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You searched for subject:( ER Stress). Showing records 1 – 30 of 197 total matches.

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NSYSU

1. Chen, Chien-wei. Down-regulation of Jab1 by ER stress in Hep3B hepatocellular carcinoma cell line.

Degree: Master, Institute of Biomedical Sciences, 2009, NSYSU

 Endoplasmic reticulum (ER) stress is the condition that unfolded or misfolded proteins accumulated in the ER which leads to the solubility stress. ER can activate… (more)

Subjects/Keywords: jab1; er stress

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APA (6th Edition):

Chen, C. (2009). Down-regulation of Jab1 by ER stress in Hep3B hepatocellular carcinoma cell line. (Thesis). NSYSU. Retrieved from http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0727109-113910

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

Chicago Manual of Style (16th Edition):

Chen, Chien-wei. “Down-regulation of Jab1 by ER stress in Hep3B hepatocellular carcinoma cell line.” 2009. Thesis, NSYSU. Accessed January 20, 2020. http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0727109-113910.

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

MLA Handbook (7th Edition):

Chen, Chien-wei. “Down-regulation of Jab1 by ER stress in Hep3B hepatocellular carcinoma cell line.” 2009. Web. 20 Jan 2020.

Vancouver:

Chen C. Down-regulation of Jab1 by ER stress in Hep3B hepatocellular carcinoma cell line. [Internet] [Thesis]. NSYSU; 2009. [cited 2020 Jan 20]. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0727109-113910.

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

Council of Science Editors:

Chen C. Down-regulation of Jab1 by ER stress in Hep3B hepatocellular carcinoma cell line. [Thesis]. NSYSU; 2009. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0727109-113910

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


University of Alberta

2. Gao, Xia. Physiological function of phosphatidylethanolamine N-methyltransferase.

Degree: PhD, Department of Biochemistry, 2015, University of Alberta

 Phosphatidylethanolamine N-methyltransferase (PEMT), a liver enriched enzyme, is responsible for approximately one third of hepatic phosphatidylcholine (PC) biosynthesis via three sequential methylations of phosphatidylethanolamine (PE).… (more)

Subjects/Keywords: ER stress; NASH; PEMT; obesity

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APA (6th Edition):

Gao, X. (2015). Physiological function of phosphatidylethanolamine N-methyltransferase. (Doctoral Dissertation). University of Alberta. Retrieved from https://era.library.ualberta.ca/files/cm900nt495

Chicago Manual of Style (16th Edition):

Gao, Xia. “Physiological function of phosphatidylethanolamine N-methyltransferase.” 2015. Doctoral Dissertation, University of Alberta. Accessed January 20, 2020. https://era.library.ualberta.ca/files/cm900nt495.

MLA Handbook (7th Edition):

Gao, Xia. “Physiological function of phosphatidylethanolamine N-methyltransferase.” 2015. Web. 20 Jan 2020.

Vancouver:

Gao X. Physiological function of phosphatidylethanolamine N-methyltransferase. [Internet] [Doctoral dissertation]. University of Alberta; 2015. [cited 2020 Jan 20]. Available from: https://era.library.ualberta.ca/files/cm900nt495.

Council of Science Editors:

Gao X. Physiological function of phosphatidylethanolamine N-methyltransferase. [Doctoral Dissertation]. University of Alberta; 2015. Available from: https://era.library.ualberta.ca/files/cm900nt495


University of Ottawa

3. Tassé, Louis-Alexandre. The Role of Sigma-1 Receptor in Modulating Endoplasmic Reticulum Stress: Putative Relevance to Alzheimer Disease .

Degree: 2018, University of Ottawa

 Alzheimer’s Disease and other neurodegenerative diseases have been linked to dysfunction in proteostasis in the endoplasmic reticulum (ER). The ER provides an exclusive environment for… (more)

Subjects/Keywords: ER stress; Sigma1-R

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APA (6th Edition):

Tassé, L. (2018). The Role of Sigma-1 Receptor in Modulating Endoplasmic Reticulum Stress: Putative Relevance to Alzheimer Disease . (Thesis). University of Ottawa. Retrieved from http://hdl.handle.net/10393/38395

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

Chicago Manual of Style (16th Edition):

Tassé, Louis-Alexandre. “The Role of Sigma-1 Receptor in Modulating Endoplasmic Reticulum Stress: Putative Relevance to Alzheimer Disease .” 2018. Thesis, University of Ottawa. Accessed January 20, 2020. http://hdl.handle.net/10393/38395.

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

MLA Handbook (7th Edition):

Tassé, Louis-Alexandre. “The Role of Sigma-1 Receptor in Modulating Endoplasmic Reticulum Stress: Putative Relevance to Alzheimer Disease .” 2018. Web. 20 Jan 2020.

Vancouver:

Tassé L. The Role of Sigma-1 Receptor in Modulating Endoplasmic Reticulum Stress: Putative Relevance to Alzheimer Disease . [Internet] [Thesis]. University of Ottawa; 2018. [cited 2020 Jan 20]. Available from: http://hdl.handle.net/10393/38395.

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

Council of Science Editors:

Tassé L. The Role of Sigma-1 Receptor in Modulating Endoplasmic Reticulum Stress: Putative Relevance to Alzheimer Disease . [Thesis]. University of Ottawa; 2018. Available from: http://hdl.handle.net/10393/38395

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


Kent State University

4. Yang, Ling. Bcl-2-associated athanogene-1 (BAG-1) Modulates the Endoplasmic Reticulum Stress Response in Chondrocytes.

Degree: PhD, College of Biomedical Sciences, 2007, Kent State University

 In eukaryotic cells, the endoplasmic reticulum (ER) is a major storage organelle for calcium and a site of synthesis and folding of secretory proteins, cell… (more)

Subjects/Keywords: BAG-1; Chondrocytes; ER stress

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APA (6th Edition):

Yang, L. (2007). Bcl-2-associated athanogene-1 (BAG-1) Modulates the Endoplasmic Reticulum Stress Response in Chondrocytes. (Doctoral Dissertation). Kent State University. Retrieved from http://rave.ohiolink.edu/etdc/view?acc_num=kent1175103480

Chicago Manual of Style (16th Edition):

Yang, Ling. “Bcl-2-associated athanogene-1 (BAG-1) Modulates the Endoplasmic Reticulum Stress Response in Chondrocytes.” 2007. Doctoral Dissertation, Kent State University. Accessed January 20, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=kent1175103480.

MLA Handbook (7th Edition):

Yang, Ling. “Bcl-2-associated athanogene-1 (BAG-1) Modulates the Endoplasmic Reticulum Stress Response in Chondrocytes.” 2007. Web. 20 Jan 2020.

Vancouver:

Yang L. Bcl-2-associated athanogene-1 (BAG-1) Modulates the Endoplasmic Reticulum Stress Response in Chondrocytes. [Internet] [Doctoral dissertation]. Kent State University; 2007. [cited 2020 Jan 20]. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=kent1175103480.

