 [del (5q)] in patients with MDS and AML. In addition to del (5q), we found that CHD1 levels are significantly lower in bone marrow cells of patients with other forms of MDS, relative to normal controls. Using CRISPR/Cas9-mediated targeted mutagenesis in zebrafish, we created chd1 homozygous mutant fish. We confirmed a marked decrease in chd1 gene expression in these mutant fish. Chd1 homozygous mutants are viable and fertile as adults, with no significant developmental or hematopoietic phenotypes observed during embryogenesis. As CHD1 can act as a tumor suppressor and is linked to the DNA damage response, we hypothesized that chd1 mutant zebrafish would be more sensitive to DNA damaging agents. Indeed, we found that chd1 mutants have increased sensitivity to ionizing radiation as evidenced by elevated brain cell death measured by whole mount imaging of live embryos and immunofluorescence for activated Caspase 3, a marker of apoptosis. We also generated chd1het; tp53het zebrafish to test whether chd1 haploinsufficiency could accelerate tumor rates in tp53 mutant fish. Single heterozygotes chd1het or tp53het usually do not form tumors at one year of age, but chd1het; tp53het double heterozygous zebrafish showed substantial tumor growth by one year of age. Taken together, our data suggest that CHD1 may play a key role in protecting genomic integrity, explaining why diminished CHD1 levels could contribute to the pathogenesis of MDS and AML. This genetic interaction may be especially crucial in patients with combined del (5q) and TP53 alterations, and could contribute to the increased severity seen in this group. Our findings suggest these and other CHD1-deficient patients may be resistant to standard therapies due to attenuated DNA damage responses, allowing their AML to survive DNA damage caused by conventional anti-cancer treatments. Disclosures No relevant conflicts of interest to declare.
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Fridolfsson, Anna-Karin, and Hans Ellegren. "Molecular Evolution of the Avian CHD1 Genes on the Z and W Sex Chromosomes." Genetics 155, no. 4 (2000): 1903–12. http://dx.doi.org/10.1093/genetics/155.4.1903.

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Abstract Genes shared between the nonrecombining parts of the two types of sex chromosomes offer a potential means to study the molecular evolution of the same gene exposed to different genomic environments. We have analyzed the molecular evolution of the coding sequence of the first pair of genes found to be shared by the avian Z (present in both sexes) and W (female-specific) sex chromosomes, CHD1Z and CHD1W. We show here that these two genes evolve independently but are highly conserved at nucleotide as well as amino acid levels, thus not indicating a female-specific role of the CHD1W gene. From comparisons of sequence data from three avian lineages, the frequency of nonsynonymous substitutions (Ka) was found to be higher for CHD1W (1.55 per 100 sites) than for CHD1Z (0.81), while the opposite was found for synonymous substitutions (Ks, 13.5 vs. 22.7). We argue that the lower effective population size and the absence of recombination on the W chromosome will generally imply that nonsynonymous substitutions accumulate faster on this chromosome than on the Z chromosome. The same should be true for the Y chromosome relative to the X chromosome in XY systems. Our data are compatible with a male-biased mutation rate, manifested by the faster rate of neutral evolution (synonymous substitutions) on the Z chromosome than on the female-specific W chromosome.
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Krogan, Nevan J., Minkyu Kim, Seong Hoon Ahn, et al. "RNA Polymerase II Elongation Factors of Saccharomyces cerevisiae: a Targeted Proteomics Approach." Molecular and Cellular Biology 22, no. 20 (2002): 6979–92. http://dx.doi.org/10.1128/mcb.22.20.6979-6992.2002.

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ABSTRACT To physically characterize the web of interactions connecting the Saccharomyces cerevisiae proteins suspected to be RNA polymerase II (RNAPII) elongation factors, subunits of Spt4/Spt5 and Spt16/Pob3 (corresponding to human DSIF and FACT), Spt6, TFIIF (Tfg1, -2, and -3), TFIIS, Rtf1, and Elongator (Elp1, -2, -3, -4, -5, and -6) were affinity purified under conditions designed to minimize loss of associated polypeptides and then identified by mass spectrometry. Spt16/Pob3 was discovered to associate with three distinct complexes: histones; Chd1/casein kinase II (CKII); and Rtf1, Paf1, Ctr9, Cdc73, and a previously uncharacterized protein, Leo1. Rtf1 and Chd1 have previously been implicated in the control of elongation, and the sensitivity to 6-azauracil of strains lacking Paf1, Cdc73, or Leo1 suggested that these proteins are involved in elongation by RNAPII as well. Confirmation came from chromatin immunoprecipitation (ChIP) assays demonstrating that all components of this complex, including Leo1, cross-linked to the promoter, coding region, and 3′ end of the ADH1 gene. In contrast, the three subunits of TFIIF cross-linked only to the promoter-containing fragment of ADH1. Spt6 interacted with the uncharacterized, essential protein Iws1 (interacts with Spt6), and Spt5 interacted either with Spt4 or with a truncated form of Spt6. ChIP on Spt6 and the novel protein Iws1 resulted in the cross-linking of both proteins to all three regions of the ADH1 gene, suggesting that Iws1 is likely an Spt6-interacting elongation factor. Spt5, Spt6, and Iws1 are phosphorylated on consensus CKII sites in vivo, conceivably by the Chd1/CKII associated with Spt16/Pob3. All the elongation factors but Elongator copurified with RNAPII.
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Dissertations / Theses on the topic "CHD1 gene"

