subject:( cholesterol)

Tulane University

1. McGraw, Claire. Cholesterol Dependent Signaling of the Adenosine A2a Receptor.

Degree: 2018, Tulane University

URL: https://digitallibrary.tulane.edu/islandora/object/tulane:79080

►

G-protein coupled receptors (GPCRs) represent the largest family of receptor proteins in the living world, having approximately 800 human genes predicted. GPCRs are therapeutically relevant,… (more)

▼

G-protein coupled receptors (GPCRs) represent the largest family of receptor proteins in the living world, having approximately 800 human genes predicted. GPCRs are therapeutically relevant, as approximately 35% of all drugs on the market target them. However, these drugs can be associated with unwanted side effects, due to ubiquitous GPCR expression throughout the body, as well as GPCRs within the same family having common ligands, but varying or contradictory responses. Although there are approximately 800 human GPCRs predicted, the high-resolution crystal structure of only 41 GPCRs are available. The first human GPCR to be crystallized was the β2-adrenergic receptor (β2AR) in 2007. Shortly thereafter an alternate crystal form of the β2AR revealed a specific cholesterol binding site between helices I, II, III and IV. From this work a cholesterol consensus motif (CCM) was established, which defined specific interactions between cholesterol and the receptor. Utilization of this CCM predicted that as many as 25% of all class A GPCRs could have a specific interaction with cholesterol at this site, including the Adenosine A2a receptor. However, the first crystal structure of the human Adenosine A2a receptor (bound to an antagonist) revealed a lipid, not cholesterol bound at the CCM. Simulations have given insight into other potential binding sites for cholesterol on the Adenosine A2a receptor’s helices 5 and 6, based on the crystal structure bound to an antagonist. Cholesterol has been shown to modulate the activity of multiple G Protein-coupled receptors (GPCRs), yet whether cholesterol acts through specific interactions, or indirectly via modifications to the membrane is not well understood. Here we report that the activity of the adenosine A2a receptor (A2aR) is dependent on cholesterol as determined by membrane cholesterol depletion with methyl-beta-cyclodextrin (MβCD). We also tested whether a specific interaction occurs between A2aR and cholesterol, by testing the impact of mutational changes to predicted cholesterol binding sites on functional consequences. Understanding how cholesterol modulates GPCRs could help in the design of superior drugs to target different cell types with varying membrane cholesterol concentrations, or in disease states where cholesterol homeostasis is disrupted. Additionally, the widespread use of cholesterol reducing drugs such as statins, has posed the new question of how plasma membrane cholesterol concentrations and activation of membrane embedded proteins are affected by these drugs.

1

Claire McGraw

Advisors/Committee Members: Robinson, Anne (Thesis advisor), School of Science & Engineering Chemical and Biomolecular Engineering (Degree granting institution).

Subjects/Keywords: GPCR; Cholesterol

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

McGraw, C. (2018). Cholesterol Dependent Signaling of the Adenosine A2a Receptor. (Thesis). Tulane University. Retrieved from https://digitallibrary.tulane.edu/islandora/object/tulane:79080

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):

McGraw, Claire. “Cholesterol Dependent Signaling of the Adenosine A2a Receptor.” 2018. Thesis, Tulane University. Accessed March 05, 2021. https://digitallibrary.tulane.edu/islandora/object/tulane:79080.

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

MLA Handbook (7^th Edition):

McGraw, Claire. “Cholesterol Dependent Signaling of the Adenosine A2a Receptor.” 2018. Web. 05 Mar 2021.

Vancouver:

McGraw C. Cholesterol Dependent Signaling of the Adenosine A2a Receptor. [Internet] [Thesis]. Tulane University; 2018. [cited 2021 Mar 05]. Available from: https://digitallibrary.tulane.edu/islandora/object/tulane:79080.

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

Council of Science Editors:

McGraw C. Cholesterol Dependent Signaling of the Adenosine A2a Receptor. [Thesis]. Tulane University; 2018. Available from: https://digitallibrary.tulane.edu/islandora/object/tulane:79080

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

Oregon State University

2. Stirniman, Ann. Serum cholesterol concentrations of women on a controlled diet.

Degree: MS, Home Economics, 1957, Oregon State University

URL: http://hdl.handle.net/1957/51701

Subjects/Keywords: Cholesterol

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Stirniman, A. (1957). Serum cholesterol concentrations of women on a controlled diet. (Masters Thesis). Oregon State University. Retrieved from http://hdl.handle.net/1957/51701

Chicago Manual of Style (16^th Edition):

Stirniman, Ann. “Serum cholesterol concentrations of women on a controlled diet.” 1957. Masters Thesis, Oregon State University. Accessed March 05, 2021. http://hdl.handle.net/1957/51701.

MLA Handbook (7^th Edition):

Stirniman, Ann. “Serum cholesterol concentrations of women on a controlled diet.” 1957. Web. 05 Mar 2021.

Vancouver:

Stirniman A. Serum cholesterol concentrations of women on a controlled diet. [Internet] [Masters thesis]. Oregon State University; 1957. [cited 2021 Mar 05]. Available from: http://hdl.handle.net/1957/51701.

Council of Science Editors:

Stirniman A. Serum cholesterol concentrations of women on a controlled diet. [Masters Thesis]. Oregon State University; 1957. Available from: http://hdl.handle.net/1957/51701

Oregon State University

3. Farid, Sheedvash Amirkia. Effect of dietary fat and cholesterol on plasma lecithin:cholesterol acyltransferase activity in man: Lecithin:cholesterol acyltransferase (LCAT).

Degree: MS, Foods and Nutrition, 1984, Oregon State University

URL: http://hdl.handle.net/1957/25888

► Effect of diets varying in amount of cholesterol and polyunsaturated to saturated fatty acid ratio (P/S) on plasma lipid levels and lecithin:cholesterol acyltransferase (LCAT) activity… (more)

Subjects/Keywords: Cholesterol

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Farid, S. A. (1984). Effect of dietary fat and cholesterol on plasma lecithin:cholesterol acyltransferase activity in man: Lecithin:cholesterol acyltransferase (LCAT). (Masters Thesis). Oregon State University. Retrieved from http://hdl.handle.net/1957/25888

Chicago Manual of Style (16^th Edition):

Farid, Sheedvash Amirkia. “Effect of dietary fat and cholesterol on plasma lecithin:cholesterol acyltransferase activity in man: Lecithin:cholesterol acyltransferase (LCAT).” 1984. Masters Thesis, Oregon State University. Accessed March 05, 2021. http://hdl.handle.net/1957/25888.

MLA Handbook (7^th Edition):

Farid, Sheedvash Amirkia. “Effect of dietary fat and cholesterol on plasma lecithin:cholesterol acyltransferase activity in man: Lecithin:cholesterol acyltransferase (LCAT).” 1984. Web. 05 Mar 2021.

Vancouver:

Farid SA. Effect of dietary fat and cholesterol on plasma lecithin:cholesterol acyltransferase activity in man: Lecithin:cholesterol acyltransferase (LCAT). [Internet] [Masters thesis]. Oregon State University; 1984. [cited 2021 Mar 05]. Available from: http://hdl.handle.net/1957/25888.

Council of Science Editors:

Farid SA. Effect of dietary fat and cholesterol on plasma lecithin:cholesterol acyltransferase activity in man: Lecithin:cholesterol acyltransferase (LCAT). [Masters Thesis]. Oregon State University; 1984. Available from: http://hdl.handle.net/1957/25888

Boston University

4. Huntsinger, Mildred Elizabeth. Cholesterol, a physical, chemical and biological study.

Degree: PhD, Biochemistry, 1935, Boston University

URL: http://hdl.handle.net/2144/9080

Subjects/Keywords: Cholesterol

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Huntsinger, M. E. (1935). Cholesterol, a physical, chemical and biological study. (Doctoral Dissertation). Boston University. Retrieved from http://hdl.handle.net/2144/9080

Chicago Manual of Style (16^th Edition):

Huntsinger, Mildred Elizabeth. “Cholesterol, a physical, chemical and biological study.” 1935. Doctoral Dissertation, Boston University. Accessed March 05, 2021. http://hdl.handle.net/2144/9080.

MLA Handbook (7^th Edition):

Huntsinger, Mildred Elizabeth. “Cholesterol, a physical, chemical and biological study.” 1935. Web. 05 Mar 2021.

Vancouver:

Huntsinger ME. Cholesterol, a physical, chemical and biological study. [Internet] [Doctoral dissertation]. Boston University; 1935. [cited 2021 Mar 05]. Available from: http://hdl.handle.net/2144/9080.

