subject:(heat shock)

University of Rochester

1. Dutta, Pranabananda. The Role of Drosophila taranis in Polycomb Mediated Transcriptional Silencing and in Maintenance of the Germline Stem Cell Niche.

Degree: PhD, 2013, University of Rochester

URL: http://hdl.handle.net/1802/26780

► The Polycomb group (PcGs) proteins are implicated in epigenetic transcriptional repression during development, stem cell maintenance and tumorigenesis. The molecular mechanism by which PcGs silence… (more)

▼ The Polycomb group (PcGs) proteins are implicated in epigenetic transcriptional repression during development, stem cell maintenance and tumorigenesis. The molecular mechanism by which PcGs silence target loci is not fully understood. Here we show that Drosophila taranis (tara) is required for positioning Pc to its target genes. Embryos lacking tara exhibit partial homeotic transformation in the cuticular segments, a phenotype associated with Pc mutants. Consistent with the homeotic transformation, tara loss of function results in misexpression of homeotic gene Ultrabithorax (Ubx) and in reduced Pc recruitment on polytene chromosomes. Moreover, Drosophila embryos lacking taranis misexpress engrailed and lose Pc binding to its Polycomb response element (PRE). These observations suggest that Tara might be involved in transcriptional regulation of Pc target genes. Mass spectrometry revealed that Tara physically interacts with Heat shock cognate70-4 (hsc4), an enhancer of Pc. We further found that taranis genetically interact with hsc4. This interaction affects the expression pattern of homeotic genes, Ubx and Abdominal-B (Abd-B) in the developing embryo. tara and hsc4 double mutant embryos show pronounced homeotic transformation similar to Pc loss of function. Our study shows taranis as an important regulator of PRE activity in the transcriptional silencing mechanism carried out by PcGs. Maintenance of tissue homeostasis requires a functional stem cell environment (a.k.a niche). The Drosophila testis provides for an excellent model for studying the stem cell niche, which contains germ line stem cells along with the somatic cyst cells and the hub cells. Here we show that taranis is required for maintaining testis niche. tara is expressed in the Drosophila testis tip. Knocking down taranis in the niche results in a loss of germline stem cells. We show that the reduction in stem cells might involve Notch signaling in the niche. Interestingly we found that tara is only required in somatic cells for their proliferation. Thus, the results suggest that taranis functions in somatic cells in the niche to regulate germ line proliferation and maintenance.

Subjects/Keywords: Engrailed; Heat Shock Cognate 4

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APA (6^th Edition):

Dutta, P. (2013). The Role of Drosophila taranis in Polycomb Mediated Transcriptional Silencing and in Maintenance of the Germline Stem Cell Niche. (Doctoral Dissertation). University of Rochester. Retrieved from http://hdl.handle.net/1802/26780

Chicago Manual of Style (16^th Edition):

Dutta, Pranabananda. “The Role of Drosophila taranis in Polycomb Mediated Transcriptional Silencing and in Maintenance of the Germline Stem Cell Niche.” 2013. Doctoral Dissertation, University of Rochester. Accessed January 18, 2021. http://hdl.handle.net/1802/26780.

MLA Handbook (7^th Edition):

Dutta, Pranabananda. “The Role of Drosophila taranis in Polycomb Mediated Transcriptional Silencing and in Maintenance of the Germline Stem Cell Niche.” 2013. Web. 18 Jan 2021.

Vancouver:

Dutta P. The Role of Drosophila taranis in Polycomb Mediated Transcriptional Silencing and in Maintenance of the Germline Stem Cell Niche. [Internet] [Doctoral dissertation]. University of Rochester; 2013. [cited 2021 Jan 18]. Available from: http://hdl.handle.net/1802/26780.

Council of Science Editors:

Dutta P. The Role of Drosophila taranis in Polycomb Mediated Transcriptional Silencing and in Maintenance of the Germline Stem Cell Niche. [Doctoral Dissertation]. University of Rochester; 2013. Available from: http://hdl.handle.net/1802/26780

Rhodes University

2. Mutsvunguma, Lorraine Zvichapera. Investigating the role of heat shock proteins (Hsps) 40, 70 and 90 in the life cycle of Theiler's murine encephalomyelitis virus (TMEV).

Degree: Faculty of Science, Biochemistry, Microbiology and Biotechnology, 2011, Rhodes University

URL: http://hdl.handle.net/10962/d1004025

► Introduction: Picornaviruses are a family of RNA viruses which are economically and clinically significant. Like many other viruses, picornaviruses utilise host cell machinery to facilitate… (more)

▼ Introduction: Picornaviruses are a family of RNA viruses which are economically and clinically significant. Like many other viruses, picornaviruses utilise host cell machinery to facilitate their replication and assembly, including heat shock proteins (Hsps). The aim of this research was to investigate the role of Hsp40, Hsp70 and Hsp90 during picornavirus infection using the cardiovirus, Theiler’s murine encephalomyelitis virus (TMEV), as a study model. Methodology: Picornavirus VP1 capsid proteins were analysed by multiple sequence alignment and multiple structural comparisons. Protein domain architecture was used to analyse Hsp90 cellular and viral client proteins. Effects of Hsp90 inhibitors, novobiocin and geldanamycin, on TMEV growth in BHK-21 cells was observed over a 48hr period. Localisation of Hsp40, Hsp90 and Hsp70 in TMEV-infected BHK-21 cells was investigated by indirect immunofluorescence and confocal microscopy. Results and Discussion: VP1 proteins of picornaviruses are highly divergent within the family at the amino acid level, which might be linked to the protein’s function in determining virus tropism and antibody neutralisation. An eight-stranded anti-parallel beta-barrel structure was found conserved in the VP1 protein structures which might be linked to the highly conserved picornavirus capsid assembly process. Absence of a common protein domain between Hsp90 viral and cellular client proteins that might be functionally connected to Hsp90, suggests that Hsp90 most likely recognises surface features rather than sequence motifs/patterns. The Hsp90 inhibitors, novobiocin and geldanamycin, had a negative effect on virus growth as virus-induced cytopathic effect was not observed in treated cell after 48hrs. TMEV 2C protein was detected by Western analysis in infected cell lysates treated with geldanamycin but not novobiocin, suggesting novobiocin affects the translation or processing of TMEV 2C. Immunofluorescence analysis of TMEV-infected cells showed a relocalisation of Hsp40 into the nucleus during infection. Overlap of Hsp40 and TMEV P1 was observed in the perinuclear region, suggesting colocalisation between these proteins. Hsp70 converged around the replication complex during infection but did not overlap with TMEV 2C. Hsp90 concentrated in the region of the replication complex where it overlapped with TMEV 2C and this redistribution was found to be dependent on the stage of infection. The overlap between Hsp90 and TMEV 2C signals observed, suggested colocalisation between the two proteins. Conclusion: This study identified Hsp90, Hsp70 and Hsp40 as possible host factors required in TMEV replication.

Subjects/Keywords: Heat shock proteins; Picornaviruses; Encephalomyelitis

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APA (6^th Edition):

Mutsvunguma, L. Z. (2011). Investigating the role of heat shock proteins (Hsps) 40, 70 and 90 in the life cycle of Theiler's murine encephalomyelitis virus (TMEV). (Thesis). Rhodes University. Retrieved from http://hdl.handle.net/10962/d1004025

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Mutsvunguma, Lorraine Zvichapera. “Investigating the role of heat shock proteins (Hsps) 40, 70 and 90 in the life cycle of Theiler's murine encephalomyelitis virus (TMEV).” 2011. Thesis, Rhodes University. Accessed January 18, 2021. http://hdl.handle.net/10962/d1004025.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Mutsvunguma, Lorraine Zvichapera. “Investigating the role of heat shock proteins (Hsps) 40, 70 and 90 in the life cycle of Theiler's murine encephalomyelitis virus (TMEV).” 2011. Web. 18 Jan 2021.

Vancouver:

Mutsvunguma LZ. Investigating the role of heat shock proteins (Hsps) 40, 70 and 90 in the life cycle of Theiler's murine encephalomyelitis virus (TMEV). [Internet] [Thesis]. Rhodes University; 2011. [cited 2021 Jan 18]. Available from: http://hdl.handle.net/10962/d1004025.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Mutsvunguma LZ. Investigating the role of heat shock proteins (Hsps) 40, 70 and 90 in the life cycle of Theiler's murine encephalomyelitis virus (TMEV). [Thesis]. Rhodes University; 2011. Available from: http://hdl.handle.net/10962/d1004025

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Penn State University

3. Hu, Wenli. INVESTIGATION OF HEAT SHOCK RESPONSES IN VARIOUS CELL LINES .

Degree: 2011, Penn State University

URL: https://submit-etda.libraries.psu.edu/catalog/11983

► Subjecting cells to elevated temperature induces heat shock responses including the inhibition of general protein synthesis and induction of specific heat shock proteins functioning mostly… (more)

Subjects/Keywords: Heat shock; cell lines

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Hu, W. (2011). INVESTIGATION OF HEAT SHOCK RESPONSES IN VARIOUS CELL LINES . (Thesis). Penn State University. Retrieved from https://submit-etda.libraries.psu.edu/catalog/11983

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Hu, Wenli. “INVESTIGATION OF HEAT SHOCK RESPONSES IN VARIOUS CELL LINES .” 2011. Thesis, Penn State University. Accessed January 18, 2021. https://submit-etda.libraries.psu.edu/catalog/11983.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Hu, Wenli. “INVESTIGATION OF HEAT SHOCK RESPONSES IN VARIOUS CELL LINES .” 2011. Web. 18 Jan 2021.

Vancouver:

Hu W. INVESTIGATION OF HEAT SHOCK RESPONSES IN VARIOUS CELL LINES . [Internet] [Thesis]. Penn State University; 2011. [cited 2021 Jan 18]. Available from: https://submit-etda.libraries.psu.edu/catalog/11983.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Hu W. INVESTIGATION OF HEAT SHOCK RESPONSES IN VARIOUS CELL LINES . [Thesis]. Penn State University; 2011. Available from: https://submit-etda.libraries.psu.edu/catalog/11983

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of the Western Cape

4. Charewa, Wellington. Increasing ethanol tolerance through the heterologous expression of the geobacillus thermoglucosiadius heat-shock proteins (GroEL/GroES) in an escherichia coli host .

Degree: 2012, University of the Western Cape

URL: http://hdl.handle.net/11394/5325

► Due to economic and environmental concerns associated with use of fossil fuels, humanity is seeking alternative fuels. Ethanol is one of the alternative fuels produced… (more)

▼ Due to economic and environmental concerns associated with use of fossil fuels, humanity is seeking alternative fuels. Ethanol is one of the alternative fuels produced commercially. Current ethanol production technologies using first generation ethanol processes is criticised for depleting the food supply and escalating food prices. Biomass is a target feedstock for use in bioethanol production and would resolve the criticism associated with the current bioethanol industry. Bacterial strains such as Geobacillus thermoglucosidasius NCIMB 11955 can be used to produce ethanol from biomass because they assimilate hexose and pentose sugars, a property that is lacking in first generation ethanol producing microbes (Saccharomyces cerevisiae and Zymomonas mobilis) (Riyanti and Rogers, 2009). Due to the low ethanol tolerance (4 % v/v (maximum)) of G. thermoglucosidasius, use of this species for bioethanol production is not economically viable. GroES and GroEL genes are involved in stress tolerance in bacteria: activation of these genes has been observed in stress induced bacteria (Rasouly and Ron, 2009). In this study the ethanol tolerance of G. thermoglucosidasius NCIMB 11955 was characterised by culturing at 45 ºC and 55 ºC in the presence of ethanol. A greater ethanol tolerance was observed at the sub-optimal growth temperature of 45 ºC. Escherichia coli metabolic systems are well understood. Aiming to improve the ethanol tolerance G. thermoglucosidasius NCIMB 11955, the GroES and GroEL genes of the organism were cloned in an expression vector and expressed in E.coli before testing their ability to confer an increased tolerance to ethanol. Proteomic analysis of the recombinant E. coli strain showed that GroES was over-expressed while GroEL was not. After over expression of GroES, the optical density of cultures was periodically measured. Over-expression of the G. thermoglucosidasius NCIMB 11955 GroES gene improved the ethanol tolerance of E. coli Rosetta pLySs growing in 4% (v/v) ethanol. Advisors/Committee Members: Cowan, Don (advisor), Taylor, Mark Paul (advisor).