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Bui, Phuongngan Thi. "Investigating the Influence of CHD1 on Gene Expression in Drosophila Melanogaster Using Position Effect Variegation." Scholarship @ Claremont, 2015. http://scholarship.claremont.edu/scripps_theses/537.

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Position Effect Variegation (PEV) is the mosaic expression of a gene that has been moved out of its optimal environment and into a different area on the chromosome. Changing a gene’s environment may have profound effects on its eligibility for proper expression, which is a complicated process regulated by many factors. The PEV phenomenon is used as an assay to study gene expression as regulated by chromatin structure. In this study, the Drosophila melanogaster white gene was used as a reporter to study the various effects of CHD1, a chromatin regulating factor, on PEV gene expression. Inspired by preliminary data generated by the Armstrong Lab where overexpression of CHD1 resulted in suppression of gene silencing of the brown gene and loss of CHD1 resulted in enhancement of gene silencing, this study uses PEV as an assay to examine whether loss of function chd1 mutant alleles function dominantly to enhance silencing of the white gene when it is placed in a repressive chromatin environment. Surprisingly, I found that a chd1 loss of function mutant allele dominantly suppressed gene silencing (meaning I saw an increase in gene expression), suggesting that the CHD1 protein is normally required for effective silencing. The results demonstrated that CHD1 is a dominant modifier of PEV gene expression. CHD1 significantly modifies gene expression by suppressing silencing of the white gene inserted into pericentric heterochromatin on the second and fourth chromosomes and an insertion into the medial region of the fourth chromosome, while it shows no significant modification of the white gene inserted into telomeric heterochromatin of the fourth chromosome. Together, these intriguing results regarding varying gene expression at different chromosomal sites show that PEV is a dynamic phenomenon meriting further research and studying the effects of CHD1 as a modifier of PEV may be influential to understanding the mechanism and characteristics of gene expression.
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Pieper, Lasse. "Das CHARGE-Syndrom – Quantifizierung eines Gonadenmosaiks und Interaktionspartnersuche des CHD7-Gens." Doctoral thesis, Niedersächsische Staats- und Universitätsbibliothek Göttingen, 2013. http://hdl.handle.net/11858/00-1735-0000-000D-F67E-1.

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Das CHARGE-Syndrom ist ein autosomal dominant vererbtes Dysmorphiesyndrom. Meistens handelt es sich um sporadische Fälle. Nur für ca. 2/3 der Betroffenen konnte als Ursache eine Mutation im CHD7-Gen nachgewiesen werden.  In dieser Arbeit wurde eine Familie untersucht, in der zwei Kinder gesunder Eltern von einem CHARGE-Syndrom betroffen sind und die Mutation c.7302dupA heterozygot aufweisen. Die  ursächliche Mutation c.7302dupA ließ sich in den väterlichen Spermien nachweisen. Ein Gonadenmosaik konnte somit beim Vater der betroffenen Kinder bestätigt werden.  Eine Methode zur DNA-Analyse an Einzelspermien wurde etabliert, mittels derer der Grad des Mosaiks näher bestimmt werden konnte. In einer Stichprobe des untersuchten Falles trugen 16 von 59 der untersuchten Einzelspermien die Mutation c.7302dupA. Aus diesem Ergebnis lässt sich ein deutlich erhöhtes Wiederholungsrisiko bei einem weiteren Kind ableiten. Eine Interaktion von CHD7 mit CHD8 konnte durch einen direkten Yeast-Two-Hybrid nachgewiesen werden. Bestätigt wurde dieses Ergebnis durch den Nachweis der Ko-Lokalisation der beiden Proteine sowie durch ein Signal in einem bimolekularen Fluoreszenzkomplement-Assay. Im direkten Yeast-Two-Hybrid ließ sich die Interaktionsstelle im CHD7 auf den AS Bereich 1950–2172 mit den Domänen SANT und CR3 mit distalen und proximalen Überhängen eingrenzen.  Durch das Einfügen einer bei einem CHARGE-Patienten identifizierten Missense-Mutation p.Trp2091Arg in den entsprechenden CHD7-Abschnitt ließ sich keine Interaktion mit CHD8 im direkten Yeast-Two-Hybrid mehr nachweisen. Die Bedeutung dieser Missense-Mutation beim Wegfall der Interaktion zwischen CHD7 und CHD8 als Ursache für das CHARGE-Syndrom ist in diesem Fall anzunehmen.
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Tai, Helen H. "The role of Xist and CHD-1 in gene silencing." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape2/PQDD_0018/NQ57070.pdf.

