subject:(TRP channels)

University of Oxford

1. Wang, Qinrui. Understanding the structure and interactions of polycystin-2 through structural and simulation studies.

Degree: PhD, 2019, University of Oxford

URL: http://ora.ox.ac.uk/objects/uuid:7caae071-ff3f-434c-ae25-8489382dcc9b ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.799926

► Polycystin-2 (PC2) is a member of the transient receptor potential (TRP) superfamily of non-selective cation channels. It has a systemic distribution with relatively high expression… (more)

▼ Polycystin-2 (PC2) is a member of the transient receptor potential (TRP) superfamily of non-selective cation channels. It has a systemic distribution with relatively high expression in kidney tubules. PC2 shares a common transmembrane fold with other TRP channels, in addition to having a extracellular/luminal domain (TOP domain) unique to TRPP and TRPML channels. Mutations in PC2 are associated with autosomal dominant polycystic kidney disease (ADPKD), which is one of the most prevalent genetic disorders in human. Despite that the genetic link between PC2 and ADPKD is well established, the molecular basis of the disease is still elusive. It has been proposed that dysfunction of ciliary PC2 is the main mechanism of pathology of PC2-associated ADPKD. Given the complex organisation of ciliary membrane, it is important to establish how PC2 interacts with specific lipids in its membrane environment. Lipid binding assay results suggest that detergent-solubilised PC2 can bind a range of phosphatidylinositol phosphates but not other simple anionic (phosphatidylserine, phosphatidic acid) or zwitterionic (phosphatidylethanolamine, phosphatidylcholine) lipids. Combining cryo-electron microscopy (cyro-EM) and multiscale molecular dynamics (MD) simulations, we identified a hydrophobic pocket in PC2 formed between S3, S4 transmembrane helices and S4-S5 linker, which showed a preference for phosphatidylinositol bisphosphate (PIP2) binding. Simulations of other members of the TRP channel family suggest this lipid-binding site may be shared amongst a number of TRP channels. In addition, our cryo-EM maps revealed a binding site for cholesterol on PC2, which is further characterised with MD simulations. These results help to position PC2 within an emerging model of the complex roles of lipids in the regulation and organisation of ciliary membranes. Moreover, we used MD simulations to probe the ion selectivity of PC2. Our results suggest that PC2 is selective for Na⁺ over Ca²⁺, and not only the selectivity filter residues but also the TOP domain contribute to the selectivity of the channel.

Subjects/Keywords: TRP channels

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APA (6^th Edition):

Wang, Q. (2019). Understanding the structure and interactions of polycystin-2 through structural and simulation studies. (Doctoral Dissertation). University of Oxford. Retrieved from http://ora.ox.ac.uk/objects/uuid:7caae071-ff3f-434c-ae25-8489382dcc9b ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.799926

Chicago Manual of Style (16^th Edition):

Wang, Qinrui. “Understanding the structure and interactions of polycystin-2 through structural and simulation studies.” 2019. Doctoral Dissertation, University of Oxford. Accessed April 17, 2021. http://ora.ox.ac.uk/objects/uuid:7caae071-ff3f-434c-ae25-8489382dcc9b ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.799926.

MLA Handbook (7^th Edition):

Wang, Qinrui. “Understanding the structure and interactions of polycystin-2 through structural and simulation studies.” 2019. Web. 17 Apr 2021.

Vancouver:

Wang Q. Understanding the structure and interactions of polycystin-2 through structural and simulation studies. [Internet] [Doctoral dissertation]. University of Oxford; 2019. [cited 2021 Apr 17]. Available from: http://ora.ox.ac.uk/objects/uuid:7caae071-ff3f-434c-ae25-8489382dcc9b ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.799926.

Council of Science Editors:

Wang Q. Understanding the structure and interactions of polycystin-2 through structural and simulation studies. [Doctoral Dissertation]. University of Oxford; 2019. Available from: http://ora.ox.ac.uk/objects/uuid:7caae071-ff3f-434c-ae25-8489382dcc9b ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.799926

Rutgers University

2. Cai, Na, 1988-. The functional interplay between TPRM7 channel-kinase autophosphorylation and its cellular regulation.

Degree: PhD, Pharmacology, Cellular and Molecular, 2018, Rutgers University

URL: https://rucore.libraries.rutgers.edu/rutgers-lib/57513/

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As a member of the transient receptor potential ion channel subfamily, TRPM7 is a remarkable ion channel in possession of its own functional kinase domain.… (more)

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As a member of the transient receptor potential ion channel subfamily, TRPM7 is a remarkable ion channel in possession of its own functional kinase domain. TRPM7 is ubiquitously expressed and permeable to divalent cations, allowing Mg2+, Ca2+, and trace metals ions such as Zn2+ to constitute the channel’s characteristic small inward current. The channel’s functional kinase domain is located at the protein’s cytosolic COOH terminus, placing TRPM7 also into a family of serine/threonine-phosphorylating alpha-kinases. It is not intuitively clear why a channel is covalently linked to a kinase, especially as it has been found that the kinase activity of TRPM7 is not required for channel gating. Previous studies have shown that TRPM7 is autophosphorylated, and yet the functional outcome of this autophosphorylation remain unknown. Motivated to understand the impact of phosphorylation on the function and regulation of this channel-kinase, I performed a comprehensive phosphoproteomic analysis of TRPM7 by mass spectrometry to identify the major in vivo phosphorylation sites on TRPM7. The results of the mass spectrometry study uncovered potential mechanisms by which the catalytic activity of TRPM7 kinase is regulated through autophosphorylation. My experiments also revealed a significant role of TRPM7’s kinase activity in regulating the posttranslational processing of TRPM7. Utilizing the TRPM7-K1646R kinase-inactive mutant, I discovered that TRPM7 kinase inactivation leads to faster protein degradation and intracellular retention of the channel in polarized epithelial cells compared to the wildtype protein. Mutational analysis of TRPM7 autophosphorylation sites further revealed a role for S1360 as a key residue mediating both protein stability and intracellular trafficking of TRPM7. In addition, I discovered that the intrinsic kinase activity of TRPM7 mediates the interaction of the channel with the signaling protein 14-3-3θ, whose binding sites on TRPM7 also contribute to the regulation of TRPM7 trafficking. Overall, these findings expand our knowledge of the in vivo phosphorylation profile of TRPM7 and, more importantly, increase our understanding of the significance of TRPM7’s kinase for functional regulation of the channel.

Advisors/Committee Members: Runnels, Loren W (chair), Walworth, Nancy C (internal member), Madura, Kiran (internal member), Jin, Shengkan (Victor) (internal member), Stock, Ann M (outside member), School of Graduate Studies.

Subjects/Keywords: TRP channels

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APA (6^th Edition):

Cai, Na, 1. (2018). The functional interplay between TPRM7 channel-kinase autophosphorylation and its cellular regulation. (Doctoral Dissertation). Rutgers University. Retrieved from https://rucore.libraries.rutgers.edu/rutgers-lib/57513/

Chicago Manual of Style (16^th Edition):

Cai, Na, 1988-. “The functional interplay between TPRM7 channel-kinase autophosphorylation and its cellular regulation.” 2018. Doctoral Dissertation, Rutgers University. Accessed April 17, 2021. https://rucore.libraries.rutgers.edu/rutgers-lib/57513/.

MLA Handbook (7^th Edition):

Cai, Na, 1988-. “The functional interplay between TPRM7 channel-kinase autophosphorylation and its cellular regulation.” 2018. Web. 17 Apr 2021.

Vancouver:

Cai, Na 1. The functional interplay between TPRM7 channel-kinase autophosphorylation and its cellular regulation. [Internet] [Doctoral dissertation]. Rutgers University; 2018. [cited 2021 Apr 17]. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/57513/.

Council of Science Editors:

Cai, Na 1. The functional interplay between TPRM7 channel-kinase autophosphorylation and its cellular regulation. [Doctoral Dissertation]. Rutgers University; 2018. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/57513/

Vanderbilt University

3. Ward, Nicholas John. The Transient Receptor Potential Vanilloid-1 Channel and Neuronal Survival in Degenerative Disease.

Degree: PhD, Neuroscience, 2014, Vanderbilt University

URL: http://hdl.handle.net/1803/13386

► Neuronal responses to stress are an important component of neurodegenerative disease and may represent targets for therapeutic intervention. In normal and pathogenic physiological conditions, members… (more)

Subjects/Keywords: neurodegeneration; glaucoma; TRPV1; TRP channels

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

APA (6^th Edition):

Ward, N. J. (2014). The Transient Receptor Potential Vanilloid-1 Channel and Neuronal Survival in Degenerative Disease. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://hdl.handle.net/1803/13386

Chicago Manual of Style (16^th Edition):

Ward, Nicholas John. “The Transient Receptor Potential Vanilloid-1 Channel and Neuronal Survival in Degenerative Disease.” 2014. Doctoral Dissertation, Vanderbilt University. Accessed April 17, 2021. http://hdl.handle.net/1803/13386.

MLA Handbook (7^th Edition):

Ward, Nicholas John. “The Transient Receptor Potential Vanilloid-1 Channel and Neuronal Survival in Degenerative Disease.” 2014. Web. 17 Apr 2021.

Vancouver:

Ward NJ. The Transient Receptor Potential Vanilloid-1 Channel and Neuronal Survival in Degenerative Disease. [Internet] [Doctoral dissertation]. Vanderbilt University; 2014. [cited 2021 Apr 17]. Available from: http://hdl.handle.net/1803/13386.

Council of Science Editors:

Ward NJ. The Transient Receptor Potential Vanilloid-1 Channel and Neuronal Survival in Degenerative Disease. [Doctoral Dissertation]. Vanderbilt University; 2014. Available from: http://hdl.handle.net/1803/13386

Columbia University

4. Benvin, Nicole Marie. Structural and Functional Studies of TRPML1 and TRPP2.

Degree: 2017, Columbia University

URL: https://doi.org/10.7916/D8NG4X0F

► In recent years, the determination of several high-resolution structures of transient receptor potential (TRP) channels has led to significant progress within this field. The primary… (more)

Subjects/Keywords: Biology; Biochemistry; Biophysics; TRP channels; Proteins – Structure

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

APA (6^th Edition):

Benvin, N. M. (2017). Structural and Functional Studies of TRPML1 and TRPP2. (Doctoral Dissertation). Columbia University. Retrieved from https://doi.org/10.7916/D8NG4X0F

Chicago Manual of Style (16^th Edition):

Benvin, Nicole Marie. “Structural and Functional Studies of TRPML1 and TRPP2.” 2017. Doctoral Dissertation, Columbia University. Accessed April 17, 2021. https://doi.org/10.7916/D8NG4X0F.

MLA Handbook (7^th Edition):

Benvin, Nicole Marie. “Structural and Functional Studies of TRPML1 and TRPP2.” 2017. Web. 17 Apr 2021.

Vancouver:

Benvin NM. Structural and Functional Studies of TRPML1 and TRPP2. [Internet] [Doctoral dissertation]. Columbia University; 2017. [cited 2021 Apr 17]. Available from: https://doi.org/10.7916/D8NG4X0F.

Council of Science Editors:

Benvin NM. Structural and Functional Studies of TRPML1 and TRPP2. [Doctoral Dissertation]. Columbia University; 2017. Available from: https://doi.org/10.7916/D8NG4X0F

Hong Kong University of Science and Technology

5. Lau, Chin Fan. Aspects of mechanoperception in dinoflagellates.

Degree: 2012, Hong Kong University of Science and Technology

URL: http://repository.ust.hk/ir/Record/1783.1-73398 ; https://doi.org/10.14711/thesis-b1190227 ; http://repository.ust.hk/ir/bitstream/1783.1-73398/1/th_redirect.html

► Mechanoperception is one of the fundamental physiological functions in many cell types. The Transient Receptor Potential (TRP) Cation channels are one of the major families… (more)

Subjects/Keywords: Dinoflagellates ; Genetics ; Cells ; Growth ; Regulation ; TRP channels

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APA (6^th Edition):

Lau, C. F. (2012). Aspects of mechanoperception in dinoflagellates. (Thesis). Hong Kong University of Science and Technology. Retrieved from http://repository.ust.hk/ir/Record/1783.1-73398 ; https://doi.org/10.14711/thesis-b1190227 ; http://repository.ust.hk/ir/bitstream/1783.1-73398/1/th_redirect.html

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):

Lau, Chin Fan. “Aspects of mechanoperception in dinoflagellates.” 2012. Thesis, Hong Kong University of Science and Technology. Accessed April 17, 2021. http://repository.ust.hk/ir/Record/1783.1-73398 ; https://doi.org/10.14711/thesis-b1190227 ; http://repository.ust.hk/ir/bitstream/1783.1-73398/1/th_redirect.html.

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

MLA Handbook (7^th Edition):

Lau, Chin Fan. “Aspects of mechanoperception in dinoflagellates.” 2012. Web. 17 Apr 2021.

Vancouver:

Lau CF. Aspects of mechanoperception in dinoflagellates. [Internet] [Thesis]. Hong Kong University of Science and Technology; 2012. [cited 2021 Apr 17]. Available from: http://repository.ust.hk/ir/Record/1783.1-73398 ; https://doi.org/10.14711/thesis-b1190227 ; http://repository.ust.hk/ir/bitstream/1783.1-73398/1/th_redirect.html.

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

Council of Science Editors:

Lau CF. Aspects of mechanoperception in dinoflagellates. [Thesis]. Hong Kong University of Science and Technology; 2012. Available from: http://repository.ust.hk/ir/Record/1783.1-73398 ; https://doi.org/10.14711/thesis-b1190227 ; http://repository.ust.hk/ir/bitstream/1783.1-73398/1/th_redirect.html

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

University of Hong Kong

6. Wang, Qian. Mechanistic study of the transient receptor potential melastain 2 (TRPM2)-Ca²⁺ signaling in ROS induced switch between apoptosis and autophagy.