Subjects/Keywords: Geobacillus; Bioethanol; Heat shock proteins

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APA (6^th Edition):

Charewa, W. (2012). Increasing ethanol tolerance through the heterologous expression of the geobacillus thermoglucosiadius heat-shock proteins (GroEL/GroES) in an escherichia coli host . (Thesis). University of the Western Cape. Retrieved from http://hdl.handle.net/11394/5325

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Charewa, Wellington. “Increasing ethanol tolerance through the heterologous expression of the geobacillus thermoglucosiadius heat-shock proteins (GroEL/GroES) in an escherichia coli host .” 2012. Thesis, University of the Western Cape. Accessed January 18, 2021. http://hdl.handle.net/11394/5325.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Charewa, Wellington. “Increasing ethanol tolerance through the heterologous expression of the geobacillus thermoglucosiadius heat-shock proteins (GroEL/GroES) in an escherichia coli host .” 2012. Web. 18 Jan 2021.

Vancouver:

Charewa W. Increasing ethanol tolerance through the heterologous expression of the geobacillus thermoglucosiadius heat-shock proteins (GroEL/GroES) in an escherichia coli host . [Internet] [Thesis]. University of the Western Cape; 2012. [cited 2021 Jan 18]. Available from: http://hdl.handle.net/11394/5325.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Charewa W. Increasing ethanol tolerance through the heterologous expression of the geobacillus thermoglucosiadius heat-shock proteins (GroEL/GroES) in an escherichia coli host . [Thesis]. University of the Western Cape; 2012. Available from: http://hdl.handle.net/11394/5325

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Latrobe University

5. Larkins, Noni Tegan. Biochemical & physiological studies of heat shock proteins in skeletal muscle.

Degree: PhD, 2011, Latrobe University

URL: http://hdl.handle.net/1959.9/533816

►

Thesis (Ph.D.) - La Trobe University, 2011

Submission note: "A thesis submitted in total fulfillment of the requirements for the degree of Doctor of Philosophy… (more)

Subjects/Keywords: Heat shock proteins.; Muscles.

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APA (6^th Edition):

Larkins, N. T. (2011). Biochemical & physiological studies of heat shock proteins in skeletal muscle. (Doctoral Dissertation). Latrobe University. Retrieved from http://hdl.handle.net/1959.9/533816

Chicago Manual of Style (16^th Edition):

Larkins, Noni Tegan. “Biochemical & physiological studies of heat shock proteins in skeletal muscle.” 2011. Doctoral Dissertation, Latrobe University. Accessed January 18, 2021. http://hdl.handle.net/1959.9/533816.

MLA Handbook (7^th Edition):

Larkins, Noni Tegan. “Biochemical & physiological studies of heat shock proteins in skeletal muscle.” 2011. Web. 18 Jan 2021.

Vancouver:

Larkins NT. Biochemical & physiological studies of heat shock proteins in skeletal muscle. [Internet] [Doctoral dissertation]. Latrobe University; 2011. [cited 2021 Jan 18]. Available from: http://hdl.handle.net/1959.9/533816.

Council of Science Editors:

Larkins NT. Biochemical & physiological studies of heat shock proteins in skeletal muscle. [Doctoral Dissertation]. Latrobe University; 2011. Available from: http://hdl.handle.net/1959.9/533816

Texas A&M University

6. Liang, Shuyin. Changes in Flower Size and Number Under Heat Stress in Rose (Rosa×Hybrida).

Degree: MS, Horticulture, 2016, Texas A&M University

URL: http://hdl.handle.net/1969.1/157975

► Roses (Rosa × hybrida) have been one of the most popular decorations for entertainment and ceremonies for the past 5,000 years, and have been used… (more)

▼ Roses (Rosa × hybrida) have been one of the most popular decorations for entertainment and ceremonies for the past 5,000 years, and have been used in the fragrance, medicinal, and food industry. Heat stress is one of the most significant abiotic stresses which negatively affects rose performance and reduces the market value of roses. This project examined the effect of heat on rose in diploid rose populations created by intercrossing heat tolerant and sensitive diploid parents. Changes in flower size were examined in a heat shock (one hour at 44°C) experiment with potted plants and in field plots by comparing flower size in cool (spring and fall) versus warm (summer) seasons. As expected, the heat treatment decreased flower diameter, petal number, and flower dry weight. Flower size traits had moderately low narrow sense heritability (0.24 - 0. 35, 0.12 - 0.33, and 0.34 - 0.37) and moderately high to high broad sense heritability (0.62 - 0.67, 0.74 - 0.91, and 0.76 - 0.81) for flower diameter, petal number, and flower dry weight respectively. The G×E variance for flower diameter and flower dry weight accounted for 37% and 27% of the variance in the field experiment indicating that the heat stress had moderate differential genotypic effects as was indicated by the analysis of variance. However the genetic variance was several fold greater than the G×E variance indicating selection for flower size would be effective in any season but for the selection of a stable flower size (heat tolerant) rose genotype, selection would be required in both the cool and warm seasons. The number of flowers per primary and secondary inflorescence had very low narrow sense (0.01 and 0.06) and moderate broad sense (0.43 and 0.34) heritability. The G×E variance for the number of flowers per primary and secondary inflorescence accounted for 55.7% and 57.0% of the total variance in the field experiment indicating selection needs to be done for within each season. Only 26% of plants had tertiary inflorescences. Advisors/Committee Members: Byrne, David H. (advisor), Pemberton, Brent H. (committee member), Murray, Seth C. (committee member), Starman, Terri W. (committee member).

Subjects/Keywords: Rosa; abiotic stress; heat tolerance; heat shock

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Liang, S. (2016). Changes in Flower Size and Number Under Heat Stress in Rose (Rosa×Hybrida). (Masters Thesis). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/157975

Chicago Manual of Style (16^th Edition):

Liang, Shuyin. “Changes in Flower Size and Number Under Heat Stress in Rose (Rosa×Hybrida).” 2016. Masters Thesis, Texas A&M University. Accessed January 18, 2021. http://hdl.handle.net/1969.1/157975.

MLA Handbook (7^th Edition):

Liang, Shuyin. “Changes in Flower Size and Number Under Heat Stress in Rose (Rosa×Hybrida).” 2016. Web. 18 Jan 2021.

Vancouver:

Liang S. Changes in Flower Size and Number Under Heat Stress in Rose (Rosa×Hybrida). [Internet] [Masters thesis]. Texas A&M University; 2016. [cited 2021 Jan 18]. Available from: http://hdl.handle.net/1969.1/157975.

Council of Science Editors:

Liang S. Changes in Flower Size and Number Under Heat Stress in Rose (Rosa×Hybrida). [Masters Thesis]. Texas A&M University; 2016. Available from: http://hdl.handle.net/1969.1/157975

Boston University

7. Beyzavi, Ali. Investigation of the heat shock response in yeast: quantitative modeling and single-cell microfluidic studies.

Degree: PhD, Mechanical Engineering, 2016, Boston University

URL: http://hdl.handle.net/2144/17084

► Heat shock response (HSR) is an ancient and highly conserved signaling pathway in cells that regulates the expression of heat shock proteins (HSPs) in the… (more)

▼ Heat shock response (HSR) is an ancient and highly conserved signaling pathway in cells that regulates the expression of heat shock proteins (HSPs) in the presence of thermal and other environmental stresses. HSPs function to prevent the formation of non-specific protein aggregates and to assist proteins in acquiring their native structures. Although HSR has been extensively studied, key aspects of this pathway remain a mystery. In particular, how HSR is activated and regulated by the master transcription factor HSF1 is not well understood. The broad goal of this thesis is to develop a quantitative framework aimed at elucidating the HSF1-mediated activation of HSR in yeast cells. Understanding this process has important implications for development, physiology and disease. Indeed, HSF1 is conserved from yeast to human, has been shown to play an important role in stress resistance, health and disease, and is a therapeutic target for neurodegenerative diseases. Broadly, there are two putative (not mutually exclusive) models for activation in response to heat shock: (1) HSF1 dissociation from chaperone proteins and (2) hyper-phosphorylation and the subsequent activation of HSF1. However the relative contribution of each of these events in the activation process is not characterized. Thus far, there is no direct evidence linking either of these two events to activation, and the relative contribution of each mechanism to the activation process has not been quantitatively characterized. To address these issues, we develop a quantitative model of HSR in yeast cells. We use the model to make a series of quantitative predictions and, in a collaborative effort, experimentally test these predictions in a yeast model of HSR. Critically, we provide the first direct evidence for chaperone dissociation of HSF1 in response to heat shock. Moreover, we find that HSF1 phosphorylation is dispensable for activation of HSR, but is able to modulate its activity. Taken together, our work leads to a model for two “orthogonal” mechanisms regulating HSR in yeast, in which chaperone dissociation acts as an ON/OFF switch, whereas phosphorylation functions to tune the gain of the response. Finally, to complement and further test this quantitative model, we develop a novel microfluidic system to explore in more depth the behavior of individual cells in the presence of heat shock inputs. This includes (1) a microfluidic device with microscale on-chip heaters enabling programmable thermal perturbations and (2) a custom image analysis platform to follow single cells through heat shock time courses. In preliminary single-cell studies, we find a relationship between HSF1 phosphorylation state and cell-to-cell variability in HSR activation level (as measured by a transcriptional reporter). These preliminary results suggest that HSF1 phosphorylation may be generating and tuning noise in the HSR in order to promote phenotypic plasticity and increased survivability of a cell population in the face of stress.

Subjects/Keywords: Engineering; Heat shock response; Microfluidics; Heat shock factor 1

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Beyzavi, A. (2016). Investigation of the heat shock response in yeast: quantitative modeling and single-cell microfluidic studies. (Doctoral Dissertation). Boston University. Retrieved from http://hdl.handle.net/2144/17084

Chicago Manual of Style (16^th Edition):

Beyzavi, Ali. “Investigation of the heat shock response in yeast: quantitative modeling and single-cell microfluidic studies.” 2016. Doctoral Dissertation, Boston University. Accessed January 18, 2021. http://hdl.handle.net/2144/17084.

MLA Handbook (7^th Edition):

Beyzavi, Ali. “Investigation of the heat shock response in yeast: quantitative modeling and single-cell microfluidic studies.” 2016. Web. 18 Jan 2021.

Vancouver:

Beyzavi A. Investigation of the heat shock response in yeast: quantitative modeling and single-cell microfluidic studies. [Internet] [Doctoral dissertation]. Boston University; 2016. [cited 2021 Jan 18]. Available from: http://hdl.handle.net/2144/17084.

