subject:(myosin light chain phosphorylation)

Temple University

1. Getz, Todd Michael. The Regulation of Phosphorylation Events in Platelets.

Degree: PhD, 2012, Temple University

URL: http://digital.library.temple.edu/u?/p245801coll10,213114

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Physiology

Platelets play a vital role in processes of hemostasis and thrombosis under physiological and pathological conditions. Following vascular damage, platelets will accumulate and stably… (more)

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Physiology

Platelets play a vital role in processes of hemostasis and thrombosis under physiological and pathological conditions. Following vascular damage, platelets will accumulate and stably adhere to exposed subendothelial matrixes. The binding of platelet surface receptor Glycoprotein VI (GPVI) to exposed collagen initiates a signaling cascade, which culminates in platelet activation. Stimulation of GPVI pathways results in the generation of thromboxane and causes the platelets to secrete their granule contents. This generated thromboxane as well as constituents released from dense granules such as ADP, and serotonin, play an essential role in potentiating the platelet response through activation of other surface receptor mediated pathways. Importantly, downstream of all these separate pathways, kinases become activated and play a crucial role in phosphorylating their substrates to elicit critical cellular responses. Previously published studies have established the importance for myosin kinase in its role for phosphorylating the myosin light chain (MLC) downstream of ADP receptors. These studies have shown MLC phosphorylation occurs rapidly and is essential for shape change following the stimulation of ADP receptors. Technological advances in antibody development have resulted in the generation of commercially available phospho-specific antibodies for MLC phosphorylated on either threonine (Thr) 18 or serine (Ser) 19. These antibodies allowed us to revisit these prior studies and address whether phosphorylation on MLC (Ser) 19 would elicit one response while phosphorylation on (Thr) 18 may result in another functional response. Our result show, that MLC is phosphorylated rapidly on (Ser) 19 and plays an important role in shape change downstream of Gq pathways, while MLC (Thr) 18 phosphorylation occurs at a slower rate downstream of G12/13 pathways and contributes to platelet dense granule secretion. Protein kinase C's (PKC) are serine/threonine kinase, which become activated following the stimulation of many of the platelet surface receptors. PKCs are classified into three groups, classical (α, βI, βII, γ), novel (δ, ε, η, θ), and atypical (ζ, ι, λ, μ) based on their cofactor requirements for activation. The classical PKCs, which require diacylglycerol and calcium for their activation were investigated using the specific inhibitor Go6976. Much to our surprise, we demonstrated that downstream of GPVI pathways, Go6976 caused non-selective inhibition of Spleen tyrosine kinase (Syk) activity. This inhibition of Syk activity resulted in a concentration-dependent reduction in phosphorylation of downstream molecules Lat and PLCγ2 as well as platelet aggregation and secretion. Stimulation of surface receptors GPVI, CLEC-2, GPIb, and FcRIIa, all lead to the activation of tyrosine kinase pathways. The role for Syk in these pathways is essential and in the absence of its activity these pathways are completely shut down. We inadvertently discovered dextran sulfate (DxS) actives platelets. Our results show that DxS…

Advisors/Committee Members: Kunapuli, Satya P., Autieri, Michael V., Driska, Steven Paul, Tsygankov, Alexander, McKenzie, Steven.

Subjects/Keywords: Physiology; Biology; Biochemistry; Dextran sulfate; Myosin light chain; Phosphorylation; Platelets; signal transduction; Syk kinase

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APA (6^th Edition):

Getz, T. M. (2012). The Regulation of Phosphorylation Events in Platelets. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,213114

Chicago Manual of Style (16^th Edition):

Getz, Todd Michael. “The Regulation of Phosphorylation Events in Platelets.” 2012. Doctoral Dissertation, Temple University. Accessed March 01, 2021. http://digital.library.temple.edu/u?/p245801coll10,213114.

MLA Handbook (7^th Edition):

Getz, Todd Michael. “The Regulation of Phosphorylation Events in Platelets.” 2012. Web. 01 Mar 2021.

Vancouver:

Getz TM. The Regulation of Phosphorylation Events in Platelets. [Internet] [Doctoral dissertation]. Temple University; 2012. [cited 2021 Mar 01]. Available from: http://digital.library.temple.edu/u?/p245801coll10,213114.

Council of Science Editors:

Getz TM. The Regulation of Phosphorylation Events in Platelets. [Doctoral Dissertation]. Temple University; 2012. Available from: http://digital.library.temple.edu/u?/p245801coll10,213114

University of Alberta

2. Aguilar, Hector N. Rho-Kinase-Mediated Diphosphorylation of Myosin Regulatory Light Chain is a Unique Biochemical Mechanism in Human Uterine Myocytes.