Council of Science Editors:

Huntsinger ME. Cholesterol, a physical, chemical and biological study. [Doctoral Dissertation]. Boston University; 1935. Available from: http://hdl.handle.net/2144/9080

5. Jia, Lin. THE ROLE OF NIEMANN-PICK C1-LIKE 1 (NPC1L1) PROTEIN IN CHOLESTEROL TRANSPORT AND METABOLIC DISEASES.

Degree: 2010, Wake Forest University

URL: http://hdl.handle.net/10339/30432

► Niemann-Pick C1-Like 1 (NPC1L1) is a polytopic transmembrane protein critical for intestinal absorption of dietary and biliary cholesterol. Ezetimibe, by inhibiting NPC1L1 function, is widely… (more)

Subjects/Keywords: Cholesterol

…Figure 1. Body weight and body weight gain of L1-KO and WT mice on the low cholesterol… …carbohydrate diet with a low (HCD-C) or a high (HCD+C) amount of cholesterol… …L1-KO and WT mice on the low cholesterol (0.02%, w/w) high fat diet (HFD-C… …x29; or on the high cholesterol (0.16%, w/w) high fat diet (HFD+C) for… …18 weeks �� …107 Figure 4. Effects of NPC1L1 deficiency on intestinal cholesterol…

8 more images…

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Jia, L. (2010). THE ROLE OF NIEMANN-PICK C1-LIKE 1 (NPC1L1) PROTEIN IN CHOLESTEROL TRANSPORT AND METABOLIC DISEASES. (Thesis). Wake Forest University. Retrieved from http://hdl.handle.net/10339/30432

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):

Jia, Lin. “THE ROLE OF NIEMANN-PICK C1-LIKE 1 (NPC1L1) PROTEIN IN CHOLESTEROL TRANSPORT AND METABOLIC DISEASES.” 2010. Thesis, Wake Forest University. Accessed March 05, 2021. http://hdl.handle.net/10339/30432.

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

MLA Handbook (7^th Edition):

Jia, Lin. “THE ROLE OF NIEMANN-PICK C1-LIKE 1 (NPC1L1) PROTEIN IN CHOLESTEROL TRANSPORT AND METABOLIC DISEASES.” 2010. Web. 05 Mar 2021.

Vancouver:

Jia L. THE ROLE OF NIEMANN-PICK C1-LIKE 1 (NPC1L1) PROTEIN IN CHOLESTEROL TRANSPORT AND METABOLIC DISEASES. [Internet] [Thesis]. Wake Forest University; 2010. [cited 2021 Mar 05]. Available from: http://hdl.handle.net/10339/30432.

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

Council of Science Editors:

Jia L. THE ROLE OF NIEMANN-PICK C1-LIKE 1 (NPC1L1) PROTEIN IN CHOLESTEROL TRANSPORT AND METABOLIC DISEASES. [Thesis]. Wake Forest University; 2010. Available from: http://hdl.handle.net/10339/30432

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

Oregon State University

6. Pescador, Josephine Organo. A method for determining free and total cholesterol in the red cell and white cell-platelet fractions in 0.4 milliliters of human blood.

Degree: MS, Home Economics, 1958, Oregon State University

URL: http://hdl.handle.net/1957/50589

Subjects/Keywords: Cholesterol

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Pescador, J. O. (1958). A method for determining free and total cholesterol in the red cell and white cell-platelet fractions in 0.4 milliliters of human blood. (Masters Thesis). Oregon State University. Retrieved from http://hdl.handle.net/1957/50589

Chicago Manual of Style (16^th Edition):

Pescador, Josephine Organo. “A method for determining free and total cholesterol in the red cell and white cell-platelet fractions in 0.4 milliliters of human blood.” 1958. Masters Thesis, Oregon State University. Accessed March 05, 2021. http://hdl.handle.net/1957/50589.

MLA Handbook (7^th Edition):

Pescador, Josephine Organo. “A method for determining free and total cholesterol in the red cell and white cell-platelet fractions in 0.4 milliliters of human blood.” 1958. Web. 05 Mar 2021.

Vancouver:

Pescador JO. A method for determining free and total cholesterol in the red cell and white cell-platelet fractions in 0.4 milliliters of human blood. [Internet] [Masters thesis]. Oregon State University; 1958. [cited 2021 Mar 05]. Available from: http://hdl.handle.net/1957/50589.

Council of Science Editors:

Pescador JO. A method for determining free and total cholesterol in the red cell and white cell-platelet fractions in 0.4 milliliters of human blood. [Masters Thesis]. Oregon State University; 1958. Available from: http://hdl.handle.net/1957/50589

University of New South Wales

7. Du, Ximing Robin. Studies of new factors involved in cholesterol homeostasis.

Degree: Biotechnology & Biomolecular Sciences, 2007, University of New South Wales

URL: http://handle.unsw.edu.au/1959.4/39827 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:1264/SOURCE02?view=true

► The regulatory pool of cholesterol is located in the endoplasmic reticulum (ER) and is key to how mammalian cells sense and respond to changes in… (more)

▼ The regulatory pool of cholesterol is located in the endoplasmic reticulum (ER) and is key to how mammalian cells sense and respond to changes in cellular cholesterol levels. The extent of cholesterol esterification by the ER-resident protein, acyl-coenzyme A:cholesterol acyl-transferase (ACAT), has become the standard method for monitoring cholesterol transport to the ER and is assumed to reflect the regulatory pool of ER cholesterol. The oxysterol, 25-hydroxycholesterol (25HC), is thought to trigger intracellular cholesterol transport to the ER. Chapter 3 of this thesis addressed whether or not cholesterol esterification necessarily reflects cholesterol movement to the cholesterol homeostatic machinery in the ER as determined by SREBP processing. Three agents that inhibited the ability of 25HC to induce cholesterol esterification (progesterone, nigericin, and monensin) did not have a corresponding effect on 25HC suppression of SREBP processing. Moreover, ACAT inhibition did not alter the sensitivity of SREBP processing to 25HC. These findings indicate that cholesterol esterification by the ER-resident protein ACAT is dissociable from cholesterol transport to the cholesterol homeostatic machinery in the ER.In order to readily analyse and quantify the processing of SREBP-2, the master regulator of cholesterol homeostasis, the second part of this study (Chapter 4) established a stable cell-line (13A/PS) that expresses the fusion protein PLAP-BP2 (secreted form of placental alkaline phosphatase joined to the luminal loop of SREBP-2 on the NH2- terminal side of Site-1). Processing of PLAP-BP2 mimics the cleavage of SREBP. The PLAP-BP2 cleavage assay was shown to be a valuable method for analysing and quantifying SREBP-2 processing. Compared to transiently transfected cells, the stable 13A/PS cells were more responsive to changes of sterol status in regards to PLAP secretion. Considering the reliability and consistency of the experiments, the 13A/PS cell-line is therefore a useful tool for the study of SREBP-2 processing.Akt is a critical regulator of cell growth, proliferation and survival that is activated by phosphatidylinositol 3-kinase (PI3K). Chapter 5 and Chapter 6 investigated the role of PI3K/Akt in activation of SREBP-2 increased in response to statin treatment and various cholesterol depletion approaches. The increase of SREBP-2 processing by statins or insulin-like growth factor-1 was blunted by treatment with a potent and specific inhibitor of PI3K, LY294002, or when a plasmid encoding a dominant-negative form of Akt (DNAkt) was expressed. Furthermore, LY294002 treatment down-regulated SREBP-2 or -1c gene targets, and decreased cholesterol and fatty acid synthesis. Fluorescence microscopy studies indicated that LY294002 disrupts transport of the SREBP escort protein, SCAP, from the ER to the Golgi. This disruption was also shown by immunofluorescence staining when DN-Akt was expressed. These data indicate that the PI3K/Akt pathway is involved in SREBP-2 transport to the Golgi, contributing to the control of…

Subjects/Keywords: Cholesterol

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Du, X. R. (2007). Studies of new factors involved in cholesterol homeostasis. (Doctoral Dissertation). University of New South Wales. Retrieved from http://handle.unsw.edu.au/1959.4/39827 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:1264/SOURCE02?view=true

Chicago Manual of Style (16^th Edition):

Du, Ximing Robin. “Studies of new factors involved in cholesterol homeostasis.” 2007. Doctoral Dissertation, University of New South Wales. Accessed March 05, 2021. http://handle.unsw.edu.au/1959.4/39827 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:1264/SOURCE02?view=true.

MLA Handbook (7^th Edition):

Du, Ximing Robin. “Studies of new factors involved in cholesterol homeostasis.” 2007. Web. 05 Mar 2021.

Vancouver:

Du XR. Studies of new factors involved in cholesterol homeostasis. [Internet] [Doctoral dissertation]. University of New South Wales; 2007. [cited 2021 Mar 05]. Available from: http://handle.unsw.edu.au/1959.4/39827 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:1264/SOURCE02?view=true.

Council of Science Editors:

Du XR. Studies of new factors involved in cholesterol homeostasis. [Doctoral Dissertation]. University of New South Wales; 2007. Available from: http://handle.unsw.edu.au/1959.4/39827 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:1264/SOURCE02?view=true

University of Alberta

8. Chung, Jiyun. Effect of Cholesterol Accumulation on the Metabolism of Amyloid Precursor Protein (APP) in Cultured N2a Cells.

Degree: MS, Department of Psychiatry, 2015, University of Alberta

URL: https://era.library.ualberta.ca/files/c4j03cz67p

► Alzheimer’s disease (AD) is a progressive neurodegenerative disorder believed to be triggered by the accumulation of β-amyloid (Aβ) peptides derived from the proteolytic processing of… (more)

Subjects/Keywords: APP; U18666A; Cholesterol

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Chung, J. (2015). Effect of Cholesterol Accumulation on the Metabolism of Amyloid Precursor Protein (APP) in Cultured N2a Cells. (Masters Thesis). University of Alberta. Retrieved from https://era.library.ualberta.ca/files/c4j03cz67p

Chicago Manual of Style (16^th Edition):

Chung, Jiyun. “Effect of Cholesterol Accumulation on the Metabolism of Amyloid Precursor Protein (APP) in Cultured N2a Cells.” 2015. Masters Thesis, University of Alberta. Accessed March 05, 2021. https://era.library.ualberta.ca/files/c4j03cz67p.