Council of Science Editors:

Beyzavi A. Investigation of the heat shock response in yeast: quantitative modeling and single-cell microfluidic studies. [Doctoral Dissertation]. Boston University; 2016. Available from: http://hdl.handle.net/2144/17084

University of Ottawa

8. Hota, Supriya. Heat Shock Factor 1 (HSF1) Modulates Inflammation and Survival Post-Myocardial Infarction.

Degree: MSc, Médecine / Medicine, 2020, University of Ottawa

URL: http://dx.doi.org/10.20381/ruor-25382

► Introduction: Myocardial Infarction (MI) is the leading cause of premature death worldwide. During MI-induced ischemia, the release of heat shock proteins (HSPs), a classic damage-associated… (more)

▼ Introduction: Myocardial Infarction (MI) is the leading cause of premature death worldwide. During MI-induced ischemia, the release of heat shock proteins (HSPs), a classic damage-associated molecular pattern (DAMP), by severely injured cells leads to prolonged inflammation through their activation of innate pattern recognition receptors, fibrosis, and subsequent contractile dysfunction. The regulation of HSPs is orchestrated by its master transcription factor, Heat Shock Factor 1 (HSF1). However, it is unknown if HSF1 is a potential integrated functional target to improve MI outcomes. We addressed this question by asking if the coordinated modulation of HSPs via genetic deletion of Hsf1 can be beneficial in MI. Hypothesis: We hypothesized that genetic deletion of Hsf1 can lead to improved survival and left ventricle (LV) remodeling through reduction of pro-inflammatory pathway activation in a murine model of MI-induced coronary artery ligation. Methods and Results: Eleven to thirteen-week-old male Hsf1-/- mice and Hsf1+/+ littermate controls were subjected to MI by left anterior descending (LAD) coronary artery ligation or sham operation. Hsf1-/- mice subjected to induced-MI had a significant higher survival rate (74%) at 28 days than WT mice post-MI in the same time frame (34%, p<0.001). Echocardiography at 3, 7, and 28 days post-MI; however, did not identify any difference in LV function between Hsf1+/+ and Hsf1-/- mice. Masson Trichrome and Picro Sirius Red staining of heart tissue sections following 7 days of sham or MI-operation indicated that MI-operated Hsf1-/- hearts had a significant smaller infarct size than Hsf1+/+ hearts at 19% compared to 32% (p<0.05), respectively; and less collagen deposition when compared to WT littermates. Cardiac expression of heat shock proteins was significantly lowered in the Hsf1-/- hearts compared to Hsf1+/+ hearts following 3 and 7 days of MI. However, no significant difference was observed in number of immune cells, cardiac gene expression of pro-inflammatory cytokines and chemokines, cardiac protein expression of NF-κB and MAPK-ERK1/2 signaling proteins, and serum IL-6 concentration between Hsf1+/+ and Hsf1-/- mice 3 days post-MI. Following 7 days of MI, there is a significant increase in the gene expression of pro-inflammatory cytokines, such as Il1b, and chemokines, such as Ccl2, in Hsf1-/- hearts than Hsf1+/+ hearts. Conclusion & Future Directions: Overall, the loss of Hsf1 improved survival and reduced infarct size following MI. However, its deletion did not affect inflammatory processes until 7 days post-MI or improved cardiac function in our specific murine MI model. Advisors/Committee Members: Liu, Peter (supervisor).

Subjects/Keywords: Myocardial Infarction; Heat Shock Factor 1; Inflammation; Heat Shock Proteins; DAMPs

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APA (6^th Edition):

Hota, S. (2020). Heat Shock Factor 1 (HSF1) Modulates Inflammation and Survival Post-Myocardial Infarction. (Masters Thesis). University of Ottawa. Retrieved from http://dx.doi.org/10.20381/ruor-25382

Chicago Manual of Style (16^th Edition):

Hota, Supriya. “Heat Shock Factor 1 (HSF1) Modulates Inflammation and Survival Post-Myocardial Infarction.” 2020. Masters Thesis, University of Ottawa. Accessed January 18, 2021. http://dx.doi.org/10.20381/ruor-25382.

MLA Handbook (7^th Edition):

Hota, Supriya. “Heat Shock Factor 1 (HSF1) Modulates Inflammation and Survival Post-Myocardial Infarction.” 2020. Web. 18 Jan 2021.

Vancouver:

Hota S. Heat Shock Factor 1 (HSF1) Modulates Inflammation and Survival Post-Myocardial Infarction. [Internet] [Masters thesis]. University of Ottawa; 2020. [cited 2021 Jan 18]. Available from: http://dx.doi.org/10.20381/ruor-25382.

Council of Science Editors:

Hota S. Heat Shock Factor 1 (HSF1) Modulates Inflammation and Survival Post-Myocardial Infarction. [Masters Thesis]. University of Ottawa; 2020. Available from: http://dx.doi.org/10.20381/ruor-25382

Indian Institute of Science

9. Raman, Swetha. Structural Studies on Heat Shock Protein 90 from Dictyostelium Discoideum and Oryza Sativa.

Degree: PhD, Faculty of Science, 2018, Indian Institute of Science

URL: http://etd.iisc.ac.in/handle/2005/3491

► Molecular chaperones are proteins that interact with and aid in stabilization and activation of other proteins. Chaperones help proteins attain their three dimensional conformation, without… (more)

▼ Molecular chaperones are proteins that interact with and aid in stabilization and activation of other proteins. Chaperones help proteins attain their three dimensional conformation, without forming a part of the final structure. Many of the chaperones are stress proteins known as Heat shock proteins (Hsps). Their expression is upregulated in response to various kinds of stress such as heat stress, oxidative stress etc., which threaten the protein homeostasis, by structurally destabilizing cellular proteins, and increasing the concentration of aggregation-prone folding intermediates. The Hsps are classified according to their molecular weight into Hsp40, Hsp60, Hsp70, Hsp90, Hsp100, and the small Hsp families. Some of them are constitutively expressed and play a fundamental role in de novo protein folding. They further aid in proteome maintenance by assisting in oligomeric assembly, protein trafficking, refolding of stress denatured protein, preventing protein aggregation and protein degradation. Heat shock protein 90 (Hsp90) are one of the important representatives of this class of proteins. Hsp90 are highly conserved class of molecular chaperones. They are found in bacteria, eukaryotes, but not in archaea. In contrast to the eukaryotes which require a functional cytoplasmic Hsp90 for viability, the bacterial counterpart (HtpG) is typically nonessential. Hsp90 is an ATP dependent chaperone. Hsp90 form dimers, with each protomer consisting of three functional domains: N- terminal, ATP binding domain, Middle domain and C-terminal domain. Hsp90 is a dynamic protein, and undergoes an elaborate conformational cycle during its ATPase cycle, which is essential for its chaperoning activity. The Hsp90 chaperone cycle is regulated by interaction with diverse cochaperones. Hsp90 interacts with specific set of substrate proteins. Many of these substrate proteins function at the heart of several cellular processes like signalling, cell cycle, apoptosis. Studies from protozoans like Leishmania, Plasmodium, Trypanosoma etc. have also implicated the role of Hsp90 in their growth and stage transitions. Thus, selective inhibition of Hsp90 has been explored as an intervention strategy against important human diseases such as cancer, malaria and other protozoan diseases. The ATP binding N-terminal domain (NTD), has been explored as the target domain for inhibition of Hsp90 using competitive inhibitors of ATP. Several chemical classes of Hsp90 inhibitors are known, including ansamycins, macrolides, purines, pyrazoles, and coumarin antibiotics. However, many inhibitors are observed to be toxic, less soluble and unstable. Hence, there is a requirement for new approach to design inhibitors which are more soluble and less toxic and serve as effective therapeutic drugs.inhibitors are observed to be toxic, less soluble and unstable. Hence, there is a requirement for new approach to design inhibitors which are more soluble and less toxic and serve as effective therapeutic drugs. The work presented in this thesis mainly concerns with the… Advisors/Committee Members: Suguna, K (advisor).

Subjects/Keywords: Dictyostelium Discoideum Heat Shock Proteins; Oryza Sativa (Rice) Heat Shock Proteins; Molecular Chaperones; Heat Shock Proteins; Heat Shock Protein 90 (Hsp90); Chaperone Proteins; Heat Shock Protein D. Discoideum (HspD); Microbial Heat Shock Proteins; Plant Heat Shock Proteins; Dictyostelium discoideum Hsp90; Oryza sativa Hsp90; Molecular Biophysics

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APA (6^th Edition):

Raman, S. (2018). Structural Studies on Heat Shock Protein 90 from Dictyostelium Discoideum and Oryza Sativa. (Doctoral Dissertation). Indian Institute of Science. Retrieved from http://etd.iisc.ac.in/handle/2005/3491

Chicago Manual of Style (16^th Edition):

Raman, Swetha. “Structural Studies on Heat Shock Protein 90 from Dictyostelium Discoideum and Oryza Sativa.” 2018. Doctoral Dissertation, Indian Institute of Science. Accessed January 18, 2021. http://etd.iisc.ac.in/handle/2005/3491.

MLA Handbook (7^th Edition):

Raman, Swetha. “Structural Studies on Heat Shock Protein 90 from Dictyostelium Discoideum and Oryza Sativa.” 2018. Web. 18 Jan 2021.

Vancouver:

Raman S. Structural Studies on Heat Shock Protein 90 from Dictyostelium Discoideum and Oryza Sativa. [Internet] [Doctoral dissertation]. Indian Institute of Science; 2018. [cited 2021 Jan 18]. Available from: http://etd.iisc.ac.in/handle/2005/3491.

Council of Science Editors:

Raman S. Structural Studies on Heat Shock Protein 90 from Dictyostelium Discoideum and Oryza Sativa. [Doctoral Dissertation]. Indian Institute of Science; 2018. Available from: http://etd.iisc.ac.in/handle/2005/3491

NSYSU

10. Liu, Shih-ming. Study of heat-shock-induced cell death in Saccharomyces cerevisiae with a deficiency of YDL100c.

Degree: Master, Biological Sciences, 2008, NSYSU

URL: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0719108-213007

► YDL100cp is the ArsA homologous protein found in Saccharomyces cerevisiae. Previous studies show that deletion of YDL100c was not lethal but unable to grow at… (more)

Subjects/Keywords: Saccharomyces cerevisiae; YDL100c; lethal heat shock

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APA (6^th Edition):

Liu, S. (2008). Study of heat-shock-induced cell death in Saccharomyces cerevisiae with a deficiency of YDL100c. (Thesis). NSYSU. Retrieved from http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0719108-213007

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Liu, Shih-ming. “Study of heat-shock-induced cell death in Saccharomyces cerevisiae with a deficiency of YDL100c.” 2008. Thesis, NSYSU. Accessed January 18, 2021. http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0719108-213007.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Liu, Shih-ming. “Study of heat-shock-induced cell death in Saccharomyces cerevisiae with a deficiency of YDL100c.” 2008. Web. 18 Jan 2021.

Vancouver:

Liu S. Study of heat-shock-induced cell death in Saccharomyces cerevisiae with a deficiency of YDL100c. [Internet] [Thesis]. NSYSU; 2008. [cited 2021 Jan 18]. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0719108-213007.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Liu S. Study of heat-shock-induced cell death in Saccharomyces cerevisiae with a deficiency of YDL100c. [Thesis]. NSYSU; 2008. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0719108-213007

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

NSYSU

11. Fu, Yaw-syan. Inhibitory Effect of Warm Water Immersion-induced Hyperthermia on Neurogenic Inflammation in Rat Airways and the Possible Mechanisms.

Degree: PhD, Biological Sciences, 2010, NSYSU

URL: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0609110-134507

► In mammals, the neurogenic inflammatory response can be induced by stimulation or activation on the peripheral sensory C-fibers to release neuropeptides from the peripheral terminals,… (more)

▼ In mammals, the neurogenic inflammatory response can be induced by stimulation or activation on the peripheral sensory C-fibers to release neuropeptides from the peripheral terminals, at the same time their afferent functions are enhanced. There are several neuropeptides stored and released from peripheral terminals of the afferent fibers, such as substance P (SP), neurokinin A, and calcitonin gene related peptide (CGRP). SP is one of the major inflammatory mediators of neurogenic inflammation that can act on neurokinin-1 receptors on smooth muscles and endothelial cells of blood vessels, causing vasodilatation, endothelial gap formation, and local plasma leakage. There are many studies and reports indicate that animals pretreated with a short period non-lethal hyperthermia can induce heat shock response and activate the expression of a group of inducible proteins called heat shock proteins (HSPs), and this stress response reduces the injury by same or other following stresses. In this study, the hyperthermia treatment (HT) was implemented by 42â hot water bath and the core body temperature of anesthetized rat was elevated and maintained around 42.0Â±0.5â for 15 min, and the normothermia control treatment (NT) was implemented by 37â warm water bath with the same period. 24 hours after NT or HT, the neurogenic plasma leakage was induced by intravascular injection with capsaicin (90 Î¼g/kg), SP (3 Î¼g/kg), or electrical stimulation on the right thoracic vagus nerve. The blood pressures of each animal were continually recorded during the neurogenic inflammation induction or sham operation. The amount of neurogenic inflammation of airway was evaluated by the area density leaky blood vessels. The leaking vessels were labeled with India ink and quantitative analysis by morphometric method. Plasma leakage was also measured by interstitial Evans blue concentration. The results indicated that HT could reduce plasma leakage and hypotension of the neurogenic inflammation that induced by capsaicin, SP or electrical stimulation on vagus nerve. Animals pretreated with aminoguanidine (a selective inhibitor of iNOS) had no significant effect on the neurogenic inflammation by following systemic SP infusion, but that could eliminate the anti-neurogenic inflammatory effect of HT. Animal applied with diphenhydramine (an antagonist of histamine H1 receptor) could attenuate the neurogenic inflammation by following systemic SP infusion, and HT could attenuate the neurogenic inflammation that with or without H1 receptor antagonist. This result indicates that NO synthesis and the activity of iNOS have few effects on neurogenic inflammation of airway, but it plays a critical factor on the initiation of heat shock response. The neurogenic inflammation induced by SP not only direct act on blood vessels but have other indirect effect by the histamine H1 receptor to enhance inflammation. Neonatal rats received high dose capsaicin treatment would induce irreversible sensory C-fiber denervation. The adult rats that were neonatally treated with… Advisors/Committee Members: Keh-Min Liu (chair), Jau-Cheng Liou (committee member), Rei-Cheng Yang (chair), Ming-Hong Tai (chair), Ching-Mei Hsu (chair), Hung-Tu Hyang (committee member).