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Loung, Le Anh. "Genetic variations in the interleukin-6(IL-6) gene : implication in coronary heart disease (CHD)." Thesis, University College London (University of London), 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.406589.

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Brajadenta, Gara Samara. "Development of a functional assay for CHD7, a protein involved in CHARGE syndrome." Thesis, Poitiers, 2019. http://www.theses.fr/2019POIT1401/document.

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Le syndrome CHARGE (CS) est une maladie génétique rare caractérisée par de nombreuses anomalies congénitales, majoritairement causées par des altérations de novo du gène CHD7. Celui-ci code pour une protéine à chromodomaines, impliquée dans le remodelage ATP-dépendant de la chromatine. La grande majorité des altérations de CHD7 consiste en allèles nuls tels que des délétions, des substitutions non-sens ou des décalages du cadre de lecture. Nous avons réalisé le premier diagnostic moléculaire d’un patient Indonésien atteint du CS, en étudiant un panel de gènes (CHD7, EFTUD2, et HOXA1) par NGS (next-generation sequencing). Nous avons identifié une nouvelle mutation non-sens hétérozygote dans l’exon 34 du gène CHD7 (c.7234G>T ou p.Glu2412Ter). Par ailleurs, il n'existe pas d’analyse fonctionnelle qui permettrait de caractériser la pathogénicité des variants de la protéine CHD7 rencontrés chez des patients. C’est pourquoi l’objectif de ce travail est de mettre au point un test fonctionnel de la protéine CHD7, sous forme sauvage ou mutée. Pour cela, nous avons généré par mutagénèse dirigée des vecteurs codant pour trois variants faux-sens de CHD7 et le variant présentant une insertion de cinq acides aminés. Ensuite, les protéines CHD7, sous forme sauvage ou variante, ont été surexprimées dans la lignée HeLa. L’expression des protéines a été mise en évidence par western blot et par immunofluorescence. Pour étudier la fonctionnalité de CHD7, nous avons quantifié par RT-qPCR les transcrits de cinq gènes (l’ADNr 45S, SOX4, SOX10, MYRF, et ID2), dont la transcription est selon le littérature régulée par CHD7. Nous avons observé que l’expression de CHD7 sauvage entraînait une diminution significative et reproductible des quantités de transcrits correspondant à tous les gènes rapporteurs. Par contre, l’expression des quatre allèles variants de CHD7 n’avait aucun impact, ce qui suggère que ces variants ne sont pas fonctionnels. Par ailleurs, nous avons appliqué notre test biologique dans des cellules de la lignée SH-SY5Y, pour lesquelles nous avons introduit une mutation faux-sens dans le génome en utilisant la technique CRISPR/Cas9. Lorsque ce variant était exprimé, les niveaux de transcription des cinq gènes rapporteurs n’étaient pas significativement différents de ceux observés dans les cellules où les deux allèles de CHD7 avaient été invalidés. Par conséquent, les variants étudiés peuvent être répertoriés comme résultant de mutations causales du CS
CHARGE syndrome (CS) is a rare genetic disease characterized by numerous congenital abnormalities, mainly caused by de novo alterations of the CHD7 gene. It encodes a chromodomain protein, involved in the ATP-dependent remodeling of chromatin. The vast majority of CHD7 alterations consists in null alleles like deletions, non-sense substitutions or frameshift-causing variations. We report the first molecular diagnosis of an Indonesian CS patient by a targeted NGS (next-generation sequencing) gene panel (CHD7, EFTUD2, and HOXA1). We identified a novel heterozygous nonsense mutation in exon 34 of CHD7 (c.7234G>T or p.Glu2412Ter). Functional analyses to confirm the pathogenicity of CHD7 variants are lacking and urgently needed. Therefore, the aim of this study was to establish a functional test for wild-type (WT) or variants of CHD7 protein found in CS patients. Using an expression vector encoding CHD7, three variants harboring an amino acid substitution and one variant with a five-amino acid insertion were generated via site-directed mutagenesis. Then CHD7 proteins, either wild-type (WT) or variants, were overexpressed in HeLa cell line. Protein expression was highlighted by western blot and immunofluorescence. We then used real-time RT-PCR to study CHD7 functionality by evaluating the transcript amounts of five genes whose expression is regulated by CHD7 according to the literature. These reporter genes are 45S rDNA, SOX4, SOX10, ID2, and MYRF. We observed that, upon WT-CHD7 expression, the reporter gene transcriptions were downregulated, whereas the four variant alleles of CHD7 had no impact. This suggests that these alleles are not polymorphisms because the variant proteins appeared non-functional. Furthermore, we applied our biological assay in SH-SY5Y cell line in which endogenous CHD7 gene was mutated using the CRISPR/Cas9 technique. Then, we observed that when a CHD7 missense variant was expressed, the transcription levels of the five reporter genes were non-significantly different, compared with the cells in which both CHD7 alleles were knocked-out. Therefore, the studied variants can be considered as disease-causing of CS
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Hamm-Baarke, Andrea. "Analyse der Informationsverarbeitung in CHL1-defizienten Mäusen mittels metabolischer Markierung, Expressionsstudien der Immediate-Early-Gene c-fos und arg3.1/arc sowie verhaltensbiologischer Tests." [S.l. : s.n.], 2003. http://deposit.ddb.de/cgi-bin/dokserv?idn=972487735.