MLA Handbook (7^th Edition):

Chung, Jiyun. “Effect of Cholesterol Accumulation on the Metabolism of Amyloid Precursor Protein (APP) in Cultured N2a Cells.” 2015. Web. 05 Mar 2021.

Vancouver:

Chung J. Effect of Cholesterol Accumulation on the Metabolism of Amyloid Precursor Protein (APP) in Cultured N2a Cells. [Internet] [Masters thesis]. University of Alberta; 2015. [cited 2021 Mar 05]. Available from: https://era.library.ualberta.ca/files/c4j03cz67p.

Council of Science Editors:

Chung J. Effect of Cholesterol Accumulation on the Metabolism of Amyloid Precursor Protein (APP) in Cultured N2a Cells. [Masters Thesis]. University of Alberta; 2015. Available from: https://era.library.ualberta.ca/files/c4j03cz67p

9. Selvamurugan C. Studies on immobilization of urease and Co immobilization of cholesterol Esterase cholesterol oxidase and Peroxidase and their clinical Applications;.

Degree: Studies on immobilization of urease and Co immobilization of cholesterol Esterase cholesterol oxidase and Peroxidase and their clinical Applications, 2014, Anna University

URL: http://shodhganga.inflibnet.ac.in/handle/10603/29401

►

Activity and stability of immobilized urease on different matrices newline Nylon 6 6 beads sepharose gel silica gel and gelatin film coated on cellulose newlineacetate… (more)

Subjects/Keywords: Esterase cholesterol oxidase

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

C, S. (2014). Studies on immobilization of urease and Co immobilization of cholesterol Esterase cholesterol oxidase and Peroxidase and their clinical Applications;. (Thesis). Anna University. Retrieved from http://shodhganga.inflibnet.ac.in/handle/10603/29401

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):

C, Selvamurugan. “Studies on immobilization of urease and Co immobilization of cholesterol Esterase cholesterol oxidase and Peroxidase and their clinical Applications;.” 2014. Thesis, Anna University. Accessed March 05, 2021. http://shodhganga.inflibnet.ac.in/handle/10603/29401.

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

MLA Handbook (7^th Edition):

C, Selvamurugan. “Studies on immobilization of urease and Co immobilization of cholesterol Esterase cholesterol oxidase and Peroxidase and their clinical Applications;.” 2014. Web. 05 Mar 2021.

Vancouver:

C S. Studies on immobilization of urease and Co immobilization of cholesterol Esterase cholesterol oxidase and Peroxidase and their clinical Applications;. [Internet] [Thesis]. Anna University; 2014. [cited 2021 Mar 05]. Available from: http://shodhganga.inflibnet.ac.in/handle/10603/29401.

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

Council of Science Editors:

C S. Studies on immobilization of urease and Co immobilization of cholesterol Esterase cholesterol oxidase and Peroxidase and their clinical Applications;. [Thesis]. Anna University; 2014. Available from: http://shodhganga.inflibnet.ac.in/handle/10603/29401

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

University of Miami

10. Reina, Samantha A. HDL Cholesterol and Stroke Risk: The Multi-Ethnic Study of Atherosclerosis.

Degree: MS, Psychology (Arts and Sciences), 2015, University of Miami

URL: https://scholarlyrepository.miami.edu/oa_theses/548

► Research shows a link between HDL cholesterol and cardiovascular disease. Evidence of the relationship between HDL cholesterol and stroke risk is mixed. Accurate identification… (more)

Subjects/Keywords: HDL cholesterol; stroke

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Reina, S. A. (2015). HDL Cholesterol and Stroke Risk: The Multi-Ethnic Study of Atherosclerosis. (Thesis). University of Miami. Retrieved from https://scholarlyrepository.miami.edu/oa_theses/548

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):

Reina, Samantha A. “HDL Cholesterol and Stroke Risk: The Multi-Ethnic Study of Atherosclerosis.” 2015. Thesis, University of Miami. Accessed March 05, 2021. https://scholarlyrepository.miami.edu/oa_theses/548.

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

MLA Handbook (7^th Edition):

Reina, Samantha A. “HDL Cholesterol and Stroke Risk: The Multi-Ethnic Study of Atherosclerosis.” 2015. Web. 05 Mar 2021.

Vancouver:

Reina SA. HDL Cholesterol and Stroke Risk: The Multi-Ethnic Study of Atherosclerosis. [Internet] [Thesis]. University of Miami; 2015. [cited 2021 Mar 05]. Available from: https://scholarlyrepository.miami.edu/oa_theses/548.

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

Council of Science Editors:

Reina SA. HDL Cholesterol and Stroke Risk: The Multi-Ethnic Study of Atherosclerosis. [Thesis]. University of Miami; 2015. Available from: https://scholarlyrepository.miami.edu/oa_theses/548

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

Victoria University of Wellington

11. Vithal, Tanisha. Investigating the function of CLU in Alzheimer's Disease in in vitro and in vivo models.

Degree: 2016, Victoria University of Wellington

URL: http://hdl.handle.net/10063/5050

► Alzheimer’s disease (AD) is a neurodegenerative disease that is responsible for 50-80% of dementia cases and is characterised by lack of visuospatial perception, impairment of… (more)

Subjects/Keywords: Clusterin; Cholesterol; Autophagy

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Vithal, T. (2016). Investigating the function of CLU in Alzheimer's Disease in in vitro and in vivo models. (Masters Thesis). Victoria University of Wellington. Retrieved from http://hdl.handle.net/10063/5050

Chicago Manual of Style (16^th Edition):

Vithal, Tanisha. “Investigating the function of CLU in Alzheimer's Disease in in vitro and in vivo models.” 2016. Masters Thesis, Victoria University of Wellington. Accessed March 05, 2021. http://hdl.handle.net/10063/5050.

MLA Handbook (7^th Edition):

Vithal, Tanisha. “Investigating the function of CLU in Alzheimer's Disease in in vitro and in vivo models.” 2016. Web. 05 Mar 2021.

Vancouver:

Vithal T. Investigating the function of CLU in Alzheimer's Disease in in vitro and in vivo models. [Internet] [Masters thesis]. Victoria University of Wellington; 2016. [cited 2021 Mar 05]. Available from: http://hdl.handle.net/10063/5050.

Council of Science Editors:

Vithal T. Investigating the function of CLU in Alzheimer's Disease in in vitro and in vivo models. [Masters Thesis]. Victoria University of Wellington; 2016. Available from: http://hdl.handle.net/10063/5050

University of New South Wales

12. Prabhu, Anika. The regulation of DHCR7 - a key enzyme in cholesterol synthesis.

Degree: Biotechnology & Biomolecular Sciences, 2016, University of New South Wales

URL: http://handle.unsw.edu.au/1959.4/57100 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:42487/SOURCE02?view=true

► Cholesterol is a vital lipid for mammalian life. It is essential for the structure of cell membranes, fetal development, and as a precursor for steroid… (more)

▼ Cholesterol is a vital lipid for mammalian life. It is essential for the structure of cell membranes, fetal development, and as a precursor for steroid hormones. However, in excess, cholesterol can be damaging to health. Thus, cellular cholesterol levels are under tight control. Previous research has focused on an early step in cholesterol synthesis: 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGCR), target of the cholesterol-lowering class of drugs known as statins. However, there is a paucity of knowledge about the other regulatory steps in the pathway.In this thesis, we investigated 7-dehydrocholesterol reductase (DHCR7); the terminal enzyme of the Kandutsch-Russell pathway of cholesterol synthesis, which converts 7-dehydrocholesterol (7DHC) into cholesterol. A deficiency in DHCR7 causes the devastating developmental disease Smith-Lemli-Opitz syndrome, highlighting the importance of the enzyme in cellular growth and development.Here, we show that DHCR7 is regulated via multiple mechanisms. At the transcriptional level, regulation occurs through dual sterol regulatory elements within the human DHCR7 promoter, which work cooperatively to control gene expression. These findings supersede previous work into the promoter of rat Dhcr7, which we have found has evolved into a more sophisticated regulatory system in higher organisms. At the post-translational level, we discovered that cholesterol induces the proteolytic degradation of DHCR7 protein. This results in the subsequent accumulation of its substrate 7DHC, which is also the precursor for vitamin D. Thus, the degradation of DHCR7 switches flux away from cholesterol synthesis into vitamin D production.Finally, we explored the role of signaling in DHCR7 regulation and identified that phosphorylation acutely controls DHCR7 activity, at a known phosphorylation site, S14. We found that inhibition of AMP-kinase and protein kinase A also ablated DHCR7 activity, through an unknown phosphorylation site. This loss of DHCR7 activity also has the potential to promote flux into vitamin D synthesis.Overall, these findings indicate that DHCR7 is an important regulatory step in cholesterol and vitamin D synthesis, playing a critical role in the homeostasis of two important molecules that are involved in human health and disease. Advisors/Committee Members: Brown, Andrew, Biotechnology & Biomolecular Sciences, Faculty of Science, UNSW.