Degree: 2014, University of Hong Kong

URL: http://hdl.handle.net/10722/206750

► Autophagy is a major catabolic pathway for maintaining cell homeostasis through degradation and recycle of macromolecules and organelles. Autophagy can be activated under environmental stress… (more)

▼ Autophagy is a major catabolic pathway for maintaining cell homeostasis through degradation and recycle of macromolecules and organelles. Autophagy can be activated under environmental stress conditions, including reactive oxygen species (ROS). TRPM2, a non-selective trans-membrane calcium channel, can be activated by ROS that, in turn, leads to intracellular 〖Ca〗^(2+) increase through 〖Ca〗^(2+) influx. It is well known that ROS regulates autophagy, and vice versa. Yet, the molecular mechanisms underlying the interplay between ROS and autophagy remain elusive. Here we studied the role of TRPM2-mediated 〖Ca〗^(2+) influx in interplay between ROS and autophagy. From our study, we found that ROS activated TRPM2 for 〖Ca〗^(2+) influx via ADPR to inhibit early autophagy induction, which ultimately led to apoptosis in TRPM2 expressing cancer cell lines. On the other hand, ROS induced autophagy, not apoptosis, for cell survival in cancer cell lines which do not express TRPM2, and autophagy inhibition, either by ATG5 knockdown or by treating cells with bafilomycin A1 (an autophagy inhibitor), converted cells to apoptosis upon ROS treatment. In addition, ROS dramatically changed mitochondrial morphology, increased mitochondrial 〖Ca〗^(2+) content, and abolished mitochondrial membrane potential in TRPM2 expressing cells. Moreover, we found that ROS-induced Ca2+ influx via TRPM2 actually activated calmodulin-dependent protein kinase II (CaMKII) to phosphorylate Ser295 on Beclin1. Phosphorylated Beclin1, in turn, decreased the association between Beclin1 and VPS34, but induced the binding between Beclin1 and BCL-2. In summary, our data demonstrated that the TRPM2/〖Ca〗^(2+)/CaMKII/ Beclin1 cascade is the molecular switch between autophagy and apoptosis in response to ROS. Since dysregulation of ROS and autophagy has been associated with a variety of human diseases, e.g. cancer, neurological disorders, heart diseases, and liver diseases, manipulating the TRPM2/〖Ca〗^(2+)/CaMKII/ Beclin1 cascade should provide novel treatment option for these diseases.

Subjects/Keywords: TRP channels; Apoptosis

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APA (6^th Edition):

Wang, Q. (2014). Mechanistic study of the transient receptor potential melastain 2 (TRPM2)-Ca²⁺ signaling in ROS induced switch between apoptosis and autophagy. (Thesis). University of Hong Kong. Retrieved from http://hdl.handle.net/10722/206750

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, Qian. “Mechanistic study of the transient receptor potential melastain 2 (TRPM2)-Ca²⁺ signaling in ROS induced switch between apoptosis and autophagy.” 2014. Thesis, University of Hong Kong. Accessed April 17, 2021. http://hdl.handle.net/10722/206750.

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, Qian. “Mechanistic study of the transient receptor potential melastain 2 (TRPM2)-Ca²⁺ signaling in ROS induced switch between apoptosis and autophagy.” 2014. Web. 17 Apr 2021.

Vancouver:

Wang Q. Mechanistic study of the transient receptor potential melastain 2 (TRPM2)-Ca²⁺ signaling in ROS induced switch between apoptosis and autophagy. [Internet] [Thesis]. University of Hong Kong; 2014. [cited 2021 Apr 17]. Available from: http://hdl.handle.net/10722/206750.

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

Council of Science Editors:

Wang Q. Mechanistic study of the transient receptor potential melastain 2 (TRPM2)-Ca²⁺ signaling in ROS induced switch between apoptosis and autophagy. [Thesis]. University of Hong Kong; 2014. Available from: http://hdl.handle.net/10722/206750

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

Rutgers University

7. Lou, Liping, 1982-. Investigation of the function and regulation of the TRPM7 ion channel in the renal proximal tubule.

Degree: PhD, TRPM7, 2019, Rutgers University

URL: https://rucore.libraries.rutgers.edu/rutgers-lib/60852/

► The TRPM7 (Transient Receptor Potential Melastatin 7) ion channel is a unique member of the TRP channel family, possessing its own functional kinase domain at… (more)

▼ The TRPM7 (Transient Receptor Potential Melastatin 7) ion channel is a unique member of the TRP channel family, possessing its own functional kinase domain at its COOH-terminus. As a Mg2+-permeable ion channel, TRPM7 has frequently been linked to the regulation of magnesium reabsorption at both the cellular and whole-body level. Mg2+ plays a pivotal role in human health and disease, and therefore, its level in the body has to be tightly regulated via ion channels and transporters in the functional unit of the kidney, the nephron. TRPM6, the close homolog of TRPM7, has been identified to be the major player regulating Mg2+ reabsorption in the distal convoluted tubule of the nephron. A major gap in our knowledge of TRPM7 is whether the channel is involved in regulating magnesium homeostasis in the proximal tubule of the nephron, where TRPM7 is highly expressed. To gain insight into the function of TRPM7 in the proximal tubule, we generated two conditional strains of proximal tubule-specific trpm7 KO mice, using PEPCK-Cre and gGT-Cre mice. The Mg2+ status of the proximal tubule trpm7 knockout mice was assessed but we did not obtain any evidence that the Mg2+ homeostasis was disrupted in the animals, indicating TRPM7 does not play a major role in proximal tubule to regulate whole-body magnesium homeostasis. However, large cavities and reduced cortical layers in the kidney anatomy of some female gGT-Cre KO trpm7 mice were observed. TRPM7 has previously been implicated in the regulation of cell-cell adhesion, having recently been found to contribute to the intercellular junction formation in the bladder urothelium. We performed transmission electron microscopy (TEM) analysis of the tissue slides obtained from the cortex of the kidneys from gGT-Cre KO trpm7 mice and found that tubule epithelial cells from the trpm7 KO mice had more impaired intercellular junctions than that from the control mice. We next investigated the relationship between TRPM7 and cell-cell adhesion process, employing the proximal tubule epithelial cell line, opossum kidney (OK) cells, as a cellular model. Mass spectrometric analysis uncovered that TRPM7 interacted with a cell adhesion protein called plakoglobin. Using immunocytochemical assays, we discovered that TRPM7 co-localized with plakoglobin and another adherens junction protein called E-cadherin. Application of the TRPM7’s channel blocker NS8593 to OK cells reduced E-cadherin expression and localization to adherens junctions. Taken together, these data suggest that TRPM7 is involved in controlling cell-cell adhesion in proximal tubule epithelial cells. In this study, we also explored the mechanism(s) by which TRPM7’s cellular localization is regulated. Using biochemical and immunocytochemical approaches, we identified a regulatory site at the COOH-terminus of TRPM7, the channel’s PDZ-binding motif, through which the localization of TRPM7 in OK cells could be regulated. Deletion of the channel’s PDZ-binding motif shortened the retention time of the mutant TRPM7 (TRPM7ΔPDZ) at adherens… Advisors/Committee Members: Runnels, Loren W (chair), Ryazanov, Alexey G (internal member), Sesti, Federico (internal member), Fan, Huizhou (outside member), School of Graduate Studies.

Subjects/Keywords: Pharmacology, Cellular and Molecular; TRP channels

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APA (6^th Edition):

Lou, Liping, 1. (2019). Investigation of the function and regulation of the TRPM7 ion channel in the renal proximal tubule. (Doctoral Dissertation). Rutgers University. Retrieved from https://rucore.libraries.rutgers.edu/rutgers-lib/60852/

Chicago Manual of Style (16^th Edition):

Lou, Liping, 1982-. “Investigation of the function and regulation of the TRPM7 ion channel in the renal proximal tubule.” 2019. Doctoral Dissertation, Rutgers University. Accessed April 17, 2021. https://rucore.libraries.rutgers.edu/rutgers-lib/60852/.

MLA Handbook (7^th Edition):

Lou, Liping, 1982-. “Investigation of the function and regulation of the TRPM7 ion channel in the renal proximal tubule.” 2019. Web. 17 Apr 2021.

Vancouver:

Lou, Liping 1. Investigation of the function and regulation of the TRPM7 ion channel in the renal proximal tubule. [Internet] [Doctoral dissertation]. Rutgers University; 2019. [cited 2021 Apr 17]. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/60852/.

Council of Science Editors:

Lou, Liping 1. Investigation of the function and regulation of the TRPM7 ion channel in the renal proximal tubule. [Doctoral Dissertation]. Rutgers University; 2019. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/60852/

Michigan State University

8. Hannon, Heidi Elise. Assessing the role of the transient receptor potential A1 channel in methylmercury-induced neurotoxicity.

Degree: 2016, Michigan State University

URL: http://etd.lib.msu.edu/islandora/object/etd:3931

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Thesis Ph. D. Michigan State University. Comparative Medicine and Integrative Biology 2016

Methylmercury (MeHg) is an environmental contaminant which bioaccumulates in aquatic food chains and,… (more)

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Thesis Ph. D. Michigan State University. Comparative Medicine and Integrative Biology 2016

Methylmercury (MeHg) is an environmental contaminant which bioaccumulates in aquatic food chains and, because fish and piscivorous animal species are global commodities, the potential for human exposure to this toxicant knows no geographic boundary. Human populations exposed to MeHg, either acutely or chronically, present with severe neurologic symptoms, with the preeminent clinical sign being distal paresthesia. The definitive mechanisms by which this pathologic state arises remains elusive, though the penultimate event is widespread degeneration somatosensory neurons of the dorsal root ganglia (DRG). Moreover, following in vivo MeHg exposure, a significant reduction in the size and number of large-fiber mechanoreceptive afferents is measurable, with a relative sparing of small-fiber nociceptive afferents and motor efferents. MeHg-induced cytotoxicity has been attributed to unregulated increase in intracellular Ca2+ concentration ([Ca2+]i); this perturbation arises in kinetically distinct phases, with sources of Ca2+ including efflux from intracellular storage organelles, and influx through Ca2+-permeable ion channels. The transient receptor potential (TRP) family of ion channels has been implicated as potential targets for MeHg due to their Ca2+ permeability, high expression in DRG neurons, and polymodal means of activation. The objective of this study was to determine whether the ankyrin 1 TRP channel isoform (TRPA1) selectively confers MeHg sensitivity on large-fiber DRG, and to characterize the contribution of TRPA1 to MeHg-induced [Ca2+]i dysregulation; TRPA1 was selected as a putative target for its role as a mechanoreceptor and potential for activation via cysteine-reactive compounds. Recombinant TRPA1, when acutely exposed to MeHg in vitro, contributed to MeHg-induced [Ca2+]i dysregulation and cell death in an extracellular Ca2+ (Ca2+e)-dependent manner. MeHg-induced [Ca2+]i elevations and neurotoxicity was also Ca2+e-dependent in acute dissociations of primary DRG, however the definitive contribution of TRPA1 as a mediator of Ca2+ influx could not be confirmed. Rather, whole-cell current recordings of large-fiber DRG revealed Na+ as the primary charge carrier in agonist-induced activation of TRPA1, and the onset of [Ca2+]i disruption was dependent upon extracellular Na+. This work contributes to our understanding of the actions of MeHg on TRP channels and implicates a role for other cations in mediating MeHg-induced [Ca2+]i dysregulation.

Description based on online resource;

Advisors/Committee Members: Atchison, William D, Barman, Susan M, Flink, Michael T, Ganey, Patricia E, Yuan, Yukun.

Subjects/Keywords: TRP channels; Methylmercury; Neurotoxicology; Toxicology; Neurosciences

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APA (6^th Edition):

Hannon, H. E. (2016). Assessing the role of the transient receptor potential A1 channel in methylmercury-induced neurotoxicity. (Thesis). Michigan State University. Retrieved from http://etd.lib.msu.edu/islandora/object/etd:3931

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):

Hannon, Heidi Elise. “Assessing the role of the transient receptor potential A1 channel in methylmercury-induced neurotoxicity.” 2016. Thesis, Michigan State University. Accessed April 17, 2021. http://etd.lib.msu.edu/islandora/object/etd:3931.

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

MLA Handbook (7^th Edition):

Hannon, Heidi Elise. “Assessing the role of the transient receptor potential A1 channel in methylmercury-induced neurotoxicity.” 2016. Web. 17 Apr 2021.

Vancouver:

Hannon HE. Assessing the role of the transient receptor potential A1 channel in methylmercury-induced neurotoxicity. [Internet] [Thesis]. Michigan State University; 2016. [cited 2021 Apr 17]. Available from: http://etd.lib.msu.edu/islandora/object/etd:3931.

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

Council of Science Editors:

Hannon HE. Assessing the role of the transient receptor potential A1 channel in methylmercury-induced neurotoxicity. [Thesis]. Michigan State University; 2016. Available from: http://etd.lib.msu.edu/islandora/object/etd:3931

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

University of Newcastle

9. Nikolaev, Yury A. Mechanosensitivity of the TRPC6 ion channel.

Degree: PhD, 2018, University of Newcastle

URL: http://hdl.handle.net/1959.13/1387381

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Research Doctorate - Doctor of Philosophy (PhD)

The transient receptor potential (TRP) ion channel family is a diverse group of channels gated by various physical… (more)

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Research Doctorate - Doctor of Philosophy (PhD)

The transient receptor potential (TRP) ion channel family is a diverse group of channels gated by various physical and chemical stimuli. One of the members, TRPC6, is a cation channel, which is expressed in ventricular cardiomyocytes (CMs). TRPC6 is gated via the G-protein-coupled receptor pathway leading to generation of diacylglycerol (DAG), which ultimately activates the ion channel. TRPC6 can also be activated by mechanical force, which for example plays a significant role in mechanotransduction of the heart. However, it is still unclear whether TRPC6 is activated directly by membrane tension or its activation is mediated via other mechanosensitive membrane structures, such as the cytoskeleton and/or the extracellular matrix. The aim of this study is to determine whether TRPC6 is an inherently mechanosensitive (MS) ion channel. First, mechanosensitivity of TRPC6 was evaluated in HEK293 cells by stretching the membrane via application of negative pressure (suction) to a patch pipette. Spontaneously active TRPC6 channel did not respond to the force. Second, using a stretch device, 15% isotropic stretch was applied to the intact cells attached to the bottom of stretchable PDMS chambers and calcium entry via TRPC6 ion channels was demonstrated. The effect, suggested mechanosensitive nature of TRPC6 channel in the cells, however, it remained unclear whether mechanosensitivity is inherent or promoted via other membrane components. To answer this question, using the purified TRPC6 protein, liposome reconstitution was carried out. Spontaneous activity of the TRPC6 single channel was demonstrated in the liposome by the patch clamp. The channel was activated according to “force-from-lipids” principle; however, application of stretch did not change the open probability of the channel. Therefore, it has been concluded that TRPC6 is not stretch activated upon application. Furthermore, the role of TRPC6 in cardiac hypertrophy was investigated. Immunostaining of TRPC6 in hypertrophic CMs revealed that the channel migrates from the intracellular t-tubules to the sarcolemma. Furthermore, the impact of MS channels on the Ca2+ homeostasis in the CMs was investigated. A new method was developed, which allowed stretching of hydrogel embedded CM in multiaxial (isotropic) directions and simultaneous measurement of Ca2+ fluorescence. Both normal and hypertrophic CMs showed a late mechanical response 300s after the stretch. MS channels were only activated after long-term induced stretch, which suggests their mechanoprotective role in the heart. The main finding of the thesis is that the TRPC6 ion channel is not inherently mechanosensitive since it is unresponsive to membrane stretch; instead it is activated by “force-from-lipids” principle without involvement of any other membrane components. Since abnormal TRPC6 activity is implicated in cardiac hypertrophy, our findings contribute to a better understanding of pathophysiological mechanisms of hypertrophy and may open up new directions…

Advisors/Committee Members: University of Newcastle. Faculty of Health & Medicine , School of Biomedical Sciences and Pharmacy.

