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University of Kansas
1.
Eastlund, Allen.
Revealing Remodeler Function: Varied and Unique.
Degree: PhD, Physics & Astronomy, 2015, University of Kansas
URL: http://hdl.handle.net/1808/19031 
► Chromatin remodelers perform a necessary and required function for the successful expression of our genetic code. By modifying, shifting, or ejecting nucleosomes from the chromatin…
(more)
▼ Chromatin remodelers perform a necessary and required function for the successful expression of our genetic code. By modifying, shifting, or ejecting nucleosomes from the
chromatin structure they allow access to the underlying DNA to the rest of the cell’s machinery. This research has focused on two major remodeler motors from major families of
chromatin remodelers: the trimeric motor domain of RSC and the motor domain of the ISWI family, ISWI. Using primarily stopped-flow spectrofluorometry, I have categorized the time-dependent motions of these motor domains along their preferred substrate, double-stranded DNA. Combined with collected ATP utilization data, I present the subsequent analysis and associated conclusions that stem from the underlying assumptions and models. Interestingly, there is little in common between the investigated proteins aside from their favored medium. While RSC exhibits modest translocation characteristics and highly effective motion with the ability for large molecular forces, ISWI is not only structurally different but highly inefficient in its motion leading to difficulties in determining its specific translocation mechanics. While
chromatin remodeling is a ubiquitous facet of eukaryotic life, there remains much to be understood about their general mechanisms.
Advisors/Committee Members: Fischer, Christopher J (advisor), Baringer, Phillip (cmtemember), Hawley, Steven (cmtemember), Johnson, Carey (cmtemember), Melott, Adrian (cmtemember).
Subjects/Keywords: Physics; Biophysics; biophysics; Chromatin; Fluorescence; Remodelers
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APA (6th Edition):
Eastlund, A. (2015). Revealing Remodeler Function: Varied and Unique. (Doctoral Dissertation). University of Kansas. Retrieved from http://hdl.handle.net/1808/19031
Chicago Manual of Style (16th Edition):
Eastlund, Allen. “Revealing Remodeler Function: Varied and Unique.” 2015. Doctoral Dissertation, University of Kansas. Accessed December 07, 2019.
http://hdl.handle.net/1808/19031.
MLA Handbook (7th Edition):
Eastlund, Allen. “Revealing Remodeler Function: Varied and Unique.” 2015. Web. 07 Dec 2019.
Vancouver:
Eastlund A. Revealing Remodeler Function: Varied and Unique. [Internet] [Doctoral dissertation]. University of Kansas; 2015. [cited 2019 Dec 07].
Available from: http://hdl.handle.net/1808/19031.
Council of Science Editors:
Eastlund A. Revealing Remodeler Function: Varied and Unique. [Doctoral Dissertation]. University of Kansas; 2015. Available from: http://hdl.handle.net/1808/19031
Purdue University
2.
Carter, Benjamin.
CHD Chromatin Remodelers Promote Epigenetic Control of Development in Arabidopsis thaliana.
Degree: PhD, Biochemistry, 2016, Purdue University
URL: https://docs.lib.purdue.edu/open_access_dissertations/1209
► Chromatin remodeling is a vital biological process that facilitates activation and repression of gene expression as well as compaction of large eukaryotic genomes into compact…
(more)
▼ Chromatin remodeling is a vital biological process that facilitates activation and repression of gene expression as well as compaction of large eukaryotic genomes into compact nuclei. The CHD3 family of
chromatin remodelers play key roles as epigenetic modifiers and transcriptional regulators in both plants and animals. PKL is a CHD3 remodeler that represses expression of seed genes during germination in Arabidopsis. Unlike animal CHD3
remodelers, PKL does not function as a member of a multi-subunit Mi-2 NuRD complex. Instead, PKL acts as a monomer in vivo and promotes the epigenetic modification H3K27me3, which is associated with transcriptional repression of tissue-specific genes by the PRC2. Thus, PKL plays an important role in promoting tissue identity by facilitating deposition and/or maintenance of H3K27me3.
Advisors/Committee Members: Joe Ogas, Stanton Gelvin, Ann Kirchmaier, Scott Briggs.
