Academic literature on the topic 'CHD1 gene'
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Journal articles on the topic "CHD1 gene"
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.
Full textRodgers, 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.
Full textPilarowski, 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.
Full textStokes, 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.
Full textSavitri, 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.
Full textTsang, 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.
Full textKareddula, 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.
Full textSinha, 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.
Full textFridolfsson, 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.
Full textKrogan, 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.
Full textDissertations / Theses on the topic "CHD1 gene"
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.
Full textPieper, 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.
Full textTai, 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.
Full textLoung, 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.
Full textBrajadenta, Gara Samara. "Development of a functional assay for CHD7, a protein involved in CHARGE syndrome." Thesis, Poitiers, 2019. http://www.theses.fr/2019POIT1401/document.
Full textCHARGE 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
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.
Full textPieper, 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.
Full textExeter, 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/.
Full textHipkiss, 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.
Full textMales 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.
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.
Full textTiivistelmä 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
Books on the topic "CHD1 gene"
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.
Full textBentham, 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.
Full textNg, Dominic S. Familial Apolipoprotein A-I Deficiency. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0036.
Full textMercado, 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.
Full textBook chapters on the topic "CHD1 gene"
Costa, Lucio G. "Receptors and Ion Channels." In Gene-Environment Interactions. John Wiley & Sons, Inc., 2006. http://dx.doi.org/10.1002/0471758043.ch11.
Full textCosta, 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.
Full textGruber, 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.
Full textCosta, Lucio G., and David L. Eaton. "Introduction." In Gene-Environment Interactions. John Wiley & Sons, Inc., 2006. http://dx.doi.org/10.1002/0471758043.ch1.
Full textAoki, 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.
Full textLu, 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.
Full textWagner, 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.
Full textMagbanua, 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.
Full textLiberles, 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.
Full textRay, 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.
Full textConference papers on the topic "CHD1 gene"
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.
Full textFatemi, 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.
Full textEgan, 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.
Full textTereshchenko, 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.
Full textFocsa, 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.
Full textZimmerman, 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.
Full textBlosser, 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.
Full textBlosser, 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.
Full textHeyking, 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.
Full textHannaway, 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.
Full textReports on the topic "CHD1 gene"
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.
Full textBochar, 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.
Full textBochar, 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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