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Pieper, Lasse [Verfasser], Wolfgang [Akademischer Betreuer] Engel, and Knut [Akademischer Betreuer] Brockmann. "Das CHARGE-Syndrom – Quantifizierung eines Gonadenmosaiks und Interaktionspartnersuche des CHD7-Gens / Lasse Pieper. Gutachter: Wolfgang Engel ; Knut Brockmann. Betreuer: Wolfgang Engel." Göttingen : Niedersächsische Staats- und Universitätsbibliothek Göttingen, 2013. http://d-nb.info/104441393X/34.

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Exeter, H. J. "The genetic architecture of secretory PLA2 (sPLA2) genes and their impact on sPLA2 activity/mass and association with CHD risk." Thesis, University College London (University of London), 2012. http://discovery.ucl.ac.uk/1380418/.

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Secretory phospholipase A2 group (sPLA2) enzymes hydrolyze the sn-2 ester bond of phospholipids, producing lysophospholipids and free fatty acids. SPLA2s have been identified as biomarkers of atherosclerosis in observational and animal studies. The aim of this study was to identify functional variants in PLA2G2A and, to a lesser extent, PLA2G5 and PLA2G10 (sPLA2 encoding genes). These variants could then serve as tools to examine their contribution to sPLA2-activity, since this is a composite measure of sPLA2-IIA,-V and –X, and associations with CHD risk/CHD traits. Two PLA2G2A SNPs were identified as being associated with sPLA2-IIA mass/sPLA2 activity. Luciferase assays, EMSA and RNA expression were used to examine their allelic differences. Rs3767221G showed ∼55% lower luciferase activity compared to rs3767221T (p = 1.22×10-35), and stronger EMSA binding of a nuclear protein compared to the T-allele. For rs11573156 C >G there were no luciferase or EMSA allelic differences. For rs11573156 there was no differential allelic lymphocyte cDNA expression for exons 5-6, but G-allele carriers (n = 7) showed a trend to lower exon 1-2 expression versus CC individuals. In the ASAP study (n = 223), a SNP acting as a proxy for rs11573156 (r2 = 0.91) on the expression array showed allelic difference of ∼25% in liver expression of total PLA2G2A (1.67×10-17). However, exon 2 specific expression was greatly reduced (4.5×10-5) compared to exons 3-6 (10-10 to 10-20), implying allele-specific exon 2 skipping as the functional basis of rs11573156 association. Rs11573156 was used as a genetic tool in a large Mendelian randomisation (MR) collaboration to establish the causality of sPLA2-IIA for CHD. While the sPLA2-IIA mass was strongly associated with CHD events, rs11573156 was not associated with outcome. Similar approaches were taken for studying PLA2G5 and PLA2G10, using eQTL data and smaller meta-analyses. Both PLA2G2A SNPs are functional. Using rs11573156 as a genetic instrument, MR suggested that sPLA2-IIA is not causally associated with CHD. Based on initial meta-analyses, neither PLA2G5 nor PLA2G10 appeared to be associated significantly with sPLA2 activity in cardiovascular related tissues. This conclusion is consistent with the outcome of the recent Phase III trial for the sPLA2 inhibitor varespladib, which was terminated due to lack of efficacy since the drug was shown to be having no significant effect on the reduction of secondary cardiovascular events.
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Hipkiss, Tim. "Brood sex ratio and sex differences in Tengmalm’s owl : (Aegolius funereus)." Doctoral thesis, Umeå University, Ecology and Environmental Science, 2002. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-8.