Council of Science Editors:

Yang L. Bcl-2-associated athanogene-1 (BAG-1) Modulates the Endoplasmic Reticulum Stress Response in Chondrocytes. [Doctoral Dissertation]. Kent State University; 2007. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=kent1175103480


University of Manchester

5. Mularczyk, Ewa. Understanding molecular pathology of chondrodysplasias: the role of ER stress.

Degree: 2011, University of Manchester

 MCDS is an autosomal dominant disorder, with a mild dwarfed phenotype and is caused by mutations in collagen X. The majority of the mutations identified… (more)

Subjects/Keywords: UPR; ER stress; chondrodysplasia

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APA (6th Edition):

Mularczyk, E. (2011). Understanding molecular pathology of chondrodysplasias: the role of ER stress. (Doctoral Dissertation). University of Manchester. Retrieved from http://www.manchester.ac.uk/escholar/uk-ac-man-scw:140302

Chicago Manual of Style (16th Edition):

Mularczyk, Ewa. “Understanding molecular pathology of chondrodysplasias: the role of ER stress.” 2011. Doctoral Dissertation, University of Manchester. Accessed January 20, 2020. http://www.manchester.ac.uk/escholar/uk-ac-man-scw:140302.

MLA Handbook (7th Edition):

Mularczyk, Ewa. “Understanding molecular pathology of chondrodysplasias: the role of ER stress.” 2011. Web. 20 Jan 2020.

Vancouver:

Mularczyk E. Understanding molecular pathology of chondrodysplasias: the role of ER stress. [Internet] [Doctoral dissertation]. University of Manchester; 2011. [cited 2020 Jan 20]. Available from: http://www.manchester.ac.uk/escholar/uk-ac-man-scw:140302.

Council of Science Editors:

Mularczyk E. Understanding molecular pathology of chondrodysplasias: the role of ER stress. [Doctoral Dissertation]. University of Manchester; 2011. Available from: http://www.manchester.ac.uk/escholar/uk-ac-man-scw:140302


University of Manchester

6. Mularczyk, Ewa. Understanding molecular pathology of chondrodysplasias : the role of ER stress.

Degree: PhD, 2012, University of Manchester

 MCDS is an autosomal dominant disorder, with a mild dwarfed phenotype and is caused by mutations in collagen X. The majority of the mutations identified… (more)

Subjects/Keywords: 616.7; UPR; ER stress; chondrodysplasia

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APA (6th Edition):

Mularczyk, E. (2012). Understanding molecular pathology of chondrodysplasias : the role of ER stress. (Doctoral Dissertation). University of Manchester. Retrieved from https://www.research.manchester.ac.uk/portal/en/theses/understanding-molecular-pathology-of-chondrodysplasias-the-role-of-er-stress(86ad2dcd-fcb6-4860-90d8-74f17996ac0d).html ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.724631

Chicago Manual of Style (16th Edition):

Mularczyk, Ewa. “Understanding molecular pathology of chondrodysplasias : the role of ER stress.” 2012. Doctoral Dissertation, University of Manchester. Accessed January 20, 2020. https://www.research.manchester.ac.uk/portal/en/theses/understanding-molecular-pathology-of-chondrodysplasias-the-role-of-er-stress(86ad2dcd-fcb6-4860-90d8-74f17996ac0d).html ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.724631.

MLA Handbook (7th Edition):

Mularczyk, Ewa. “Understanding molecular pathology of chondrodysplasias : the role of ER stress.” 2012. Web. 20 Jan 2020.

Vancouver:

Mularczyk E. Understanding molecular pathology of chondrodysplasias : the role of ER stress. [Internet] [Doctoral dissertation]. University of Manchester; 2012. [cited 2020 Jan 20]. Available from: https://www.research.manchester.ac.uk/portal/en/theses/understanding-molecular-pathology-of-chondrodysplasias-the-role-of-er-stress(86ad2dcd-fcb6-4860-90d8-74f17996ac0d).html ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.724631.

Council of Science Editors:

Mularczyk E. Understanding molecular pathology of chondrodysplasias : the role of ER stress. [Doctoral Dissertation]. University of Manchester; 2012. Available from: https://www.research.manchester.ac.uk/portal/en/theses/understanding-molecular-pathology-of-chondrodysplasias-the-role-of-er-stress(86ad2dcd-fcb6-4860-90d8-74f17996ac0d).html ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.724631


Kansas State University

7. Zhu, Xiaoxi. Intracellular localization, biochemical and biophysical properties of human Armet.

Degree: MS, Department of Biochemistry, 2011, Kansas State University

 Armet is a bifunctional protein widely distributed in animal species, vertebrate and invertebrate. It is an evidently part of the Unfolded Protein Response (UPR) and… (more)

Subjects/Keywords: Armet; ER stress; Biochemistry (0487)

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APA (6th Edition):

Zhu, X. (2011). Intracellular localization, biochemical and biophysical properties of human Armet. (Masters Thesis). Kansas State University. Retrieved from http://hdl.handle.net/2097/8107

Chicago Manual of Style (16th Edition):

Zhu, Xiaoxi. “Intracellular localization, biochemical and biophysical properties of human Armet.” 2011. Masters Thesis, Kansas State University. Accessed January 20, 2020. http://hdl.handle.net/2097/8107.

MLA Handbook (7th Edition):

Zhu, Xiaoxi. “Intracellular localization, biochemical and biophysical properties of human Armet.” 2011. Web. 20 Jan 2020.

Vancouver:

Zhu X. Intracellular localization, biochemical and biophysical properties of human Armet. [Internet] [Masters thesis]. Kansas State University; 2011. [cited 2020 Jan 20]. Available from: http://hdl.handle.net/2097/8107.

Council of Science Editors:

Zhu X. Intracellular localization, biochemical and biophysical properties of human Armet. [Masters Thesis]. Kansas State University; 2011. Available from: http://hdl.handle.net/2097/8107


Cornell University

8. He, Yin. Investigating Mammalian Unfolded Protein Response: The Physiology And Regulatory Mechanisms Of Ire1Alpha-Xbp1 Signaling .

Degree: 2013, Cornell University

 The endoplasmic reticulum (ER) serves as the site of protein synthesis, folding, maturation, modification, secretion, and degradation for approximately one-third of the proteome. Disruptions in… (more)

Subjects/Keywords: ER stress; UPR; IRE1alpha; XBP1

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APA (6th Edition):

He, Y. (2013). Investigating Mammalian Unfolded Protein Response: The Physiology And Regulatory Mechanisms Of Ire1Alpha-Xbp1 Signaling . (Thesis). Cornell University. Retrieved from http://hdl.handle.net/1813/34097

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

Chicago Manual of Style (16th Edition):

He, Yin. “Investigating Mammalian Unfolded Protein Response: The Physiology And Regulatory Mechanisms Of Ire1Alpha-Xbp1 Signaling .” 2013. Thesis, Cornell University. Accessed January 20, 2020. http://hdl.handle.net/1813/34097.