Subjects/Keywords: TRP ion channels; mechanosensitive ion channels; TRPC6; cardiac hypertrophy; cardiomyocyte

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APA (6^th Edition):

Nikolaev, Y. A. (2018). Mechanosensitivity of the TRPC6 ion channel. (Doctoral Dissertation). University of Newcastle. Retrieved from http://hdl.handle.net/1959.13/1387381

Chicago Manual of Style (16^th Edition):

Nikolaev, Yury A. “Mechanosensitivity of the TRPC6 ion channel.” 2018. Doctoral Dissertation, University of Newcastle. Accessed April 17, 2021. http://hdl.handle.net/1959.13/1387381.

MLA Handbook (7^th Edition):

Nikolaev, Yury A. “Mechanosensitivity of the TRPC6 ion channel.” 2018. Web. 17 Apr 2021.

Vancouver:

Nikolaev YA. Mechanosensitivity of the TRPC6 ion channel. [Internet] [Doctoral dissertation]. University of Newcastle; 2018. [cited 2021 Apr 17]. Available from: http://hdl.handle.net/1959.13/1387381.

Council of Science Editors:

Nikolaev YA. Mechanosensitivity of the TRPC6 ion channel. [Doctoral Dissertation]. University of Newcastle; 2018. Available from: http://hdl.handle.net/1959.13/1387381

Columbia University

10. Saotome, Kei. Structural Studies of a Mammalian Epithelial Calcium Channel.

Degree: 2016, Columbia University

URL: https://doi.org/10.7916/D80C4W8P

► Calcium plays an essential role in the physiology and biochemistry of many biological functions, including excitation-contraction coupling, neuronal signaling, and fertilization. In mammals, the calcium… (more)

▼ Calcium plays an essential role in the physiology and biochemistry of many biological functions, including excitation-contraction coupling, neuronal signaling, and fertilization. In mammals, the calcium content in various tissues, organs, and cell types is tightly regulated to maintain homeostasis. A chief process controlling calcium levels is absorption of the ion from the lumen by epithelial cells that line organs including the intestines and kidney. Calcium entry at the apical membrane constitutes the first step of epithelial calcium absorption. Two highly calcium-selective transient receptor potential vanilloid (TRPV) channels, TRPV5 and TRPV6, are the pore-forming subunits responsible for epithelial calcium entry in kidney and intestine, respectively. Genetic knockout of TRPV5 or TRPV6 in animals leads to phenotypes related to defective calcium homeostasis, including lowered serum calcium levels, decreased calcium absorption, reduced bone density, impaired sperm motility, and decreased maternal-fetal calcium transfer. In humans, aberrant TRPV5/6 expression is associated with preeclampsia and calcium nephrolithiasis (kidney stones). Additionally, TRPV6 expression level is upregulated in carcinomas of prostate, colon, breast, thyroid, and ovary, suggesting a role for TRPV6 in cancer survival. A detailed understanding of epithelial calcium entry is hindered by a lack of high-resolution structural information on intact channels. This dissertation presents structural analyses of the epithelial calcium channel TRPV6. We applied modern membrane protein screening and expression techniques, including fluorescence-detection size exclusion chromatography (FSEC) and baculovirus mediated mammalian cell transduction (BacMam), to identify optimal TRPV6 constructs and purification schemes for crystallization. Using a surface mutagenesis approach guided by lower-resolution structural solutions, we engineered a rat TRPV6 mutant (TRPV6cryst) that permitted solving a 3.25 Å resolution crystal structure. We used fluorescent calcium indicator assays to show that TRPV6cryst retains the permeation and ionic block properties of the wild type channel. The tetrameric structure of TRPV6cryst reveals a transmembrane domain architecture similar to voltage gated ion channels, with the ion conducting pore coincident with the overall four-fold symmetry axis. A ring of aspartate (D541) residues, shown in previous studies as a critical determinant of calcium selectivity, forms a narrow constriction at the extracellular pore entrance, or selectivity filter. Methionine (M577) side chains in the lower portion of the channel pore plug the conduction pathway and define the closed state of the channel. The ankyrin repeat domain, linker domain, N-terminal helix, and C-terminal hook form an intracellular skirt surrounding a cavity that lies beneath the pore axis. Close interactions between these domains, in large part mediated by the N-terminal helix, suggest that they are involved in allosteric modulation or concerted movements…

Subjects/Keywords: Calcium – Physiological effect; Biochemistry; TRP channels; Calcium channels

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APA (6^th Edition):

Saotome, K. (2016). Structural Studies of a Mammalian Epithelial Calcium Channel. (Doctoral Dissertation). Columbia University. Retrieved from https://doi.org/10.7916/D80C4W8P

Chicago Manual of Style (16^th Edition):

Saotome, Kei. “Structural Studies of a Mammalian Epithelial Calcium Channel.” 2016. Doctoral Dissertation, Columbia University. Accessed April 17, 2021. https://doi.org/10.7916/D80C4W8P.

MLA Handbook (7^th Edition):

Saotome, Kei. “Structural Studies of a Mammalian Epithelial Calcium Channel.” 2016. Web. 17 Apr 2021.

Vancouver:

Saotome K. Structural Studies of a Mammalian Epithelial Calcium Channel. [Internet] [Doctoral dissertation]. Columbia University; 2016. [cited 2021 Apr 17]. Available from: https://doi.org/10.7916/D80C4W8P.

Council of Science Editors:

Saotome K. Structural Studies of a Mammalian Epithelial Calcium Channel. [Doctoral Dissertation]. Columbia University; 2016. Available from: https://doi.org/10.7916/D80C4W8P

Columbia University

11. McGoldrick, Luke Lawrence Reedy. Structural Analyses of the Transient Receptor Potential Channels TRPV3 and TRPV6.

Degree: 2019, Columbia University

URL: https://doi.org/10.7916/d8-d1x5-rw78

► Transient receptor potential (TRP) channels comprise a superfamily of cation-selective ion channels that are largely calcium (Ca2+) permeable and that play diverse physiological roles ranging… (more)

▼ Transient receptor potential (TRP) channels comprise a superfamily of cation-selective ion channels that are largely calcium (Ca2+) permeable and that play diverse physiological roles ranging from nociception in primary afferent neurons to the absorption of dietary Ca2+. The 28 mammalian TRP channels are categorized into 6 subfamilies. The vanilloid subfamily is named for its founding member, TRPV1, the capsaicin receptor, and has 6 members. TRPV1-4 are all heat sensitive ion channels whereas TRPV5 and TRPV6 are involved in renal Ca2+ reabsorption and Ca2+ absorption in the intestine, respectively. In our structural studies, we have focused on TRPV3 and TRPV6. TRPV6 is a highly Ca2+ selective TRP channel (PCa/PNa ~ 130) that functions in active Ca2+ absorption in the intestine. Its expression is upregulated by vitamin D and is, on the molecular level, regulated by PIP2 and calmodulin (CaM). Previously, the structure of TRPV6 was solved using X-ray crystallography. Using the crystal structure, a negatively charged extracellular vestibule was identified and anomalous diffraction was used to identify ion binding sites in the pore. Also, at the top of the selectivity filter, four aspartates were identified that coordinate Ca2+ entering the pore and confer to TRPV6 its selectivity for Ca2+. However, only the structure of the rat orthologue was solved and only in the closed, apo state. We used cryo-electron microscopy (cryo-EM) to solve structures of the human orthologue of TRPV6 in the open and closed (we used the mutation R470E to close the channel) states. The closed-to-open TRPV6 transition is accompanied by the formation of short π-helices in the middle of the pore-lining S6 helices, which in turn results in their turning and a different set of residues facing the pore. Additionally, the formation of the π-helices results in kinking of the S6 helices, which further widens the pore. TRPV6 is constitutively active when expressed heterologously. In other words, the addition of external stimuli is not necessary for the activation of the channel. Therefore, its activity needs to be regulated to prevent toxic Ca2+ overload. One mechanism by which this occurs is through its regulation by CaM. CaM has been shown to bind TRPV6 and regulate its function, however, the way it binds to and regulates TRPV6 remained unknown. To uncover this mechanism, we solved the structure of TRPV6 bound to CaM. We found that CaM binds TRPV6 in a 1:1 stoichiometric ratio and that CaM directly blocks the TRPV6 pore by inserting a positively charged lysine into a tera-tryptophan cage at the bottom of the pore. As a result, the channel adopts an inactivated conformation; although the pore-lining S6 helices still contain local π-helices, they are pulled closer together, narrowing the pore and further blocking it with hydrophobic side chains. We have also conducted studies of TRPV3. Unlike TRPV6, TRPV3 is a heat-activated vanilloid TRP channel. TRPV3 is expressed highly in keratinocytes where it has been implicated in wound healing and…

Subjects/Keywords: Biochemistry; Molecular biology; TRP channels; Structure-activity relationships (Biochemistry); Ion channels

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

APA (6^th Edition):

McGoldrick, L. L. R. (2019). Structural Analyses of the Transient Receptor Potential Channels TRPV3 and TRPV6. (Doctoral Dissertation). Columbia University. Retrieved from https://doi.org/10.7916/d8-d1x5-rw78

Chicago Manual of Style (16^th Edition):

McGoldrick, Luke Lawrence Reedy. “Structural Analyses of the Transient Receptor Potential Channels TRPV3 and TRPV6.” 2019. Doctoral Dissertation, Columbia University. Accessed April 17, 2021. https://doi.org/10.7916/d8-d1x5-rw78.

MLA Handbook (7^th Edition):

McGoldrick, Luke Lawrence Reedy. “Structural Analyses of the Transient Receptor Potential Channels TRPV3 and TRPV6.” 2019. Web. 17 Apr 2021.

Vancouver:

McGoldrick LLR. Structural Analyses of the Transient Receptor Potential Channels TRPV3 and TRPV6. [Internet] [Doctoral dissertation]. Columbia University; 2019. [cited 2021 Apr 17]. Available from: https://doi.org/10.7916/d8-d1x5-rw78.

Council of Science Editors:

McGoldrick LLR. Structural Analyses of the Transient Receptor Potential Channels TRPV3 and TRPV6. [Doctoral Dissertation]. Columbia University; 2019. Available from: https://doi.org/10.7916/d8-d1x5-rw78

12. 渡邊, 成樹. Trpm7 Protein Contributes to Intercellular Junction Formation in Mouse Urothelium : TRPM7蛋白のマウス尿路上皮細胞間結合の形成への関与.

Degree: 博士（医学）, 2017, Asahikawa Medical University / 旭川医科大学

URL: http://amcor.asahikawa-med.ac.jp/modules/xoonips/detail.php?id=20170630_K512

► Trpm7 is a divalent cation-permeable channel that has been reported to be involved in magnesium homeostasis as well as cellular adhesion and migration. We generated… (more)

Subjects/Keywords: animal model; cell junction; epithelial cell; inflammation; transient receptor potential channels (TRP channels)

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APA (6^th Edition):

渡邊, �. (2017). Trpm7 Protein Contributes to Intercellular Junction Formation in Mouse Urothelium : TRPM7蛋白のマウス尿路上皮細胞間結合の形成への関与. (Thesis). Asahikawa Medical University / 旭川医科大学. Retrieved from http://amcor.asahikawa-med.ac.jp/modules/xoonips/detail.php?id=20170630_K512

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):

渡邊, 成樹. “Trpm7 Protein Contributes to Intercellular Junction Formation in Mouse Urothelium : TRPM7蛋白のマウス尿路上皮細胞間結合の形成への関与.” 2017. Thesis, Asahikawa Medical University / 旭川医科大学. Accessed April 17, 2021. http://amcor.asahikawa-med.ac.jp/modules/xoonips/detail.php?id=20170630_K512.

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

MLA Handbook (7^th Edition):

渡邊, 成樹. “Trpm7 Protein Contributes to Intercellular Junction Formation in Mouse Urothelium : TRPM7蛋白のマウス尿路上皮細胞間結合の形成への関与.” 2017. Web. 17 Apr 2021.

Vancouver:

渡邊 �. Trpm7 Protein Contributes to Intercellular Junction Formation in Mouse Urothelium : TRPM7蛋白のマウス尿路上皮細胞間結合の形成への関与. [Internet] [Thesis]. Asahikawa Medical University / 旭川医科大学; 2017. [cited 2021 Apr 17]. Available from: http://amcor.asahikawa-med.ac.jp/modules/xoonips/detail.php?id=20170630_K512.