Subjects/Keywords: heat shock response; neurogenic inflammation; airway

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Fu, Y. (2010). Inhibitory Effect of Warm Water Immersion-induced Hyperthermia on Neurogenic Inflammation in Rat Airways and the Possible Mechanisms. (Doctoral Dissertation). NSYSU. Retrieved from http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0609110-134507

Chicago Manual of Style (16^th Edition):

Fu, Yaw-syan. “Inhibitory Effect of Warm Water Immersion-induced Hyperthermia on Neurogenic Inflammation in Rat Airways and the Possible Mechanisms.” 2010. Doctoral Dissertation, NSYSU. Accessed January 18, 2021. http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0609110-134507.

MLA Handbook (7^th Edition):

Fu, Yaw-syan. “Inhibitory Effect of Warm Water Immersion-induced Hyperthermia on Neurogenic Inflammation in Rat Airways and the Possible Mechanisms.” 2010. Web. 18 Jan 2021.

Vancouver:

Fu Y. Inhibitory Effect of Warm Water Immersion-induced Hyperthermia on Neurogenic Inflammation in Rat Airways and the Possible Mechanisms. [Internet] [Doctoral dissertation]. NSYSU; 2010. [cited 2021 Jan 18]. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0609110-134507.

Council of Science Editors:

Fu Y. Inhibitory Effect of Warm Water Immersion-induced Hyperthermia on Neurogenic Inflammation in Rat Airways and the Possible Mechanisms. [Doctoral Dissertation]. NSYSU; 2010. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0609110-134507

NSYSU

12. Yang, Ya-Ting. Burkholderia pseudomallei heat shock protein (groEL) DNA vaccination provides Th1 immune response with cross-protection to Burkholderia cenocepacia for BALB/c mice.

Degree: Master, Biological Sciences, 2012, NSYSU

URL: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0910112-163807

► The immunogenicity and protective efficacy of a DNA vaccine encoding a truncated groEL heat shock gene (pcDNA3/groEL) from Burkholderia pseudomallei was evaluated in vaccinated BALB/c… (more)

Subjects/Keywords: Melioidosis; heat shock proteins; DNA vaccine; Burkholderia

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APA (6^th Edition):

Yang, Y. (2012). Burkholderia pseudomallei heat shock protein (groEL) DNA vaccination provides Th1 immune response with cross-protection to Burkholderia cenocepacia for BALB/c mice. (Thesis). NSYSU. Retrieved from http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0910112-163807

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Yang, Ya-Ting. “Burkholderia pseudomallei heat shock protein (groEL) DNA vaccination provides Th1 immune response with cross-protection to Burkholderia cenocepacia for BALB/c mice.” 2012. Thesis, NSYSU. Accessed January 18, 2021. http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0910112-163807.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Yang, Ya-Ting. “Burkholderia pseudomallei heat shock protein (groEL) DNA vaccination provides Th1 immune response with cross-protection to Burkholderia cenocepacia for BALB/c mice.” 2012. Web. 18 Jan 2021.

Vancouver:

Yang Y. Burkholderia pseudomallei heat shock protein (groEL) DNA vaccination provides Th1 immune response with cross-protection to Burkholderia cenocepacia for BALB/c mice. [Internet] [Thesis]. NSYSU; 2012. [cited 2021 Jan 18]. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0910112-163807.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Yang Y. Burkholderia pseudomallei heat shock protein (groEL) DNA vaccination provides Th1 immune response with cross-protection to Burkholderia cenocepacia for BALB/c mice. [Thesis]. NSYSU; 2012. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0910112-163807

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Drexel University

13. Khaira, Depinder Kaur. Proteomic scale effect of HSP90 inhibition with 17-AAG and radicicol.

Degree: 2011, Drexel University

URL: http://hdl.handle.net/1860/3728

►

Heat Shock Protein 90 is a molecular chaperone with a function of folding the proteins involved in cell signaling, such as transcription factors and protein… (more)

▼

Heat Shock Protein 90 is a molecular chaperone with a function of folding the proteins involved in cell signaling, such as transcription factors and protein kinases. Under stressful conditions, HSP90 stabilizes its client proteins and provides protection to the cell against cellular stressors such as in cancer cells. Through mutations, cancer cells become dependent on oncogenic pathways. Then the most malignant tumor cells are selected for cloning. As this malignant process proceeds, there is a need for the up-regulation of HSP90. The dependency of the cancer cells on HSP90 increases to a great extent as HSP90 protects the overexpressed and unstable oncogenic proteins. Therefore, it makes sense to say that if we inhibit HSP90 it would be beneficial for all types of cancer. The promising anti-tumor activity of 17-allylamino-17demethoxygeldanamycin (17AAG) and Radicicol results from the inhibition of HSP90. Proteomic analysis was done to study the effect of HSP90 inhibitors after 24 hours of drug treatment. Lung epithelial cancer cells were given a treatment of 60nM of 17AAG and 600nM of Radicicol. Mass Spectrometry (LC-MS/MS) and Western Blotting were used to analyze the drug treated and untreated samples. The drugs bind at the ATP pocket of HSP90 and disrupt the HSP90 complex that stabilizes the client proteins. An increase in the expression of HSP90 and HSP70 is observed. This might mean that the complex that assists in folding of the client proteins is disrupted which can be beneficial, as the cancer cells would be deprived of the oncogenic proteins that they rely on. Furthermore, the results from drug treated A549 cells were compared to Mesenchymal Stem Cells (MSC’s). This can help in studying the effect of drugs on a wider variety of cells. MSC’s are undifferentiated cells; which can differentiate into various cell types, example adipocytes, chondrocytes and cardiomyocytes. Giving the drug treatment to MSC’s would help us in understanding the effect of the drugs on the cells and whether the cells were harmed or not. This information can prove to be beneficial before testing the drugs in people. Hence treating MSC with 17-AAG and Radicicol would help in testing the safety and quality of the drugs.

M.S., Biomedical Engineering – Drexel University, 2011

Advisors/Committee Members: Kriete, Andres.

Subjects/Keywords: Biomedical engineering; Heat shock proteins; Transcription factors

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APA (6^th Edition):

Khaira, D. K. (2011). Proteomic scale effect of HSP90 inhibition with 17-AAG and radicicol. (Thesis). Drexel University. Retrieved from http://hdl.handle.net/1860/3728

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Khaira, Depinder Kaur. “Proteomic scale effect of HSP90 inhibition with 17-AAG and radicicol.” 2011. Thesis, Drexel University. Accessed January 18, 2021. http://hdl.handle.net/1860/3728.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Khaira, Depinder Kaur. “Proteomic scale effect of HSP90 inhibition with 17-AAG and radicicol.” 2011. Web. 18 Jan 2021.

Vancouver:

Khaira DK. Proteomic scale effect of HSP90 inhibition with 17-AAG and radicicol. [Internet] [Thesis]. Drexel University; 2011. [cited 2021 Jan 18]. Available from: http://hdl.handle.net/1860/3728.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Khaira DK. Proteomic scale effect of HSP90 inhibition with 17-AAG and radicicol. [Thesis]. Drexel University; 2011. Available from: http://hdl.handle.net/1860/3728

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Texas A&M University

14. Lyons, Brandon Nicholas. Insecticide Resistance of Alphitobius diaperinus (Coleoptera: Tenebrionidae) to β-Cyfluthrin And Associated Heat Tolerance.

Degree: MS, Entomology, 2014, Texas A&M University

URL: http://hdl.handle.net/1969.1/152761

► The lesser mealworm Alphitobius diaperinus (Panzer) (Coleoptera: Tenebrionidae) is an important economic pest to poultry producers globally that cause structural damage and spread pathogens to… (more)

▼ The lesser mealworm Alphitobius diaperinus (Panzer) (Coleoptera: Tenebrionidae) is an important economic pest to poultry producers globally that cause structural damage and spread pathogens to poultry. Adult lesser mealworms were collected from three farms in Mt. Pleasant, TX, USA (A-C) and three farms in Franklin, TX, USA (D-F) in order to assess insecticide resistance across populations, as well its relationship to heat tolerance. Filter papers were treated with a range of doses of the active ingredient (AI) β-Cyfluthrin. Farms B and E displayed much higher LD_(50) of 0.320 mg/mL and 0.627 mg/mL respectively compared to the remaining four farms, which ranged from 0.048-0.161mg/mL. In addition, a field bioassay was conducted to determine adult beetle susceptibility to label rates of formulated permethrin, Vector Ban Plus™ and a pyrethroid, Tempo SC Ultra™. These insecticides were applied to commonly found surfaces in poultry operations (concrete, wood chip particle board, and pressure treated wood). Adult beetles were exposed to the treated surfaces for 2 h and then placed in untreated sterile petri dishes. “Mortality” refers to mortality and morbidity recorded together at 2, 24, and 48 h post-exposure for both bioassays. Insecticide resistance varied greatly based on observation period and compound. The range of mean mortalities measured at 2 h regardless of surface type for Tempo SC Ultra™ was 58-100% and for Vector Ban Plus™ 17-100%. The mean mortality range at 24 h regardless of surface for Tempo SC Ultra™ (91-100%) had less than 10% variation, while Vector Ban Plus™ (0.00-49.73%) displayed almost 50% variation. The mean mortality range at 48 h regardless of surface for Tempo SC Ultra™ (72-100%) showed high knockdown and increased in variation by 30%, and Vector Ban Plus™ (0-29%) had a similar variation, but with low knockdown. Mortality was similar for Tempo SC Ultra™ for each substrate. β-Cyfluthrin (AI) had varying effectiveness depending on the population’s resistance levels, however all the farms tested had LD_(50) well above the equivalent formulation dosage of 0.02mg/mL. The β-Cyfluthrin formulation had high mortality on all the surfaces tested highlighting the importance of the other ingredients in a formulation. Heat tolerance experiments were conducted on the F_(1) progeny of populations B, D, and E (n=14). The heat shock results were inconclusive. Modification to the experimental design may be needed to yield comparable results. Advisors/Committee Members: Teel, Pete (advisor), Tomberlin, Jeff (advisor), Crippen, Tawni (committee member), Coufal, Craig (committee member), Swiger, Sonja (committee member).

Subjects/Keywords: lesser mealworm; insecticide resistance; heat shock

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APA (6^th Edition):

Lyons, B. N. (2014). Insecticide Resistance of Alphitobius diaperinus (Coleoptera: Tenebrionidae) to β-Cyfluthrin And Associated Heat Tolerance. (Masters Thesis). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/152761

Chicago Manual of Style (16^th Edition):

Lyons, Brandon Nicholas. “Insecticide Resistance of Alphitobius diaperinus (Coleoptera: Tenebrionidae) to β-Cyfluthrin And Associated Heat Tolerance.” 2014. Masters Thesis, Texas A&M University. Accessed January 18, 2021. http://hdl.handle.net/1969.1/152761.