Degree: PhD, Department of Physiology, 2011, University of Alberta

URL: https://era.library.ualberta.ca/files/vt150j556

► Rationale: Smooth muscle (SM) contraction results from activation of the cellular contractile machinery by phosphorylation of myosin regulatory light chain (RLC) at S19 (pRLC) by… (more)

▼ Rationale: Smooth muscle (SM) contraction results from activation of the cellular contractile machinery by phosphorylation of myosin regulatory light chain (RLC) at S19 (pRLC) by RLC kinase (MLCK). Subsequent phosphorylation at T18 yields diphosphorylated-RLC (ppRLC), which has been shown to enhance the myosin ATPase activity, and therefore might have implications for the ability of the muscle to generate tension. In uterine myocytes, the extent of diphosphorylation is greater than that observed in vascular myocytes. In preliminary experiments using cultured human uterine smooth muscle cells (hUSMC), we observed that rho-kinase (ROK) inhibition caused a marked reduction in ppRLC, but surprisingly, not pRLC. Therefore we pursued a quantitative comparison in ROK-mediated phosphorylation of RLC in hUSMC and human vascular myocytes (hVSMC). Objectives: 1) to develop and validate quantitative methods for assessment of phosphorylated RLC, and 2) to apply these methods in studies comparing ROK-mediated phosphorylation of RLC in hUSMC and hVSMC. Findings: We have developed and validated two assays for quantitative measurements of phosphorylated RLC using phospho-specific antibodies: 1) a high-throughput in-cell western assay, and 2) western blotting-based quantification of RLC-phospho-states after separation with phos-tag SDS-PAGE. These techniques revealed that hUSMC differ from hVSMC in their primary phosphorylation responses to stimulation. hUSMC respond to oxytocin with increased pRLC and ppRLC, whereas hVSMC respond to endothelin-1 with increased pRLC only. In hUSMC, only ppRLC was sensitive to ROK inhibition using a pharmacologic inhibitor, and this occurred at approximately 100-fold lower concentration of ROK inhibitor than that required to achieve an equivalent reduction of pRLC in hVSMC. Conclusions: In hUSMC, ROK phosphorylates RLC at T18 downstream of MLCK-mediated phosphorylation at S19. This sequential phosphorylation of RLC forms ppRLC. This role of ROK activity appears unique to hUSMC and is a fundamental difference from hVSMC. These findings suggest the possibility of a uterine-specific therapeutic avenue for prevention or arrest of preterm labor achieved by targeting ROK to reduce ppRLC levels in hUSMC. Our data also suggest that ROK inhibition might avoid the prohibitive side effects of currently used agents for preterm labour, of which the most common and serious is hypotension that results from unwanted vascular relaxation.

Subjects/Keywords: Phos-tag; Contractility; Uterus; In-cell Western; rhoA; Myosin Regulatory Light Chain; MYPT1; Myometrium; Oxytocin; Phosphorylation; endothelin-1; Rho-Kinase

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

APA (6^th Edition):

Aguilar, H. N. (2011). Rho-Kinase-Mediated Diphosphorylation of Myosin Regulatory Light Chain is a Unique Biochemical Mechanism in Human Uterine Myocytes. (Doctoral Dissertation). University of Alberta. Retrieved from https://era.library.ualberta.ca/files/vt150j556

Chicago Manual of Style (16^th Edition):

Aguilar, Hector N. “Rho-Kinase-Mediated Diphosphorylation of Myosin Regulatory Light Chain is a Unique Biochemical Mechanism in Human Uterine Myocytes.” 2011. Doctoral Dissertation, University of Alberta. Accessed March 01, 2021. https://era.library.ualberta.ca/files/vt150j556.

MLA Handbook (7^th Edition):

Aguilar, Hector N. “Rho-Kinase-Mediated Diphosphorylation of Myosin Regulatory Light Chain is a Unique Biochemical Mechanism in Human Uterine Myocytes.” 2011. Web. 01 Mar 2021.

Vancouver:

Aguilar HN. Rho-Kinase-Mediated Diphosphorylation of Myosin Regulatory Light Chain is a Unique Biochemical Mechanism in Human Uterine Myocytes. [Internet] [Doctoral dissertation]. University of Alberta; 2011. [cited 2021 Mar 01]. Available from: https://era.library.ualberta.ca/files/vt150j556.