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

Council of Science Editors:

渡邊 �. Trpm7 Protein Contributes to Intercellular Junction Formation in Mouse Urothelium : TRPM7蛋白のマウス尿路上皮細胞間結合の形成への関与. [Thesis]. Asahikawa Medical University / 旭川医科大学; 2017. Available from: http://amcor.asahikawa-med.ac.jp/modules/xoonips/detail.php?id=20170630_K512

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

University of Pennsylvania

13. Hughes, Taylor. Trpv5: Structure, Function And Drug Discovery.

Degree: 2019, University of Pennsylvania

URL: https://repository.upenn.edu/edissertations/3385

► The transient receptor potential vanilloid 5 (TRPV5) channel is a highly calcium selective ion channel that regulates systemic calcium homeostasis by acting as a critical… (more)

Subjects/Keywords: Cryo-EM; Drug discovery; Ion Channels; Structural biology; TRP channels; TRPV5; Biochemistry; Molecular Biology; Pharmacology

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

APA (6^th Edition):

Hughes, T. (2019). Trpv5: Structure, Function And Drug Discovery. (Thesis). University of Pennsylvania. Retrieved from https://repository.upenn.edu/edissertations/3385

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):

Hughes, Taylor. “Trpv5: Structure, Function And Drug Discovery.” 2019. Thesis, University of Pennsylvania. Accessed April 17, 2021. https://repository.upenn.edu/edissertations/3385.

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

MLA Handbook (7^th Edition):

Hughes, Taylor. “Trpv5: Structure, Function And Drug Discovery.” 2019. Web. 17 Apr 2021.

Vancouver:

Hughes T. Trpv5: Structure, Function And Drug Discovery. [Internet] [Thesis]. University of Pennsylvania; 2019. [cited 2021 Apr 17]. Available from: https://repository.upenn.edu/edissertations/3385.

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

Council of Science Editors:

Hughes T. Trpv5: Structure, Function And Drug Discovery. [Thesis]. University of Pennsylvania; 2019. Available from: https://repository.upenn.edu/edissertations/3385

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

University of Tasmania

14. Gasperini, RJ. Homer, TRP channels and calcium : the signalling triad of growth cone motility.

Degree: 2008, University of Tasmania

URL: https://eprints.utas.edu.au/19858/1/whole_GasperiniRobertJohn2008_thesis.pdf ; Gasperini, RJ ORCID: 0000-0001-6859-1247 <https://orcid.org/0000-0001-6859-1247> 2008 , 'Homer, TRP channels and calcium : the signalling triad of growth cone motility', PhD thesis, University of Tasmania.

► The nervous system is an elaborate network of intricate circuits linking, monitoring and controlling all functions in the body. This circuitry, established early in development,… (more)

▼ The nervous system is an elaborate network of intricate circuits linking, monitoring and controlling all functions in the body. This circuitry, established early in development, is defined by a process known as axon guidance. The precision and accuracy of this circuitry is ultimately a correlate of the navigational capabilities of specialised structures at the distal tips of extending axons, the growth cones. Growth cones are equipped with an array of fine antennal projections, or filipodia, sensitive to a variety of attractive or repulsive signals. These guidance cues are detected and interpreted by intracellular signal transduction mechanisms that mediate cytoskeletal rearrangements within the growth cone, ultimately providing directional control of growth cone trajectories. Guidance cues may be diffusible molecules from distant target tissues or components of contacting cells, however, the complete repertoire of molecules that transduce these extracellular signals to the cytosolic cytoskeletal machinery are yet to be fully understood. Neurons have evolved a variety of important intracellular signal transduction pathways, many of which rely on calcium as a key second messenger molecule. Many crucial pre- and post-synaptic functions in neurons are mediated by changes in intracellular calcium concentration ([Ca(²⁺)]i,) including filipodial protrusion and neurite elongation. Indeed, spatial [Ca(²⁺)]i gradients within the growth cone are crucial for the appropriate recognition and motile responses to the key guidance molecules netrin-1 and brain derived neurotrophic factor (BDNF). Cytosolic calcium is highly regulated with the key calcium buffering organelle being the endoplasmic reticulum (ER). The mechanisms regulating the transduction of extracellular guidance signals to changes in ER mediated calcium release, however, are still to be determined. This thesis describes work focusing on the elucidation of a molecular correlate of such a mechanism. Homer proteins are best known as facilitators of receptor clustering and signalling at the post synaptic density. Long form Homer (H1b/c) forms dimers via C-terminal coiled-coil domains, cross-linking multiple signalling partners through N-terminal, enabled-VASP homology (EVH1) domains. This molecular motif enables Homer proteins to couple cell-surface receptors such as metabotropic glutamate receptors (mGluR) and transient receptor potential cation channels (TRPC) to intracellular calcium stores via inositol triphosphate (IP(₃)R) and ryanodine (RyR) receptors. Homer is necessary for axon pathfinding in the amphibian visual system in vivo, in a mechanism that to date, has remained elusive. The unique binding characteristics of this synaptic molecule, the subcellular location and physiological relevance of its binding partners makes Homer a good candidate molecule to facilitate the coupling of extracellular guidance cues to changes in [Ca(⁺⁺)]i. This study addresses the following questions: What is the biochemical nature of Homer function in axon…

Subjects/Keywords: TRP channels; Proteins; Molecular neurobiology

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APA (6^th Edition):

Gasperini, R. (2008). Homer, TRP channels and calcium : the signalling triad of growth cone motility. (Thesis). University of Tasmania. Retrieved from https://eprints.utas.edu.au/19858/1/whole_GasperiniRobertJohn2008_thesis.pdf ; Gasperini, RJ ORCID: 0000-0001-6859-1247 <https://orcid.org/0000-0001-6859-1247> 2008 , 'Homer, TRP channels and calcium : the signalling triad of growth cone motility', PhD thesis, University of Tasmania.

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):

Gasperini, RJ. “Homer, TRP channels and calcium : the signalling triad of growth cone motility.” 2008. Thesis, University of Tasmania. Accessed April 17, 2021. https://eprints.utas.edu.au/19858/1/whole_GasperiniRobertJohn2008_thesis.pdf ; Gasperini, RJ ORCID: 0000-0001-6859-1247 <https://orcid.org/0000-0001-6859-1247> 2008 , 'Homer, TRP channels and calcium : the signalling triad of growth cone motility', PhD thesis, University of Tasmania..

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

MLA Handbook (7^th Edition):

Gasperini, RJ. “Homer, TRP channels and calcium : the signalling triad of growth cone motility.” 2008. Web. 17 Apr 2021.

Vancouver:

Gasperini R. Homer, TRP channels and calcium : the signalling triad of growth cone motility. [Internet] [Thesis]. University of Tasmania; 2008. [cited 2021 Apr 17]. Available from: https://eprints.utas.edu.au/19858/1/whole_GasperiniRobertJohn2008_thesis.pdf ; Gasperini, RJ ORCID: 0000-0001-6859-1247 <https://orcid.org/0000-0001-6859-1247> 2008 , 'Homer, TRP channels and calcium : the signalling triad of growth cone motility', PhD thesis, University of Tasmania..

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

Council of Science Editors:

Gasperini R. Homer, TRP channels and calcium : the signalling triad of growth cone motility. [Thesis]. University of Tasmania; 2008. Available from: https://eprints.utas.edu.au/19858/1/whole_GasperiniRobertJohn2008_thesis.pdf ; Gasperini, RJ ORCID: 0000-0001-6859-1247 <https://orcid.org/0000-0001-6859-1247> 2008 , 'Homer, TRP channels and calcium : the signalling triad of growth cone motility', PhD thesis, University of Tasmania.

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

University of Toronto

15. Tong, Steven. The Role of Oxidative Stress on Neural TRPC3, TRPC5, TRPC6 Expression and/or Function and Relevance to Bipolar Disorder.

Degree: 2012, University of Toronto

URL: http://hdl.handle.net/1807/32495

►

The etiology of bipolar disorder (BD) is multidimensional and thought to involve several factors that increase neuronal oxidative stress and disrupt intracellular calcium homeostasis. As… (more)

Subjects/Keywords: Bipolar Disorder; Oxidative Stress; TRP Channels; Calcium; 0317

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APA (6^th Edition):

Tong, S. (2012). The Role of Oxidative Stress on Neural TRPC3, TRPC5, TRPC6 Expression and/or Function and Relevance to Bipolar Disorder. (Masters Thesis). University of Toronto. Retrieved from http://hdl.handle.net/1807/32495

Chicago Manual of Style (16^th Edition):

Tong, Steven. “The Role of Oxidative Stress on Neural TRPC3, TRPC5, TRPC6 Expression and/or Function and Relevance to Bipolar Disorder.” 2012. Masters Thesis, University of Toronto. Accessed April 17, 2021. http://hdl.handle.net/1807/32495.

MLA Handbook (7^th Edition):

Tong, Steven. “The Role of Oxidative Stress on Neural TRPC3, TRPC5, TRPC6 Expression and/or Function and Relevance to Bipolar Disorder.” 2012. Web. 17 Apr 2021.

Vancouver:

Tong S. The Role of Oxidative Stress on Neural TRPC3, TRPC5, TRPC6 Expression and/or Function and Relevance to Bipolar Disorder. [Internet] [Masters thesis]. University of Toronto; 2012. [cited 2021 Apr 17]. Available from: http://hdl.handle.net/1807/32495.

Council of Science Editors:

Tong S. The Role of Oxidative Stress on Neural TRPC3, TRPC5, TRPC6 Expression and/or Function and Relevance to Bipolar Disorder. [Masters Thesis]. University of Toronto; 2012. Available from: http://hdl.handle.net/1807/32495

University of Delaware

16. Hurd, Lauren M. Elucidating the role of Transient Receptor Potential Channel Vanilloid 4 (TRPV4) mutation on channel activity and chondrocyte function in metatropic dysplasia.

Degree: PhD, University of Delaware, Department of Biological Sciences, 2015, University of Delaware

URL: http://udspace.udel.edu/handle/19716/17450

► Metatropic dysplasia (MD) is a severe skeletal dysplasia that results in a significant impact on quality of life in patients diagnosed with disease. MD is… (more)

▼ Metatropic dysplasia (MD) is a severe skeletal dysplasia that results in a significant impact on quality of life in patients diagnosed with disease. MD is characterized by striking skeletal changes which include general shortening of long bones, widened metaphysis, and halberd shaped pelvis. Over time, patients display wedging of vertebral bodies (platyspondyly), and progressive kyphoscoliosis. These spinal changes result in reduced spinal integrity with cervical vertebrae instability, spinal stenosis and a reduced respiratory capacity. Mutations in non-selective cation channel, Transient Receptor Potential Channel Vanilloid 4 (TRPV4) have been found to cause MD. TRPV4 associated channelopathies also include peripheral neuropathies and other skeletal dysplasias that range in clinical severity and symptomatic phenotype. As a result, causation, classification and development of TRPV4 channelopathies are very complex. TRPV4 channel activity is integral in the Ca2+ mediated response to a large variety of sensory stimulation from the extracellular environment. TRPV4 activity can also be regulated by changes in temperature, nociception and natural and synthetic ligands, such as arachidonic acid metabolites and phorbol esters. It is most classically studied as a regulator of Ca 2+ response to changes in osmotic and mechanical forces. The spatial, temporal and intensive properties of [Ca2+ ]i as well as spontaneous Ca2+ oscillations can have a profound effect on cell behavior. In the musculoskeletal system, TRPV4 Ca2+ signaling regulates the chondrogenic response to osmotic signals and anabolic chondrogenic response under mechanical loads. TRPV4 also plays a chondroprotective role in normal articular cartilage and is imperative to maintaining joint health. Loss of TRPV4 often results in osteoarthritis. Whereas most information pertains to normal TRPV4 physiology and signaling, the effect of TRPV4 mutation in terms on skeletal development has only recently been studied. Histological analysis of growth plates from lethal variants of MD revealed a highly unorganized growth plate with reduced hypertrophic regions and delayed endochondral ossification, suggesting that mutational TRPV4 activity disrupts ordered chondrogenesis. Expression of TRPV4 mutations in numerous cell types alludes to gain-of function activity that results in increased basal and stimulated intracellular Ca 2+ ([Ca2+ ]i ) activity, as well as constitutively open channel gating. However, most studies have been performed in non-endogenous cell types that are either transfected or transformed. To better understand channel properties directly affected by disease, we studied the effect of two TRPV4 mutations, p.Pro799Leu and p.Gly800Asp on Ca2+ channel activity and chondrocyte function in cells directly isolated from patients with metatropic dysplasia. P.Pro799Leu is considered a mutational hotspot and there is a high prevalence of this specific mutation in disease, whereas p.Gly800Asp is a novel severe mutation identified by our group. We hypothesize that… Advisors/Committee Members: Duncan, Randall L.Funanage, Vicky L..

Subjects/Keywords: Dysplasia.; Human skeleton – Abnormalities.; TRP channels.; Cartilage cells.

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

APA (6^th Edition):

Hurd, L. M. (2015). Elucidating the role of Transient Receptor Potential Channel Vanilloid 4 (TRPV4) mutation on channel activity and chondrocyte function in metatropic dysplasia. (Doctoral Dissertation). University of Delaware. Retrieved from http://udspace.udel.edu/handle/19716/17450

Chicago Manual of Style (16^th Edition):

Hurd, Lauren M. “Elucidating the role of Transient Receptor Potential Channel Vanilloid 4 (TRPV4) mutation on channel activity and chondrocyte function in metatropic dysplasia.” 2015. Doctoral Dissertation, University of Delaware. Accessed April 17, 2021. http://udspace.udel.edu/handle/19716/17450.

MLA Handbook (7^th Edition):

Hurd, Lauren M. “Elucidating the role of Transient Receptor Potential Channel Vanilloid 4 (TRPV4) mutation on channel activity and chondrocyte function in metatropic dysplasia.” 2015. Web. 17 Apr 2021.

Vancouver:

Hurd LM. Elucidating the role of Transient Receptor Potential Channel Vanilloid 4 (TRPV4) mutation on channel activity and chondrocyte function in metatropic dysplasia. [Internet] [Doctoral dissertation]. University of Delaware; 2015. [cited 2021 Apr 17]. Available from: http://udspace.udel.edu/handle/19716/17450.

Council of Science Editors:

Hurd LM. Elucidating the role of Transient Receptor Potential Channel Vanilloid 4 (TRPV4) mutation on channel activity and chondrocyte function in metatropic dysplasia. [Doctoral Dissertation]. University of Delaware; 2015. Available from: http://udspace.udel.edu/handle/19716/17450

Univerzitet u Beogradu

17. Srebro , Dragana P., 1986-. Farmakodinamska ispitivanja magnezijum-sulfata i dizocilpina u modelima somatskog i visceralnog bola kod pacova.