MLA Handbook (7^th Edition):

Lyons, Brandon Nicholas. “Insecticide Resistance of Alphitobius diaperinus (Coleoptera: Tenebrionidae) to β-Cyfluthrin And Associated Heat Tolerance.” 2014. Web. 18 Jan 2021.

Vancouver:

Lyons BN. Insecticide Resistance of Alphitobius diaperinus (Coleoptera: Tenebrionidae) to β-Cyfluthrin And Associated Heat Tolerance. [Internet] [Masters thesis]. Texas A&M University; 2014. [cited 2021 Jan 18]. Available from: http://hdl.handle.net/1969.1/152761.

Council of Science Editors:

Lyons BN. Insecticide Resistance of Alphitobius diaperinus (Coleoptera: Tenebrionidae) to β-Cyfluthrin And Associated Heat Tolerance. [Masters Thesis]. Texas A&M University; 2014. Available from: http://hdl.handle.net/1969.1/152761

University of Johannesburg

15. Boshoff, Tuschka. Heat shock protein 70 (hsp70) gene polymorphism: implications for tuberculosis susceptibility in the Cape Coloured population from South Africa.

Degree: PhD, 2011, University of Johannesburg

URL: http://hdl.handle.net/10210/3946

► Heat shock proteins (HSP) (in particular hsp70) are increasingly synthesised during and following exposure to stressful insults, playing an important role in protection and adaptation.… (more)

▼ Heat shock proteins (HSP) (in particular hsp70) are increasingly synthesised during and following exposure to stressful insults, playing an important role in protection and adaptation. Protective effects of HSP concerning infection and immunity include self/non-self discrimination, enhancement of the immune response, immune protection, thermotolerance and cytoprotection from inflammatory mediators (reactive oxygen species and cytokines). Considering the general protective role of hsp70 and its specific immunological functions, including antigen processing and presentation, variation in hsp 70 genes may contribute towards differential coping with stress and disease susceptibility. In humans, three members of the hsp70 gene family, hspl0-1, hsp70-2 and hsp70-hom, were mapped to the MHC class Ill region approximately 280 kbp centromeric to the TNFa gene and 92 kbp telomeric to the C2 gene. Polymorphisms in MHC-Iocalized hsp70 genes have been implicated in susceptibility to a number of diseases, independently or in combination with class II polymorphisms due to linkage disequilibrium (LD). MHC alleles are most often associated with immunosuppressive diseases. Tuberculosis (TB) has a strong immunological basis, involving cell-mediated immunity with human leukocyte antigen (HLA) variants implicated in its susceptibility/resistance. In the light of the above, the role of hsp70 polymorphism in TB susceptibility, alone or in combination with MHC class II alleles, was investigated through the following objectives: 1) Typing of hsp70 gene polymorphism (hsp70-1, hsp70-2 and hsp70-hom) in controls and TB cases from the Cape Coloured population of South Africa 2) Comparison between Cape Coloureds and Caucasoid populations with regard to hsp70 allele and genotype distribution 3) Studying linkage disequilibrium between members of MHC class II (HLADRB1) and Ill (hsp70) alleles in the Cape Coloureds 4) Simulation of MHC class II and Ill haplotypes in this particular population Hsp70 polymorphism was studied in controls (n=106) and TB cases (n=107) from the complex hybrid Cape Coloured population inhabiting the Western Cape region of South Africa - a population showing increased susceptibility to TB. PCR-RFLP and PAGE analysis were used to determine the hsp70 allele frequencies and genotype distribution of the individuals studied, while linkage disequilibrium between MHC class II and Ill, and within class Ill alleles, was investigated using the software "Graphical Overview of Linkage Disequilibruim" (GOLD). Haplotypes comprising MHC class II and Ill alleles were simulated using the software PHASE.

Subjects/Keywords: Heat shock proteins; Tuberculosis; Disease susceptibility

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Boshoff, T. (2011). Heat shock protein 70 (hsp70) gene polymorphism: implications for tuberculosis susceptibility in the Cape Coloured population from South Africa. (Doctoral Dissertation). University of Johannesburg. Retrieved from http://hdl.handle.net/10210/3946

Chicago Manual of Style (16^th Edition):

Boshoff, Tuschka. “Heat shock protein 70 (hsp70) gene polymorphism: implications for tuberculosis susceptibility in the Cape Coloured population from South Africa.” 2011. Doctoral Dissertation, University of Johannesburg. Accessed January 18, 2021. http://hdl.handle.net/10210/3946.

MLA Handbook (7^th Edition):

Boshoff, Tuschka. “Heat shock protein 70 (hsp70) gene polymorphism: implications for tuberculosis susceptibility in the Cape Coloured population from South Africa.” 2011. Web. 18 Jan 2021.

Vancouver:

Boshoff T. Heat shock protein 70 (hsp70) gene polymorphism: implications for tuberculosis susceptibility in the Cape Coloured population from South Africa. [Internet] [Doctoral dissertation]. University of Johannesburg; 2011. [cited 2021 Jan 18]. Available from: http://hdl.handle.net/10210/3946.

Council of Science Editors:

Boshoff T. Heat shock protein 70 (hsp70) gene polymorphism: implications for tuberculosis susceptibility in the Cape Coloured population from South Africa. [Doctoral Dissertation]. University of Johannesburg; 2011. Available from: http://hdl.handle.net/10210/3946

University of Wollongong

16. Cox, Dezerae. The interaction of small heat shock molecular chaperone proteins with a-synuclein.

Degree: PhD, 2016, University of Wollongong

URL: 0601 BIOCHEMISTRY AND CELL BIOLOGY ; https://ro.uow.edu.au/theses/4823

► Protein homeostasis, or proteostasis, is the process of maintaining the conformational and functional integrity of the proteome. Proteostasis is preserved in the face of… (more)

Subjects/Keywords: protein aggregation; neurodegeneration; heat shock proteins

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APA (6^th Edition):

Cox, D. (2016). The interaction of small heat shock molecular chaperone proteins with a-synuclein. (Doctoral Dissertation). University of Wollongong. Retrieved from 0601 BIOCHEMISTRY AND CELL BIOLOGY ; https://ro.uow.edu.au/theses/4823

Chicago Manual of Style (16^th Edition):

Cox, Dezerae. “The interaction of small heat shock molecular chaperone proteins with a-synuclein.” 2016. Doctoral Dissertation, University of Wollongong. Accessed January 18, 2021. 0601 BIOCHEMISTRY AND CELL BIOLOGY ; https://ro.uow.edu.au/theses/4823.

MLA Handbook (7^th Edition):

Cox, Dezerae. “The interaction of small heat shock molecular chaperone proteins with a-synuclein.” 2016. Web. 18 Jan 2021.

Vancouver:

Cox D. The interaction of small heat shock molecular chaperone proteins with a-synuclein. [Internet] [Doctoral dissertation]. University of Wollongong; 2016. [cited 2021 Jan 18]. Available from: 0601 BIOCHEMISTRY AND CELL BIOLOGY ; https://ro.uow.edu.au/theses/4823.

Council of Science Editors:

Cox D. The interaction of small heat shock molecular chaperone proteins with a-synuclein. [Doctoral Dissertation]. University of Wollongong; 2016. Available from: 0601 BIOCHEMISTRY AND CELL BIOLOGY ; https://ro.uow.edu.au/theses/4823

University of Waikato

17. Kaur, Supreet. In vitro study of heat shock protein 60 expression and mitochondrial morphology in response to mitochondrial stress in HeLa cells .

Degree: 2015, University of Waikato

URL: http://hdl.handle.net/10289/10578

► Diabetes mellitus ( DM) is a metabolic disorder and affecting worldwide as stated by WHO that diabetes will be seventh leading cause of death in… (more)

▼ Diabetes mellitus ( DM) is a metabolic disorder and affecting worldwide as stated by WHO that diabetes will be seventh leading cause of death in 2030. Diabetes mellitus is characterized by hyperglycaemia and the production of reactive oxygen species that damages proteins, lipids and DNA. This further elicits mitochondrial specific stress, resulting in increased production of HSP60 which is a mitochondrial stress protein. The aim of this study was to investigate the mitochondrial morphology changes and heat shock protein responses of HeLa cells subjected to physiological levels of hyperglycaemia (25mM). HeLa cell growth was found to be slightly reduced with increasing glucose concentrations (10mM – 25mM ) as compared to the control (5mM). Furthermore, high glucose conditions (25mM) also affected mitochondrial activity as statistically significantly decreased mitochondrial dehydrogenase activity was observed as compared to the control. These results altogether conclude that high glucose (25mM) acted as a mitochondrial stressor. Mitochondria is a dynamic organelle that fuses and divides according to environmental stimuli and energy requirements. As a result the shape of mitochondria varies from small ovals to tubules and reticular networks. These events are mainly controlled by fission and fusion proteins and regulatory machinery. Therefore mitochondrial morphology was also analyzed by using confocal microscopy to determine the effects of high glucose (25mM) on mitochondrial morphology as compared to the control. It was found that the majority of mitochondria in the control (5mM) was tubular as compared to high glucose which showed increased mitochondrial fragmentation suggesting that growing cells in the presence of hyperglycemic conditions lead to mitochondrial stress. Mitochondrial specific stress results in selective induction of molecular chaperone, HSP60 which is mainly localized in the matrix of mitochondria. So furthermore , the expression of HSP60 was investigated. Consistent western blots results showed upregulation of HSP60 with heat shocked protein set as a positive control but not with high glucose concentration (25mM). Interestingly, HSP70 expression was found to be upregulated with high glucose (25mM) as compared to control therefore it can be concluded that there were more general cellular stress as compared to mitochondrial specific stress. This study concluded that high glucose (25mM) effects HeLa cell growth and mitochondrial activity as well as mitochondrial morphology . There are various evidence which links oxidative stress and mitochondrial dynamics and observed increased production of ROS along with short and fragmented mitochondria in high glucose conditions. Advisors/Committee Members: Martinus, Ryan Dennis (advisor).

Subjects/Keywords: Diabetes; Heat shock protein 60; mitochondrial morphology

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Kaur, S. (2015). In vitro study of heat shock protein 60 expression and mitochondrial morphology in response to mitochondrial stress in HeLa cells . (Masters Thesis). University of Waikato. Retrieved from http://hdl.handle.net/10289/10578

Chicago Manual of Style (16^th Edition):

Kaur, Supreet. “In vitro study of heat shock protein 60 expression and mitochondrial morphology in response to mitochondrial stress in HeLa cells .” 2015. Masters Thesis, University of Waikato. Accessed January 18, 2021. http://hdl.handle.net/10289/10578.

MLA Handbook (7^th Edition):

Kaur, Supreet. “In vitro study of heat shock protein 60 expression and mitochondrial morphology in response to mitochondrial stress in HeLa cells .” 2015. Web. 18 Jan 2021.

Vancouver:

Kaur S. In vitro study of heat shock protein 60 expression and mitochondrial morphology in response to mitochondrial stress in HeLa cells . [Internet] [Masters thesis]. University of Waikato; 2015. [cited 2021 Jan 18]. Available from: http://hdl.handle.net/10289/10578.

Council of Science Editors:

Kaur S. In vitro study of heat shock protein 60 expression and mitochondrial morphology in response to mitochondrial stress in HeLa cells . [Masters Thesis]. University of Waikato; 2015. Available from: http://hdl.handle.net/10289/10578

University of Toronto

18. Salerno, Stephanie Angela. The Effect of Estrogen Deprivation on the Cellular Stress Response following Muscle Damage.