Subjects/Keywords: Arabidopsis; Chromatin Remodelers; H2A.Z; H3K27me3; PICKLE; PKR2
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APA (6th Edition):
Carter, B. (2016). CHD Chromatin Remodelers Promote Epigenetic Control of Development in Arabidopsis thaliana. (Doctoral Dissertation). Purdue University. Retrieved from https://docs.lib.purdue.edu/open_access_dissertations/1209
Chicago Manual of Style (16th Edition):
Carter, Benjamin. “CHD Chromatin Remodelers Promote Epigenetic Control of Development in Arabidopsis thaliana.” 2016. Doctoral Dissertation, Purdue University. Accessed December 07, 2019.
https://docs.lib.purdue.edu/open_access_dissertations/1209.
MLA Handbook (7th Edition):
Carter, Benjamin. “CHD Chromatin Remodelers Promote Epigenetic Control of Development in Arabidopsis thaliana.” 2016. Web. 07 Dec 2019.
Vancouver:
Carter B. CHD Chromatin Remodelers Promote Epigenetic Control of Development in Arabidopsis thaliana. [Internet] [Doctoral dissertation]. Purdue University; 2016. [cited 2019 Dec 07].
Available from: https://docs.lib.purdue.edu/open_access_dissertations/1209.
Council of Science Editors:
Carter B. CHD Chromatin Remodelers Promote Epigenetic Control of Development in Arabidopsis thaliana. [Doctoral Dissertation]. Purdue University; 2016. Available from: https://docs.lib.purdue.edu/open_access_dissertations/1209
University of Edinburgh
3.
Varzandeh, Simon.
Structural and biochemical insights into the ATP-dependent chromatin remodeler LSH.
Degree: PhD, 2017, University of Edinburgh
URL: http://hdl.handle.net/1842/29515
► Chromatin remodelling proteins support a variety of cellular functions and utilise the energy from ATP hydrolysis to either reposition or evict nucleosomes. One such protein,…
(more)
▼ Chromatin remodelling proteins support a variety of cellular functions and utilise the energy from ATP hydrolysis to either reposition or evict nucleosomes. One such protein, Lymphoid specific helicase (LSH), regulates DNA methylation in mammalian cells cooperatively with DNA Methyltransferase 3B (DNMT3B) through binding of the N-terminal domain of LSH. The correct functioning of LSH is essential for heterochromatin formation, with a knockout of LSH causing perinatal lethality or severe developmental abnormalities. There is little biochemical data and no structural data on LSH. Therefore, we aim to determine the structural characteristics and regulatory mechanism of LSH in vitro. LSH was expressed in an optimised insect cell system which increased protein yield 25-fold with greater than 95% purity. LSH is monomeric with increased thermal stability upon ATP or ADP binding. Full length LSH could not be crystallised therefore a core ATPase region of LSH missing the N-terminal domain was identified through limited proteolysis. This also provided evidence the N-terminal domain of LSH is disordered, which was proven through biophysical characterisation of LSH1-176. Expression of the LSH ATPase region was weak and the protein was unstable; suggesting the N-terminal domain of LSH is required for LSH stability. Therefore, complementary structural methods were used to study LSH. Crosslinking mass-spectrometry revealed the N and C termini are in close proximity, suggesting flexible linking regions, which was supported by limited proteolysis experiments. Negative staining Electron Microscopy defined LSH as a tri-lobal and elongated structure which could harbour the ATPase region in the two spherical lobes. 3D modelling of SAXS data obtained of LSH was in agreement with EM data. To understand molecular mechanisms of LSH, functional studies investigating LSH:DNA and LSH:DNMT3B interactions were performed. LSH had a KD for dsDNA of 0.4 μM in solution. LSH does not bind ssDNA nor does it have a greater affinity for methylated dsDNA. LSH was found to bind the dsDNA overhangs of nucleosomes but not to core nucleosomes, suggesting LSH solely interacts with DNA in chromatin and not histones. A stable complex of LSH:DNMT3B could not be achieved in vitro, however, other components for complex formation may have been missing. This study has improved our understanding of LSH structure, biophysical properties and its biochemical interaction with DNA and nucleosomes. This study has laid the foundations for the structural investigations of a LSH:nucleosome and potentially a LSH:DNMT3B complex in vitro to gain a greater understanding of how functional domains of LSH regulates its enzymatic function.