Subjects/Keywords: Cholesterol; DHCR7; Enzyme

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Prabhu, A. (2016). The regulation of DHCR7 - a key enzyme in cholesterol synthesis. (Doctoral Dissertation). University of New South Wales. Retrieved from http://handle.unsw.edu.au/1959.4/57100 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:42487/SOURCE02?view=true

Chicago Manual of Style (16^th Edition):

Prabhu, Anika. “The regulation of DHCR7 - a key enzyme in cholesterol synthesis.” 2016. Doctoral Dissertation, University of New South Wales. Accessed March 05, 2021. http://handle.unsw.edu.au/1959.4/57100 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:42487/SOURCE02?view=true.

MLA Handbook (7^th Edition):

Prabhu, Anika. “The regulation of DHCR7 - a key enzyme in cholesterol synthesis.” 2016. Web. 05 Mar 2021.

Vancouver:

Prabhu A. The regulation of DHCR7 - a key enzyme in cholesterol synthesis. [Internet] [Doctoral dissertation]. University of New South Wales; 2016. [cited 2021 Mar 05]. Available from: http://handle.unsw.edu.au/1959.4/57100 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:42487/SOURCE02?view=true.

Council of Science Editors:

Prabhu A. The regulation of DHCR7 - a key enzyme in cholesterol synthesis. [Doctoral Dissertation]. University of New South Wales; 2016. Available from: http://handle.unsw.edu.au/1959.4/57100 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:42487/SOURCE02?view=true

13. Karmakar, Sanat. Structure and phase behaviour of lipid cholesterol membranes; -.

Degree: Research, 2005, Jawaharlal Nehru University

URL: http://shodhganga.inflibnet.ac.in/handle/10603/28768

non

Bibliography p.159-160

Advisors/Committee Members: Raghunathan, V A.

Subjects/Keywords: lipid-cholesterol; cholesterol; cholesterol membranes

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Karmakar, S. (2005). Structure and phase behaviour of lipid cholesterol membranes; -. (Thesis). Jawaharlal Nehru University. Retrieved from http://shodhganga.inflibnet.ac.in/handle/10603/28768

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):

Karmakar, Sanat. “Structure and phase behaviour of lipid cholesterol membranes; -.” 2005. Thesis, Jawaharlal Nehru University. Accessed March 05, 2021. http://shodhganga.inflibnet.ac.in/handle/10603/28768.

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

MLA Handbook (7^th Edition):

Karmakar, Sanat. “Structure and phase behaviour of lipid cholesterol membranes; -.” 2005. Web. 05 Mar 2021.

Vancouver:

Karmakar S. Structure and phase behaviour of lipid cholesterol membranes; -. [Internet] [Thesis]. Jawaharlal Nehru University; 2005. [cited 2021 Mar 05]. Available from: http://shodhganga.inflibnet.ac.in/handle/10603/28768.

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

Council of Science Editors:

Karmakar S. Structure and phase behaviour of lipid cholesterol membranes; -. [Thesis]. Jawaharlal Nehru University; 2005. Available from: http://shodhganga.inflibnet.ac.in/handle/10603/28768

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

Durban University of Technology

14. Joseph, Jeanine Dorothy. Homoeopathy in hypercholesterolaemia.

Degree: 1994, Durban University of Technology

URL: http://hdl.handle.net/10321/1804

►

Dissertation submitted in partial compliance with the requirements for the Master's Diploma in Technology: Homoeopathy, Technikon Natal, 1994.

The purpose of this study was to… (more)

Subjects/Keywords: Homeopathy; Cholesterol

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Joseph, J. D. (1994). Homoeopathy in hypercholesterolaemia. (Thesis). Durban University of Technology. Retrieved from http://hdl.handle.net/10321/1804

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):

Joseph, Jeanine Dorothy. “Homoeopathy in hypercholesterolaemia.” 1994. Thesis, Durban University of Technology. Accessed March 05, 2021. http://hdl.handle.net/10321/1804.

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

MLA Handbook (7^th Edition):

Joseph, Jeanine Dorothy. “Homoeopathy in hypercholesterolaemia.” 1994. Web. 05 Mar 2021.

Vancouver:

Joseph JD. Homoeopathy in hypercholesterolaemia. [Internet] [Thesis]. Durban University of Technology; 1994. [cited 2021 Mar 05]. Available from: http://hdl.handle.net/10321/1804.

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

Council of Science Editors:

Joseph JD. Homoeopathy in hypercholesterolaemia. [Thesis]. Durban University of Technology; 1994. Available from: http://hdl.handle.net/10321/1804

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

Durban University of Technology

15. Hillermann, Roland. Hypercholesterolemia : the role of homoeopathy.

Degree: 1996, Durban University of Technology

URL: http://hdl.handle.net/10321/1855

►

A dissertation submitted in partial compliance with the requirements for the Master's Degree in Technology: Homoeopathy, Technikon Natal, 1996.

The purpose of this study was… (more)

▼

A dissertation submitted in partial compliance with the requirements for the Master's Degree in Technology: Homoeopathy, Technikon Natal, 1996.

The purpose of this study was to evaluate the efficacy of Taraxacum 5CH in the treatment of hypercholesterolemic patients, in terms of measuring the extent of change in serum total cholesterol (TC), low density lipoprotein (LOL) and high density lipoprotein levels (HOL). The expected result was a resultant lowering of bath the TC and LOL levels, as well as an increase of the HOL levels. Convenience sampling was employed to draw patients from Technikon Natal, a Durban company and the general public from the greater Durban area. Only persons with raised TC and LOL levels were accepted into the trial. Of these one half constituted the control group and received only placebo, the remaining half made up the trial group and were treated with Taraxacum 5CH. The remedies were prepared and dispensed by a qualified pharmacist. Venous blood was obtained from all subjects before the trial and monthly, for three consecutive months, during the trial. A reputable pathology laboratory was employed to obtain lipogram studies of all blood samples. The participants were asked not to change their then present diets or lifestyles. Performing paired T-tests on the initial versus the final values of the control group revealed no statistically significant changes in the TC, LOL and HOL levels, whereas in the trial group a significant reduction was computed for the TC and LOL levels, as well as an insignificant increase of the HOL levels. Unpaired T-tests showed that the trial and control groups were not significantly different at the beginning ot the trial, but were found to have changed to become significantly different by the end of the trial with respects to TC and LOL levels. The HOL levels were dissimilar initially, but were shown to be significantly similar at the end of the trial.

M

Advisors/Committee Members: Till, Hettie.

Subjects/Keywords: Homeopathy; Cholesterol

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Hillermann, R. (1996). Hypercholesterolemia : the role of homoeopathy. (Thesis). Durban University of Technology. Retrieved from http://hdl.handle.net/10321/1855

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):

Hillermann, Roland. “Hypercholesterolemia : the role of homoeopathy.” 1996. Thesis, Durban University of Technology. Accessed March 05, 2021. http://hdl.handle.net/10321/1855.

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

MLA Handbook (7^th Edition):

Hillermann, Roland. “Hypercholesterolemia : the role of homoeopathy.” 1996. Web. 05 Mar 2021.

Vancouver:

Hillermann R. Hypercholesterolemia : the role of homoeopathy. [Internet] [Thesis]. Durban University of Technology; 1996. [cited 2021 Mar 05]. Available from: http://hdl.handle.net/10321/1855.

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

Council of Science Editors:

Hillermann R. Hypercholesterolemia : the role of homoeopathy. [Thesis]. Durban University of Technology; 1996. Available from: http://hdl.handle.net/10321/1855

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

Oregon State University

16. Elzoheiry, Azza A. The metabolic fate of lipoprotein cholesterol in isolated rat liver parenchymal cells.

Degree: PhD, Foods and Nutrition, 1984, Oregon State University

URL: http://hdl.handle.net/1957/27150

► The metabolic fate of cholesterol delivered to rat hepatocytes by rat plasma lipoproteins was determined. Binding and degradation of rat low and high density lipoproteins… (more)

▼ The metabolic fate of cholesterol delivered to rat hepatocytes by rat plasma lipoproteins was determined. Binding and degradation of rat low and high density lipoproteins (LDL and HDL) in rat hepatocytes were studied. ¹²⁵I-labelled LDL and HDL were incubated with cells in the presence of varying concentrations of unlabelled lipoproteins for two hours at 37°C. The amount of ¹²⁵I-LDL and ¹²⁵I-HDL binding and degradation decreased by increasing concentrations of respective unlabelled lipoproteins. The presence of 50-fold excess of unlabelled LDL or HDL resulted in a reduction of ¹²⁵I-LDL and ¹²⁵I-HDL bindings by 66-82%, and degradations by 63-88%, respectively. Equilibrium dissociation constants (K [subscript d]) determined by Scatchard analysis for HDL (.15 x 10⁻⁸M) and LDL (1.04 x 10⁻⁸M) revealed that HDL have approximately 7-fold higher binding affinity for receptors on cell surface than LDL. Specific use of LDL and HDL-cholesterol for bile acid synthesis by rat hepatocytes was investigated. When LDL and HDL labelled with ³H-LDL cholesterol was transformed to bile acids mostly as lithocholic, chenodeoxy and deoxycholic acids. A technique developed for isolation of hepatocytes from rat liver was described. Once isolated by the technique most cells retained their microscopic structural integrity, and excluded trypan blue. The viability was 93%, which decreased to 86% after four hours of incubation. The presented data demonstrated that both HDL and LDL bind to specific receptors on hepatocytes and undergo proteolytic degradation in rats. The study also showed that the binding affinity of HDL to hepatic receptors was much greater than that of LDL but in total binding LDL uptake was four times greater than HDL, suggesting the presence of two specific binding sites for HDL and LDL. The first direct evidence for the preferential utilization of HDL-cholesterol for biosynthesis of bile acids in vivo is presented. This finding is compatible with the current concept of HDL as the protective lipoprotein against developing coronary heart disease. Advisors/Committee Members: Oh, Suk Y. (advisor), Maksud, Michael G. (committee member).