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

MLA Handbook (7th Edition):

He, Yin. “Investigating Mammalian Unfolded Protein Response: The Physiology And Regulatory Mechanisms Of Ire1Alpha-Xbp1 Signaling .” 2013. Web. 20 Jan 2020.

Vancouver:

He Y. Investigating Mammalian Unfolded Protein Response: The Physiology And Regulatory Mechanisms Of Ire1Alpha-Xbp1 Signaling . [Internet] [Thesis]. Cornell University; 2013. [cited 2020 Jan 20]. Available from: http://hdl.handle.net/1813/34097.

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

Council of Science Editors:

He Y. Investigating Mammalian Unfolded Protein Response: The Physiology And Regulatory Mechanisms Of Ire1Alpha-Xbp1 Signaling . [Thesis]. Cornell University; 2013. Available from: http://hdl.handle.net/1813/34097

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


University of Toronto

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

Degree: 2011, University of Toronto

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

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APA (6th 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 (16th Edition):

Hager, Lauren. “Lecithin:Cholesterol Acyltransferase Deficiency Protects against Cholesterol-induced Hepatic Endoplasmic Reticulum Stress in Mice.” 2011. Masters Thesis, University of Toronto. Accessed January 20, 2020. http://hdl.handle.net/1807/30620.

MLA Handbook (7th Edition):

Hager, Lauren. “Lecithin:Cholesterol Acyltransferase Deficiency Protects against Cholesterol-induced Hepatic Endoplasmic Reticulum Stress in Mice.” 2011. Web. 20 Jan 2020.

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 2020 Jan 20]. 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 Newcastle

10. Tay, Kwang Hong. Targeting adaptative mechanisms to endoplasmic reticulum stress in melanoma.

Degree: PhD, 2014, University of Newcastle

Research Doctorate - Doctor of Philosophy (PhD)

Melanoma is a skin cancer that remains a major public health problem in Australia because of high incidence,… (more)

Subjects/Keywords: melanoma; ER stress; apoptosis; thesis by publication

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APA (6th Edition):

Tay, K. H. (2014). Targeting adaptative mechanisms to endoplasmic reticulum stress in melanoma. (Doctoral Dissertation). University of Newcastle. Retrieved from http://hdl.handle.net/1959.13/1043155

Chicago Manual of Style (16th Edition):

Tay, Kwang Hong. “Targeting adaptative mechanisms to endoplasmic reticulum stress in melanoma.” 2014. Doctoral Dissertation, University of Newcastle. Accessed January 20, 2020. http://hdl.handle.net/1959.13/1043155.

MLA Handbook (7th Edition):

Tay, Kwang Hong. “Targeting adaptative mechanisms to endoplasmic reticulum stress in melanoma.” 2014. Web. 20 Jan 2020.

Vancouver:

Tay KH. Targeting adaptative mechanisms to endoplasmic reticulum stress in melanoma. [Internet] [Doctoral dissertation]. University of Newcastle; 2014. [cited 2020 Jan 20]. Available from: http://hdl.handle.net/1959.13/1043155.

Council of Science Editors:

Tay KH. Targeting adaptative mechanisms to endoplasmic reticulum stress in melanoma. [Doctoral Dissertation]. University of Newcastle; 2014. Available from: http://hdl.handle.net/1959.13/1043155


Penn State University

11. Zhu, Bokai. Modulation Of Skin Cancer By Peroxisome Proliferator-activated Receptor Beta/delta.

Degree: PhD, Molecular Medicine, 2012, Penn State University

 Ligand activation of peroxisome proliferator–activated receptor-β/δ (PPARβ/δ) inhibits chemically-induced skin tumorigenesis and Pparβ/δ-null mice exhibit enhanced chemically-induced skin tumorigenesis compared to wild-type mice. Since over… (more)

Subjects/Keywords: PPARb/d; HRAS; Mitosis; Senescence; ER stress

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APA (6th Edition):

Zhu, B. (2012). Modulation Of Skin Cancer By Peroxisome Proliferator-activated Receptor Beta/delta. (Doctoral Dissertation). Penn State University. Retrieved from https://etda.libraries.psu.edu/catalog/15143

Chicago Manual of Style (16th Edition):

Zhu, Bokai. “Modulation Of Skin Cancer By Peroxisome Proliferator-activated Receptor Beta/delta.” 2012. Doctoral Dissertation, Penn State University. Accessed January 20, 2020. https://etda.libraries.psu.edu/catalog/15143.

MLA Handbook (7th Edition):

Zhu, Bokai. “Modulation Of Skin Cancer By Peroxisome Proliferator-activated Receptor Beta/delta.” 2012. Web. 20 Jan 2020.

Vancouver:

Zhu B. Modulation Of Skin Cancer By Peroxisome Proliferator-activated Receptor Beta/delta. [Internet] [Doctoral dissertation]. Penn State University; 2012. [cited 2020 Jan 20]. Available from: https://etda.libraries.psu.edu/catalog/15143.

Council of Science Editors:

Zhu B. Modulation Of Skin Cancer By Peroxisome Proliferator-activated Receptor Beta/delta. [Doctoral Dissertation]. Penn State University; 2012. Available from: https://etda.libraries.psu.edu/catalog/15143


University of California – San Diego

12. Rodvold, Jeffrey James. Anatomy of the cell extrinsic effects of endoplasmic reticulum stress in tumor facilitation.

Degree: Biomedical Sciences, 2017, University of California – San Diego

 The tumor microenvironment is harbor to a variety of insults that privilege tumor cells to co-opt host immunity. Many of these insults, including nutrient deprivation… (more)

Subjects/Keywords: Biology; ER stress; Tumor immunology; UPR

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APA (6th Edition):

Rodvold, J. J. (2017). Anatomy of the cell extrinsic effects of endoplasmic reticulum stress in tumor facilitation. (Thesis). University of California – San Diego. Retrieved from http://www.escholarship.org/uc/item/49z0t0b1

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

Chicago Manual of Style (16th Edition):

Rodvold, Jeffrey James. “Anatomy of the cell extrinsic effects of endoplasmic reticulum stress in tumor facilitation.” 2017. Thesis, University of California – San Diego. Accessed January 20, 2020. http://www.escholarship.org/uc/item/49z0t0b1.

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

MLA Handbook (7th Edition):

Rodvold, Jeffrey James. “Anatomy of the cell extrinsic effects of endoplasmic reticulum stress in tumor facilitation.” 2017. Web. 20 Jan 2020.

Vancouver:

Rodvold JJ. Anatomy of the cell extrinsic effects of endoplasmic reticulum stress in tumor facilitation. [Internet] [Thesis]. University of California – San Diego; 2017. [cited 2020 Jan 20]. Available from: http://www.escholarship.org/uc/item/49z0t0b1.

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

Council of Science Editors:

Rodvold JJ. Anatomy of the cell extrinsic effects of endoplasmic reticulum stress in tumor facilitation. [Thesis]. University of California – San Diego; 2017. Available from: http://www.escholarship.org/uc/item/49z0t0b1

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


University of Manchester

13. Mullan, Lorna. Stimulation of intracellular proteolytic degradation as a means of reducing ER stress in a model of skeletal dysplasia.