Degree: Medicinski fakultet, 2016, Univerzitet u Beogradu

URL: https://fedorabg.bg.ac.rs/fedora/get/o:11645/bdef:Content/get

Medicina - Farmakologija / Medicine - Pharmacology

Magnezijum je mineral koji u organizmu ima brojne uloge. On je kofaktor u više od 300 enzimskih reakcija, održava membranski potencijal, ima modulatorno dejstvo na jonske kanale, neurotransmisiju, i drugo...

Subjects/Keywords: magnesium sulfate; dizocilpine; NMDA antagonist; TRP channels; inflammatory pain; edema

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

APA (6^th Edition):

Srebro , Dragana P., 1. (2016). Farmakodinamska ispitivanja magnezijum-sulfata i dizocilpina u modelima somatskog i visceralnog bola kod pacova. (Thesis). Univerzitet u Beogradu. Retrieved from https://fedorabg.bg.ac.rs/fedora/get/o:11645/bdef:Content/get

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

Chicago Manual of Style (16^th Edition):

Srebro , Dragana P., 1986-. “Farmakodinamska ispitivanja magnezijum-sulfata i dizocilpina u modelima somatskog i visceralnog bola kod pacova.” 2016. Thesis, Univerzitet u Beogradu. Accessed April 17, 2021. https://fedorabg.bg.ac.rs/fedora/get/o:11645/bdef:Content/get.

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

MLA Handbook (7^th Edition):

Srebro , Dragana P., 1986-. “Farmakodinamska ispitivanja magnezijum-sulfata i dizocilpina u modelima somatskog i visceralnog bola kod pacova.” 2016. Web. 17 Apr 2021.

Vancouver:

Srebro , Dragana P. 1. Farmakodinamska ispitivanja magnezijum-sulfata i dizocilpina u modelima somatskog i visceralnog bola kod pacova. [Internet] [Thesis]. Univerzitet u Beogradu; 2016. [cited 2021 Apr 17]. Available from: https://fedorabg.bg.ac.rs/fedora/get/o:11645/bdef:Content/get.

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

Council of Science Editors:

Srebro , Dragana P. 1. Farmakodinamska ispitivanja magnezijum-sulfata i dizocilpina u modelima somatskog i visceralnog bola kod pacova. [Thesis]. Univerzitet u Beogradu; 2016. Available from: https://fedorabg.bg.ac.rs/fedora/get/o:11645/bdef:Content/get

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

University of Oxford

18. Hanson, Sonya M. Structural, biochemical and computational studies of TRP channel transmembrane domain modularity.

Degree: PhD, 2014, University of Oxford

URL: http://ora.ox.ac.uk/objects/uuid:328269a9-11c0-4d5b-9cb7-d7433cf4d6c4 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.640060

► Transient receptor potential (TRP) channels are expressed throughout the central nervous system and have a unique ability to detect a wide range of stimuli including… (more)

▼ Transient receptor potential (TRP) channels are expressed throughout the central nervous system and have a unique ability to detect a wide range of stimuli including changes in voltage, temperature, pH, lipid environment, small molecule agonists, and mechanical stress. While it is known that TRP channels contain the same six transmembrane helix (S1-S6), tetrameric architecture as voltage-gated channels, the degree to which functional and structural analogies are relevant remains poorly understood. This thesis describes a multidisciplinary approach toward understanding the structure and function of TRP channel transmembrane domains by focusing on the S1-S4 transmembrane helices of the TRPV1. This focus is inspired by the voltage-sensor domain (VSD) of the S1-S4 helices of voltage-gated channels, for which a range of studies show functional and structural independence. While some TRP channels are voltage-sensitive, their S4 helix does not contain the positive string of amino acids of canonical VSDs. However, the S1-S4 helices are functionally significant as the binding site of small molecule ligands in both TRPV1 and TRPM8 (for capsaicin and menthol, respectively). The question of TRP channel transmembrane domain modularity is addressed in this thesis by expression and purification trials as well as radioligand-binding assays. It is demonstrated that the S1-S4 and S1-S6 helices of TRPV1 can be properly inserted, overexpressed, and show signs of stability upon detergent-extraction from Saccharomyces cerevisiae membranes. However the TRPV1 S1-S4 and S1-S6 helices do not show wildtype (WT)-like binding in [³H]-RTX binding assays. These results indicate that the TRPV1 transmembrane domains are likely structural but not functional domains. The S. cerevisiae expression system remained promising for the overexpression of TRP transmembrane domains as well as the production of functional, though not stable upon detergent-extraction, WT TRPV1. This WT TRPV1 was subsequently found to functionally bind both RTX, used in ligand binding assays, as well as the double-knot toxin (DkTx), targeted to the pore domain (the S5-S6 helices). An effect of DkTx on RTX binding affinity demonstrates an allosteric interaction indicative of a possible tighter packing between the two transmembrane domains than is seen in voltage-gated channels containing the canonical VSD. Computational approaches additionally allowed for the investigation of the intramembrane capsaicin binding site in the TRPV1 S1-S4 helices, crucial to the initial motivations of this study. While the literature locates the capsaicin binding site to the TRPV1 S1-S4 helices, a `binding pocket' has yet to be defined, with regards to the orientation of bound capsaicin and its access route to the site via the bilayer. Using molecular dynamics (MD) simulations the preferred location of capsaicin within the bilayer is defined, as well as the elucidiation of capsaicin flip-flop between bilayer leaflets as a key event prior to TRPV1 binding. A transient binding was also…

Subjects/Keywords: 572; Molecular biophysics (biochemistry); TRP channels; capsaicin; membrane protein; ion channel

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

APA (6^th Edition):

Hanson, S. M. (2014). Structural, biochemical and computational studies of TRP channel transmembrane domain modularity. (Doctoral Dissertation). University of Oxford. Retrieved from http://ora.ox.ac.uk/objects/uuid:328269a9-11c0-4d5b-9cb7-d7433cf4d6c4 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.640060

Chicago Manual of Style (16^th Edition):

Hanson, Sonya M. “Structural, biochemical and computational studies of TRP channel transmembrane domain modularity.” 2014. Doctoral Dissertation, University of Oxford. Accessed April 17, 2021. http://ora.ox.ac.uk/objects/uuid:328269a9-11c0-4d5b-9cb7-d7433cf4d6c4 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.640060.

MLA Handbook (7^th Edition):

Hanson, Sonya M. “Structural, biochemical and computational studies of TRP channel transmembrane domain modularity.” 2014. Web. 17 Apr 2021.

Vancouver:

Hanson SM. Structural, biochemical and computational studies of TRP channel transmembrane domain modularity. [Internet] [Doctoral dissertation]. University of Oxford; 2014. [cited 2021 Apr 17]. Available from: http://ora.ox.ac.uk/objects/uuid:328269a9-11c0-4d5b-9cb7-d7433cf4d6c4 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.640060.

Council of Science Editors:

Hanson SM. Structural, biochemical and computational studies of TRP channel transmembrane domain modularity. [Doctoral Dissertation]. University of Oxford; 2014. Available from: http://ora.ox.ac.uk/objects/uuid:328269a9-11c0-4d5b-9cb7-d7433cf4d6c4 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.640060

George Mason University

19. Armengol, Kevin. The Cellular and Molecular Basis of Noxious Cold Detection in Drosophila melanogaster Larvae .

Degree: 2015, George Mason University

URL: http://hdl.handle.net/1920/9803

► Nociception, the process of encoding and transmitting noxious stimuli within a nervous system, is an essential mechanism through which organisms are alerted to potentially life-threatening… (more)

▼ Nociception, the process of encoding and transmitting noxious stimuli within a nervous system, is an essential mechanism through which organisms are alerted to potentially life-threatening insults or conditions that originate externally or internally and may lead to incipient tissue damage. These insults can be classified into three broad types of stimuli: chemical, mechanical and thermal. Despite significant progress in this field of study, our understanding of the neural bases of noxious cold detection remains poorly understood. The Drosophila melanogaster larval peripheral nervous system (PNS) has emerged as an excellent model system for studying both the cellular and molecular mechanisms of nociception, particularly with regards to noxious heat and mechanical stimuli. Using this model system, we have implemented a systems neuroscience approach to dissect the underlying cellular, genetic, molecular, and behavioral bases of noxious cold detection. We have developed the first behavioral assay for investigating cold nociception in Drosophila and have identified unique noxious cold-evoked behavioral responses. These cold-specific behaviors require synaptic transmission predominantly from class III dendritic arborization (da) sensory neurons. Optogenetic activation of class III neurons, independent of thermal stimulation, is sufficient to behaviorally phenocopy noxious cold-evoked behavior. Moreover, GCaMP6 functional analyses reveal specific activation of class III da neurons in response to noxious cold stimulation. At a molecular level, microarray analyses revealed these neurons are enriched with a broad spectrum of ion channels, including numerous Transient Receptor Potential (TRP) channels. Mutant and cell-type specific RNAi analyses reveal that select TRP channels Trpm, nompC and Pkd2 are required for normal cold-evoked behaviors and function in the transduction step of noxious cold stimulation. Collectively, our results establish a novel systems-level framework for exploring cellular and molecular mechanisms underlying thermosensory nociception. Advisors/Committee Members: Cox, Daniel N (advisor).

Subjects/Keywords: noxious cold; da neurons; TRP channels; calcium imaging; aptogenetics; behavior

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

APA (6^th Edition):

Armengol, K. (2015). The Cellular and Molecular Basis of Noxious Cold Detection in Drosophila melanogaster Larvae . (Thesis). George Mason University. Retrieved from http://hdl.handle.net/1920/9803

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):

Armengol, Kevin. “The Cellular and Molecular Basis of Noxious Cold Detection in Drosophila melanogaster Larvae .” 2015. Thesis, George Mason University. Accessed April 17, 2021. http://hdl.handle.net/1920/9803.

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

MLA Handbook (7^th Edition):

Armengol, Kevin. “The Cellular and Molecular Basis of Noxious Cold Detection in Drosophila melanogaster Larvae .” 2015. Web. 17 Apr 2021.

Vancouver:

Armengol K. The Cellular and Molecular Basis of Noxious Cold Detection in Drosophila melanogaster Larvae . [Internet] [Thesis]. George Mason University; 2015. [cited 2021 Apr 17]. Available from: http://hdl.handle.net/1920/9803.

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

Council of Science Editors:

Armengol K. The Cellular and Molecular Basis of Noxious Cold Detection in Drosophila melanogaster Larvae . [Thesis]. George Mason University; 2015. Available from: http://hdl.handle.net/1920/9803

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

Hong Kong University of Science and Technology

20. Li, Ching Ki. Characterization of a TRPP complex and its interacting components acting in sex pheromone perception of male C. elegans.

Degree: 2013, Hong Kong University of Science and Technology

URL: http://repository.ust.hk/ir/Record/1783.1-7857 ; https://doi.org/10.14711/thesis-b1213356 ; http://repository.ust.hk/ir/bitstream/1783.1-7857/1/th_redirect.html

► In nature, chemical communication between animals is important for species survival. Finding a mating partner in dioecious species is one of these survival strategies. Caenorhabditis… (more)

▼ In nature, chemical communication between animals is important for species survival. Finding a mating partner in dioecious species is one of these survival strategies. Caenorhabditis remanei females produce a sex pheromone with long-range attractiveness for both C. remanei and C. elegans males. Using C. elegans as a model for studying this chemotactic behavior, two polycystin genes lov-1 and pkd-2, were shown to be required for sex pheromone sensation. These genes encode a transient receptor potential polycystin (TRPP) ion channel complex, which is localized to the ciliary structures implicated in sensation underlying both developmental and physiological processes. TRPP complex in human is important in kidney’s function, and their mutations are associated with autosomal dominant polycystic kidney disease (ADPKD). In mice, this protein complex is involved in determining left-right asymmetry during organogenesis. In C. elegans, the TRPP complex is localized to the ciliated endings of male-specific CEM neurons, which were previously shown to be required for sex pheromone chemotaxis through laser ablation and genetic analyses. In this study, I confined the acting site of PKD-2 to neuronal cilia in which odorants interact with their corresponding receptors. I also performed an electrophysiological assay to correlate the chemical stimuli with polycystin proteins in CEM neurons. These findings support the notion that the TRPP complex is activated by sex pheromone with intracellular signal relay. Importantly, these give us a glimpse into the chemosensory role of CEM neurons, the function of which remains elusive. In addition, I screened for additional mediators of polycystin signaling. Interestingly, atp-2 (ATP synthase subunit) was found to be acting in polycystin signaling to regulate sex pheromone chemotaxis. This ATP synthase subunit is co-localized with polycystin proteins to the neuronal ciliary compartment and is probably playing an unanticipated role to modulate C. elegans sexual behavior.

Subjects/Keywords: TRP channels ; Caenorhabditis elegans – Genetics ; Polycystic kidney disease

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

APA (6^th Edition):

Li, C. K. (2013). Characterization of a TRPP complex and its interacting components acting in sex pheromone perception of male C. elegans. (Thesis). Hong Kong University of Science and Technology. Retrieved from http://repository.ust.hk/ir/Record/1783.1-7857 ; https://doi.org/10.14711/thesis-b1213356 ; http://repository.ust.hk/ir/bitstream/1783.1-7857/1/th_redirect.html

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):

Li, Ching Ki. “Characterization of a TRPP complex and its interacting components acting in sex pheromone perception of male C. elegans.” 2013. Thesis, Hong Kong University of Science and Technology. Accessed April 17, 2021. http://repository.ust.hk/ir/Record/1783.1-7857 ; https://doi.org/10.14711/thesis-b1213356 ; http://repository.ust.hk/ir/bitstream/1783.1-7857/1/th_redirect.html.

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

MLA Handbook (7^th Edition):

Li, Ching Ki. “Characterization of a TRPP complex and its interacting components acting in sex pheromone perception of male C. elegans.” 2013. Web. 17 Apr 2021.

Vancouver:

Li CK. Characterization of a TRPP complex and its interacting components acting in sex pheromone perception of male C. elegans. [Internet] [Thesis]. Hong Kong University of Science and Technology; 2013. [cited 2021 Apr 17]. Available from: http://repository.ust.hk/ir/Record/1783.1-7857 ; https://doi.org/10.14711/thesis-b1213356 ; http://repository.ust.hk/ir/bitstream/1783.1-7857/1/th_redirect.html.