Subjects/Keywords: Cholesterol – Metabolism

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Elzoheiry, A. A. (1984). The metabolic fate of lipoprotein cholesterol in isolated rat liver parenchymal cells. (Doctoral Dissertation). Oregon State University. Retrieved from http://hdl.handle.net/1957/27150

Chicago Manual of Style (16^th Edition):

Elzoheiry, Azza A. “The metabolic fate of lipoprotein cholesterol in isolated rat liver parenchymal cells.” 1984. Doctoral Dissertation, Oregon State University. Accessed March 05, 2021. http://hdl.handle.net/1957/27150.

MLA Handbook (7^th Edition):

Elzoheiry, Azza A. “The metabolic fate of lipoprotein cholesterol in isolated rat liver parenchymal cells.” 1984. Web. 05 Mar 2021.

Vancouver:

Elzoheiry AA. The metabolic fate of lipoprotein cholesterol in isolated rat liver parenchymal cells. [Internet] [Doctoral dissertation]. Oregon State University; 1984. [cited 2021 Mar 05]. Available from: http://hdl.handle.net/1957/27150.

Council of Science Editors:

Elzoheiry AA. The metabolic fate of lipoprotein cholesterol in isolated rat liver parenchymal cells. [Doctoral Dissertation]. Oregon State University; 1984. Available from: http://hdl.handle.net/1957/27150

Dalhousie University

17. Robinson, Carolyn-Ann. The effect of phosphorylation on oxysterol-binding protein (OSBP) sterol binding activity.

Degree: MS, Department of Biochemistry & Molecular Biology, 2012, Dalhousie University

URL: http://hdl.handle.net/10222/15489

► Oxysterol binding protein (OSBP) binds 25-hydroxycholesterol (25OH) and cholesterol, which regulates PH and FFAT domain interaction with the Golgi apparatus and endoplasmic reticulum, respectively. Adjacent… (more)

Subjects/Keywords: cholesterol; oxysterol; sterol transport; phosphorylation

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Robinson, C. (2012). The effect of phosphorylation on oxysterol-binding protein (OSBP) sterol binding activity. (Masters Thesis). Dalhousie University. Retrieved from http://hdl.handle.net/10222/15489

Chicago Manual of Style (16^th Edition):

Robinson, Carolyn-Ann. “The effect of phosphorylation on oxysterol-binding protein (OSBP) sterol binding activity.” 2012. Masters Thesis, Dalhousie University. Accessed March 05, 2021. http://hdl.handle.net/10222/15489.

MLA Handbook (7^th Edition):

Robinson, Carolyn-Ann. “The effect of phosphorylation on oxysterol-binding protein (OSBP) sterol binding activity.” 2012. Web. 05 Mar 2021.

Vancouver:

Robinson C. The effect of phosphorylation on oxysterol-binding protein (OSBP) sterol binding activity. [Internet] [Masters thesis]. Dalhousie University; 2012. [cited 2021 Mar 05]. Available from: http://hdl.handle.net/10222/15489.

Council of Science Editors:

Robinson C. The effect of phosphorylation on oxysterol-binding protein (OSBP) sterol binding activity. [Masters Thesis]. Dalhousie University; 2012. Available from: http://hdl.handle.net/10222/15489

UCLA

18. Sallam, Tamer. Characterization of Novel Liver X Receptor Regulatory Circuits.

Degree: Molec, Cell, & Integ Physiology, 2014, UCLA

URL: http://www.escholarship.org/uc/item/1608s1wp

► The liver X receptors (LXRs) are members of the nuclear receptors superfamily of transcription factors. Multiple lines of evidence established LXRs as crucial regulators of… (more)

Subjects/Keywords: Medicine; Cholesterol; Nuclear Receptor

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Sallam, T. (2014). Characterization of Novel Liver X Receptor Regulatory Circuits. (Thesis). UCLA. Retrieved from http://www.escholarship.org/uc/item/1608s1wp

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):

Sallam, Tamer. “Characterization of Novel Liver X Receptor Regulatory Circuits.” 2014. Thesis, UCLA. Accessed March 05, 2021. http://www.escholarship.org/uc/item/1608s1wp.

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

MLA Handbook (7^th Edition):

Sallam, Tamer. “Characterization of Novel Liver X Receptor Regulatory Circuits.” 2014. Web. 05 Mar 2021.

Vancouver:

Sallam T. Characterization of Novel Liver X Receptor Regulatory Circuits. [Internet] [Thesis]. UCLA; 2014. [cited 2021 Mar 05]. Available from: http://www.escholarship.org/uc/item/1608s1wp.

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

Council of Science Editors:

Sallam T. Characterization of Novel Liver X Receptor Regulatory Circuits. [Thesis]. UCLA; 2014. Available from: http://www.escholarship.org/uc/item/1608s1wp

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

University of Rochester

19. Thach, Chia Tha. Modulation of Cellular Signaling Upon Cholesterol Depletion and Nanoparticle Exposure.

Degree: PhD, 2013, University of Rochester

URL: http://hdl.handle.net/1802/26782

► With the increase in the production of engineered nanomaterials, researchers are discovering that there is a direct impact of these nanomaterials on the cell membrane.… (more)

▼ With the increase in the production of engineered nanomaterials, researchers are discovering that there is a direct impact of these nanomaterials on the cell membrane. The cell membrane contains many different types of lipids and proteins responsible for numerous cell functions. The assembly of cholesterols and sphingolipids within the membrane forms microdomain structures known as lipid rafts. Lipid rafts embed many receptors that are involved in regulating cytokine production. Studies have shown that engineered nanomaterials can erode the membrane and create holes. We hypothesized that nanoparticles can interfere with cellular signaling by inhibiting the assembly of receptors on the lipid rafts. Using alveolar epithelial cells containing an Interleukin-8 promoter Luciferase construct, we were able to evaluate the ability of charged nanoparticles to alter cytokine gene expression elicited by a secondary stimulus. We exposed cells to charged nanoparticles, followed with stimulation of the IL-8 promoter with the proinflammatory cytokine tumor necrosis factor-α (TNF-α). We then used endocytic inhibitors and cholesterol depletors to determine if the nanoparticles rely on endocytosis and membrane cholesterol to alter the TNF-α stimulated IL-8 promoter. We found that cationic nanoparticles were able to reduce the IL-8 promoter activity despite exposure to the endocytic inhibitors. When membrane cholesterol was removed from the cells, all the effects of the nanoparticles disappeared. Furthermore, cationic nanoparticles disrupt signaling by inducing receptor aggregation and reducing NF-κB translocation. These effects were cholesterol dependent. Our studies demonstrated that not only can nanoparticles induce cytotoxicity, they can have the potential to interfere with cellular signaling. Since particles are now being considered for applications in both consumer and medical products, it is important to evaluate whether the particles may possess these biological effects.

Subjects/Keywords: Nanoparticles; Cellular signaling; Chemokines; Cholesterol

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Thach, C. T. (2013). Modulation of Cellular Signaling Upon Cholesterol Depletion and Nanoparticle Exposure. (Doctoral Dissertation). University of Rochester. Retrieved from http://hdl.handle.net/1802/26782

Chicago Manual of Style (16^th Edition):

Thach, Chia Tha. “Modulation of Cellular Signaling Upon Cholesterol Depletion and Nanoparticle Exposure.” 2013. Doctoral Dissertation, University of Rochester. Accessed March 05, 2021. http://hdl.handle.net/1802/26782.

MLA Handbook (7^th Edition):

Thach, Chia Tha. “Modulation of Cellular Signaling Upon Cholesterol Depletion and Nanoparticle Exposure.” 2013. Web. 05 Mar 2021.

Vancouver:

Thach CT. Modulation of Cellular Signaling Upon Cholesterol Depletion and Nanoparticle Exposure. [Internet] [Doctoral dissertation]. University of Rochester; 2013. [cited 2021 Mar 05]. Available from: http://hdl.handle.net/1802/26782.

Council of Science Editors:

Thach CT. Modulation of Cellular Signaling Upon Cholesterol Depletion and Nanoparticle Exposure. [Doctoral Dissertation]. University of Rochester; 2013. Available from: http://hdl.handle.net/1802/26782

University of Alberta

20. Gao, Xia. Biochemical Characterization of ATP-Binding Cassette Transporter G1 Mediated Cholesterol Efflux.

Degree: MS, Medical Sciences-Paediatrics, 2012, University of Alberta

URL: https://era.library.ualberta.ca/files/bv73c0887

► ABCG1 mediates cholesterol efflux onto lipidated apolipoprotein A-I and plays an important role in macrophage reverse cholesterol transport, thereby preventing atherosclerosis. However, how ABCG1 mediates… (more)

Subjects/Keywords: ABCG1; cysteine; palmitoylation; cholesterol

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Gao, X. (2012). Biochemical Characterization of ATP-Binding Cassette Transporter G1 Mediated Cholesterol Efflux. (Masters Thesis). University of Alberta. Retrieved from https://era.library.ualberta.ca/files/bv73c0887

Chicago Manual of Style (16^th Edition):

Gao, Xia. “Biochemical Characterization of ATP-Binding Cassette Transporter G1 Mediated Cholesterol Efflux.” 2012. Masters Thesis, University of Alberta. Accessed March 05, 2021. https://era.library.ualberta.ca/files/bv73c0887.