Degree: 2015, University of Manchester

 MCDS is an autosomal dominant skeletal dysplasia disorder caused by mutations in collagen X. In most cases, mutations in collagen X result in a misfolded… (more)

Subjects/Keywords: MCDS; ER stress; chondrodysplasia; collagen X

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APA (6th Edition):

Mullan, L. (2015). Stimulation of intracellular proteolytic degradation as a means of reducing ER stress in a model of skeletal dysplasia. (Doctoral Dissertation). University of Manchester. Retrieved from http://www.manchester.ac.uk/escholar/uk-ac-man-scw:274429

Chicago Manual of Style (16th Edition):

Mullan, Lorna. “Stimulation of intracellular proteolytic degradation as a means of reducing ER stress in a model of skeletal dysplasia.” 2015. Doctoral Dissertation, University of Manchester. Accessed January 20, 2020. http://www.manchester.ac.uk/escholar/uk-ac-man-scw:274429.

MLA Handbook (7th Edition):

Mullan, Lorna. “Stimulation of intracellular proteolytic degradation as a means of reducing ER stress in a model of skeletal dysplasia.” 2015. Web. 20 Jan 2020.

Vancouver:

Mullan L. Stimulation of intracellular proteolytic degradation as a means of reducing ER stress in a model of skeletal dysplasia. [Internet] [Doctoral dissertation]. University of Manchester; 2015. [cited 2020 Jan 20]. Available from: http://www.manchester.ac.uk/escholar/uk-ac-man-scw:274429.

Council of Science Editors:

Mullan L. Stimulation of intracellular proteolytic degradation as a means of reducing ER stress in a model of skeletal dysplasia. [Doctoral Dissertation]. University of Manchester; 2015. Available from: http://www.manchester.ac.uk/escholar/uk-ac-man-scw:274429


McMaster University

14. Naiel, Safaa. The Role of Endoplasmic Reticulum Stress in the Development of Essential Hypertension.

Degree: MSc, 2017, McMaster University

Essential hypertension is the leading contributor to premature death worldwide. Endoplasmic reticulum (ER) stress has recently been implicated in diseased blood vessels and hypertension. It… (more)

Subjects/Keywords: ER Stress; 4-PBA; Hypertension; SHR

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APA (6th Edition):

Naiel, S. (2017). The Role of Endoplasmic Reticulum Stress in the Development of Essential Hypertension. (Masters Thesis). McMaster University. Retrieved from http://hdl.handle.net/11375/22174

Chicago Manual of Style (16th Edition):

Naiel, Safaa. “The Role of Endoplasmic Reticulum Stress in the Development of Essential Hypertension.” 2017. Masters Thesis, McMaster University. Accessed January 20, 2020. http://hdl.handle.net/11375/22174.

MLA Handbook (7th Edition):

Naiel, Safaa. “The Role of Endoplasmic Reticulum Stress in the Development of Essential Hypertension.” 2017. Web. 20 Jan 2020.

Vancouver:

Naiel S. The Role of Endoplasmic Reticulum Stress in the Development of Essential Hypertension. [Internet] [Masters thesis]. McMaster University; 2017. [cited 2020 Jan 20]. Available from: http://hdl.handle.net/11375/22174.

Council of Science Editors:

Naiel S. The Role of Endoplasmic Reticulum Stress in the Development of Essential Hypertension. [Masters Thesis]. McMaster University; 2017. Available from: http://hdl.handle.net/11375/22174


University of Manchester

15. Mullan, Lorna A. Stimulation of intracellular proteolytic degradation as a means of reducing ER stress in a model of skeletal dysplasia.

Degree: PhD, 2015, University of Manchester

 MCDS is an autosomal dominant skeletal dysplasia disorder caused by mutations in collagen X. In most cases, mutations in collagen X result in a misfolded… (more)

Subjects/Keywords: 616.7; collagen X; chondrodysplasia; MCDS; ER stress

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APA (6th Edition):

Mullan, L. A. (2015). Stimulation of intracellular proteolytic degradation as a means of reducing ER stress in a model of skeletal dysplasia. (Doctoral Dissertation). University of Manchester. Retrieved from https://www.research.manchester.ac.uk/portal/en/theses/stimulation-of-intracellular-proteolytic-degradation-as-a-means-of-reducing-er-stress-in-a-model-of-skeletal-dysplasia(b2bb722a-4c5b-4cae-8624-c83aeddd3d2a).html ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.724635

Chicago Manual of Style (16th Edition):

Mullan, Lorna A. “Stimulation of intracellular proteolytic degradation as a means of reducing ER stress in a model of skeletal dysplasia.” 2015. Doctoral Dissertation, University of Manchester. Accessed January 20, 2020. https://www.research.manchester.ac.uk/portal/en/theses/stimulation-of-intracellular-proteolytic-degradation-as-a-means-of-reducing-er-stress-in-a-model-of-skeletal-dysplasia(b2bb722a-4c5b-4cae-8624-c83aeddd3d2a).html ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.724635.

MLA Handbook (7th Edition):

Mullan, Lorna A. “Stimulation of intracellular proteolytic degradation as a means of reducing ER stress in a model of skeletal dysplasia.” 2015. Web. 20 Jan 2020.

Vancouver:

Mullan LA. Stimulation of intracellular proteolytic degradation as a means of reducing ER stress in a model of skeletal dysplasia. [Internet] [Doctoral dissertation]. University of Manchester; 2015. [cited 2020 Jan 20]. Available from: https://www.research.manchester.ac.uk/portal/en/theses/stimulation-of-intracellular-proteolytic-degradation-as-a-means-of-reducing-er-stress-in-a-model-of-skeletal-dysplasia(b2bb722a-4c5b-4cae-8624-c83aeddd3d2a).html ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.724635.

Council of Science Editors:

Mullan LA. Stimulation of intracellular proteolytic degradation as a means of reducing ER stress in a model of skeletal dysplasia. [Doctoral Dissertation]. University of Manchester; 2015. Available from: https://www.research.manchester.ac.uk/portal/en/theses/stimulation-of-intracellular-proteolytic-degradation-as-a-means-of-reducing-er-stress-in-a-model-of-skeletal-dysplasia(b2bb722a-4c5b-4cae-8624-c83aeddd3d2a).html ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.724635


University of Texas Medical Branch – Galveston

16. [No author]. Novel Insights Into Normal Aryl Hydrocarbon Receptor Biology Through the Regulation of Stanniocalcin 2 .