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Males and females differ in morphology and behaviour, so that selection acts differently on the two sexes. This changes the relative reproductive success of males and females, and it is beneficial for parents to bias the sex ratio of their broods in favour of the sex with the best survival and breeding prospects. Differences between the sexes and brood sex ratio in Tengmalm’s owl (Aegolius funereus) in northern Sweden were investigated, using a molecular sexing technique based on PCRamplification of sex-linked CHD1 genes. Among owls caught during autumn migration, females were commoner than males, especially within juveniles. However, in contrast to earlier studies, it was shown that adult males sometimes undertake migratory movements indicatory of nomadism. Measurements of these owls revealed that sexual size dimorphism in Tengmalm’s owl is not as great as previously reported from studies carried out during the breeding season. Females were slightly larger (4% by mass) than males, probably owing to the different roles of males and females during breeding, when this dimorphism is greater. The size difference between male and female nestlings was found to be similar to that for adults in autumn, and to investigate whether this led to differential mortality, the effect of supplementary feeding on mortality of male and female nestlings was studied. Supplementary feeding reduced male mortality when vole abundance was low, and it was concluded that larger female nestlings out-competed their smaller brothers, who then suffered increased mortality when food was scarce. Recruitment of male nestlings into the breeding population declined with decreasing food supply at the time of fledging, a pattern not observed in females. Juvenile males were therefore more vulnerable to food shortage than females, both in the nest and after fledging. Mean brood sex ratio varied significantly among years characterized by different phases of the vole cycle and associated vole abundance. Broods were male-biased (63% males) in a year when the food supply was favourable during spring and summer, neutral (50%) in a year with an intermediate food supply, and female-biased (35% males) in a year when food was in short supply. Parents appeared to adaptively adjust the sex ratio of their broods according to the relative mortality risk and reproductive potential of sons and daughters.

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Solyom, S. (Szilvia). "BRCA/Fanconi anemia pathway genes in hereditary predisposition to breast cancer." Doctoral thesis, Oulun yliopisto, 2011. http://urn.fi/urn:isbn:9789514294099.