Degree: 2017, University of Toronto

URL: http://hdl.handle.net/1807/77887

►

TA muscles from ovary-intact (OVI; n=12) and ovariectomized (OVX; n=12) female Sprague-Dawley rats were subjected to either 20 or 40 LCs. No differences in any… (more)

Subjects/Keywords: Estrogen; Heat Shock Proteins; Skeletal Muscle; 0379

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APA (6^th Edition):

Salerno, S. A. (2017). The Effect of Estrogen Deprivation on the Cellular Stress Response following Muscle Damage. (Masters Thesis). University of Toronto. Retrieved from http://hdl.handle.net/1807/77887

Chicago Manual of Style (16^th Edition):

Salerno, Stephanie Angela. “The Effect of Estrogen Deprivation on the Cellular Stress Response following Muscle Damage.” 2017. Masters Thesis, University of Toronto. Accessed January 18, 2021. http://hdl.handle.net/1807/77887.

MLA Handbook (7^th Edition):

Salerno, Stephanie Angela. “The Effect of Estrogen Deprivation on the Cellular Stress Response following Muscle Damage.” 2017. Web. 18 Jan 2021.

Vancouver:

Salerno SA. The Effect of Estrogen Deprivation on the Cellular Stress Response following Muscle Damage. [Internet] [Masters thesis]. University of Toronto; 2017. [cited 2021 Jan 18]. Available from: http://hdl.handle.net/1807/77887.

Council of Science Editors:

Salerno SA. The Effect of Estrogen Deprivation on the Cellular Stress Response following Muscle Damage. [Masters Thesis]. University of Toronto; 2017. Available from: http://hdl.handle.net/1807/77887

IUPUI

19. Hammack, Lindsay J. 20S proteasome assembly: alternative pathways and complexes.

Degree: 2017, IUPUI

URL: http://hdl.handle.net/1805/15096

►

Indiana University-Purdue University Indianapolis (IUPUI)

The ubiquitin-proteasome system is responsible for the targeted degradation of proteins within the cell. The 26S proteasome, which is the… (more)

Subjects/Keywords: Proteasome; Protein Assembly; Heat shock protein

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APA (6^th Edition):

Hammack, L. J. (2017). 20S proteasome assembly: alternative pathways and complexes. (Thesis). IUPUI. Retrieved from http://hdl.handle.net/1805/15096

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Hammack, Lindsay J. “20S proteasome assembly: alternative pathways and complexes.” 2017. Thesis, IUPUI. Accessed January 18, 2021. http://hdl.handle.net/1805/15096.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Hammack, Lindsay J. “20S proteasome assembly: alternative pathways and complexes.” 2017. Web. 18 Jan 2021.

Vancouver:

Hammack LJ. 20S proteasome assembly: alternative pathways and complexes. [Internet] [Thesis]. IUPUI; 2017. [cited 2021 Jan 18]. Available from: http://hdl.handle.net/1805/15096.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Hammack LJ. 20S proteasome assembly: alternative pathways and complexes. [Thesis]. IUPUI; 2017. Available from: http://hdl.handle.net/1805/15096

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Victoria University of Wellington

20. Andreassend, Sarah Kateyln. The Synthesis of Malonganenone Analogues for Antiparasitic Structure-Activity Relationship Analyses.

Degree: 2017, Victoria University of Wellington

URL: http://hdl.handle.net/10063/9269

► The most lethal causative species of malaria, Plasmodium falciparum, has been reported as developing resistance against current antimalarial drugs in South-East Asia. New antimalarial drugs,… (more)

Subjects/Keywords: Malaria; Heat shock protein; Prenylated alkaloid

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APA (6^th Edition):

Andreassend, S. K. (2017). The Synthesis of Malonganenone Analogues for Antiparasitic Structure-Activity Relationship Analyses. (Masters Thesis). Victoria University of Wellington. Retrieved from http://hdl.handle.net/10063/9269

Chicago Manual of Style (16^th Edition):

Andreassend, Sarah Kateyln. “The Synthesis of Malonganenone Analogues for Antiparasitic Structure-Activity Relationship Analyses.” 2017. Masters Thesis, Victoria University of Wellington. Accessed January 18, 2021. http://hdl.handle.net/10063/9269.

MLA Handbook (7^th Edition):

Andreassend, Sarah Kateyln. “The Synthesis of Malonganenone Analogues for Antiparasitic Structure-Activity Relationship Analyses.” 2017. Web. 18 Jan 2021.

Vancouver:

Andreassend SK. The Synthesis of Malonganenone Analogues for Antiparasitic Structure-Activity Relationship Analyses. [Internet] [Masters thesis]. Victoria University of Wellington; 2017. [cited 2021 Jan 18]. Available from: http://hdl.handle.net/10063/9269.

Council of Science Editors:

Andreassend SK. The Synthesis of Malonganenone Analogues for Antiparasitic Structure-Activity Relationship Analyses. [Masters Thesis]. Victoria University of Wellington; 2017. Available from: http://hdl.handle.net/10063/9269

Michigan State University

21. Kam, David Michael. Hemorrhage, the stress response, and the heat shock response.

Degree: MS, Department of Surgery, 1995, Michigan State University

URL: http://etd.lib.msu.edu/islandora/object/etd:25632

Subjects/Keywords: Heat shock proteins

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APA (6^th Edition):

Kam, D. M. (1995). Hemorrhage, the stress response, and the heat shock response. (Masters Thesis). Michigan State University. Retrieved from http://etd.lib.msu.edu/islandora/object/etd:25632

Chicago Manual of Style (16^th Edition):

Kam, David Michael. “Hemorrhage, the stress response, and the heat shock response.” 1995. Masters Thesis, Michigan State University. Accessed January 18, 2021. http://etd.lib.msu.edu/islandora/object/etd:25632.

MLA Handbook (7^th Edition):

Kam, David Michael. “Hemorrhage, the stress response, and the heat shock response.” 1995. Web. 18 Jan 2021.

Vancouver:

Kam DM. Hemorrhage, the stress response, and the heat shock response. [Internet] [Masters thesis]. Michigan State University; 1995. [cited 2021 Jan 18]. Available from: http://etd.lib.msu.edu/islandora/object/etd:25632.

Council of Science Editors:

Kam DM. Hemorrhage, the stress response, and the heat shock response. [Masters Thesis]. Michigan State University; 1995. Available from: http://etd.lib.msu.edu/islandora/object/etd:25632

University of Texas – Austin

22. -1697-0146. Heat shock-induced cell death.

Degree: PhD, Pharmaceutical Sciences, 2016, University of Texas – Austin

URL: http://dx.doi.org/10.26153/tsw/10809

► Hyperthermia or heat shock therapy has been utilized in clinical cancer therapy in combination with surgery, chemotherapy, or radiotherapy for the treatment of various types… (more)

Subjects/Keywords: Heat shock; Lysosome; Bim; Cell death

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APA (6^th Edition):

-1697-0146. (2016). Heat shock-induced cell death. (Doctoral Dissertation). University of Texas – Austin. Retrieved from http://dx.doi.org/10.26153/tsw/10809

Note: this citation may be lacking information needed for this citation format:
Author name may be incomplete

Chicago Manual of Style (16^th Edition):

-1697-0146. “Heat shock-induced cell death.” 2016. Doctoral Dissertation, University of Texas – Austin. Accessed January 18, 2021. http://dx.doi.org/10.26153/tsw/10809.

Note: this citation may be lacking information needed for this citation format:
Author name may be incomplete

MLA Handbook (7^th Edition):

-1697-0146. “Heat shock-induced cell death.” 2016. Web. 18 Jan 2021.

Note: this citation may be lacking information needed for this citation format:
Author name may be incomplete

Vancouver:

-1697-0146. Heat shock-induced cell death. [Internet] [Doctoral dissertation]. University of Texas – Austin; 2016. [cited 2021 Jan 18]. Available from: http://dx.doi.org/10.26153/tsw/10809.

Note: this citation may be lacking information needed for this citation format:
Author name may be incomplete

Council of Science Editors:

-1697-0146. Heat shock-induced cell death. [Doctoral Dissertation]. University of Texas – Austin; 2016. Available from: http://dx.doi.org/10.26153/tsw/10809

Note: this citation may be lacking information needed for this citation format:
Author name may be incomplete

University of New Mexico

23. Lanphere, Kathryn. The early time course of autophagy in human peripheral blood mononuclear cells following endurance exercise.

Degree: Health, Exercise, and Sports Sciences, 2014, University of New Mexico

URL: http://hdl.handle.net/1928/23558

► Exercise disrupts homeostasis and leads to the induction of an important catabolic system called autophagy. Autophagy is a beneficial cell survival process that is induced… (more)

▼ Exercise disrupts homeostasis and leads to the induction of an important catabolic system called autophagy. Autophagy is a beneficial cell survival process that is induced in periods of starvation. The purposes of this study are to (1) determine the time course of autophagy activation following endurance exercise at 70% of VO2max in a warm environment and (2) to determine if exercising at 50% of VO2max induces autophagy in a warm environment. Methods. Eight endurance trained subjects (2 females) participated in this study and completed a moderate intensity exercise (MIE) trial for 1h (50% of VO2max ), and a high intensity exercise (HIE) trial for 1h (70% of VO2max ). Results. Core temperature and heart rate during HIE was higher during 10-60 and 5-60 minutes, respectively, when compared to the same time during MIE and pre-HIE, p < 0.01. IL-6 levels were increased (p < 0.01) 0h post-exercise and 1h post-exercise HIE versus pre-exercise. IL-6 was increased following MIE 0h post-exercise, when compared to pre-exercise, p < 0.01. Decreases (p < 0.05) in plasma insulin were found following HIE at 2h, when compared to pre-exercise. Decreases in plasma insulin were also found at 4h post-exercise following MIE when compared to pre-exercise, p < 0.05. HIE increased (p < 0.05) autophagy marker LC3-II at 0h , 2h, and 4h post-exercise when compared to pre-exercise. MIE increased LC3-II at 1h post-exercise when compared to pre-exercise. LC3b decreased following MIE at 1h (p < 0.01) and was increased at 2h, post-exercise when compared to baseline. HSPA1A was decreased at 1h following HIE, when compared to baseline, p < 0.01. HSP70 and LC3-II were moderately and significantly related during MIE, p < 0.01. Increased Akt phosphorylation occurred 2h post-MIE when compared to pre-exercise levels, p < 0.01. Conclusions. Our data suggest that autophagy can be stimulated by exercise at both 50% VO2max and 70% VO2max. MIE induced phosphorylation of Akt post-exercise and may be activated independent of circulating insulin levels. It is unknown how or if the decreased levels we observed in plasma insulin and increases in IL-6 influence autophagy in PBMCs following exercise. Advisors/Committee Members: Mermier, Christine, Dokladny, Karol, Schneider, Suzanne, Ann, Gibson, Moseley, Pope.

Subjects/Keywords: autophagy; mTOR; endurance exercise; heat shock protein

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Lanphere, K. (2014). The early time course of autophagy in human peripheral blood mononuclear cells following endurance exercise. (Doctoral Dissertation). University of New Mexico. Retrieved from http://hdl.handle.net/1928/23558

Chicago Manual of Style (16^th Edition):

Lanphere, Kathryn. “The early time course of autophagy in human peripheral blood mononuclear cells following endurance exercise.” 2014. Doctoral Dissertation, University of New Mexico. Accessed January 18, 2021. http://hdl.handle.net/1928/23558.

MLA Handbook (7^th Edition):

Lanphere, Kathryn. “The early time course of autophagy in human peripheral blood mononuclear cells following endurance exercise.” 2014. Web. 18 Jan 2021.

Vancouver:

Lanphere K. The early time course of autophagy in human peripheral blood mononuclear cells following endurance exercise. [Internet] [Doctoral dissertation]. University of New Mexico; 2014. [cited 2021 Jan 18]. Available from: http://hdl.handle.net/1928/23558.

Council of Science Editors:

Lanphere K. The early time course of autophagy in human peripheral blood mononuclear cells following endurance exercise. [Doctoral Dissertation]. University of New Mexico; 2014. Available from: http://hdl.handle.net/1928/23558

University of New Mexico

24. Zuhl, Micah. The effect of oral glutamine supplementation on gut permeability and heat shock protein regulation in runners with a history of gastrointestinal distress.