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

Council of Science Editors:

Li CK. Characterization of a TRPP complex and its interacting components acting in sex pheromone perception of male C. elegans. [Thesis]. Hong Kong University of Science and Technology; 2013. Available from: http://repository.ust.hk/ir/Record/1783.1-7857 ; https://doi.org/10.14711/thesis-b1213356 ; http://repository.ust.hk/ir/bitstream/1783.1-7857/1/th_redirect.html

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

University of Hong Kong

21. Che, Hui. Functional transient receptor potential channels in human preadipocytes and cardiac c-kit⁺ progenitor cells.

Degree: 2013, University of Hong Kong

URL: http://hdl.handle.net/10722/196436

► Transient receptor potential (TRP) channels play important roles in cellular physiology and biology. The present PhD project investigated the functional expression of TRPV and TRPM… (more)

▼ Transient receptor potential (TRP) channels play important roles in cellular physiology and biology. The present PhD project investigated the functional expression of TRPV and TRPM channels in human preadipocytes and cardiac c-kit+ progenitor cells and their roles in regulating cell proliferation, adipogenic differentiation or migration. In addition, the role of store-operated Ca2+ entry (SOCE) channels in regulating cell proliferation and migration was also studied in human cardiac c-kit+ progenitor cells using multiple approaches including whole-cell patch voltage-clamp, confocal microscope, molecular biology, etc. We found that TRPV2, TRPV4 and TRPM7 channels were abundantly expressed in human preadipocytes. Activation of TRPV2 channels by probenecid caused a long-lasting intracellular Ca2+ transient, while activation of TRPV4 channels by 4-PDD induced Ca2+ oscillations. TRPM7 current was recorded with a Mg2+-free pipette solution, and inhibited by 2-aminoethyl diphenyl borate (2-APB). Silence of TRPV2 or TRPM7, but not TRPV4, with the specific shRNA, reduced cell proliferation via inhibiting cyclin D1, cyclin E, and p-ERK1/2. Individually silencing these three channels decreased adipogenic differentiation by reducing p-Akt kinase. The results indicate that TRPV2, TRPV4 and TRPM7 are involved in adipogenesis, while TRPV2 and TRPM7, but not TRPV4, regulate cell proliferation in human preadipocytes. In second part of the thesis, abundant expression of TRPV2, TRPV4, and TRPM7 channels was demonstrated in human cardiac c-kit+ progenitor cells. Similar to human preadipocytes, probenecid and 4-PDD activated Ca2+ signaling, and TRPM7 current recorded with a Mg2+-free pipette solution was inhibited by 2-APB. Silencing TRPV2 or TRPM7, but not TRPV4, inhibited cell proliferation by arresting cells at G0/G1 phase with a reduced cyclin D, cyclin E, and p-ERK1/2. Cell migration was decreased with silence of TRPV2, TRV4 or TRPM7 via inhibiting p-Akt kinase. The results show that TRPV2, TRPV4 and TRPM7 mediate cell migration, while TRPV2 and TRPM7, but not TRPV4 channels, participate in regulating cell proliferation. In third part of the thesis, we demonstrated that SOCE channels were composed of TRPC1, STIM1 and Orai1 by protein-protein interaction. Silence of TRPC1, STIM1, or Orai1 with specific siRNA reduced Ca2+ influx through SOCE channels, decreased cell proliferation by inhibiting cyclin D1 and cyclin E, and slowed down cell migration via reducing p-Akt kinase. These results suggest that TRPC1, STIM1 and Orai1 are the major components of SOCE channels in human cardiac c-kit+ cells. SOCE channels play an essential role in regulating cell proliferation and migration. Collectively, this PhD project has demonstrated for the first time that 1) TRPV2, TRPV4, and TRPM7 are abundantly expressed in human preadipocytes and cardiac c-kit+ progenitor cells. 2) These TRP channels regulate adipogenic differentiation in preadipocytes and migration in cardiac c-kit+ progenitor cells. 3) TRPV2 and TRPM7, but not TRPV4, are… Advisors/Committee Members: Tse, HF (advisor), Li, GR (advisor).

Subjects/Keywords: TRP channels; Stem cells

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

APA (6^th Edition):

Che, H. (2013). Functional transient receptor potential channels in human preadipocytes and cardiac c-kit⁺ progenitor cells. (Thesis). University of Hong Kong. Retrieved from http://hdl.handle.net/10722/196436

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):

Che, Hui. “Functional transient receptor potential channels in human preadipocytes and cardiac c-kit⁺ progenitor cells.” 2013. Thesis, University of Hong Kong. Accessed April 17, 2021. http://hdl.handle.net/10722/196436.

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

MLA Handbook (7^th Edition):

Che, Hui. “Functional transient receptor potential channels in human preadipocytes and cardiac c-kit⁺ progenitor cells.” 2013. Web. 17 Apr 2021.

Vancouver:

Che H. Functional transient receptor potential channels in human preadipocytes and cardiac c-kit⁺ progenitor cells. [Internet] [Thesis]. University of Hong Kong; 2013. [cited 2021 Apr 17]. Available from: http://hdl.handle.net/10722/196436.

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

Council of Science Editors:

Che H. Functional transient receptor potential channels in human preadipocytes and cardiac c-kit⁺ progenitor cells. [Thesis]. University of Hong Kong; 2013. Available from: http://hdl.handle.net/10722/196436

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

Rice University

22. Polali, Sruthi. Novel Mechanisms for Magnetogenetic Neuromodulation.

Degree: MS, Natural Sciences, 2017, Rice University

URL: http://hdl.handle.net/1911/105466

► Magnetogenetic tools permit wireless stimulation of specific neurons located deep inside the brain of freely moving animals: a capability that improves the study of neural… (more)

▼ Magnetogenetic tools permit wireless stimulation of specific neurons located deep inside the brain of freely moving animals: a capability that improves the study of neural activity and its correlation to behavior. Recently, a fully genetically encoded, magnetically sensitive protein chimera consisting of ferritin and TRPV4, dubbed Magneto2.0, was shown to elicit action potentials in neurons when exposed to a magnetic field. The iron-sequestering protein, ferritin serves as the magnetically sensitive domain in this chimera, while TRPV4 is a cation selective channel that responds to mechanical and temperature stimuli. While it was suggested that the mode of operation was through mechanical stimulation of the channel by ferritin, later calculations show that the forces exerted by ferritin nanoparticles are orders of magnitude lower than what is required for channel gating. We propose an alternate mechanisms based on the magnetocaloric effect to explain how paramagnetic ferritin could gate the thermally sensitive TRPV4. A magnetic field reduces the entropy of the ferritin nanoparticles when its magnetic spins align, resulting in an increase in temperature that in turn gates the heat-sensitive TRPV4 channel. We support our theory with calculations and experimental data that demonstrate that the observed responses are indeed thermally mediated. To further prove the magnetocaloric mechanism, we designed a novel magnetogenetic channel consisting of fusion of ferritin and cold-sensitive channel TRPM8, dubbed MagM8. This channel is activated due to decrease in temperature caused by increase in entropy during demagnetization of ferritin. In addition to reconciling biological observations with physical properties of genetically encoded magnetic nanoparticles, our explanation will also aid the design of new magnetogenetic tools with improved magnetic sensitivity. Advisors/Committee Members: Robinson, Jacob (advisor), Natelson, Douglas (committee member), Clementi, Cecilia (committee member), Kemere, Caleb (committee member).

Subjects/Keywords: Magnetogenetic; Neuromodulation; Magnetocaloric; Magnetic Stimulation; TRP channels; Ferritin

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APA (6^th Edition):

Polali, S. (2017). Novel Mechanisms for Magnetogenetic Neuromodulation. (Masters Thesis). Rice University. Retrieved from http://hdl.handle.net/1911/105466

Chicago Manual of Style (16^th Edition):

Polali, Sruthi. “Novel Mechanisms for Magnetogenetic Neuromodulation.” 2017. Masters Thesis, Rice University. Accessed April 17, 2021. http://hdl.handle.net/1911/105466.

MLA Handbook (7^th Edition):

Polali, Sruthi. “Novel Mechanisms for Magnetogenetic Neuromodulation.” 2017. Web. 17 Apr 2021.

Vancouver:

Polali S. Novel Mechanisms for Magnetogenetic Neuromodulation. [Internet] [Masters thesis]. Rice University; 2017. [cited 2021 Apr 17]. Available from: http://hdl.handle.net/1911/105466.

Council of Science Editors:

Polali S. Novel Mechanisms for Magnetogenetic Neuromodulation. [Masters Thesis]. Rice University; 2017. Available from: http://hdl.handle.net/1911/105466

23. Almeida, Mônica Moura de. Efeitos cardiovasculares induzidos pelo óleo essencial de mentha x-villosa hudson (oemv), rotundifolona e mentol em ratos espontaneamente hipertensos – o papel dos canais potencial receptor transiente (trp).

Degree: 2015, Universidade Federal da Paraíba; Programa de Pós-Graduação em Produtos Naturais e Sintéticos Bioativos; UFPB; Brasil; Farmacologia

URL: https://repositorio.ufpb.br/jspui/handle/tede/9496

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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior - CAPES

The monoterpenes found in essential oils from plants act on transient receptor potential channels (TRP). Some TRP channels with altered expression in hypertensive rats may be new therapeutic targets for the control of hypertension. Aim: Compare the responses induced by Essential Oil of Mentha x villosa Hudson (OEMV), rotundifolone and menthol in Spontaneously Hypertensive rats (SHR) and normotensive Wistar Kyoto (WKY), evaluating the role of TRP channels. Methods and Results: In vivo (blood pressure measurement and heart rate), in vitro (measure of the frequency and force of contraction in the atria and the isometric tension in superior mesenteric arteries) and biochemical (PCR and Western blot) studies were used. The OEMV (3, 5, 10 and 20 mg/kg), the rotundifolone (10, 20 and 30 mg/kg) and the menthol (3, 5, 10 and 20 mg/kg) induced significant hypotensive and bradycardic response in non-anesthetized SHR and WKY rats. The reduction in the diastolic blood pressure was significantly greater than the decrease in the systolic blood pressure, suggesting a greater action on the vascular component of blood pressure. However, the significant bradycardic effect and reduction in the systolic blood pressure also suggest an action on the cardiac component. Furthermore, the decrease in the blood pressure and heart rate induced by rotundifolone and by menthol were significantly more potent in SHR. The action of OEMV, the rotundifolone and menthol in the right atrium (with spontaneous activity) and left (electrically stimulated) showed negative inotropic and chronotropic effects and culminating in complete inhibition of cardiac activity. Moreover, the negative inotropic effect was more potent in SHR and protein TRPM8 channel showed increased expression in the ventricles (left > right) and atria (left > right) of SHR rats. Also, OEMV, rotundifolone and menthol induced vasorelaxant response in superior mesenteric arteries of SHR and WKY rats, precontracted with PHE. The major mechanism involves the endothelium-independent route, which was more potent in SHR. The mechanism of the endothelium-independent vasorelaxant response induced by rotundifolone and menthol probably involves TRPM8 channels, which showed increased expression in SHR, and TRPC1, TRPC3 and TRPC6 channels. However, the response…

Advisors/Committee Members: Medeiros, Isac Almeida de.

Subjects/Keywords: Rotundifolona; Mentol; Ratos SHR; Cardiovascular; Canais TRP; Rotundifolone; Menthol; SHR rats; Cardiovascular; TRP channels; CIENCIAS BIOLOGICAS::FARMACOLOGIA

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APA (6^th Edition):

Almeida, M. M. d. (2015). Efeitos cardiovasculares induzidos pelo óleo essencial de mentha x-villosa hudson (oemv), rotundifolona e mentol em ratos espontaneamente hipertensos – o papel dos canais potencial receptor transiente (trp). (Doctoral Dissertation). Universidade Federal da Paraíba; Programa de Pós-Graduação em Produtos Naturais e Sintéticos Bioativos; UFPB; Brasil; Farmacologia. Retrieved from https://repositorio.ufpb.br/jspui/handle/tede/9496

Chicago Manual of Style (16^th Edition):

Almeida, Mônica Moura de. “Efeitos cardiovasculares induzidos pelo óleo essencial de mentha x-villosa hudson (oemv), rotundifolona e mentol em ratos espontaneamente hipertensos – o papel dos canais potencial receptor transiente (trp).” 2015. Doctoral Dissertation, Universidade Federal da Paraíba; Programa de Pós-Graduação em Produtos Naturais e Sintéticos Bioativos; UFPB; Brasil; Farmacologia. Accessed April 17, 2021. https://repositorio.ufpb.br/jspui/handle/tede/9496.

MLA Handbook (7^th Edition):

Almeida, Mônica Moura de. “Efeitos cardiovasculares induzidos pelo óleo essencial de mentha x-villosa hudson (oemv), rotundifolona e mentol em ratos espontaneamente hipertensos – o papel dos canais potencial receptor transiente (trp).” 2015. Web. 17 Apr 2021.

Vancouver:

Almeida MMd. Efeitos cardiovasculares induzidos pelo óleo essencial de mentha x-villosa hudson (oemv), rotundifolona e mentol em ratos espontaneamente hipertensos – o papel dos canais potencial receptor transiente (trp). [Internet] [Doctoral dissertation]. Universidade Federal da Paraíba; Programa de Pós-Graduação em Produtos Naturais e Sintéticos Bioativos; UFPB; Brasil; Farmacologia; 2015. [cited 2021 Apr 17]. Available from: https://repositorio.ufpb.br/jspui/handle/tede/9496.

Council of Science Editors:

Almeida MMd. Efeitos cardiovasculares induzidos pelo óleo essencial de mentha x-villosa hudson (oemv), rotundifolona e mentol em ratos espontaneamente hipertensos – o papel dos canais potencial receptor transiente (trp). [Doctoral Dissertation]. Universidade Federal da Paraíba; Programa de Pós-Graduação em Produtos Naturais e Sintéticos Bioativos; UFPB; Brasil; Farmacologia; 2015. Available from: https://repositorio.ufpb.br/jspui/handle/tede/9496

Texas Medical Center

24. Turner, Heather N. Cellular and genetic bases of cold nociception and nociceptive sensitization in Drosophila larvae.

