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You searched for +publisher:"Rutgers University" +contributor:("Sesti, Federico"). Showing records 1 – 3 of 3 total matches.

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Rutgers University

1. 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

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 (6th 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 (16th 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 11, 2021. https://rucore.libraries.rutgers.edu/rutgers-lib/60852/.

MLA Handbook (7th Edition):

Lou, Liping, 1982-. “Investigation of the function and regulation of the TRPM7 ion channel in the renal proximal tubule.” 2019. Web. 11 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 11]. 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/

2. Royal, Remi, 1989-. Limiting oxidation in potassium channel kv2.1 using cysteine-alanine mutation.

Degree: MS, Physiology and Integrative Biology, 2013, Rutgers University

The Kv2.1 (KCNB1) channel is expressed in the cortex and hippocampus. Interaction between cysteine residues of the kv2.1 channel plays a role in the formation of disulfide bonds. Disulfide bond formation following oxidative stress suggests that cysteine interaction in voltage-gated K+ channel kv2.1 plays a key role in the oxidation of kv2.1. Previous research has shown that oxidation of potassium (K+) channels by reactive oxygen species (ROS) is a major factor in the loss of neuronal function [6]. The purpose of this study was to use cysteine-alanine mutations to prevent oxidation of K+ channel kv2.1. In this thesis, the anti-oxidant properties of the double mutant C73AC29A were investigated. The affects were observed using site-directed mutagenesis and the polymerase chain reaction (PCR). PCR was utilized to form a double mutant between C73A and C29A. SDS-Page and Western Blot analysis were used to analyze whether there was more or less oxidation in the double mutant C73AC29A compared to that of the kv2.1 control. The double mutant C73AC29A showed protective properties, showing less oxidation than the kv2.1 control when placed under oxidative stress. Findings suggest that C73AC29A could provide protection from oxidation-induced loss of function in the kv2.1 channel. Advisors/Committee Members: Royal, Remi, 1989- (author), Sesti, Federico (chair), Jacinto, Estela (internal member), Fan, Huizhou (internal member).

Subjects/Keywords: Potassium channels; Potassium – Oxidation

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

APA (6th Edition):

Royal, Remi, 1. (2013). Limiting oxidation in potassium channel kv2.1 using cysteine-alanine mutation. (Masters Thesis). Rutgers University. Retrieved from http://hdl.rutgers.edu/1782.1/rucore10001600001.ETD.000067828

Chicago Manual of Style (16th Edition):

Royal, Remi, 1989-. “Limiting oxidation in potassium channel kv2.1 using cysteine-alanine mutation.” 2013. Masters Thesis, Rutgers University. Accessed April 11, 2021. http://hdl.rutgers.edu/1782.1/rucore10001600001.ETD.000067828.

MLA Handbook (7th Edition):

Royal, Remi, 1989-. “Limiting oxidation in potassium channel kv2.1 using cysteine-alanine mutation.” 2013. Web. 11 Apr 2021.

Vancouver:

Royal, Remi 1. Limiting oxidation in potassium channel kv2.1 using cysteine-alanine mutation. [Internet] [Masters thesis]. Rutgers University; 2013. [cited 2021 Apr 11]. Available from: http://hdl.rutgers.edu/1782.1/rucore10001600001.ETD.000067828.

Council of Science Editors:

Royal, Remi 1. Limiting oxidation in potassium channel kv2.1 using cysteine-alanine mutation. [Masters Thesis]. Rutgers University; 2013. Available from: http://hdl.rutgers.edu/1782.1/rucore10001600001.ETD.000067828

3. Tutak, Wojtek, 1978-. Single walled carbon nanotube networks as substrates for bone cells.

Degree: PhD, Materials Science and Engineering, 2010, Rutgers University

A central effort in biomedical research concerns the development of materials for sustaining and controlling cell growth. Carbon nanotube based substrates have been shown to support the growth of different kinds of cells. However the underlying molecular mechanisms remain poorly defined. To address the fundamental question of mechanisms by which nanotubes promote bone mitosis and histogenesis, primary calvariae osteoblastic cells were grown on single walled carbon nanotube (SWNT) network substrates. Using a combination of biochemical and optical techniques, we demonstrate here that SWNT networks promote cell development through two distinct steps. Initially, SWNTs are absorbed in a process that resembles endocytosis, inducing acute toxicity. Nanotube mediated cell destruction, however, induces a release of endogenous factors that act to boost the activity of the surviving cells by stimulating the synthesis of extracellular matrix. In the second part of the research, minimally invasive SWNT matrices were used to further investigate network properties for biomedical applications without extensive presence of cytotoxicity. In the literature, carbon nanotube based substrates have been shown to support the growth of different cell types and, as such, have raised considerable interest in view of their possible use in biomedical applications. Nanotube matrices that are embedded in polymers cause inherent changes in nanotube chemical and physical film properties. Thus, it is critical to understand how the physical properties of the pristine networks affect the biology of the host tissue. Here, we investigated how the physical and chemical properties of SWNT networks impact the response of MC3T3-E1 bone osteoblasts. We found that two fundamental steps in cell growth: initial attachment to the substrate and proliferation, are strongly dependent on the energy and roughness of the surface, respectively. Thus, fine-tuning the properties of the film may represent a strategy to optimize the response of the biological host. Outlined above results led to a next set of experiments in which in-situ, real time cell interactions with SWNT films were investigated. Direct electrical measurements on SWNT thin films on changing osteoblastic cell growth were conducted. The experiments indicated that in fact the nanotube films have capability of hosting and sensing initial cell material interactions.

Advisors/Committee Members: Tutak, Wojtek, 1978- (author), Chhowalla, Manish (chair), Lehman, Richard (internal member), Mann, Adrian (internal member), Klein, Lisa (internal member), Sesti, Federico (outside member).

Subjects/Keywords: Cells – Growth – Regulation; Nanotubes; Osteoclasts

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

APA (6th Edition):

Tutak, Wojtek, 1. (2010). Single walled carbon nanotube networks as substrates for bone cells. (Doctoral Dissertation). Rutgers University. Retrieved from http://hdl.rutgers.edu/1782.1/rucore10001600001.ETD.000056809

Chicago Manual of Style (16th Edition):

Tutak, Wojtek, 1978-. “Single walled carbon nanotube networks as substrates for bone cells.” 2010. Doctoral Dissertation, Rutgers University. Accessed April 11, 2021. http://hdl.rutgers.edu/1782.1/rucore10001600001.ETD.000056809.

MLA Handbook (7th Edition):

Tutak, Wojtek, 1978-. “Single walled carbon nanotube networks as substrates for bone cells.” 2010. Web. 11 Apr 2021.

Vancouver:

Tutak, Wojtek 1. Single walled carbon nanotube networks as substrates for bone cells. [Internet] [Doctoral dissertation]. Rutgers University; 2010. [cited 2021 Apr 11]. Available from: http://hdl.rutgers.edu/1782.1/rucore10001600001.ETD.000056809.

Council of Science Editors:

Tutak, Wojtek 1. Single walled carbon nanotube networks as substrates for bone cells. [Doctoral Dissertation]. Rutgers University; 2010. Available from: http://hdl.rutgers.edu/1782.1/rucore10001600001.ETD.000056809

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