Degree: Health, Exercise, and Sports Sciences, 2013, University of New Mexico

URL: http://hdl.handle.net/1928/22082

► Gastrointestinal (GI) permeability increases during high intensity exercise leading to endotoxin leakage, and a pro-inflammatory immune response. The purpose of this study are to assess… (more)

▼ Gastrointestinal (GI) permeability increases during high intensity exercise leading to endotoxin leakage, and a pro-inflammatory immune response. The purpose of this study are to assess whether oral glutamine supplementation (1) reduces exercise induced permeability through up-regulation of the heat shock response resulting in occludin stabilization, and (2) depresses the exercise induced inflammatory response. Methods. Eight human subjects (n=8) participated in baseline (PRE) testing, a glutamine (GLN), and placebo (PLA) supplementation trial in a double blind design. After PRE measurements, subjects ingested .9g/kg fat free mass of glutamine per day or a sugar free lemon placebo drink for seven days with a one-month washout period between trials. A 60-min treadmill run at 70% of maximal oxygen consumption was performed at 30°C in an environmental chamber at the end of each supplementation period. Intestinal permeability was assessed at rest and during each trial through urine concentrations of lactulose and rhamnose. Plasma glutamine, plasma endotoxin, and peripheral blood mononuclear cell levels of heat shock protein 70 (HSP70), and nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor, alpha (IκB-α) were measured pre-exercise, post-exercise, 2hr post-exercise, and 4hr post-exercise. Cultured caco-2 human intestinal epithelial cells supplemented with three concentrations of GLN (0, 4, and 6mmol/L) were exposed to heat stress (41\xbaC) to simulate exercise and control (37\xbaC) conditions. HSP70, heat shock factor 1 (HSF-1), and occludin were measured from each culture. Results: Core temperature was not different between exercise trials (39.40 ± .39 vs. 39.54 ± .22 for PLA vs. GLN, respectively, p>0.05). Resting plasma glutamine levels were significantly higher in the GLN trial versus PLA (1.893 ± 0.245mmol.L vs. 0.8285 ± 0.078 mmol.L, p<0.05). Permeability as the ratio of lactulose to rhamnose was significantly higher in the PLA trial when compared to PRE (.0604 ± .0470 vs. .0218 ±.0084, respectively, p<0.05). Permeability was not statistically different between GLN trial and PRE (.0272 ± .0074 vs. .0218 ± .0084, respectively, p>0.05). PBMC expression of IκB-α and HSP70 were higher at the 4hr post-exercise time point in the GLN trial when compared to the 4hr mark in the PLA (.9839 ± .1587 vs. 1.520 ±.2294 and 2.083 ± .6712 vs. 2.895 ± .8444, p<0.05 for IKB-α and HSP70, respectively). Plasma endotoxin was higher compared to pre-exercise at the 2hr post-exercise in the PLA trial (2.883 ± 0.4310 pg.ml vs. 4.550 ± 0.3350 pg.ml, p<0.05 respectively) and significantly higher when compared to the 2hr post-exercise mark in GLN trial (4.550 ± 0.3350 pg/ml vs. 2.883 ± .4314 pg/ml, p<0.05). Results of cell culture: HSP70 expression in Caco-2 cells was higher in the 6mmol 41\xbaC trial when compared to the 0mmol 41\xbaC trial (1.973 ± 0.163 vs. 1.133 ± 0.064, p<0.05,… Advisors/Committee Members: Mermier, Christine, Schneider, Suzanne, Kravitz, Len, Dokladny, Karol, Moseley, Pope.

Subjects/Keywords: Gastrointestinal Permeability; Exercise; Heat Shock Proteins

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APA (6^th Edition):

Zuhl, M. (2013). The effect of oral glutamine supplementation on gut permeability and heat shock protein regulation in runners with a history of gastrointestinal distress. (Doctoral Dissertation). University of New Mexico. Retrieved from http://hdl.handle.net/1928/22082

Chicago Manual of Style (16^th Edition):

Zuhl, Micah. “The effect of oral glutamine supplementation on gut permeability and heat shock protein regulation in runners with a history of gastrointestinal distress.” 2013. Doctoral Dissertation, University of New Mexico. Accessed January 18, 2021. http://hdl.handle.net/1928/22082.

MLA Handbook (7^th Edition):

Zuhl, Micah. “The effect of oral glutamine supplementation on gut permeability and heat shock protein regulation in runners with a history of gastrointestinal distress.” 2013. Web. 18 Jan 2021.

Vancouver:

Zuhl M. The effect of oral glutamine supplementation on gut permeability and heat shock protein regulation in runners with a history of gastrointestinal distress. [Internet] [Doctoral dissertation]. University of New Mexico; 2013. [cited 2021 Jan 18]. Available from: http://hdl.handle.net/1928/22082.

Council of Science Editors:

Zuhl M. The effect of oral glutamine supplementation on gut permeability and heat shock protein regulation in runners with a history of gastrointestinal distress. [Doctoral Dissertation]. University of New Mexico; 2013. Available from: http://hdl.handle.net/1928/22082

25. Boler, Melissa L. Drosophila Can Overcome the Loss of One Allele of Hsp110 by Over Expression of the Hsp110 Protein from the Other Allele.

Degree: 2015, Buffalo State College

URL: https://digitalcommons.buffalostate.edu/forensic_science_theses/6

► Heat shock proteins are a class of molecular chaperone protein that assist in the refolding of misfolded proteins and escorting terminally misfolded (or aggregated) proteins… (more)

Subjects/Keywords: Heat shock proteins; Hsp70; Hsp70Cb/Hsp110; Drosophila

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APA (6^th Edition):

Boler, M. L. (2015). Drosophila Can Overcome the Loss of One Allele of Hsp110 by Over Expression of the Hsp110 Protein from the Other Allele. (Thesis). Buffalo State College. Retrieved from https://digitalcommons.buffalostate.edu/forensic_science_theses/6

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Boler, Melissa L. “Drosophila Can Overcome the Loss of One Allele of Hsp110 by Over Expression of the Hsp110 Protein from the Other Allele.” 2015. Thesis, Buffalo State College. Accessed January 18, 2021. https://digitalcommons.buffalostate.edu/forensic_science_theses/6.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Boler, Melissa L. “Drosophila Can Overcome the Loss of One Allele of Hsp110 by Over Expression of the Hsp110 Protein from the Other Allele.” 2015. Web. 18 Jan 2021.

Vancouver:

Boler ML. Drosophila Can Overcome the Loss of One Allele of Hsp110 by Over Expression of the Hsp110 Protein from the Other Allele. [Internet] [Thesis]. Buffalo State College; 2015. [cited 2021 Jan 18]. Available from: https://digitalcommons.buffalostate.edu/forensic_science_theses/6.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Boler ML. Drosophila Can Overcome the Loss of One Allele of Hsp110 by Over Expression of the Hsp110 Protein from the Other Allele. [Thesis]. Buffalo State College; 2015. Available from: https://digitalcommons.buffalostate.edu/forensic_science_theses/6

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

McGill University

26. Wang, Ying. Interaction of human heat shock factor-1 transcription with promotor DNA.

Degree: MS, Department of Biology, 1993, McGill University

URL: https://escholarship.mcgill.ca/downloads/jm214r460.pdf ; https://escholarship.mcgill.ca/concern/theses/hh63sz256

► Prokaryotic and eukaryotic cells respond to potentially damaging stimuli such as elevated temperature by the rapid, vigorous and transient acceleration in the rate of expression… (more)

Subjects/Keywords: Heat shock proteins

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APA (6^th Edition):

Wang, Y. (1993). Interaction of human heat shock factor-1 transcription with promotor DNA. (Masters Thesis). McGill University. Retrieved from https://escholarship.mcgill.ca/downloads/jm214r460.pdf ; https://escholarship.mcgill.ca/concern/theses/hh63sz256

Chicago Manual of Style (16^th Edition):

Wang, Ying. “Interaction of human heat shock factor-1 transcription with promotor DNA.” 1993. Masters Thesis, McGill University. Accessed January 18, 2021. https://escholarship.mcgill.ca/downloads/jm214r460.pdf ; https://escholarship.mcgill.ca/concern/theses/hh63sz256.

MLA Handbook (7^th Edition):

Wang, Ying. “Interaction of human heat shock factor-1 transcription with promotor DNA.” 1993. Web. 18 Jan 2021.

Vancouver:

Wang Y. Interaction of human heat shock factor-1 transcription with promotor DNA. [Internet] [Masters thesis]. McGill University; 1993. [cited 2021 Jan 18]. Available from: https://escholarship.mcgill.ca/downloads/jm214r460.pdf ; https://escholarship.mcgill.ca/concern/theses/hh63sz256.

Council of Science Editors:

Wang Y. Interaction of human heat shock factor-1 transcription with promotor DNA. [Masters Thesis]. McGill University; 1993. Available from: https://escholarship.mcgill.ca/downloads/jm214r460.pdf ; https://escholarship.mcgill.ca/concern/theses/hh63sz256

Virginia Tech

27. Gross, Tiffany Lauren. Aedes aegypti Heat Shock 70 Genes and their Inducible Promoters.

Degree: PhD, Entomology, 2011, Virginia Tech

URL: http://hdl.handle.net/10919/28305

► Aedes aegypti is an important vector of the viruses that cause dengue fever, dengue hemorrhagic fever, and yellow fever. In depth genetic studies of vector… (more)

▼ Aedes aegypti is an important vector of the viruses that cause dengue fever, dengue hemorrhagic fever, and yellow fever. In depth genetic studies of vector species have been made possible due to the availability of genome sequences and techniques for producing stably transformed mosquitoes. These resources have also contributed to the establishment of new genetics-based approaches to the control of vector borne disease. Genetic studies of Ae. aegypti have benefited from the ability to drive targeted transgene expression, however a ubiquitous inducible promoter has not been identified in this mosquito. The Drosophila melanogaster heat shock 70 promoter has been shown to drive inducible expression in heterologous systems; however, DmHsp70 possesses significant basal activity in Aedes aegypti. This study characterized the sequence and expression of the heat shock 70 genes of Aedes aegypti. AaHsp70 genes were found to be organized in two clusters, each comprised of three divergent pairs. AaHsp70 genes exhibited robust expression upon heat shock in larvae, pupae, and adults as well as in heads, salivary glands, midguts and ovaries. Genomic regions upstream of AaHsp70 genes were found to drive heat-inducible expression of a reporter in both cell and embryo assays. Deletion analysis of AaHsp70-derived promoters yielded two ~1.5 kb genomic fragments that maintained robust heat inducibility in these systems. Aedes aegypti were transformed with AaHsp70-luciferase gene cassettes using the transposable element Mos1. AaHsp70-luciferase transcripts accumulated specifically after heat shock, and displayed a pattern of rapid induction and decay similar to endogenous AaHsp70 genes. Heat-induced expression of luciferase was observed in transgenic larvae, pupae and adults as well as heads, midguts and ovaries but not salivary glands, with levels varying between transgenic strains. The effect of heat shock on the endogenous RNAi pathway as well as the effect of blood feeding on the expression of AaHsp70 genes was investigated, though reproducible results could not be obtained using the assays employed. In conclusion, the heat shock 70 gene family of Aedes aegypti was identified and characterized. The AaHsp70 promoters described could be valuable for gene function studies as well as for the precise timing of the expression of anti-pathogen molecules. Advisors/Committee Members: Adelman, Zachary N. (committeechair), Sharakhov, Igor V. (committee member), Dolan, Erin L. (committee member), Zhu, Jinsong (committee member), Myles, Kevin M. (committee member).

Subjects/Keywords: Aedes aegypti; heat shock; hsp70; inducible promoter

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APA (6^th Edition):

Gross, T. L. (2011). Aedes aegypti Heat Shock 70 Genes and their Inducible Promoters. (Doctoral Dissertation). Virginia Tech. Retrieved from http://hdl.handle.net/10919/28305

Chicago Manual of Style (16^th Edition):

Gross, Tiffany Lauren. “Aedes aegypti Heat Shock 70 Genes and their Inducible Promoters.” 2011. Doctoral Dissertation, Virginia Tech. Accessed January 18, 2021. http://hdl.handle.net/10919/28305.