Degree: 2013, University of Texas Medical Branch – Galveston

 Proper hepatocyte function is vital for survival; hence unrepaired destruction of the parenchymal tissue leading to liver decompensation is devastating. Therefore, understanding the homeostatic process… (more)

Subjects/Keywords: AhR; Stc2; Hepatocytes; Apoptosis; ER Stress

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APA (6th Edition):

author], [. (2013). Novel Insights Into Normal Aryl Hydrocarbon Receptor Biology Through the Regulation of Stanniocalcin 2 . (Thesis). University of Texas Medical Branch – Galveston. Retrieved from http://hdl.handle.net/2152.3/542

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

Chicago Manual of Style (16th Edition):

author], [No. “Novel Insights Into Normal Aryl Hydrocarbon Receptor Biology Through the Regulation of Stanniocalcin 2 .” 2013. Thesis, University of Texas Medical Branch – Galveston. Accessed January 20, 2020. http://hdl.handle.net/2152.3/542.

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

MLA Handbook (7th Edition):

author], [No. “Novel Insights Into Normal Aryl Hydrocarbon Receptor Biology Through the Regulation of Stanniocalcin 2 .” 2013. Web. 20 Jan 2020.

Vancouver:

author] [. Novel Insights Into Normal Aryl Hydrocarbon Receptor Biology Through the Regulation of Stanniocalcin 2 . [Internet] [Thesis]. University of Texas Medical Branch – Galveston; 2013. [cited 2020 Jan 20]. Available from: http://hdl.handle.net/2152.3/542.

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

Council of Science Editors:

author] [. Novel Insights Into Normal Aryl Hydrocarbon Receptor Biology Through the Regulation of Stanniocalcin 2 . [Thesis]. University of Texas Medical Branch – Galveston; 2013. Available from: http://hdl.handle.net/2152.3/542

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


Vanderbilt University

17. Burman, Ankita. Unraveling the Role of Endoplasmic Reticulum Stress in Idiopathic Pulmonary Fibrosis (IPF).

Degree: PhD, Cell and Developmental Biology, 2019, Vanderbilt University

 Endoplasmic reticulum (ER) stress in type II AECs has been associated with pathogenesis of IPF; however, factors inducing ER stress and downstream mechanisms through which… (more)

Subjects/Keywords: UPR; IPF; ER stress; Pulmonary. Fibrosis; Lung

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APA (6th Edition):

Burman, A. (2019). Unraveling the Role of Endoplasmic Reticulum Stress in Idiopathic Pulmonary Fibrosis (IPF). (Doctoral Dissertation). Vanderbilt University. Retrieved from http://etd.library.vanderbilt.edu/available/etd-01112019-155241/ ;

Chicago Manual of Style (16th Edition):

Burman, Ankita. “Unraveling the Role of Endoplasmic Reticulum Stress in Idiopathic Pulmonary Fibrosis (IPF).” 2019. Doctoral Dissertation, Vanderbilt University. Accessed January 20, 2020. http://etd.library.vanderbilt.edu/available/etd-01112019-155241/ ;.

MLA Handbook (7th Edition):

Burman, Ankita. “Unraveling the Role of Endoplasmic Reticulum Stress in Idiopathic Pulmonary Fibrosis (IPF).” 2019. Web. 20 Jan 2020.

Vancouver:

Burman A. Unraveling the Role of Endoplasmic Reticulum Stress in Idiopathic Pulmonary Fibrosis (IPF). [Internet] [Doctoral dissertation]. Vanderbilt University; 2019. [cited 2020 Jan 20]. Available from: http://etd.library.vanderbilt.edu/available/etd-01112019-155241/ ;.

Council of Science Editors:

Burman A. Unraveling the Role of Endoplasmic Reticulum Stress in Idiopathic Pulmonary Fibrosis (IPF). [Doctoral Dissertation]. Vanderbilt University; 2019. Available from: http://etd.library.vanderbilt.edu/available/etd-01112019-155241/ ;


University of Toronto

18. Anyiwe, Kikanwa Brenda Lydia Hope. Sensitization to Death Receptor Stimuli and Anchorage-dependent Cell Death through Induction of Endoplasmic Reticulum Stress.

Degree: 2011, University of Toronto

Activation of the unfolded protein response follows induction of endoplasmic reticulum (ER) stress, resulting in widespread inhibition of protein expression. FLIP protein is particularly sensitive… (more)

Subjects/Keywords: ER stress; death receptor stimuli; FLIP; 0760

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APA (6th Edition):

Anyiwe, K. B. L. H. (2011). Sensitization to Death Receptor Stimuli and Anchorage-dependent Cell Death through Induction of Endoplasmic Reticulum Stress. (Masters Thesis). University of Toronto. Retrieved from http://hdl.handle.net/1807/29467

Chicago Manual of Style (16th Edition):

Anyiwe, Kikanwa Brenda Lydia Hope. “Sensitization to Death Receptor Stimuli and Anchorage-dependent Cell Death through Induction of Endoplasmic Reticulum Stress.” 2011. Masters Thesis, University of Toronto. Accessed January 20, 2020. http://hdl.handle.net/1807/29467.

MLA Handbook (7th Edition):

Anyiwe, Kikanwa Brenda Lydia Hope. “Sensitization to Death Receptor Stimuli and Anchorage-dependent Cell Death through Induction of Endoplasmic Reticulum Stress.” 2011. Web. 20 Jan 2020.

Vancouver:

Anyiwe KBLH. Sensitization to Death Receptor Stimuli and Anchorage-dependent Cell Death through Induction of Endoplasmic Reticulum Stress. [Internet] [Masters thesis]. University of Toronto; 2011. [cited 2020 Jan 20]. Available from: http://hdl.handle.net/1807/29467.

Council of Science Editors:

Anyiwe KBLH. Sensitization to Death Receptor Stimuli and Anchorage-dependent Cell Death through Induction of Endoplasmic Reticulum Stress. [Masters Thesis]. University of Toronto; 2011. Available from: http://hdl.handle.net/1807/29467


University of Guelph

19. Morgan, Larry. The Role of Cytochrome P450 2A5 During Endoplasmic Reticulum Stress .

Degree: 2014, University of Guelph

 Cytochrome P450 2A5 (CYP2A5) is a murine orthologue of human CYP2A6 and is predominantly found within the endoplasmic reticulum (ER) of the liver. CYP2A5 differs… (more)

Subjects/Keywords: CYP2A5; ER Stress; Hepatocytes; Nrf2; Heme; Bilirubin

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APA (6th Edition):

Morgan, L. (2014). The Role of Cytochrome P450 2A5 During Endoplasmic Reticulum Stress . (Thesis). University of Guelph. Retrieved from https://atrium.lib.uoguelph.ca/xmlui/handle/10214/7827

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

Chicago Manual of Style (16th Edition):

Morgan, Larry. “The Role of Cytochrome P450 2A5 During Endoplasmic Reticulum Stress .” 2014. Thesis, University of Guelph. Accessed January 20, 2020. https://atrium.lib.uoguelph.ca/xmlui/handle/10214/7827.

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

MLA Handbook (7th Edition):

Morgan, Larry. “The Role of Cytochrome P450 2A5 During Endoplasmic Reticulum Stress .” 2014. Web. 20 Jan 2020.