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Abstract Two major genes are involved in hereditary predisposition to breast and ovarian cancer – BRCA1 and BRCA2. However, germline mutations in these tumor suppressors account for a maximum 20% of the familial breast cancer cases. A significant portion of the genes predisposing to this disease is unknown and therefore needs to be discovered. The aim of this study was to identify novel breast cancer susceptibility genes from the interweaving BRCA/Fanconi anemia (FA) pathway. Five candidate genes – MERIT40, ABRAXAS, BRIP1, CHK1, and FANCA – were screened for mutations by utilizing conformation-sensitive gel electrophoresis and sequencing, or with multiplex ligation-dependent probe amplification in blood DNA samples of Finnish familial breast cancer patients. Investigation of the MERIT40 gene revealed novel nucleotide changes, being the first report on mutation screening of this gene. None of the observed alterations, however, appeared to be disease related, suggesting that germline mutations in MERIT40 are rare or absent in breast cancer patients. A missense alteration (c.1082G>A, leading to Arg361Gln) was identified in ABRAXAS in 3 out of 125 Northern Finnish breast cancer families (2.4%), but not in any of the 867 healthy controls. The prevalence of the mutation between familial and control cases was statistically significantly different (p=0.002). ABRAXAS c.1082G>A appears to have pathological significance based on its exclusive occurrence in cancer cases, evolutionary conservation, disruption of a putative nuclear localization signal, reduced nuclear localization of the protein, and defective accumulation at DNA damage sites. The BRIP1 (FANCJ) and CHK1 genes were screened for large genomic rearrangements, but no abnormalities were detected, ruling out a significant contribution to breast cancer susceptibility in the Northern Finnish population. A novel large heterozygous deletion was identified in the FANCA gene in one out of 100 breast cancer families, removing the promoter and the first 12 exons. The deletion allele was not present in the tested controls, suggesting that it might contribute to breast cancer susceptibility. This is the first report on the association of a large-size germline deletion in a gene acting in the upstream part of the FA signaling pathway with familial breast cancer
Tiivistelmä BRCA1 ja BRCA2 ovat kaksi tärkeintä perinnöllisen rinta- ja munasarjasyövän alttiusgeeniä. Niissä esiintyvät ituradan muutokset selittävät kuitenkin vain noin 20 % familiaalisista rintasyöpätapauksista. Suurin osa alttiusgeeneistä on edelleen tunnistamatta ja näitä tekijöitä etsitään aktiivisesti. Tämän tutkimuksen tarkoituksena on ollut tunnistaa uusia alttiustekijöitä toisiinsa läheisesti liittyviltä BRCA/Fanconin anemia (FA) signaalinsiirtoreiteiltä. Viisi kandidaattigeeniä - MERIT40, ABRAXAS, BRIP1, CHK1 ja FANCA – kartoitettiin mutaatioiden suhteen suomalaisissa rintasyöpäperheissä käyttämällä konformaatiosensitiivistä geelielektroforeesia ja sekvensointia, tai multiplex ligation-dependent probe amplification- menetelmää. MERIT40-geenissä havaittiin useita aikaisemmin raportoimattomia nukleotidimuutoksia, mutta yhdenkään niistä ei havaittu liittyvän rintasyöpäalttiuteen. MERIT40-geenimuutosten mahdollista yhteyttä rintasyöpäalttiuteen ei ole tutkittu aikaisemmin. ABRAXAS-geenissä havaittiin missense-mutaatio (c.1082G>A, joka johtaa Arg361Gln aminohappokorvautumiseen) kolmessa pohjoissuomalaisessa rintasyöpäperheessä (3/125, 2.4 %). Muutosta ei havaittu terveissä kontrolleissa (N=867), ja ero mutaation esiintyvyydessä familiaalisten rintasyöpätapausten ja terveiden kontrollien välillä oli tilastollisesti merkitsevä (p=0.002). ABRAXAS c.1082G>A-muutos on todennäköisesti patogeeninen, sillä kyseinen aminohappopaikka on evolutiivisesti konservoitunut ja sijaitsee todennäköisellä tumaanohjaussignaalialueella. Funktionaaliset kokeet osoittivat, että mutatoitunut proteiinituote lokalisoitui villityypin proteiinia heikommin tumaan ja sen ohjautuminen DNA-vaurioalueille oli puutteellista. BRIP1- (FANCJ) ja CHK1-geeneistä etsittiin laajoja genomisia uudelleenjärjestelyjä, mutta niitä ei havaittu. Näin ollen kyseisillä muutoksilla ei ole merkittävää roolia perinnöllisessä rintasyöpäalttiudessa suomalaisessa väestössä. FANCA-geenissä havaittiin laaja heterotsygoottinen deleetio yhdessä tutkitusta 100 rintasyöpäperheestä. Deleetio poistaa geenin promoottorialueen lisäksi sen 12 ensimmäistä eksonia. Deleetioalleelia ei havaittu terveissä kontrolleissa, joten se mahdollisesti liittyy perinnölliseen rintasyöpäalttiuteen. Tutkimus on ensimmäinen, jossa raportoidaan laaja genominen deleetio FA-signaalinsiirtoreitin ylävirran geenissä familiaalisessa rintasyövässä
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Books on the topic "CHD1 gene"

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Prasad, Supritha, and Edwin H. Cook. Novel Approaches for Treating Pediatric Psychiatric Disorders. Edited by Dennis S. Charney, Eric J. Nestler, Pamela Sklar, and Joseph D. Buxbaum. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190681425.003.0067.

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Multifactorial mechanisms, including varying degrees of polygenic risk, contribute to most child onset psychiatric disorders. Methods to better understand the biological impact of inherited low-risk variation are emerging, and these studies may be useful to develop novel treatments for childhood onset psychiatric disorders. In some neurodevelopmental disorders, specifically autism spectrum disorder (ASD) and intellectual disability (ID), recurrent spontaneously mutated genes have been identified. This leads to the current focus on individual, high-risk targets (e.g., SHANK3, FMR1, MECP2, CHD8) for development of novel treatments. This chapter summarizes and begins to compare neurobiological data from several distinct single gene disorders as a means to guide further therapeutic development based on overlapping pathways of interest.
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Bentham, James R. The genetics of congenital heart disease. Edited by José Maria Pérez-Pomares, Robert G. Kelly, Maurice van den Hoff, et al. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198757269.003.0022.

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Congenital heart disease (CHD) is defined as a structural cardiac malformation resulting from an abnormality of development; 8% of CHD is inherited in a Mendelian fashion and 12% results from chromosomal imbalance. Recurrence risk and new research suggest that even the remaining 80% of patients without an identifiable familial or syndromic basis for disease may have an identifiable genetic cause. The potential to understand these mechanisms is increasing with the advent of new sequencing techniques which have identified multiple or single rare variants and/or copy number variants clustering in cardiac developmental genes as well as common variants that may also contribute to disease, for example by altering metabolic pathways. Work in model organisms such as mouse and zebrafish has been pivotal in identifying CHD candidate genes. Future challenges involve translating the discoveries made in mouse models to human CHD genetics and manipulating potentially protective pathways to prevent disease.
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Ng, Dominic S. Familial Apolipoprotein A-I Deficiency. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0036.