MLA Handbook (7^th Edition):

Gao, Xia. “Biochemical Characterization of ATP-Binding Cassette Transporter G1 Mediated Cholesterol Efflux.” 2012. Web. 05 Mar 2021.

Vancouver:

Gao X. Biochemical Characterization of ATP-Binding Cassette Transporter G1 Mediated Cholesterol Efflux. [Internet] [Masters thesis]. University of Alberta; 2012. [cited 2021 Mar 05]. Available from: https://era.library.ualberta.ca/files/bv73c0887.

Council of Science Editors:

Gao X. Biochemical Characterization of ATP-Binding Cassette Transporter G1 Mediated Cholesterol Efflux. [Masters Thesis]. University of Alberta; 2012. Available from: https://era.library.ualberta.ca/files/bv73c0887

21. Gupta, Sanjay. To test the reprodusibility of changes induced in lipid lipoprotein profile after high cholesterol fat diet in healthy individuals;.

Degree: Medicine, 1993, Bundelkhand University

URL: http://shodhganga.inflibnet.ac.in/handle/10603/19873

To test the reprodusibility of changes induced in lipid-lipoprotein profile after high cholesterol fat diet in healthy individuals newline

Bibliography p.126-135, Appendix p.136-140

Advisors/Committee Members: Arora,R C and Agarwal, Navnit and Arora, Sunita.

Subjects/Keywords: lipid-lipoprotein; cholesterol; Health

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Gupta, S. (1993). To test the reprodusibility of changes induced in lipid lipoprotein profile after high cholesterol fat diet in healthy individuals;. (Thesis). Bundelkhand University. Retrieved from http://shodhganga.inflibnet.ac.in/handle/10603/19873

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):

Gupta, Sanjay. “To test the reprodusibility of changes induced in lipid lipoprotein profile after high cholesterol fat diet in healthy individuals;.” 1993. Thesis, Bundelkhand University. Accessed March 05, 2021. http://shodhganga.inflibnet.ac.in/handle/10603/19873.

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

MLA Handbook (7^th Edition):

Gupta, Sanjay. “To test the reprodusibility of changes induced in lipid lipoprotein profile after high cholesterol fat diet in healthy individuals;.” 1993. Web. 05 Mar 2021.

Vancouver:

Gupta S. To test the reprodusibility of changes induced in lipid lipoprotein profile after high cholesterol fat diet in healthy individuals;. [Internet] [Thesis]. Bundelkhand University; 1993. [cited 2021 Mar 05]. Available from: http://shodhganga.inflibnet.ac.in/handle/10603/19873.

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

Council of Science Editors:

Gupta S. To test the reprodusibility of changes induced in lipid lipoprotein profile after high cholesterol fat diet in healthy individuals;. [Thesis]. Bundelkhand University; 1993. Available from: http://shodhganga.inflibnet.ac.in/handle/10603/19873

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

22. Suri, Ashok Kumar. To test the reprodusibility of changes induced in lipid lipoprotein profile after high cholesterol fat diet in healthy individuals;.

Degree: Medicine, 2014, Bundelkhand University

URL: http://shodhganga.inflibnet.ac.in/handle/10603/19886

To test the reprodusibility of changes induced in lipid-lipoprotein profile after high cholesterol fat diet in healthy individuals newline

Bibliography p.84-92

Advisors/Committee Members: Arora,R C and Agarwal, Navnit and Arora, Sunita.

Subjects/Keywords: lipid-lipoprotein; Health; cholesterol

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Suri, A. K. (2014). To test the reprodusibility of changes induced in lipid lipoprotein profile after high cholesterol fat diet in healthy individuals;. (Thesis). Bundelkhand University. Retrieved from http://shodhganga.inflibnet.ac.in/handle/10603/19886

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):

Suri, Ashok Kumar. “To test the reprodusibility of changes induced in lipid lipoprotein profile after high cholesterol fat diet in healthy individuals;.” 2014. Thesis, Bundelkhand University. Accessed March 05, 2021. http://shodhganga.inflibnet.ac.in/handle/10603/19886.

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

MLA Handbook (7^th Edition):

Suri, Ashok Kumar. “To test the reprodusibility of changes induced in lipid lipoprotein profile after high cholesterol fat diet in healthy individuals;.” 2014. Web. 05 Mar 2021.

Vancouver:

Suri AK. To test the reprodusibility of changes induced in lipid lipoprotein profile after high cholesterol fat diet in healthy individuals;. [Internet] [Thesis]. Bundelkhand University; 2014. [cited 2021 Mar 05]. Available from: http://shodhganga.inflibnet.ac.in/handle/10603/19886.

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

Council of Science Editors:

Suri AK. To test the reprodusibility of changes induced in lipid lipoprotein profile after high cholesterol fat diet in healthy individuals;. [Thesis]. Bundelkhand University; 2014. Available from: http://shodhganga.inflibnet.ac.in/handle/10603/19886

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

Texas A&M University

23. Lee, Teak Veng. Dietary Cholesterol and Resistance Training as Countermeasures to Accelerated Muscle Loss.

Degree: PhD, Kinesiology, 2015, Texas A&M University

URL: http://hdl.handle.net/1969.1/156299

► Cholesterol plays an important role in physiology, serving as a membrane constituent and steroid hormone precursor. Recently, cholesterol has also been associated with skeletal muscle… (more)

▼ Cholesterol plays an important role in physiology, serving as a membrane constituent and steroid hormone precursor. Recently, cholesterol has also been associated with skeletal muscle homeostasis, leading to the purpose of this research, which was to examine the role of cholesterol metabolism during perturbations of skeletal muscle homeostasis. We evaluated skeletal muscle responses and proteins involved in cholesterol metabolism [sterol regulatory element-binding protein-2 (SREBP-2) and low-density lipoprotein-receptor (LDL-R)] under conditions of unloading, exercise and dietary cholesterol (D-CL) administration. We hypothesized that skeletal muscle mass, fractional synthesis rates (FSR), SREBP-2, and LDL-R would be lower in unloaded muscle while exercise and D-CL would have a positive effect. The first study examined the effect of hindlimb unloading (HU) on muscle mass, SREBP-2, and LDL-R. HU animals showed lower muscle mass and a trend towards lower gastrocnemius SREBP-2 than cage controls (CC). The second study examined the effect of D-CL and resistance training (RT) on lean mass, FSR, SREBP-2, and LDL-R in ambulatory rats. Unexpectedly, rats performing exercise without added resistance [(RT-Control (RTC)] had greater lean mass responses than the RT groups. However, RT groups had higher plantaris to body mass ratio and FSR than RTC (plantaris FSR only) and CC (both variables) animals. RT plus high D-CL administration resulted in greater plantaris FSR than the RT group consuming normal D-CL. Quadriceps SREBP-2 trended towards an increase in response to RT. The third study investigated the effect of D-CL and RT on muscle mass, FSR, SREBP-2, and LDL-R in the context of HU. HU and HU rats performing RT had lower muscle mass than CC. HU rats showed higher liver mature LDL-R than CC but showed a trend towards lower gastrocnemius SREBP-2 than CC. There was no difference in FSR among activity or D-CL groups. These studies show evidence of shifts in content of proteins related to cholesterol metabolism and muscle FSR when muscle activity is manipulated from RT to complete unloading. However, effects such as elevated FSR with RT and high D-CL were not consistent throughout the studies, leaving doubt of the effect of activity on cholesterol metabolism. Advisors/Committee Members: Riechman, Steven E (advisor), Fluckey, James D (committee member), Smith, Stephen B (committee member), Woodman, Christopher R (committee member).

Subjects/Keywords: Dietary Cholesterol; Resistance Training; Unloading

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Lee, T. V. (2015). Dietary Cholesterol and Resistance Training as Countermeasures to Accelerated Muscle Loss. (Doctoral Dissertation). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/156299

Chicago Manual of Style (16^th Edition):

Lee, Teak Veng. “Dietary Cholesterol and Resistance Training as Countermeasures to Accelerated Muscle Loss.” 2015. Doctoral Dissertation, Texas A&M University. Accessed March 05, 2021. http://hdl.handle.net/1969.1/156299.

MLA Handbook (7^th Edition):

Lee, Teak Veng. “Dietary Cholesterol and Resistance Training as Countermeasures to Accelerated Muscle Loss.” 2015. Web. 05 Mar 2021.

Vancouver:

Lee TV. Dietary Cholesterol and Resistance Training as Countermeasures to Accelerated Muscle Loss. [Internet] [Doctoral dissertation]. Texas A&M University; 2015. [cited 2021 Mar 05]. Available from: http://hdl.handle.net/1969.1/156299.