Vancouver:

Morgan L. The Role of Cytochrome P450 2A5 During Endoplasmic Reticulum Stress . [Internet] [Thesis]. University of Guelph; 2014. [cited 2020 Jan 20]. Available from: https://atrium.lib.uoguelph.ca/xmlui/handle/10214/7827.

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

Council of Science Editors:

Morgan L. The Role of Cytochrome P450 2A5 During Endoplasmic Reticulum Stress . [Thesis]. University of Guelph; 2014. Available from: https://atrium.lib.uoguelph.ca/xmlui/handle/10214/7827

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


University of Helsinki

20. Montonen, Ella. CDNF:n vaikutukset solulimakalvoston stressiin ja kliinisiin oireisiin amyotrofisen lateraaliskleroosin hiirimallissa.

Degree: Farmaceutiska fakulteten, 2015, University of Helsinki

Endoplasmic reticulum stress (ER-stress) is the result of accumulation of unfolded and misfolded proteins in the ER. The unfolded proteins activate the unfolded protein response… (more)

Subjects/Keywords: CDNF; ALS; UPR; ER-stress; unfolded proteins; ER-stressi; UPR-reitti; laskostumattomat proteiinit; Farmakologi; Pharmacology; Farmakologia; CDNF; ALS; UPR; ER-stress; unfolded proteins; ER-stressi; UPR-reitti; laskostumattomat proteiinit

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APA (6th Edition):

Montonen, E. (2015). CDNF:n vaikutukset solulimakalvoston stressiin ja kliinisiin oireisiin amyotrofisen lateraaliskleroosin hiirimallissa. (Masters Thesis). University of Helsinki. Retrieved from http://hdl.handle.net/10138/158359

Chicago Manual of Style (16th Edition):

Montonen, Ella. “CDNF:n vaikutukset solulimakalvoston stressiin ja kliinisiin oireisiin amyotrofisen lateraaliskleroosin hiirimallissa.” 2015. Masters Thesis, University of Helsinki. Accessed January 20, 2020. http://hdl.handle.net/10138/158359.

MLA Handbook (7th Edition):

Montonen, Ella. “CDNF:n vaikutukset solulimakalvoston stressiin ja kliinisiin oireisiin amyotrofisen lateraaliskleroosin hiirimallissa.” 2015. Web. 20 Jan 2020.

Vancouver:

Montonen E. CDNF:n vaikutukset solulimakalvoston stressiin ja kliinisiin oireisiin amyotrofisen lateraaliskleroosin hiirimallissa. [Internet] [Masters thesis]. University of Helsinki; 2015. [cited 2020 Jan 20]. Available from: http://hdl.handle.net/10138/158359.

Council of Science Editors:

Montonen E. CDNF:n vaikutukset solulimakalvoston stressiin ja kliinisiin oireisiin amyotrofisen lateraaliskleroosin hiirimallissa. [Masters Thesis]. University of Helsinki; 2015. Available from: http://hdl.handle.net/10138/158359


University of Utah

21. Moore, Kristin A. The mechanisms and function of regulated ire1-dependent decay during endoplasmic reticulum stress.

Degree: PhD, Biology, 2016, University of Utah

 The endoplasmic reticulum (ER) is a dynamic organelle that is responsible for the folding and quality control of proteins within the endomembrane system. Both physiological… (more)

Subjects/Keywords: Blos1; Endoplasmic reticulum (ER); ER stress; mRNA degradation; Regulated-Ire1 Dependent Decay; Unfolded Protein Response

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APA (6th Edition):

Moore, K. A. (2016). The mechanisms and function of regulated ire1-dependent decay during endoplasmic reticulum stress. (Doctoral Dissertation). University of Utah. Retrieved from http://content.lib.utah.edu/cdm/singleitem/collection/etd3/id/4104/rec/2602

Chicago Manual of Style (16th Edition):

Moore, Kristin A. “The mechanisms and function of regulated ire1-dependent decay during endoplasmic reticulum stress.” 2016. Doctoral Dissertation, University of Utah. Accessed January 20, 2020. http://content.lib.utah.edu/cdm/singleitem/collection/etd3/id/4104/rec/2602.

MLA Handbook (7th Edition):

Moore, Kristin A. “The mechanisms and function of regulated ire1-dependent decay during endoplasmic reticulum stress.” 2016. Web. 20 Jan 2020.

Vancouver:

Moore KA. The mechanisms and function of regulated ire1-dependent decay during endoplasmic reticulum stress. [Internet] [Doctoral dissertation]. University of Utah; 2016. [cited 2020 Jan 20]. Available from: http://content.lib.utah.edu/cdm/singleitem/collection/etd3/id/4104/rec/2602.

Council of Science Editors:

Moore KA. The mechanisms and function of regulated ire1-dependent decay during endoplasmic reticulum stress. [Doctoral Dissertation]. University of Utah; 2016. Available from: http://content.lib.utah.edu/cdm/singleitem/collection/etd3/id/4104/rec/2602


McMaster University

22. Ayaub, Ehab. Investigating Strategies to Modulate Macrophage Function to Prevent the Progression of Fibrotic Lung Disease.

Degree: PhD, 2017, McMaster University

 Tissue fibrosis occurs in the advanced stages of various chronic diseases and can account for 45% of all deaths related to chronic diseases worldwide. The… (more)

Subjects/Keywords: Lung; Fibrosis; Macrophages; ER stress; Unfolded Protein Response; GRP78; ER expansion; IL-6

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APA (6th Edition):

Ayaub, E. (2017). Investigating Strategies to Modulate Macrophage Function to Prevent the Progression of Fibrotic Lung Disease. (Doctoral Dissertation). McMaster University. Retrieved from http://hdl.handle.net/11375/21998

Chicago Manual of Style (16th Edition):

Ayaub, Ehab. “Investigating Strategies to Modulate Macrophage Function to Prevent the Progression of Fibrotic Lung Disease.” 2017. Doctoral Dissertation, McMaster University. Accessed January 20, 2020. http://hdl.handle.net/11375/21998.

MLA Handbook (7th Edition):

Ayaub, Ehab. “Investigating Strategies to Modulate Macrophage Function to Prevent the Progression of Fibrotic Lung Disease.” 2017. Web. 20 Jan 2020.

Vancouver:

Ayaub E. Investigating Strategies to Modulate Macrophage Function to Prevent the Progression of Fibrotic Lung Disease. [Internet] [Doctoral dissertation]. McMaster University; 2017. [cited 2020 Jan 20]. Available from: http://hdl.handle.net/11375/21998.