MLA Handbook (7^th Edition):

Gross, Tiffany Lauren. “Aedes aegypti Heat Shock 70 Genes and their Inducible Promoters.” 2011. Web. 18 Jan 2021.

Vancouver:

Gross TL. Aedes aegypti Heat Shock 70 Genes and their Inducible Promoters. [Internet] [Doctoral dissertation]. Virginia Tech; 2011. [cited 2021 Jan 18]. Available from: http://hdl.handle.net/10919/28305.

Council of Science Editors:

Gross TL. Aedes aegypti Heat Shock 70 Genes and their Inducible Promoters. [Doctoral Dissertation]. Virginia Tech; 2011. Available from: http://hdl.handle.net/10919/28305

28. Ghosh Dastidar, Sayantani. Molecular Mechanisms Of Transcriptional Responses In Stress-Induced Human Cells.

Degree: PhD, Biomedical Sciences, 2020, University of North Dakota

URL: https://commons.und.edu/theses/3097

► Precise regulation of gene expression is essential for maintaining cell homeostasis and survival. Rapid responses to intracellular or extracellular stimuli involve highly regulated genome-wide… (more)

▼ Precise regulation of gene expression is essential for maintaining cell homeostasis and survival. Rapid responses to intracellular or extracellular stimuli involve highly regulated genome-wide changes in the transcriptional landscape. However, works on transcriptional regulation thus far has been primarily focused on genes and gene promoters. Consequently, ubiquitous transcription outside of genes has been greatly neglected. Therefore, in order to understand genome-wide transcriptional changes with stimuli, we looked at transcription factor distribution, RNA Polymerase II (Pol II) dynamics, histone changes, chromatin accessibility at both promoters and promoter-distal regions along with changes in gene transcription. With this approach, we were able to create a more comprehensive picture of how cells respond when exposed to stimuli. Previous studies in mouse and human cells have shown with heat stress at elevated temperature, there is massive genome-wide binding of transcription factor HSF1 (Heat-Shock Factor 1) (Mahat et al., 2016; Vihervaara et al., 2017). Genome-wide analyses revealed there are approximately 280,000 HSF1 binding elements in the human genome. However, with heat-shock, HSF1 binds to less than 4% of these sites indicating HSF1 binding might be context-dependent. To address whether HSF1 binding depends upon stimulus and/or cell-type, we exposed two different cell types, MCF7 breast cancer and K562 chronic myelogenous leukemia cells to a heat-dependent (heat stress at 43°C) and a heat-independent stress (Arsenic) and compared genome-wide changes in HSF1 distribution, histone marks, RNA Pol II and nascent transcription. We found HSF1 binds across the entire human genome during HSR and is a highly sensitive indicator of global heat-shock response (HSR) among the marks we tested. This genome-wide HSF1 binding is independent of stress type but is dependent on cell type. This cell type specific difference in HSF1 binding is more prominent at distal intergenic regions rather than at promoters. The mechanism of this difference in HSF1 binding in different cell types might not be dependent on chromatin accessibility as detected by ATAC-sequencing but might be potentially pre-determined at ground state of cells maintaining cells in a poised state for rapid orchestration of HSR. We next studied the dynamics of RNA Polymerase (Pol II) regulation and gene expression under different stresses and different human cell types. HSR has been associated with massive repression of gene expression due to elevated temperature (Mahat et al., 2016; Vihervaara et al., 2017). We found this repression is cell type dependent and takes place by distinct cell-specific mechanisms. Regulation of gene expression at the level of Pol II can occur at two steps: (i) during recruitment of Pol II at promoter and (ii) during release of Pol II from promoter-paused site to gene body. We found this mechanism of recruitment versus release at promoter differs between cell types and can, in turn, explain the… Advisors/Committee Members: Sergei Nechaev, Min Wu.

Subjects/Keywords: Enhancer; Heat Shock; Histones; Inflammation; Promoter; Transcription

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Ghosh Dastidar, S. (2020). Molecular Mechanisms Of Transcriptional Responses In Stress-Induced Human Cells. (Doctoral Dissertation). University of North Dakota. Retrieved from https://commons.und.edu/theses/3097

Chicago Manual of Style (16^th Edition):

Ghosh Dastidar, Sayantani. “Molecular Mechanisms Of Transcriptional Responses In Stress-Induced Human Cells.” 2020. Doctoral Dissertation, University of North Dakota. Accessed January 18, 2021. https://commons.und.edu/theses/3097.

MLA Handbook (7^th Edition):

Ghosh Dastidar, Sayantani. “Molecular Mechanisms Of Transcriptional Responses In Stress-Induced Human Cells.” 2020. Web. 18 Jan 2021.

Vancouver:

Ghosh Dastidar S. Molecular Mechanisms Of Transcriptional Responses In Stress-Induced Human Cells. [Internet] [Doctoral dissertation]. University of North Dakota; 2020. [cited 2021 Jan 18]. Available from: https://commons.und.edu/theses/3097.

Council of Science Editors:

Ghosh Dastidar S. Molecular Mechanisms Of Transcriptional Responses In Stress-Induced Human Cells. [Doctoral Dissertation]. University of North Dakota; 2020. Available from: https://commons.und.edu/theses/3097

Univerzitet u Beogradu

29. Elzaedi, Younis M., 1968-. Uloga vanćelijskih proteina toplotnog stresa u inflamaciji povezanoj sa posttraumatskim stresnim poremećajem.

Degree: Biološki fakultet, 2015, Univerzitet u Beogradu

URL: https://fedorabg.bg.ac.rs/fedora/get/o:7903/bdef:Content/get

►

Biology - Biochemistry and Molecular Biology / Biologija - Biohemija i molekularna biologija

Posttraumatski stresni poremećaj (PTSP) je psihijatrijska bolest koja se može razviti posle… (more)

▼

Biology - Biochemistry and Molecular Biology / Biologija - Biohemija i molekularna biologija

Posttraumatski stresni poremećaj (PTSP) je psihijatrijska bolest koja se može razviti posle izlaganja traumatskom događaju. PTSP predstavlja veliko medicinsko i ekonomsko opterećenje za društvo, zbog relativno velike učestalosti i komorbiditeta sa mnogim drugim psihijatrijskim i somatskim bolestima. Smatra se da se najbolji rezultati u razumevanju patogeneze PTSP-a i njegovoj dijagnostici i terapiji mogu postići integrisanjem psiholoških, bioloških i farmakoterapeutskih pristupa. Aktuelna istraživanja sugerišu da je PTSP povezan sa neuroendokrinim poremećajima i promenama imunskih funkcija. Smatra se da je hiperosetljivost hipotalamo-hipofizno-adrenokortikalne (HHA) ose na kortizol neuroendokrini „pečat“ PTSP-a, dok je priroda imunskih poremećaja povezanih sa PTSP-om još uvek nejasna. Većina studija pokazala je da je PTSP povezan sa pojačanom inflamacijom, ali su objavljeni i podaci o nepromenjenom inflamatornom statusu, pa čak i smanjenom nivou inflamatornih markera u cirkulaciji PTSP pacijenata. Pretpostavlja se da pojačana inflamacija kod osoba obolelih od PTSP-a može biti posledica nedovoljne imunosupresije kortizolom. Međutim, podaci o nivou kortizola i funkcionisanju kortizolskih receptora kod pacijenata sa PTSP-om nisu konzistentni. Izlaganje različitim stresorima indukuje sintezu unutarćelijskih proteina toplotnog stresa (HSP) čije funkcije potpomažu preživljavanje ćelija. Tokom mnogo godina HSP su posmatrani kao unutarćelijski proteini, ali sada se zna da ih mnoge sisarske ćelije oslobađaju u cirkulaciju, gde mogu da aktiviraju pro-inflamatorne odgovore. Uzimajući da pojačana inflamacija koja je povezana sa PTSP-om verovatno nije posledica umanjenog anti-inflamatornog delovanja kortizola, mi smo pretpostavili da ona može biti posledica indukcije i oslobađanja Hsp60 i Hsp70 psihološkom traumom. Cilj ove studije bio je da se povežu parametri inflamatornog statusa sa nivoima kortizola i HSP u cirkulaciji, kao i da se otkriju moguće veze između inflamatornih markera i vanćelijskih HSP sa izlaganjem traumi, simptomima PTSP-a, osetljivošću i otpornošću na PTSP...

Advisors/Committee Members: Veličković, Nataša.

Subjects/Keywords: posttraumatic stress disorder; heat shock proteins; extracellular heat shock proteins; cytokines; glucocorticoid receptor; cortisol

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Elzaedi, Younis M., 1. (2015). Uloga vanćelijskih proteina toplotnog stresa u inflamaciji povezanoj sa posttraumatskim stresnim poremećajem. (Thesis). Univerzitet u Beogradu. Retrieved from https://fedorabg.bg.ac.rs/fedora/get/o:7903/bdef:Content/get

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Elzaedi, Younis M., 1968-. “Uloga vanćelijskih proteina toplotnog stresa u inflamaciji povezanoj sa posttraumatskim stresnim poremećajem.” 2015. Thesis, Univerzitet u Beogradu. Accessed January 18, 2021. https://fedorabg.bg.ac.rs/fedora/get/o:7903/bdef:Content/get.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Elzaedi, Younis M., 1968-. “Uloga vanćelijskih proteina toplotnog stresa u inflamaciji povezanoj sa posttraumatskim stresnim poremećajem.” 2015. Web. 18 Jan 2021.

Vancouver:

Elzaedi, Younis M. 1. Uloga vanćelijskih proteina toplotnog stresa u inflamaciji povezanoj sa posttraumatskim stresnim poremećajem. [Internet] [Thesis]. Univerzitet u Beogradu; 2015. [cited 2021 Jan 18]. Available from: https://fedorabg.bg.ac.rs/fedora/get/o:7903/bdef:Content/get.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Elzaedi, Younis M. 1. Uloga vanćelijskih proteina toplotnog stresa u inflamaciji povezanoj sa posttraumatskim stresnim poremećajem. [Thesis]. Univerzitet u Beogradu; 2015. Available from: https://fedorabg.bg.ac.rs/fedora/get/o:7903/bdef:Content/get

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of South Florida

30. Mendez, Jamie Elizabeth. Investigation of Hsf1 Interacting Partners via a Genome-wide Yeast Two-hybrid Screen.

Degree: 2013, University of South Florida

URL: https://scholarcommons.usf.edu/etd/4543

► Heat shock factor 1 (HSF1) is the master transcriptional regulator of the heat shock response (HSR), an evolutionarily conserved cellular stress response. HSF1 promotes the… (more)

Subjects/Keywords: C. elegans; heat shock factor 1; Heat shock response; RNA interference; Saccharomyces cerevisiae; Biology

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❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Mendez, J. E. (2013). Investigation of Hsf1 Interacting Partners via a Genome-wide Yeast Two-hybrid Screen. (Thesis). University of South Florida. Retrieved from https://scholarcommons.usf.edu/etd/4543

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Mendez, Jamie Elizabeth. “Investigation of Hsf1 Interacting Partners via a Genome-wide Yeast Two-hybrid Screen.” 2013. Thesis, University of South Florida. Accessed January 18, 2021. https://scholarcommons.usf.edu/etd/4543.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Mendez, Jamie Elizabeth. “Investigation of Hsf1 Interacting Partners via a Genome-wide Yeast Two-hybrid Screen.” 2013. Web. 18 Jan 2021.

Vancouver:

Mendez JE. Investigation of Hsf1 Interacting Partners via a Genome-wide Yeast Two-hybrid Screen. [Internet] [Thesis]. University of South Florida; 2013. [cited 2021 Jan 18]. Available from: https://scholarcommons.usf.edu/etd/4543.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Mendez JE. Investigation of Hsf1 Interacting Partners via a Genome-wide Yeast Two-hybrid Screen. [Thesis]. University of South Florida; 2013. Available from: https://scholarcommons.usf.edu/etd/4543

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Open Access Theses and Dissertations