Degree: PhD, 2016, Texas Medical Center

URL: https://digitalcommons.library.tmc.edu/utgsbs_dissertations/714

► Organisms from flies to mammals utilize thermoreceptors to detect and respond to noxious thermal stimuli. Although much is understood about noxious heat avoidance, our… (more)

▼ Organisms from flies to mammals utilize thermoreceptors to detect and respond to noxious thermal stimuli. Although much is understood about noxious heat avoidance, our understanding of the basic biology of noxious cold perception is gravely minimal. Numerous clinical conditions disrupt the sensory machinery, such as in patients suffering from tissue damage (from wound or sunburn), or injury to the peripheral nerves, as in patients with diabetes or undergoing chemotherapy. Our goal is to determine the genetic basis for noxious cold perception and injury-induced nociceptive sensitization using the genetically tractable Drosophila model. Using a novel "cold probe" tool and assay we found larvae produce a mutually exclusive set of reactive behaviors to a defined noxious cold stimulus (3-12 ºC), including a full-body contraction and the bending of anterior and posterior segments to make a U-Shape. These behaviors are distinct from normal locomotion, responses to gentle touch, noxious heat or harsh mechanical stimuli. Through genetic manipulation, we found cold responses require specific classes of peripheral sensory neurons and receptors, which differ depending on the cold-evoked behavior. Our data indicates these cold-sensing neurons are multimodal, and the level of cellular activation determines the behavioral output to different stimuli. To study cold nociceptive sensitization, we used a "sunburn assay" which exposes the dorsal side of the larva to UV-damage, and found larvae display a dramatic shift in cold responses after injury. This behavioral shift requires similar sets of peripheral sensory neurons and receptors specific to each sensitized cold-evoked behavior. Lastly, we found the Tumor Necrosis Factor (TNF) and Tachykinin (Tk) pathways, both involved in sensitization to noxious heat, may also play a role UV-induced cold sensitization. We have established the first system to study noxious cold and cold sensitization in Drosophila. Our unique tool and assay will allow us to further uncover the conserved molecular and genetic players involved in this process. Advisors/Committee Members: Michael J. Galko, Ph.D., Edgar T. Walters, Ph.D., Howard Gutstein, M.D..

Subjects/Keywords: Drosophila; nociception; pain; thermosensation; cold; sensitization; neurons; TRP channels; genetics; neuroscience; Molecular and Cellular Neuroscience

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

APA (6^th Edition):

Turner, H. N. (2016). Cellular and genetic bases of cold nociception and nociceptive sensitization in Drosophila larvae. (Doctoral Dissertation). Texas Medical Center. Retrieved from https://digitalcommons.library.tmc.edu/utgsbs_dissertations/714

Chicago Manual of Style (16^th Edition):

Turner, Heather N. “Cellular and genetic bases of cold nociception and nociceptive sensitization in Drosophila larvae.” 2016. Doctoral Dissertation, Texas Medical Center. Accessed April 17, 2021. https://digitalcommons.library.tmc.edu/utgsbs_dissertations/714.

MLA Handbook (7^th Edition):

Turner, Heather N. “Cellular and genetic bases of cold nociception and nociceptive sensitization in Drosophila larvae.” 2016. Web. 17 Apr 2021.

Vancouver:

Turner HN. Cellular and genetic bases of cold nociception and nociceptive sensitization in Drosophila larvae. [Internet] [Doctoral dissertation]. Texas Medical Center; 2016. [cited 2021 Apr 17]. Available from: https://digitalcommons.library.tmc.edu/utgsbs_dissertations/714.

Council of Science Editors:

Turner HN. Cellular and genetic bases of cold nociception and nociceptive sensitization in Drosophila larvae. [Doctoral Dissertation]. Texas Medical Center; 2016. Available from: https://digitalcommons.library.tmc.edu/utgsbs_dissertations/714

University of Hawaii – Manoa

25. Bessac, Bret Fajans. Divalent cation channels with intrinsic alpha-kinase activity.

Degree: PhD, 2009, University of Hawaii – Manoa

URL: http://hdl.handle.net/10125/12115

Electronic reproduction.

Also available by subscription via World Wide Web

xvi, 113, pp leaves, bound ill. (some col.) 29 cm

Subjects/Keywords: TRP channels; Protein kinases; Chemical bonds

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

APA (6^th Edition):

Bessac, B. F. (2009). Divalent cation channels with intrinsic alpha-kinase activity. (Doctoral Dissertation). University of Hawaii – Manoa. Retrieved from http://hdl.handle.net/10125/12115

Chicago Manual of Style (16^th Edition):

Bessac, Bret Fajans. “Divalent cation channels with intrinsic alpha-kinase activity.” 2009. Doctoral Dissertation, University of Hawaii – Manoa. Accessed April 17, 2021. http://hdl.handle.net/10125/12115.

MLA Handbook (7^th Edition):

Bessac, Bret Fajans. “Divalent cation channels with intrinsic alpha-kinase activity.” 2009. Web. 17 Apr 2021.

Vancouver:

Bessac BF. Divalent cation channels with intrinsic alpha-kinase activity. [Internet] [Doctoral dissertation]. University of Hawaii – Manoa; 2009. [cited 2021 Apr 17]. Available from: http://hdl.handle.net/10125/12115.

Council of Science Editors:

Bessac BF. Divalent cation channels with intrinsic alpha-kinase activity. [Doctoral Dissertation]. University of Hawaii – Manoa; 2009. Available from: http://hdl.handle.net/10125/12115

Duke University

26. Sosa Pagan, Jason Omar. Temperature Activation Mechanism of TRP Ion Channels .

Degree: 2017, Duke University

URL: http://hdl.handle.net/10161/14474

► Organisms need to sense temperature to avoid detrimental damage to cells and tissues. In mammals, this is thought to be mediated, at least in… (more)

▼ Organisms need to sense temperature to avoid detrimental damage to cells and tissues. In mammals, this is thought to be mediated, at least in part, by several members of the transient receptor potential (TRP) superfamily of ion channels. TRP channels are outwardly rectifying channels with 6 transmembrane segments that assemble as a tetramer. Some TRP channels are activated by cold or heat, chemicals, and depolarizing voltages. Temperature sensitive TRP channels are expressed in a variety of cell types including keratinocytes and medium- to small-diameter nociceptors where they are involved in the detection of noxious chemicals, inflammatory mediators, and temperature. In response to noxious stimuli, TRP channels mediate the depolarization of nociceptors ultimately leading to the perception of pain. Due to their critical role in nociception they are excellent candidates for the development of analgesic drugs that can be used as treatments for different pain modalities. However, drugs that target these ion channels have many unwanted side effects that include hypo or hyperthermia. Clearly, a thorough understanding of the structures and mechanism that mediate temperature activation of TRP channels is needed for the clever development of novel drugs that do not evoked these side effects. Although countless studies have tried to identify the structures and mechanisms that confer temperature sensitivity to TRP channels, no consensus about these have been attained. One recent proposed mechanism assumes that temperature activation is driven by the exposure of hydrophobic residues to solvent. This mechanism further predicts that residues are exposed to solvent in a coordinated way, but without necessarily being near each other. However, there is little experimental evidence supporting this mechanism in TRP channels. Here I tackle these questions using a variety of approaches: First, I tested the sufficiency of the pore domain of TRPV1 towards temperature sensitivity using minimal ‘pore-only’ channels, but found that my minimalistic approach does not yield functional channels. I then tested the sufficiency of the entire ankyrin repeat 6, or single-point mutation on the same repeat of drosophila TRPA1 for inverting the temperature directionality of the channel, but found that the structure was not sufficient to make heat-activated drosophila TRPA1 cold sensitive. Lastly, I took a combinatorial approach and used random mutagenesis, coupled to high-throughput screening and massive parallel sequencing to identify and characterize mutations from ~7,300 randomly mutated TRPV1 clones. I found that residues important for temperature activation are randomly spread throughout the entire sequence of the channel indicating that temperature does not activate the channel by acting on a single coherent domain, but rather in the entire protein. This implies that it will be very complicated to develop analgesic drugs that do not affect the temperature activation mechanism since residues throughout the protein are involved in… Advisors/Committee Members: Grandl, Jorg (advisor).

Subjects/Keywords: Biophysics; Neurosciences; Deep sequencing; High throughput screening; Ion channels; Random mutagenesis; Temperature activation; TRP

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

APA (6^th Edition):

Sosa Pagan, J. O. (2017). Temperature Activation Mechanism of TRP Ion Channels . (Thesis). Duke University. Retrieved from http://hdl.handle.net/10161/14474

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):

Sosa Pagan, Jason Omar. “Temperature Activation Mechanism of TRP Ion Channels .” 2017. Thesis, Duke University. Accessed April 17, 2021. http://hdl.handle.net/10161/14474.

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

MLA Handbook (7^th Edition):

Sosa Pagan, Jason Omar. “Temperature Activation Mechanism of TRP Ion Channels .” 2017. Web. 17 Apr 2021.

Vancouver:

Sosa Pagan JO. Temperature Activation Mechanism of TRP Ion Channels . [Internet] [Thesis]. Duke University; 2017. [cited 2021 Apr 17]. Available from: http://hdl.handle.net/10161/14474.

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

Council of Science Editors:

Sosa Pagan JO. Temperature Activation Mechanism of TRP Ion Channels . [Thesis]. Duke University; 2017. Available from: http://hdl.handle.net/10161/14474

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

University of Lund

27. Survery, Sabeen. Characterization of Membrane Proteins: From a gated plant aquaporin to animal ion channel receptors.

Degree: 2015, University of Lund

URL: https://lup.lub.lu.se/record/5415972 ; https://portal.research.lu.se/ws/files/5824246/5421734.pdf

► Membrane proteins play several important roles in a cell. Among these proteins are aquaporins (AQPs) and transient receptor potential (TRP) ion channels that mediate water… (more)

▼ Membrane proteins play several important roles in a cell. Among these proteins are aquaporins (AQPs) and transient receptor potential (TRP) ion channels that mediate water transport, temperature and noxious chemical sensation, respectively. The function of some AQPs, for example the spinach isoform SoPIP2;1 is regulated by pH, phosphorylation and heavy metals such as mercury. However, the mechanisms by which mercury activate or inhibits AQPs are poorly understood. We suggest that mercury binds to SoPIP2;1 close to the C-terminal end and that the binding of mercury results in destabilization of the C-terminal region. This may affect its interaction with the residues forming the gate and therefore lead to an increase of the water permeability of SoPIP2;1 (Paper II). SoPIP2;1 is a highly selective water channel and can be produced as a functional protein in high yield in a heterologous system which suggest that SoPIP2;1 is a good choice for insertion in biomimetic membranes to be used for water purification. However, the stability of SoPIP2;1 in artificial membranes needed to be demonstrated. Thus we determined the stability of SoPIP2;1 in different lipids and identified E. coli polar lipids as the best system for reconstitution of SoPIP2;1. The results will contribute towards the effort to use SoPIP2;1 in biomimetic water filtration technology (Paper I). The animal TRP ion channel subtype A1 (TRPA1) from fruit fly, snake and mosquito has been implicated in warm temperature sensation. However, the threshold temperature which activates human TRPA1 (hTRPA1) is controversial. We addressed this issue by reconstituting the purified hTRPA1 in artificial lipid membranes. The purified hTRPA1 was found to be activated by cold temperatures and electrophilic chemicals. The results resolve the controversy surrounding the threshold temperature for the activation of hTRPA1 (Paper IV). The Anopheles gambiae TRPA1 (AgTRPA1) was found to be activated by heat and electrophilic compounds when reconstituted in artificial membranes after purification. The temperature activation as well as the binding of electrophilic ligands to AgTRPA1 resulted in the quenching of fluorescence suggesting that thermal and chemical activation brought about similar conformational changes of the protein and perhaps reflect the dynamic change in the conformation of residues involved in the gating process (Paper III). We also demonstrated that the N-terminal domain of both human and mosquito TRPA1 is not essential for thermal/chemical sensation (Paper III and Paper IV) as opposed to previous reports.

Subjects/Keywords: Biological Sciences; MIPs; AQPs; TRP ion channels; water transport; themo sensor; Electrophiles

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

APA (6^th Edition):

Survery, S. (2015). Characterization of Membrane Proteins: From a gated plant aquaporin to animal ion channel receptors. (Doctoral Dissertation). University of Lund. Retrieved from https://lup.lub.lu.se/record/5415972 ; https://portal.research.lu.se/ws/files/5824246/5421734.pdf

Chicago Manual of Style (16^th Edition):

Survery, Sabeen. “Characterization of Membrane Proteins: From a gated plant aquaporin to animal ion channel receptors.” 2015. Doctoral Dissertation, University of Lund. Accessed April 17, 2021. https://lup.lub.lu.se/record/5415972 ; https://portal.research.lu.se/ws/files/5824246/5421734.pdf.

MLA Handbook (7^th Edition):

Survery, Sabeen. “Characterization of Membrane Proteins: From a gated plant aquaporin to animal ion channel receptors.” 2015. Web. 17 Apr 2021.

Vancouver:

Survery S. Characterization of Membrane Proteins: From a gated plant aquaporin to animal ion channel receptors. [Internet] [Doctoral dissertation]. University of Lund; 2015. [cited 2021 Apr 17]. Available from: https://lup.lub.lu.se/record/5415972 ; https://portal.research.lu.se/ws/files/5824246/5421734.pdf.

Council of Science Editors:

Survery S. Characterization of Membrane Proteins: From a gated plant aquaporin to animal ion channel receptors. [Doctoral Dissertation]. University of Lund; 2015. Available from: https://lup.lub.lu.se/record/5415972 ; https://portal.research.lu.se/ws/files/5824246/5421734.pdf

University of Hong Kong

28. Zhang, Yanhui. Modulation of transient outward potassium channels by protein tyrosinekinases and demonstration of TRPC and TRPM channels in human atrialmyocytes.