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Apolipoprotein (apo) A-I is the key structural protein of high-density lipoprotein (HDL) and is necessary for sustaining the circulating level of HDL. It has also been studied extensively for its role in mediating many of the antiatherosclerotic and antithrombotic properties of HDL. More than 50 naturally occurring mutations and variants have been described, and they usually result in marked HDL deficiency in a gene-dose dependent manner. However, the propensity to develop accelerated coronary heart disease (CHD) is highly heterogeneous. Mutations resulting in inability to synthesize apo A-I tend to be associated with early CHD, while mutations resulting in structurally altered apo A-I are generally not associated. Furthermore, a number of apo A-I variants, for example apo A-I Iowa or apo A-I Helsinki, have been linked to amyloidosis, resulting in potentially serious morbid complications.
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Mercado, Pilar, Jamey E. Eklund, and Jennifer L. Anderson. Charge Syndrome. Edited by Kirk Lalwani, Ira Todd Cohen, Ellen Y. Choi, and Vidya T. Raman. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190685157.003.0003.

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The major diagnostic features of CHARGE syndrome include coloboma of the eyes, choanal atresia or stenosis, distinctive external ears, cranial nerve abnormalities, and absent or small semicircular canals. The mnemonic refers to coloboma of the eye, heart defects, atresia of choanae, retardation of growth and development, cenitalia hypoplasia, and ear abnormalities and deafness. There is no defined etiology, though a de novo mutation on the CHD 7 gene located on Chromosome 8 is responsible for more than 50% of CHARGE cases. The incidence of CHARGE is about 1:10,000 live births with an equal distribution between males and females. The anesthetic implications of this syndrome are many and vary with the patient’s phenotype. A potential difficult airway, congenital heart defects, choanal atresia, and cranial nerve abnormalities present the most significant issues for the anesthesiologist. A multidisciplinary team must be established early to properly care for these complex patients.
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Book chapters on the topic "CHD1 gene"

1

Costa, Lucio G. "Receptors and Ion Channels." In Gene-Environment Interactions. John Wiley & Sons, Inc., 2006. http://dx.doi.org/10.1002/0471758043.ch11.

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Costa, Lucio G., and David L. Eaton. "Overview of Section IV." In Gene-Environment Interactions. John Wiley & Sons, Inc., 2006. http://dx.doi.org/10.1002/0471758043.ch21.

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Gruber, Sabine, and Alexandra Hüsken. "Control of Cleistogamy and Seed Dormancy for Biological Gene Containment in Oilseed Rape (Brassica napusL.)." In Plant Gene Containment. Blackwell Publishing Ltd., 2012. http://dx.doi.org/10.1002/9781118352670.ch11.

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Costa, Lucio G., and David L. Eaton. "Introduction." In Gene-Environment Interactions. John Wiley & Sons, Inc., 2006. http://dx.doi.org/10.1002/0471758043.ch1.

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Aoki, Jennifer A., and James L. Manley. "The Role of Cotranscriptional Recruitment of RNA-Binding Proteins in the Maintenance of Genomic Stability." In Posttranscriptional Gene Regulation. Wiley-VCH Verlag GmbH & Co. KGaA, 2013. http://dx.doi.org/10.1002/9783527665433.ch1.

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Lu, Bao-Rong, and Wei Wang. "Potential Environmental Impacts of Transgene Flow in Rice with a Particular View on Herbicide Resistance." In Plant Gene Containment. Blackwell Publishing Ltd., 2012. http://dx.doi.org/10.1002/9781118352670.ch1.

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Wagner, Andreas. "On the Energy and Material Cost of Gene Duplication." In Evolution after Gene Duplication. John Wiley & Sons, Inc., 2011. http://dx.doi.org/10.1002/9780470619902.ch11.

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Magbanua, Mark Jesus M., Kevin Dawson, Liping Huang, et al. "Nutrient-Gene Interactions Involving Soy Peptide and Chemopreventive Genes in Prostate Epithelial Cells." In Nutritional Genomics. John Wiley & Sons, Inc., 2006. http://dx.doi.org/10.1002/0471781797.ch11.

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Liberles, David A., Grigory Kolesov, and Katharina Dittmar. "Understanding Gene Duplication Through Biochemistry and Population Genetics." In Evolution after Gene Duplication. John Wiley & Sons, Inc., 2011. http://dx.doi.org/10.1002/9780470619902.ch1.

