Spelling suggestions: "subject:"acetylation."" "subject:"scetylation.""
1 |
Kinetics and mechanisms of acetylation of hydroxy compounds N-methylimidazole as a catalyst /Pandit, Nivedita Krishnakumar. January 1980 (has links)
Thesis (Ph. D.)--University of Wisconsin--Madison, 1980. / Typescript. Vita. eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references.
|
2 |
Genetic and genomic studies of histone H3 methylation and acetylationJin, Yi. January 2008 (has links) (PDF)
Thesis (Ph. D.)--Washington State University, December 2008. / Title from PDF title page (viewed on Feb. 18, 2010). "Department of Molecular Plant Sciences." Includes bibliographical references.
|
3 |
The effect of structure and conformation of the side chain on the rate of acetylation of 12 [alpha]-hydroxy-5B steroidsAtkinson, Kenneth Frederick January 1974 (has links)
This document only includes an excerpt of the corresponding thesis or dissertation. To request a digital scan of the full text, please contact the Ruth Lilly Medical Library's Interlibrary Loan Department (rlmlill@iu.edu).
|
4 |
The effects of narcotics and other substances on tissue oxidations and on biological acetylationsJohnson, Willard J. January 1952 (has links)
Note:
|
5 |
Formation and reactions of methylol celluloseBaker, Timothy J. 01 January 1979 (has links)
No description available.
|
6 |
Effect of p300 HAT Activity on Myogenic DifferentiationHamed, Munerah 23 January 2013 (has links)
Skeletal muscle specification and differentiation programs are regulated by the myogenic regulatory factors which include Myf5, MyoD, myogenin and Mrf4. Upstream of the MRFs, the transcription co-activators and other intracellular and extracellular signals play crucial roles in regulating skeletal myogenesis. Histone acetyltransferase activity of p300 is required for Myf5 and MyoD expression. Furthermore, the MyoD core enhancer region is indispensable for MyoD expression. However, the mechanism by which p300 activates MyoD gene expression is to be determined. The histone acetyltransferase activity of p300 can be inhibited by small molecule inhibitors such as curcumin. Thus, using the inhibitor approach on stem cells is useful to investigate the role of p300 in activating MyoD expression during myogenesis. We here show that curcumin was able to inhibit stem cell determination and differentiation into skeletal myocytes. We also show that p300 is present, and histone acetylation is high at the core enhancer region. Therefore, we provide evidence that p300 is directly involved in MyoD gene expression during skeletal myogenesis.
|
7 |
Examining the effects of SERCA2a acetylation in the heartSusser, Shanel 14 January 2016 (has links)
The sarcoplasmic reticulum Ca2+-ATPase (SERCA2a) is responsible for calcium transport in the heart and its dysfunction in heart disease and diabetes make it a target for treatment strategies. SERCA2a structure can be modified post-translationally by the addition of an acetyl protein via acetylation. Sirtuin3 (SIRT) is a deacetylase, which may interact with SERCA2a to reverse its acetylation. The aim of this study was to determine if SERCA2a function is altered by acetylation, if this occurs in the diabetic heart, and if SIRT3 influences SERCA2a acetylation. Our data indicates that modification to three SERCA2a acetylation sites impairs its activity in a cell culture model and that SERCA2a acetylation occurs at higher levels in the diabetic heart. Furthermore, SERCA2a is acetylated at higher levels in absence of SIRT3, suggesting that SIRT3 activity influences SERCA2a. Our data identifies possible therapeutic strategies to target and reduce SERCA2a acetylation in the diabetic heart. / February 2016
|
8 |
Effect of p300 HAT Activity on Myogenic DifferentiationHamed, Munerah January 2013 (has links)
Skeletal muscle specification and differentiation programs are regulated by the myogenic regulatory factors which include Myf5, MyoD, myogenin and Mrf4. Upstream of the MRFs, the transcription co-activators and other intracellular and extracellular signals play crucial roles in regulating skeletal myogenesis. Histone acetyltransferase activity of p300 is required for Myf5 and MyoD expression. Furthermore, the MyoD core enhancer region is indispensable for MyoD expression. However, the mechanism by which p300 activates MyoD gene expression is to be determined. The histone acetyltransferase activity of p300 can be inhibited by small molecule inhibitors such as curcumin. Thus, using the inhibitor approach on stem cells is useful to investigate the role of p300 in activating MyoD expression during myogenesis. We here show that curcumin was able to inhibit stem cell determination and differentiation into skeletal myocytes. We also show that p300 is present, and histone acetylation is high at the core enhancer region. Therefore, we provide evidence that p300 is directly involved in MyoD gene expression during skeletal myogenesis.
|
9 |
HPV replication regulation by acetylation of a conserved lysine in the E2 proteinThomas, Yanique Serge Gillana 26 June 2017 (has links)
Indiana University-Purdue University Indianapolis (IUPUI) / Papillomaviruses (PVs) are non-enveloped DNA viruses that are the primary
etiological agents of cervical and oropharyngeal cancers. Vaccines for
H(human)PV have proven to be effective prophylactic treatments; however, there
is no treatment available for those currently infected. To develop new therapies,
we require a clear understanding of viral pathogenesis and regulation.
The Papillomavirus E2 protein is a sequence specific DNA binding protein that
recruits cellular factors to its genome in infected epithelial cells. E2 also binds to
and loads the viral E1 DNA helicase at the origin of replication. Post-translational
modifications of PV E2 have been identified as potential regulators of E2
functions. We recently reported lysine (K) 111 as a target of p300 acetylation in
B(bovine)PV that is involved in the regulation of viral transcription. K111 is
conserved in most papillomaviruses, so we pursued a mutational approach to
query the functional significance of lysine in HPV E2. Amino acid substitutions
that prevent acetylation, including arginine, were unable to stimulate transcription
and E1 mediated DNA replication. The arginine K111 mutant retained E2
transcriptional repression, nuclear localization, DNA and chromatin binding, and
association with E2 binding partners involved in PV transcription and replication. When directly investigating origin unwinding, the replication defective E2 K111R
mutant recruited E1 to the viral replication origin, but surprisingly, unwinding of
the duplex DNA did not occur. In contrast, the glutamine K111 mutant increased
origin melting and stimulated replication compared to wild type E2. We have
identified Topoisomerase I as a key host factor involved in viral replication whose
recruitment is dependent on K111 acetylation, and propose a new model for viral
origin dynamics during replication initiation. This work reveals a novel activity of
E2 necessary for denaturing the viral origin that likely depends on acetylation of highly conserved lysine 111.
|
10 |
Intramolecular catalysis in the acetylation of 7a-hydroxy-5b-steroidsBaker, James Francis January 1975 (has links)
This document only includes an excerpt of the corresponding thesis or dissertation. To request a digital scan of the full text, please contact the Ruth Lilly Medical Library's Interlibrary Loan Department (rlmlill@iu.edu).
|
Page generated in 0.0644 seconds