Degree: 2011, University of Hong Kong

URL: http://hdl.handle.net/10722/174323

► My PhD project investigated the regulation of human cardiac transient outward potassium current (Ito) by protein tyrosine kinases (PTKs) and the functional expression of transient… (more)

▼ My PhD project investigated the regulation of human cardiac transient outward potassium current (Ito) by protein tyrosine kinases (PTKs) and the functional expression of transient receptor potential (TRP) channels in human atrial myocytes to make an advanced understanding of human cardiac electrophysiology and pathophysiology. The modulation of human cardiac Itoby PTKs was studied in human atrial myocytes and HEK 293 cells expressing hKv4.3 (coding human cardiac Ito). We found that the broad-spectrum PTK inhibitor genistein, the selective EGFR kinase inhibitor AG556, and the Src-family kinases inhibitor PP2 inhibited human atrial Itoand the inhibitory effect was countered by the protein tyrosine phosphatase (PTP) inhibitor orthovanadate. Similar results were observed in hKv4.3-HEK cells. Interestingly, tyrosine phosphorylation of hKv4.3channels was reduced by genistein, AG556, and PP2,and the reduction was antagonized by orthovanadate. The mutant Y136F of hKv4.3 lost the inhibitory response to AG556, whileY108F lost the response to PP2.The double mutant Y108F-Y136F hKv4.3 failed to respond to both AG556 and PP2, and exhibited a dramatic reduction of tyrosine phosphorylation. These results indicate that native cardiac Itois regulated by both EGFR and Src family kinases. In the second part, we studied whether TRPC channels would mediate the nonselective cation current described previously in human atrial myocytes. It was found that TRPC1 channel activator thapsigargin activated the current, and the effect was suppressed by La3+or prevented by intracellular anti-TRPC1 antibody. Endothelin-1 and angiotensin II stimulated the current, andthe effect was inhibited by La3+and/or 2-APB. RT-PCR and Western blot analysis revealed that in addition to the TRPC1 channels mediating the nonselective cation current, the components of store-operated Ca2+channels (SOCs), STIM1 and Orai1 were abundantly expressed in human atria. The interaction of TRPC1, STIM1, and Orai1 was confirmed by co-immunoprecipitation. Interestingly, we found that protein expression of TRPC1 and STIM1, but not Orai1, was up-regulated in human atria with atrial fibrillation. The third part of the project determined whether TRPM7 channels were expressed in human atrial myocytes, since this channel was reported in human atrial fibroblasts, conferring atrial fibrosis in human atria with atrial fibrillation. We found a TRPM7 -like current which was potentiated by acidic pH, and inhibited by La3+and 2-APB, and a Ca2+-activated TRPM4 current. RT-PCR and Western blot analysis confirmed the expression of TRPM7 and TRPM4 channels in human atria. Moreover, we found TRPM7 protein, but not TRPM4 protein was significantly up-regulated in human atria with atrial fibrillation, suggesting the potential participation of TRPM7 channels in atrial remodeling of human atria with atrial fibrillation. Collectively, this PhD thesis project has demonstrated for the first time that human cardiac Itois modulated by EGFR kinase and Src kinases via phosphorylating Y136and Y108,… Advisors/Committee Members: Li, GR (advisor), Tse, HF (advisor).

Subjects/Keywords: TRP channels.; Potassium channels.; Protein-tyrosine kinase.; Atrial fibrillation.

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

APA (6^th Edition):

Zhang, Y. (2011). Modulation of transient outward potassium channels by protein tyrosinekinases and demonstration of TRPC and TRPM channels in human atrialmyocytes. (Thesis). University of Hong Kong. Retrieved from http://hdl.handle.net/10722/174323

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):

Zhang, Yanhui. “Modulation of transient outward potassium channels by protein tyrosinekinases and demonstration of TRPC and TRPM channels in human atrialmyocytes.” 2011. Thesis, University of Hong Kong. Accessed April 17, 2021. http://hdl.handle.net/10722/174323.

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

MLA Handbook (7^th Edition):

Zhang, Yanhui. “Modulation of transient outward potassium channels by protein tyrosinekinases and demonstration of TRPC and TRPM channels in human atrialmyocytes.” 2011. Web. 17 Apr 2021.

Vancouver:

Zhang Y. Modulation of transient outward potassium channels by protein tyrosinekinases and demonstration of TRPC and TRPM channels in human atrialmyocytes. [Internet] [Thesis]. University of Hong Kong; 2011. [cited 2021 Apr 17]. Available from: http://hdl.handle.net/10722/174323.

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

Council of Science Editors:

Zhang Y. Modulation of transient outward potassium channels by protein tyrosinekinases and demonstration of TRPC and TRPM channels in human atrialmyocytes. [Thesis]. University of Hong Kong; 2011. Available from: http://hdl.handle.net/10722/174323

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

29. Nathana Fernandes Mezzalira. Efeito da Luz e Temperatura Sobre a Expressão de Genes do Relógio em Mamífero: Tecidos Periféricos como Modelo de Estudo.

Degree: 2015, University of São Paulo

URL: http://www.teses.usp.br/teses/disponiveis/41/41135/tde-15032016-105421/

► O surgimento e a evolução da vida na terra foram possíveis graças ao desenvolvimento de mecanismos temporais precisos capazes de ajustar os processos fisiológicos que… (more)

▼ O surgimento e a evolução da vida na terra foram possíveis graças ao desenvolvimento de mecanismos temporais precisos capazes de ajustar os processos fisiológicos que ocorriam no interior do organismo com os ciclos ambientais, promovendo assim, ganhos na capacidade adaptativa e reprodutiva dos indivíduos. Neste contexto, luz e temperatura são as duas pistas temporais mais relevantes para resetar o relógio endógeno e, aparentemente, esses dois zeitgebers trabalham juntos para manter os ritmos circadianos. Uma ampla gama de fotorreceptores e fotopigmentos evoluiu no sentido de perceber com alta sensibilidade a informação fótica fornecida pelo ambiente e, recentemente, foi demonstrado que a detecção de temperatura também pode ser exercida pelos fotopigmentos rodopsina e melanopsina, sendo mediada por canais TRP (Shen et al., 2011). Consideramos as células B16-F10 Per1::Luc como um modelo promissor para o estudo de luz e temperatura em relógios periféricos, uma vez que essa linhagem expressa os dois fotopigmentos apontados com função de termorreceptores em Drosophila. Nossos estudos nos permitiram verificar que a luz não atua como um agente sincronizador nessas células, que se mantiveram em livre curso mesmo após um pulso de 10 min de luz azul (650 lux). Por outro lado, um pulso de temperatura de 2,5º C acima da temperatura de manutenção por 1h atuou ajustando a expressão do gene Per1, imprimindo um ritmo circadiano, diferentemente do observado no controle. Com base nessas informações, hipotetizamos que a informação de luz, percebida via melanopsina na retina de mamíferos, levaria a regulação da temperatura circadiana pelo NSQ, e a temperatura corporal, por sua vez, poderia atuar como uma pista interna para a sincronização dos tecidos periféricos, tendo os canais TRP como mediadores. Para responder esta questão, utilizamos camundongos WT e TrpV1 KO submetidos a diferentes protocolos de luz e avaliamos a expressão de genes do relógio Per1, Per2, Clock e Bmal1 e dos canais TrpV1 e TrpA1 em tecidos periféricos. Identificamos que a glândula suprarrenal, fígado e tecido adiposo marrom possuem uma maquinaria do relógio tipicamente ativa e acreditamos que a oscilação dos genes de relógio observada nesses tecidos é expressiva. Interessantemente, vimos também que o TrpV1, além de ser expresso nos tecidos analisados em animais WT, apresenta uma transcrição rítmica no fígado e tecido adiposo marrom de animais em LD, corroborando nossa hipótese de que canais TRP atuam como mediadores da informação de luz aos tecidos periféricos. Dadas as diferenças encontradas entre os animais WT e TrpV1 KO, sugerimos que a presença do canal TRPV1 pode ser essencial, embora seu grau de envolvimento varie de acordo com o tecido. No que diz respeito ao canal TRPA1, encontramos dois resultados que merecem ser destacados. Primeiramente, identificamos no fígado de camundongos TrpV1 KO mantidos em LD uma provável compensação da expressão de TrpA1 na ausência de TrpV1 e, curiosamente, que o tecido adiposo marrom não expressa o canal TrpA1. Considerando os… Advisors/Committee Members: Ana Maria de Lauro Castrucci, Jose Cipolla Neto, Silvia Cristina Ribeiro de Souza.

Subjects/Keywords: B16-F10 Per1::Luc; Canais TRP; Genes do relógio; Luz; Mus musculus; Relógios periféricos; Temperatura; B16-F10 Per1::Luc; Clock genes; Light; Mus musculus; Peripheral clocks; Temperature; TRP channels

Record Details Similar Records Cite « Share

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

APA (6^th Edition):

Mezzalira, N. F. (2015). Efeito da Luz e Temperatura Sobre a Expressão de Genes do Relógio em Mamífero: Tecidos Periféricos como Modelo de Estudo. (Masters Thesis). University of São Paulo. Retrieved from http://www.teses.usp.br/teses/disponiveis/41/41135/tde-15032016-105421/

Chicago Manual of Style (16^th Edition):

Mezzalira, Nathana Fernandes. “Efeito da Luz e Temperatura Sobre a Expressão de Genes do Relógio em Mamífero: Tecidos Periféricos como Modelo de Estudo.” 2015. Masters Thesis, University of São Paulo. Accessed April 17, 2021. http://www.teses.usp.br/teses/disponiveis/41/41135/tde-15032016-105421/.

MLA Handbook (7^th Edition):

Mezzalira, Nathana Fernandes. “Efeito da Luz e Temperatura Sobre a Expressão de Genes do Relógio em Mamífero: Tecidos Periféricos como Modelo de Estudo.” 2015. Web. 17 Apr 2021.

Vancouver:

Mezzalira NF. Efeito da Luz e Temperatura Sobre a Expressão de Genes do Relógio em Mamífero: Tecidos Periféricos como Modelo de Estudo. [Internet] [Masters thesis]. University of São Paulo; 2015. [cited 2021 Apr 17]. Available from: http://www.teses.usp.br/teses/disponiveis/41/41135/tde-15032016-105421/.

Council of Science Editors:

Mezzalira NF. Efeito da Luz e Temperatura Sobre a Expressão de Genes do Relógio em Mamífero: Tecidos Periféricos como Modelo de Estudo. [Masters Thesis]. University of São Paulo; 2015. Available from: http://www.teses.usp.br/teses/disponiveis/41/41135/tde-15032016-105421/

Queens University

30. Sturgeon, Raymond. Lipid signalling modulates neuroendocrine cell excitability and cation channel function .

Degree: Physiology, Queens University

URL: http://hdl.handle.net/1974/24913

► Ion channel function and modulation determine the strength and duration of periods of enhanced neuronal activity and excitability that control and shape behaviour. The bag… (more)

▼ Ion channel function and modulation determine the strength and duration of periods of enhanced neuronal activity and excitability that control and shape behaviour. The bag cell neurons of the hermaphroditic sea snail, Aplysia californica, provide a model to examine the regulation of ion channel function. Reproduction is initiated when bag cell neurons secrete egg-laying hormone during a protracted depolarization and afterdischarge. Early in the afterdischarge, phospholipase C (PLC) hydrolyzes phosphatidylinositol-4,5-bisphosphate (PIP2) into inositol trisphosphate (IP3) and diacylglycerol (DAG). In cultured bag cell neurons, activating PLC with N-(3-trifluoromethylphenyl)-2,4,6-trimethylbenzenesulfonamide (m-3M3FBS), or adding a DAG analogue, 1-oleoyl-2-acetyl-sn-glycerol (OAG), induced depolarization and spiking, mediated by a large, prolonged, Ca2+-permeable, inward current (IOAG) through a non-selective, voltage-independent cation channel that reversed near -20 mV and was enhanced by intracellular IP3. Furthermore, IOAG required basal PKC activity prior to the current, though OAG failed to trigger PKC. Molecular biology revealed a transient receptor potential (TRP) channel in bag cell neurons with secondary structure conserved in other TRPC5 channels. Designated ApTRPC5, when expressed in HEK cells it was a voltage-independent, non-selective cation current gated by PLC-coupled receptors or OAG. A separate source of depolarization for the afterdischarge is a voltage-gated, Ca2+-activated, non-selective cation channel. The effect of exogenous OAG and IP3, as well as PLC activation via m-3M3FBS, was investigated at the single channel level. OAG transiently elevated open probability (PO), and co-application of IP3 boosted and prolonged this response. Exposure to OAG and IP3 also left-shifted channel voltage-dependence; moreover, PLC activation using m-3M3FBS increased PO in excised patches, suggesting PLC may be physically localized to the channel. The Ca2+-activation of this channel desensitized during continued exposure to high Ca2+, which is reminiscent of PIP2-mediated desensitization seen in some TRPM channels. Accordingly, addition of a PIP2 analogue, di-C8-PIP2, ablated Ca2+ desensitization, while inhibiting the hydrolysis of PIP2 by PLC, with U73122, mirrored that effect. The phosphoinositol signalling cascade regulates multiple TRP-like channels during the afterdischarge, providing a means to facilitate prolonged depolarization and reproductive behaviour. Because TRP channels are modulated by phosphoinositols in numerous organisms, these results have implications for neuroendocrine function throughout the animal kingdom.

Subjects/Keywords: Aplysia ; Electrophysiology ; Cation channel ; Neuroendocrine cells ; TRP Channels

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APA (6^th Edition):

Sturgeon, R. (n.d.). Lipid signalling modulates neuroendocrine cell excitability and cation channel function . (Thesis). Queens University. Retrieved from http://hdl.handle.net/1974/24913

Note: this citation may be lacking information needed for this citation format:
No year of publication.
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Sturgeon, Raymond. “Lipid signalling modulates neuroendocrine cell excitability and cation channel function .” Thesis, Queens University. Accessed April 17, 2021. http://hdl.handle.net/1974/24913.

Note: this citation may be lacking information needed for this citation format:
No year of publication.
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Sturgeon, Raymond. “Lipid signalling modulates neuroendocrine cell excitability and cation channel function .” Web. 17 Apr 2021.

Note: this citation may be lacking information needed for this citation format:
No year of publication.

Vancouver:

Sturgeon R. Lipid signalling modulates neuroendocrine cell excitability and cation channel function . [Internet] [Thesis]. Queens University; [cited 2021 Apr 17]. Available from: http://hdl.handle.net/1974/24913.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
No year of publication.

Council of Science Editors:

Sturgeon R. Lipid signalling modulates neuroendocrine cell excitability and cation channel function . [Thesis]. Queens University; Available from: http://hdl.handle.net/1974/24913

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
No year of publication.

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