Council of Science Editors:

Lee TV. Dietary Cholesterol and Resistance Training as Countermeasures to Accelerated Muscle Loss. [Doctoral Dissertation]. Texas A&M University; 2015. Available from: http://hdl.handle.net/1969.1/156299

Texas A&M University

24. Tan, Qiulin. Inhibition of cholesterol biosynthesis under hypoxia.

Degree: MS, Toxicology, 2006, Texas A&M University

URL: http://hdl.handle.net/1969.1/3101

► Oxygen balance is very important and tightly regulated in mammals. Under hypoxia, hypoxia inducible factor 1(HIF-1) dimerizes with hypoxia inducible factor 1± (HIF-) and activates… (more)

Subjects/Keywords: cholesterol; hypoxia

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Tan, Q. (2006). Inhibition of cholesterol biosynthesis under hypoxia. (Masters Thesis). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/3101

Chicago Manual of Style (16^th Edition):

Tan, Qiulin. “Inhibition of cholesterol biosynthesis under hypoxia.” 2006. Masters Thesis, Texas A&M University. Accessed March 05, 2021. http://hdl.handle.net/1969.1/3101.

MLA Handbook (7^th Edition):

Tan, Qiulin. “Inhibition of cholesterol biosynthesis under hypoxia.” 2006. Web. 05 Mar 2021.

Vancouver:

Tan Q. Inhibition of cholesterol biosynthesis under hypoxia. [Internet] [Masters thesis]. Texas A&M University; 2006. [cited 2021 Mar 05]. Available from: http://hdl.handle.net/1969.1/3101.

Council of Science Editors:

Tan Q. Inhibition of cholesterol biosynthesis under hypoxia. [Masters Thesis]. Texas A&M University; 2006. Available from: http://hdl.handle.net/1969.1/3101

Penn State University

25. Sterling, Nicholas William. Tracking and Understanding Parkinson’s Disease Progression Through the Lens of Quantitative Magnetic Resonance Imaging.

Degree: 2016, Penn State University

URL: https://submit-etda.libraries.psu.edu/catalog/27705

► Parkinson's disease (PD) is an age-related neurodegenerative disorder that typically begins with prodromal non-motor symptoms (such as loss of olfaction and sleep dysfunction) and relatively… (more)

▼ Parkinson's disease (PD) is an age-related neurodegenerative disorder that typically begins with prodromal non-motor symptoms (such as loss of olfaction and sleep dysfunction) and relatively subtle motor changes (such as reduced arm swing). The current clinical diagnosis is based on the presence of classic motor symptoms such as bradykinesia, rigidity, and tremor at rest. As PD progresses, many patients develop severe motor (including gait and postural changes) and cognitive disability which ultimately lead to the loss of independence. The current treatment of PD is mainly based on management of symptoms, and there is no known therapy that can halt or reverse the progression of neuropathology. As life expectancies increase globally, PD is expected to double in prevalence over the next 25 years. Neuroprotective strategies that can modify the course of the disease, therefore, are critically needed. Past efforts to identify, understand and evaluate potentially neuroprotective treatments for PD, however, have been hindered by the lack of cellular or animal model that exactly mimic human disease, and the lack of objective and reliable in vivo markers of PD-related pathology in humans. The goals of this research were to identify structural magnetic resonance imaging (MRI) markers of PD progression and utilize these markers to understand the factors that may influence the progression of PD. After providing an introduction that underscores the importance of my research goals (Section I) and the strengths and limitations of the approaches that I used (versus the current art of the field), I discuss in Section II the use of structural magnetic resonance imaging to explore gray matter changes in various stages of PD. Striatal atrophy was found to be related to early changes in PD, and cortical atrophy (particularly loss of cortical folding) was found to be associated with worsening clinical symptoms and longer disease duration. These findings were consistent with the known pathologic trajectory of PD, where PD-related pathology affects brainstem and nigrostriatal structures well before the time of diagnosis, and Lewy pathology subsequently progresses in an ascending fashion to later involve higher-level cortex structures. In Section III, I examine the relationships between cortical gray matter atrophy and changes in subcortical white matter. Poorer subcortical white matter diffusion characteristics were found to be associated with cortical atrophy in PD, and opposite associations were found in control subjects. These data provided the foundation for Section IV, where I utilized these newly described cortical imaging markers, along with changes in cognitive function, to explore the role of plasma cholesterol in PD. The link between plasma low density lipoprotein (LDL) cholesterol and PD had been pioneered by my research mentor’s laboratory, and the studies described in this dissertation are the first attempts to associate LDL-cholesterol with specific in vivo cortical changes in PD. This relationship, if proven, may be a… Advisors/Committee Members: Xuemei Huang, Dissertation Advisor/Co-Advisor, Xuemei Huang, Committee Chair/Co-Chair, Thomas Allen Lloyd, Committee Member, Diane M Thiboutot, Committee Member, Ming Wang, Committee Member, Martin Styner, Special Member.

Subjects/Keywords: Parkinson's disease; cholesterol; imaging; neuroprotection

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Sterling, N. W. (2016). Tracking and Understanding Parkinson’s Disease Progression Through the Lens of Quantitative Magnetic Resonance Imaging. (Thesis). Penn State University. Retrieved from https://submit-etda.libraries.psu.edu/catalog/27705

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):

Sterling, Nicholas William. “Tracking and Understanding Parkinson’s Disease Progression Through the Lens of Quantitative Magnetic Resonance Imaging.” 2016. Thesis, Penn State University. Accessed March 05, 2021. https://submit-etda.libraries.psu.edu/catalog/27705.

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

MLA Handbook (7^th Edition):

Sterling, Nicholas William. “Tracking and Understanding Parkinson’s Disease Progression Through the Lens of Quantitative Magnetic Resonance Imaging.” 2016. Web. 05 Mar 2021.

Vancouver:

Sterling NW. Tracking and Understanding Parkinson’s Disease Progression Through the Lens of Quantitative Magnetic Resonance Imaging. [Internet] [Thesis]. Penn State University; 2016. [cited 2021 Mar 05]. Available from: https://submit-etda.libraries.psu.edu/catalog/27705.

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

Council of Science Editors:

Sterling NW. Tracking and Understanding Parkinson’s Disease Progression Through the Lens of Quantitative Magnetic Resonance Imaging. [Thesis]. Penn State University; 2016. Available from: https://submit-etda.libraries.psu.edu/catalog/27705

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

Texas Tech University

26. Hein, Matthew. Measurement of the Maximum Cholesterol Solubility in Binary Lipid Bilayers Containing POPE and POPC Via Light Scattering Method.

Degree: MS, Physics - Applied Physics, 2016, Texas Tech University

URL: http://hdl.handle.net/2346/82259

► Cholesterol is a significant component of animal cell membranes, and its presence has the effects of not only adding rigidity to the lipid bilayer, but… (more)

Subjects/Keywords: cholesterol; phospholipid; POPE; POPC

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Hein, M. (2016). Measurement of the Maximum Cholesterol Solubility in Binary Lipid Bilayers Containing POPE and POPC Via Light Scattering Method. (Masters Thesis). Texas Tech University. Retrieved from http://hdl.handle.net/2346/82259

Chicago Manual of Style (16^th Edition):

Hein, Matthew. “Measurement of the Maximum Cholesterol Solubility in Binary Lipid Bilayers Containing POPE and POPC Via Light Scattering Method.” 2016. Masters Thesis, Texas Tech University. Accessed March 05, 2021. http://hdl.handle.net/2346/82259.

MLA Handbook (7^th Edition):

Hein, Matthew. “Measurement of the Maximum Cholesterol Solubility in Binary Lipid Bilayers Containing POPE and POPC Via Light Scattering Method.” 2016. Web. 05 Mar 2021.

Vancouver:

Hein M. Measurement of the Maximum Cholesterol Solubility in Binary Lipid Bilayers Containing POPE and POPC Via Light Scattering Method. [Internet] [Masters thesis]. Texas Tech University; 2016. [cited 2021 Mar 05]. Available from: http://hdl.handle.net/2346/82259.

Council of Science Editors:

Hein M. Measurement of the Maximum Cholesterol Solubility in Binary Lipid Bilayers Containing POPE and POPC Via Light Scattering Method. [Masters Thesis]. Texas Tech University; 2016. Available from: http://hdl.handle.net/2346/82259

University of Toronto

27. Hager, Lauren. Lecithin:Cholesterol Acyltransferase Deficiency Protects against Cholesterol-induced Hepatic Endoplasmic Reticulum Stress in Mice.

Degree: 2011, University of Toronto

URL: http://hdl.handle.net/1807/30620

►

Our laboratory has recently reported that lecithin:cholesterol acyltransferase (LCAT) deficient mice are hypersensitive to insulin and resistant to diet-induced obesity, particularly in the LDL receptor… (more)

Subjects/Keywords: cholesterol; ER stress; 0433

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Hager, L. (2011). Lecithin:Cholesterol Acyltransferase Deficiency Protects against Cholesterol-induced Hepatic Endoplasmic Reticulum Stress in Mice. (Masters Thesis). University of Toronto. Retrieved from http://hdl.handle.net/1807/30620

Chicago Manual of Style (16^th Edition):

Hager, Lauren. “Lecithin:Cholesterol Acyltransferase Deficiency Protects against Cholesterol-induced Hepatic Endoplasmic Reticulum Stress in Mice.” 2011. Masters Thesis, University of Toronto. Accessed March 05, 2021. http://hdl.handle.net/1807/30620.

MLA Handbook (7^th Edition):

Hager, Lauren. “Lecithin:Cholesterol Acyltransferase Deficiency Protects against Cholesterol-induced Hepatic Endoplasmic Reticulum Stress in Mice.” 2011. Web. 05 Mar 2021.