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Ray, Kunal, Arijit Mukhopadhyay, and Mainak Sengupta. "Gene Discovery by Direct Genome Sequencing." In Gene Discovery for Disease Models. John Wiley & Sons, Inc., 2012. http://dx.doi.org/10.1002/9780470933947.ch11.

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Conference papers on the topic "CHD1 gene"

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Nasr, Amal, Aya Omar, Maha Alser, Huseyin Yalcin, and Fatiha Benslimane. "Unraveling Gene Expression Profiles of Cardiac Genes that Participate in Embryonic development of Congenital Heart Defects using Chick Embryo." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2020. http://dx.doi.org/10.29117/quarfe.2020.0196.

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Hypoplastic left heart syndrome (HLHS) is a rare but serious subtype of congenital heart defect (CHDs) at which the hemodynamics are disturbed. In this project, HLHS was introduced surgically by left atrial ligation (LAL) to embryonic chicks and the subsequent effects of it were studied. Different tests were done post-LAL to study cardiac morphology, function, and gene expression of cardiac markers.
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Fatemi, Mehrnaz, Hassan Brim, Krisham kumar, and Hassan Ashktorab. "Abstract 5018: Transcriptional and functional analysis of the CHD5 gene in Colorectal Cancer." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-5018.

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Egan, Christopher M., Ulrika Nyman, Julie Skotte, et al. "Abstract PR12: CHD5 is required for neurogenesis and has a dual role in facilitating gene expression and Polycomb gene repression." In Abstracts: AACR Special Conference on Chromatin and Epigenetics in Cancer - June 19-22, 2013; Atlanta, GA. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.cec13-pr12.

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Tereshchenko, Irina V., Hua Zhong, Marina Chekmareva, et al. "Abstract 2233: Rearrangement of ERG and CHD1 genes in prostate cancer as a marker of tumor heterogeneity." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-2233.

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Focsa, IO, M. Ioana, I. Streata, et al. "P140 Clinical caracterization of a new case with chromosome 3 terminal microdeletion, involving chl1 gene." In 8th Europaediatrics Congress jointly held with, The 13th National Congress of Romanian Pediatrics Society, 7–10 June 2017, Palace of Parliament, Romania, Paediatrics building bridges across Europe. BMJ Publishing Group Ltd and Royal College of Paediatrics and Child Health, 2017. http://dx.doi.org/10.1136/archdischild-2017-313273.228.

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Zimmerman, Mark W., Shuning He, Jimann Shin, et al. "Abstract 2433: Loss of chd5-mediated gene repression synergizes with MYCN to accelerate neuroblastoma tumorigenesis in zebrafish." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-2433.

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Blosser, Wayne D., Jack A. Dempsey, Ann M. McNulty, et al. "Abstract 2535: Enhanced gene expression of replication fork and other E2F targets genes is associated with sensitivity and, paradoxically, also with acquired drug resistance, to the Chk1 inhibitor prexasertib." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-2535.

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Blosser, Wayne D., Jack A. Dempsey, Ann M. McNulty, et al. "Abstract 2535: Enhanced gene expression of replication fork and other E2F targets genes is associated with sensitivity and, paradoxically, also with acquired drug resistance, to the Chk1 inhibitor prexasertib." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-2535.

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Heyking, Kristina von, Annette Fasan, Stefan Burdach, and Günther H. Richter. "Abstract 3973: BRICHOS genes CHM1 and ITM2A maintain an undifferentiated, invasive phenotype in Ewing sarcoma." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-3973.

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Hannaway, Nicola L., Jill E. Hunter, Alastair Greystoke, and Neil D. Perkins. "Abstract 2548: DNA damage response gene expression in CHK1 inhibitor responsive and resistant mouse models of MYC driven B-cell lymphoma." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-2548.

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Reports on the topic "CHD1 gene"

1

Bochar, Daniel A. CHD8, A Novel Beta-Catenin Associated Chromatin Remodeling Enzyme, Regulates Androgen Receptor Mediated Gene Transcription. Defense Technical Information Center, 2008. http://dx.doi.org/10.21236/ada483296.

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Bochar, Daniel A. CHD8, A Novel Beta-Catenin Associated Chromatin Remodeling Enzyme, Regulates Androgen Receptor Mediated Gene Transcription. Defense Technical Information Center, 2010. http://dx.doi.org/10.21236/ada529449.

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Bochar, Daniel A. CHD8, A Novel Beta-Catenin Associated Chromatin Remodeling Enzyme, Regulates Androgen Receptor Mediated Gene Transcription. Defense Technical Information Center, 2009. http://dx.doi.org/10.21236/ada504104.

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