Council of Science Editors:

Ayaub E. Investigating Strategies to Modulate Macrophage Function to Prevent the Progression of Fibrotic Lung Disease. [Doctoral Dissertation]. McMaster University; 2017. Available from: http://hdl.handle.net/11375/21998


University of Rochester

23. Gewandter, Jennifer. Studies in Oxidative Damage-induced Signaling: A Focus Outside the Nucleus.

Degree: PhD, 2011, University of Rochester

 Oxidative stress, or increased reactive oxygen species (ROS), damages cellular macromolecules and activates signaling cascades that modulate cell fate. Oxidative damage and induction of these… (more)

Subjects/Keywords: Oxidative Stress; Oxidative Damage; Mitochondrial DNA Damage; ER Stress

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APA (6th Edition):

Gewandter, J. (2011). Studies in Oxidative Damage-induced Signaling: A Focus Outside the Nucleus. (Doctoral Dissertation). University of Rochester. Retrieved from http://hdl.handle.net/1802/17665

Chicago Manual of Style (16th Edition):

Gewandter, Jennifer. “Studies in Oxidative Damage-induced Signaling: A Focus Outside the Nucleus.” 2011. Doctoral Dissertation, University of Rochester. Accessed January 20, 2020. http://hdl.handle.net/1802/17665.

MLA Handbook (7th Edition):

Gewandter, Jennifer. “Studies in Oxidative Damage-induced Signaling: A Focus Outside the Nucleus.” 2011. Web. 20 Jan 2020.

Vancouver:

Gewandter J. Studies in Oxidative Damage-induced Signaling: A Focus Outside the Nucleus. [Internet] [Doctoral dissertation]. University of Rochester; 2011. [cited 2020 Jan 20]. Available from: http://hdl.handle.net/1802/17665.

Council of Science Editors:

Gewandter J. Studies in Oxidative Damage-induced Signaling: A Focus Outside the Nucleus. [Doctoral Dissertation]. University of Rochester; 2011. Available from: http://hdl.handle.net/1802/17665


University of Southern California

24. Hu, Jay. Pathways of cell death in response to HIV protease cocktail Ritonavir/Lopinavir in primary hepatocytes.

Degree: MS, Biochemistry and Molecular Biology, 2015, University of Southern California

 Highly Active Anti Retroviral Therapy (HAART) has become an integral part of modern Human Immunodeficiency Virus (HIV) and Acquired Immunodeficiency Syndrome (AIDS) treatment. Liver damage… (more)

Subjects/Keywords: hepatocytes; ER stress; oxidative stress; Nrf2; HIV protease inhibitor

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APA (6th Edition):

Hu, J. (2015). Pathways of cell death in response to HIV protease cocktail Ritonavir/Lopinavir in primary hepatocytes. (Masters Thesis). University of Southern California. Retrieved from http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/574755/rec/4950

Chicago Manual of Style (16th Edition):

Hu, Jay. “Pathways of cell death in response to HIV protease cocktail Ritonavir/Lopinavir in primary hepatocytes.” 2015. Masters Thesis, University of Southern California. Accessed January 20, 2020. http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/574755/rec/4950.

MLA Handbook (7th Edition):

Hu, Jay. “Pathways of cell death in response to HIV protease cocktail Ritonavir/Lopinavir in primary hepatocytes.” 2015. Web. 20 Jan 2020.

Vancouver:

Hu J. Pathways of cell death in response to HIV protease cocktail Ritonavir/Lopinavir in primary hepatocytes. [Internet] [Masters thesis]. University of Southern California; 2015. [cited 2020 Jan 20]. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/574755/rec/4950.

Council of Science Editors:

Hu J. Pathways of cell death in response to HIV protease cocktail Ritonavir/Lopinavir in primary hepatocytes. [Masters Thesis]. University of Southern California; 2015. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/574755/rec/4950


University of Manchester

25. Jumuddin, Farra Aidah Binti. ANTIOXIDANT PROPERTIES OF NQO2.

Degree: 2017, University of Manchester

 Dihydronicotinamide riboside (NRH) quinone oxidoreductase 2 (NQO2) is involved in quinone metabolism reducing quinone to hydroquinone. Quinones are products of oestrogen metabolism and are responsible… (more)

Subjects/Keywords: Quinone oxidoreductase (NQO2); oestrogen receptor; ROS; oxidative stress; ER stress; antioxidant

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APA (6th Edition):

Jumuddin, F. A. B. (2017). ANTIOXIDANT PROPERTIES OF NQO2. (Doctoral Dissertation). University of Manchester. Retrieved from http://www.manchester.ac.uk/escholar/uk-ac-man-scw:311808

Chicago Manual of Style (16th Edition):

Jumuddin, Farra Aidah Binti. “ANTIOXIDANT PROPERTIES OF NQO2.” 2017. Doctoral Dissertation, University of Manchester. Accessed January 20, 2020. http://www.manchester.ac.uk/escholar/uk-ac-man-scw:311808.

MLA Handbook (7th Edition):

Jumuddin, Farra Aidah Binti. “ANTIOXIDANT PROPERTIES OF NQO2.” 2017. Web. 20 Jan 2020.

Vancouver:

Jumuddin FAB. ANTIOXIDANT PROPERTIES OF NQO2. [Internet] [Doctoral dissertation]. University of Manchester; 2017. [cited 2020 Jan 20]. Available from: http://www.manchester.ac.uk/escholar/uk-ac-man-scw:311808.

Council of Science Editors:

Jumuddin FAB. ANTIOXIDANT PROPERTIES OF NQO2. [Doctoral Dissertation]. University of Manchester; 2017. Available from: http://www.manchester.ac.uk/escholar/uk-ac-man-scw:311808


National University of Ireland – Galway

26. Kennedy, Donna. The regulation of ER stress induced cell death by HSPB1 (hsp27) .

Degree: 2013, National University of Ireland – Galway

 Endoplasmic reticulum (ER) stress is associated with several human pathologies including neurodegenerative disorders. ER stress results in accumulation of unfolded proteins which activates the unfolded… (more)

Subjects/Keywords: Cell stress; Heat shock; ER stress; Department of Biochemistry

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APA (6th Edition):

Kennedy, D. (2013). The regulation of ER stress induced cell death by HSPB1 (hsp27) . (Thesis). National University of Ireland – Galway. Retrieved from http://hdl.handle.net/10379/4487

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

Chicago Manual of Style (16th Edition):

Kennedy, Donna. “The regulation of ER stress induced cell death by HSPB1 (hsp27) .” 2013. Thesis, National University of Ireland – Galway. Accessed January 20, 2020. http://hdl.handle.net/10379/4487.

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

MLA Handbook (7th Edition):

Kennedy, Donna. “The regulation of ER stress induced cell death by HSPB1 (hsp27) .” 2013. Web. 20 Jan 2020.

Vancouver:

Kennedy D. The regulation of ER stress induced cell death by HSPB1 (hsp27) . [Internet] [Thesis]. National University of Ireland – Galway; 2013. [cited 2020 Jan 20]. Available from: http://hdl.handle.net/10379/4487.