Subjects/Keywords: nucleosomes; chromatin remodelers; Lymphoid Specific Helicase; DNA methyltransferase 3B; DNMT3B
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APA ·
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APA (6th Edition):
Varzandeh, S. (2017). Structural and biochemical insights into the ATP-dependent chromatin remodeler LSH. (Doctoral Dissertation). University of Edinburgh. Retrieved from http://hdl.handle.net/1842/29515
Chicago Manual of Style (16th Edition):
Varzandeh, Simon. “Structural and biochemical insights into the ATP-dependent chromatin remodeler LSH.” 2017. Doctoral Dissertation, University of Edinburgh. Accessed December 07, 2019.
http://hdl.handle.net/1842/29515.
MLA Handbook (7th Edition):
Varzandeh, Simon. “Structural and biochemical insights into the ATP-dependent chromatin remodeler LSH.” 2017. Web. 07 Dec 2019.
Vancouver:
Varzandeh S. Structural and biochemical insights into the ATP-dependent chromatin remodeler LSH. [Internet] [Doctoral dissertation]. University of Edinburgh; 2017. [cited 2019 Dec 07].
Available from: http://hdl.handle.net/1842/29515.
Council of Science Editors:
Varzandeh S. Structural and biochemical insights into the ATP-dependent chromatin remodeler LSH. [Doctoral Dissertation]. University of Edinburgh; 2017. Available from: http://hdl.handle.net/1842/29515
Cornell University
4.
Kartha, Nithya.
CHARACTERIZING THE ROLE OF THE CHROMATIN REMODELING COMPONENT ARID1A AS A SUPPRESSOR OF SPORADIC MAMMARY TUMORS IN MICE
.
Degree: 2017, Cornell University
URL: http://hdl.handle.net/1813/56907
► The American Cancer Society estimates that in the year 2017, approximately 40,000 women will die from breast cancer. The vast majority of these breast cancer…
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▼ The American Cancer Society estimates that in the year 2017, approximately 40,000 women will die from breast cancer. The vast majority of these breast cancer cases (80-85%) are sporadic in nature, developing spontaneously within the lifetime of a woman. While there is a significant amount of knowledge regarding the genetic drivers of hereditary breast cancers, there is very little known about the genes responsible for driving sporadic breast cancers, largely in part due to the dearth of appropriate mouse models of this disease. The C3H-MCM4Chaos3(Chaos3) mouse model bears a single endogenous mutation in a gene encoding a component of the MCM2-7 replication helicase, which our lab has previously shown results in a state of chronic replication stress and downstream genomic instability, leading to a strain-specific phenotype of female mice developing spontaneous mammary adenocarcinomas. In my graduate research work, I have utilized this powerful and unique mouse model to determine the genetic drivers of these sporadic mammary tumors (MTs), based on relevance to human breast cancer data available publicly. My analyses of recurrent genomic alterations present in these Chaos3 MTs revealed that the majority of them (>80%) contained heterozygous deletions of a gene encoding the
chromatin remodeling component Arid1a. Importantly, ARID1A is also frequently deleted (monoallelically) in a significant
subset of human breast cancers (between 30-50%, depending on the specific study cited), based on data from The Cancer Genome Atlas (TCGA). I have characterized the pathways being altered upon overexpression of Arid1a in Chaos3 MT cells, and have identified potential direct transcriptional targets of Arid1a regulation using this in vitro system. I have further shown that the heterozygous loss of Arid1a is a critical maintenance factor for MT growth in this model, and that endogenous induction of Arid1a expression to wild-type levels is sufficient to significantly slow down MT cell proliferation in vitro. This is suggestive of a haploinsufficient role for Arid1a tumor suppression, in a manner similar to TP53, and offers an intriguing therapeutic opportunity of inducing the remaining ARID1A allele to potentially reduce MT growth in the subset of human breast cancers that retain an intact copy of this powerful tumor suppressor gene.
Advisors/Committee Members: Coonrod, Scott A. (committeeMember), Weiss, Robert S. (committeeMember).