Vancouver:

Hager L. Lecithin:Cholesterol Acyltransferase Deficiency Protects against Cholesterol-induced Hepatic Endoplasmic Reticulum Stress in Mice. [Internet] [Masters thesis]. University of Toronto; 2011. [cited 2021 Mar 05]. Available from: http://hdl.handle.net/1807/30620.

Council of Science Editors:

Hager L. Lecithin:Cholesterol Acyltransferase Deficiency Protects against Cholesterol-induced Hepatic Endoplasmic Reticulum Stress in Mice. [Masters Thesis]. University of Toronto; 2011. Available from: http://hdl.handle.net/1807/30620

University of Texas Southwestern Medical Center

28. Gay, Austin Tyler. Protein Sensors for Membrane Cholesterol.

Degree: 2016, University of Texas Southwestern Medical Center

URL: http://hdl.handle.net/2152.5/5722

► The cholesterol content of animal cells is maintained within narrow limits. This regulation applies not only to the overall cholesterol level in the cell, but… (more)

Subjects/Keywords: Bacterial Toxins; Cholesterol; Lipid Bilayers

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Gay, A. T. (2016). Protein Sensors for Membrane Cholesterol. (Thesis). University of Texas Southwestern Medical Center. Retrieved from http://hdl.handle.net/2152.5/5722

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):

Gay, Austin Tyler. “Protein Sensors for Membrane Cholesterol.” 2016. Thesis, University of Texas Southwestern Medical Center. Accessed March 05, 2021. http://hdl.handle.net/2152.5/5722.

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

MLA Handbook (7^th Edition):

Gay, Austin Tyler. “Protein Sensors for Membrane Cholesterol.” 2016. Web. 05 Mar 2021.

Vancouver:

Gay AT. Protein Sensors for Membrane Cholesterol. [Internet] [Thesis]. University of Texas Southwestern Medical Center; 2016. [cited 2021 Mar 05]. Available from: http://hdl.handle.net/2152.5/5722.

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

Council of Science Editors:

Gay AT. Protein Sensors for Membrane Cholesterol. [Thesis]. University of Texas Southwestern Medical Center; 2016. Available from: http://hdl.handle.net/2152.5/5722

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

University of Texas Southwestern Medical Center

29. Wang, Michael Leechun. The Hydrophobic Handoff Between NPC2 and the N-Terminal Domain of NPC1 in the Export of Cholesterol from Lysosomes.

Degree: 2013, University of Texas Southwestern Medical Center

URL: http://hdl.handle.net/2152.5/1708

► Low density lipoproteins (LDL) and related plasma lipoproteins deliver cholesterol to cells by receptor-mediated endocytosis. The lipoprotein is degraded in late endosomes and lysosomes where… (more)

▼ Low density lipoproteins (LDL) and related plasma lipoproteins deliver cholesterol to cells by receptor-mediated endocytosis. The lipoprotein is degraded in late endosomes and lysosomes where its cholesterol is released. Egress of cholesterol from late endosomes and lysosomes (hereafter referred to as lysosomes) requires two proteins: Niemann-Pick C2 (NPC2), a soluble protein of 132 amino acids; and NPC1, an intrinsic membrane protein of 1278 amino acids and 13 postulated membrane-spanning helices that span the lysosomal membrane. Recessive loss-of-function mutations in either NPC2 or NPC1 produce NPC disease, which causes death in childhood owing to cholesterol accumulation in lysosomes of liver, brain, and lung. Consistent with their cholesterol export role, NPC2 and NPC1 both bind cholesterol. The cholesterol binding site on NPC1 is located in the NH2-terminal domain (NTD), which projects into the lysosomal lumen. This domain, designated NPC1(NTD), can be expressed in vitro as a soluble protein of 240 amino acids that retains cholesterol binding activity. This thesis studies NPC2 and NPC1(NTD) in detail as summarized below. Two major differences exist between the cholesterol binding of NPC2 and NPC1(NTD). 1) Competitive binding studies and crystal structures indicate that the two proteins bind cholesterol in opposite orientations. NPC2 binds the iso-octyl side chain, leaving the 3ß hydroxyl exposed, whereas NPC1 binds the 3ß-hydroxyl, leaving the side chain partially exposed. 2) Kinetic studies of cholesterol binding reveal that NPC2 binds and releases cholesterol rapidly (half-time < 2 min at 4 °C), while NPC1(NTD) binds cholesterol very slowly (half-time > 2 hr at 4 °C). Its rapid cholesterol binding allows NPC2 to transfer cholesterol to and from liposomes. Unlike NPC2, NPC1(NTD) cannot rapidly transfer its bound cholesterol to liposomes. However, NPC1(NTD) can accomplish this delivery when NPC2 is present. Furthermore, cholesterol binding to NPC1(NTD) is accelerated by >15-fold when the sterol is first bound to NPC2 and then transferred to NPC1(NTD). These data led us to advance a model in which NPC2 can mediate bi-directional transfer of cholesterol to or from NPC1(NTD). In cells, we envision that NPC2 accepts cholesterol in the lysosomal lumen and transports it to membrane-bound NPC1, thus accounting for the requirement for both proteins for lysosomal cholesterol export. Amino acid residues important or binding or transfer of cholesterol on NPC2 and NPC1(NTD) were identified through alanine scan mutagenesis. For both NPC2 and NPC1(NTD), residues that decreased binding mapped to areas surrounding the binding pockets on the crystal structures; residues that decreased transfer, but not binding, mapped to discrete surface patches near the opening of the binding pockets. These surface patches may be sites where the two proteins interact to transfer cholesterol. The most severe mutations disrupting binding were P120S for NPC2 and P202A/F203A for NPC1(NTD); and those that disrupted transfer were V81D… Advisors/Committee Members: Brown, Michael S., Goldstein, Joseph L., Thomas, Philip J., Roth, Michael G., Hofmann, Sandra L., Liang, Guosheng.

Subjects/Keywords: Carrier Proteins; Cholesterol; Glycoproteins; Lysosomes

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Wang, M. L. (2013). The Hydrophobic Handoff Between NPC2 and the N-Terminal Domain of NPC1 in the Export of Cholesterol from Lysosomes. (Thesis). University of Texas Southwestern Medical Center. Retrieved from http://hdl.handle.net/2152.5/1708

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):

Wang, Michael Leechun. “The Hydrophobic Handoff Between NPC2 and the N-Terminal Domain of NPC1 in the Export of Cholesterol from Lysosomes.” 2013. Thesis, University of Texas Southwestern Medical Center. Accessed March 05, 2021. http://hdl.handle.net/2152.5/1708.

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

MLA Handbook (7^th Edition):

Wang, Michael Leechun. “The Hydrophobic Handoff Between NPC2 and the N-Terminal Domain of NPC1 in the Export of Cholesterol from Lysosomes.” 2013. Web. 05 Mar 2021.

Vancouver:

Wang ML. The Hydrophobic Handoff Between NPC2 and the N-Terminal Domain of NPC1 in the Export of Cholesterol from Lysosomes. [Internet] [Thesis]. University of Texas Southwestern Medical Center; 2013. [cited 2021 Mar 05]. Available from: http://hdl.handle.net/2152.5/1708.

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

Council of Science Editors:

Wang ML. The Hydrophobic Handoff Between NPC2 and the N-Terminal Domain of NPC1 in the Export of Cholesterol from Lysosomes. [Thesis]. University of Texas Southwestern Medical Center; 2013. Available from: http://hdl.handle.net/2152.5/1708

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

University of Texas Southwestern Medical Center

30. Farooqi, Midhat Saleem. The Role of Insig-Mediated Cholesterol Homeostasis in Mouse Hair Development.

Degree: 2012, University of Texas Southwestern Medical Center

URL: http://hdl.handle.net/2152.5/1108

► Insig-1 and Insig-2, two very homologous proteins, are indispensable for feedback inhibition of cholesterol biosynthesis. Mice null for both Insigs drastically overproduce cholesterol and its… (more)

Subjects/Keywords: Membrane Proteins; Hair Disease; Cholesterol

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Farooqi, M. S. (2012). The Role of Insig-Mediated Cholesterol Homeostasis in Mouse Hair Development. (Thesis). University of Texas Southwestern Medical Center. Retrieved from http://hdl.handle.net/2152.5/1108

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):

Farooqi, Midhat Saleem. “The Role of Insig-Mediated Cholesterol Homeostasis in Mouse Hair Development.” 2012. Thesis, University of Texas Southwestern Medical Center. Accessed March 05, 2021. http://hdl.handle.net/2152.5/1108.

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

MLA Handbook (7^th Edition):

Farooqi, Midhat Saleem. “The Role of Insig-Mediated Cholesterol Homeostasis in Mouse Hair Development.” 2012. Web. 05 Mar 2021.

Vancouver:

Farooqi MS. The Role of Insig-Mediated Cholesterol Homeostasis in Mouse Hair Development. [Internet] [Thesis]. University of Texas Southwestern Medical Center; 2012. [cited 2021 Mar 05]. Available from: http://hdl.handle.net/2152.5/1108.

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

Council of Science Editors:

Farooqi MS. The Role of Insig-Mediated Cholesterol Homeostasis in Mouse Hair Development. [Thesis]. University of Texas Southwestern Medical Center; 2012. Available from: http://hdl.handle.net/2152.5/1108

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

		in
And / Or
		in
And / Or
		in
And / Or
		in

Open Access Theses and Dissertations