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

Council of Science Editors:

Kennedy D. The regulation of ER stress induced cell death by HSPB1 (hsp27) . [Thesis]. National University of Ireland – Galway; 2013. Available from: http://hdl.handle.net/10379/4487

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


National University of Ireland – Galway

27. Cleary, Patricia. Investigation of IRE1/XBP1s pathway and its potential as a therapeutic target in breast cancer .

Degree: 2015, National University of Ireland – Galway

 X-Box binding protein 1 (XBP1) is an integral component of the unfolded protein response (UPR), a pro-survival mechanism, triggered by the onset of endoplasmic reticulum… (more)

Subjects/Keywords: ER stress, Breast Cancer, IRE1, XBP1, Sestrin 2; ER stress; Breast cancer; IRE1; XBP1; Sestrin 2; Biochemistry

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APA (6th Edition):

Cleary, P. (2015). Investigation of IRE1/XBP1s pathway and its potential as a therapeutic target in breast cancer . (Thesis). National University of Ireland – Galway. Retrieved from http://hdl.handle.net/10379/5461

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

Chicago Manual of Style (16th Edition):

Cleary, Patricia. “Investigation of IRE1/XBP1s pathway and its potential as a therapeutic target in breast cancer .” 2015. Thesis, National University of Ireland – Galway. Accessed January 20, 2020. http://hdl.handle.net/10379/5461.

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

MLA Handbook (7th Edition):

Cleary, Patricia. “Investigation of IRE1/XBP1s pathway and its potential as a therapeutic target in breast cancer .” 2015. Web. 20 Jan 2020.

Vancouver:

Cleary P. Investigation of IRE1/XBP1s pathway and its potential as a therapeutic target in breast cancer . [Internet] [Thesis]. National University of Ireland – Galway; 2015. [cited 2020 Jan 20]. Available from: http://hdl.handle.net/10379/5461.

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

Council of Science Editors:

Cleary P. Investigation of IRE1/XBP1s pathway and its potential as a therapeutic target in breast cancer . [Thesis]. National University of Ireland – Galway; 2015. Available from: http://hdl.handle.net/10379/5461

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


NSYSU

28. Guo, Bo-Lin. The neuroprotective effects of marine-derived compound via the regulation of unfolded protein response and autophagy pathway.

Degree: Master, Marine Biotechnology and Resources, 2017, NSYSU

 Parkinson's disease (PD) is a degenerative disorder of the central nervous system. Symptoms of PD include resting tremor, rigidity, bradykinesia, and posture instability. Motor symptoms… (more)

Subjects/Keywords: Parkinson's disease; ER stress; autophagy; UPR; 6-OHDA

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

APA (6th Edition):

Guo, B. (2017). The neuroprotective effects of marine-derived compound via the regulation of unfolded protein response and autophagy pathway. (Thesis). NSYSU. Retrieved from http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0631117-233150

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

Chicago Manual of Style (16th Edition):

Guo, Bo-Lin. “The neuroprotective effects of marine-derived compound via the regulation of unfolded protein response and autophagy pathway.” 2017. Thesis, NSYSU. Accessed January 20, 2020. http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0631117-233150.

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

MLA Handbook (7th Edition):

Guo, Bo-Lin. “The neuroprotective effects of marine-derived compound via the regulation of unfolded protein response and autophagy pathway.” 2017. Web. 20 Jan 2020.

Vancouver:

Guo B. The neuroprotective effects of marine-derived compound via the regulation of unfolded protein response and autophagy pathway. [Internet] [Thesis]. NSYSU; 2017. [cited 2020 Jan 20]. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0631117-233150.

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

Council of Science Editors:

Guo B. The neuroprotective effects of marine-derived compound via the regulation of unfolded protein response and autophagy pathway. [Thesis]. NSYSU; 2017. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0631117-233150

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


University of Newcastle

29. Jiang, Chen Chen. Regulation of endoplasmic reticulum stress induced Apoptosis in human melanoma.

Degree: PhD, 2008, University of Newcastle

Research Doctorate - Doctor of Philosophy (PhD)

Melanoma is a skin cancer that remains a major public health problem in Australia because of its high… (more)

Subjects/Keywords: ER stress; apoptosis; melanoma

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

APA (6th Edition):

Jiang, C. C. (2008). Regulation of endoplasmic reticulum stress induced Apoptosis in human melanoma. (Doctoral Dissertation). University of Newcastle. Retrieved from http://hdl.handle.net/1959.13/31434

Chicago Manual of Style (16th Edition):

Jiang, Chen Chen. “Regulation of endoplasmic reticulum stress induced Apoptosis in human melanoma.” 2008. Doctoral Dissertation, University of Newcastle. Accessed January 20, 2020. http://hdl.handle.net/1959.13/31434.

MLA Handbook (7th Edition):

Jiang, Chen Chen. “Regulation of endoplasmic reticulum stress induced Apoptosis in human melanoma.” 2008. Web. 20 Jan 2020.

Vancouver:

Jiang CC. Regulation of endoplasmic reticulum stress induced Apoptosis in human melanoma. [Internet] [Doctoral dissertation]. University of Newcastle; 2008. [cited 2020 Jan 20]. Available from: http://hdl.handle.net/1959.13/31434.

Council of Science Editors:

Jiang CC. Regulation of endoplasmic reticulum stress induced Apoptosis in human melanoma. [Doctoral Dissertation]. University of Newcastle; 2008. Available from: http://hdl.handle.net/1959.13/31434


University of Notre Dame

30. Jenifer B. Gifford. GRP78 Associated Chemoresistance Affects Drug Response in Pancreatic Ductal Adenocarcinoma</h1>.

Degree: PhD, Biological Sciences, 2017, University of Notre Dame

  Pancreatic Ductal Adenocarcinoma (PDAC) is the 3rd leading cause of cancer related death and has a five year survival rate below 8%. This poor… (more)

Subjects/Keywords: ER Stress; Chemoresistance; BiP; Pancreatic; Chemotherapy; GRP78; Cancer; IT-139

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

APA (6th Edition):

Gifford, J. B. (2017). GRP78 Associated Chemoresistance Affects Drug Response in Pancreatic Ductal Adenocarcinoma</h1>. (Doctoral Dissertation). University of Notre Dame. Retrieved from https://curate.nd.edu/show/gm80ht27s0n

Chicago Manual of Style (16th Edition):

Gifford, Jenifer B.. “GRP78 Associated Chemoresistance Affects Drug Response in Pancreatic Ductal Adenocarcinoma</h1>.” 2017. Doctoral Dissertation, University of Notre Dame. Accessed January 20, 2020. https://curate.nd.edu/show/gm80ht27s0n.

MLA Handbook (7th Edition):

Gifford, Jenifer B.. “GRP78 Associated Chemoresistance Affects Drug Response in Pancreatic Ductal Adenocarcinoma</h1>.” 2017. Web. 20 Jan 2020.

Vancouver:

Gifford JB. GRP78 Associated Chemoresistance Affects Drug Response in Pancreatic Ductal Adenocarcinoma</h1>. [Internet] [Doctoral dissertation]. University of Notre Dame; 2017. [cited 2020 Jan 20]. Available from: https://curate.nd.edu/show/gm80ht27s0n.

Council of Science Editors:

Gifford JB. GRP78 Associated Chemoresistance Affects Drug Response in Pancreatic Ductal Adenocarcinoma</h1>. [Doctoral Dissertation]. University of Notre Dame; 2017. Available from: https://curate.nd.edu/show/gm80ht27s0n

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