Subjects/Keywords: Genetics;
Breast cancer;
Molecular biology;
Arid1a;
Chromatin remodelers;
Mouse model;
SWI/SNF;
Biochemistry
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APA ·
Chicago ·
MLA ·
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CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Kartha, N. (2017). CHARACTERIZING THE ROLE OF THE CHROMATIN REMODELING COMPONENT ARID1A AS A SUPPRESSOR OF SPORADIC MAMMARY TUMORS IN MICE
. (Thesis). Cornell University. Retrieved from http://hdl.handle.net/1813/56907
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Kartha, Nithya. “CHARACTERIZING THE ROLE OF THE CHROMATIN REMODELING COMPONENT ARID1A AS A SUPPRESSOR OF SPORADIC MAMMARY TUMORS IN MICE
.” 2017. Thesis, Cornell University. Accessed December 07, 2019.
http://hdl.handle.net/1813/56907.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Kartha, Nithya. “CHARACTERIZING THE ROLE OF THE CHROMATIN REMODELING COMPONENT ARID1A AS A SUPPRESSOR OF SPORADIC MAMMARY TUMORS IN MICE
.” 2017. Web. 07 Dec 2019.
Vancouver:
Kartha N. CHARACTERIZING THE ROLE OF THE CHROMATIN REMODELING COMPONENT ARID1A AS A SUPPRESSOR OF SPORADIC MAMMARY TUMORS IN MICE
. [Internet] [Thesis]. Cornell University; 2017. [cited 2019 Dec 07].
Available from: http://hdl.handle.net/1813/56907.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Kartha N. CHARACTERIZING THE ROLE OF THE CHROMATIN REMODELING COMPONENT ARID1A AS A SUPPRESSOR OF SPORADIC MAMMARY TUMORS IN MICE
. [Thesis]. Cornell University; 2017. Available from: http://hdl.handle.net/1813/56907
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Leiden University
5.
Helfricht, A.
Chromatin modifiers in DNA repair and human disease.
Degree: 2016, Leiden University
URL: http://hdl.handle.net/1887/43800
► Upon the induction of DNA damage, cells initiate a protective response, referred to as the DNA damage response (DDR), to repair DNA damage and maintain…
(more)
▼ Upon the induction of DNA damage, cells initiate a protective response, referred to as the
DNA damage response (DDR), to repair DNA damage and maintain genome integrity. This
response is driven and regulated by posttranslational protein modifications and
chromatin
remodeling events. Mutations or aberrant expression of
chromatin modifying proteins not
only impacts on the DDR, but also causes human diseases with severe clinical phenotypes,
illustrating the importance of these proteins for genome stability maintenance and human
health. Largely unclear is, however, which and how
chromatin modifying enzymes control
the complex DDR pathways and in this manner prevent the onset of disease. To this end,
we employed cross-disciplinary approaches that combined cell biological, biochemical and
microscopic methods to identify histone modifying enzymes,
chromatin remodelers as well
as other DDR proteins and elucidate their mechanistic role in the response to DNA doublestrand
breaks (DSBs) and disease prevention.
Advisors/Committee Members: Supervisor: S.M. van der Maarel Co-Supervisor: H. van Attikum, Vertegaal, A.C.O..
Subjects/Keywords: Chromatin remodelers; DNA damage response; DSB repair; Immunodeficiency; CF syndrome; Chromatin remodelers; DNA damage response; DSB repair; Immunodeficiency; CF syndrome
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APA ·
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APA (6th Edition):
Helfricht, A. (2016). Chromatin modifiers in DNA repair and human disease. (Doctoral Dissertation). Leiden University. Retrieved from http://hdl.handle.net/1887/43800
Chicago Manual of Style (16th Edition):
Helfricht, A. “Chromatin modifiers in DNA repair and human disease.” 2016. Doctoral Dissertation, Leiden University. Accessed December 07, 2019.
http://hdl.handle.net/1887/43800.
MLA Handbook (7th Edition):
Helfricht, A. “Chromatin modifiers in DNA repair and human disease.” 2016. Web. 07 Dec 2019.
Vancouver:
Helfricht A. Chromatin modifiers in DNA repair and human disease. [Internet] [Doctoral dissertation]. Leiden University; 2016. [cited 2019 Dec 07].
Available from: http://hdl.handle.net/1887/43800.
Council of Science Editors:
Helfricht A. Chromatin modifiers in DNA repair and human disease. [Doctoral Dissertation]. Leiden University; 2016. Available from: http://hdl.handle.net/1887/43800
. 
Open Access Theses and Dissertations