Council of Science Editors:

Aguilar HN. Rho-Kinase-Mediated Diphosphorylation of Myosin Regulatory Light Chain is a Unique Biochemical Mechanism in Human Uterine Myocytes. [Doctoral Dissertation]. University of Alberta; 2011. Available from: https://era.library.ualberta.ca/files/vt150j556

University of Saskatchewan

3. de Jesus Cadete, Virgilio. Ischemia/reperfusion-induced changes in cardiac contractile proteins.

Degree: 2012, University of Saskatchewan

URL: http://hdl.handle.net/10388/ETD-2012-08-555

► Heart disease, often results in the development of ischemia/reperfusion (I/R) injury, and is one of the major causes of morbidity and mortality. I/R injury is… (more)

▼ Heart disease, often results in the development of ischemia/reperfusion (I/R) injury, and is one of the major causes of morbidity and mortality. I/R injury is usually characterized by the development of cardiac contractile dysfunction, which is one of the major indicators of recovery. The understanding of the mechanisms underlying the development cardiac contractile dysfunction in response to I/R is crucial for the prevention and treatment of I/R injury. Using a proteomics approach to an isolated heart model we identified myosin light chain 1 (MLC1) as an important contractile protein, phosphorylated by myosin light chain kinase (MLCK) and degraded by matrix metalloproteinase-2 (MMP-2) due to I/R. Prevention of MLC1 phosphorylation, with an MLCK inhibitor (ML-7) or a myosin light chain phosphatase – MLCP – stimulator (Y-27632), and degradation with an MMPs inhibitor (doxycycline) protects the heart from contractile dysfunction, associated with a preservation of MLC1 protein levels. The combined use of these three drugs (ML-7, Y-27632 and doxycycline) at subthreshold concentrations resulted in a full protection of both contractile function and MLC1 in hearts subjected to I/R. The MLCP indirect activator Y-27632 (a Rho kinase inhibitor) showed the best degree of protection of contractile function at full protective doses, independent of MLC1 preservation. A proteomics approach revealed that the administration of Y-27632 to hearts subjected to I/R results, not only in a protection of MLC1 from phosphorylation and degradation, but also a modulation of enzymes involved in energy production (lactate dehydrogenase and glyceraldehyde 3-phosphate dehydrogenase). This modulation of energy metabolism is potentially an importa effect of Rho kinase inhibitors, secondary to direct protection of cardiac contractile proteins from degradation in response to I/R. The data presented here show a novel paradigm in the development of I/R-induced cardiac contractile dysfunction. Moreover, we establish a new therapeutic approach (multidrug treatment) that can be of crucial importance in the development of new preventive or treatment strategies against cardiac injury. Advisors/Committee Members: Sawicki, Grzegorz, Desai, Kaushik, Richardson, J Steven, Gopalakrishnan, Venkat, Grochulski, Pawel.

Subjects/Keywords: ischemia/reperfusion injury; myosin light chain 1; matrix metalloproteinase-2, cardioprotection; synergy; posttranslational modifications; phosphorylation; Y-27632

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APA (6^th Edition):

de Jesus Cadete, V. (2012). Ischemia/reperfusion-induced changes in cardiac contractile proteins. (Thesis). University of Saskatchewan. Retrieved from http://hdl.handle.net/10388/ETD-2012-08-555

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):

de Jesus Cadete, Virgilio. “Ischemia/reperfusion-induced changes in cardiac contractile proteins.” 2012. Thesis, University of Saskatchewan. Accessed March 01, 2021. http://hdl.handle.net/10388/ETD-2012-08-555.

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

MLA Handbook (7^th Edition):

de Jesus Cadete, Virgilio. “Ischemia/reperfusion-induced changes in cardiac contractile proteins.” 2012. Web. 01 Mar 2021.

Vancouver:

de Jesus Cadete V. Ischemia/reperfusion-induced changes in cardiac contractile proteins. [Internet] [Thesis]. University of Saskatchewan; 2012. [cited 2021 Mar 01]. Available from: http://hdl.handle.net/10388/ETD-2012-08-555.

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

Council of Science Editors:

de Jesus Cadete V. Ischemia/reperfusion-induced changes in cardiac contractile proteins. [Thesis]. University of Saskatchewan; 2012. Available from: http://hdl.handle.net/10388/ETD-2012-08-555

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

Virginia Commonwealth University

4. Anderson, Charles Dudley, Jr. Kinase pathways underlying muscarinic activation of colonic longitudinal muscle.

Degree: PhD, Physiology, 2011, Virginia Commonwealth University

URL: https://doi.org/10.25772/G0W4-2V09 ; https://scholarscompass.vcu.edu/etd/2365

► The longitudinal muscle layer in gut is the functional opponent to the circular muscle layer during the peristalsis reflex. Differences in innervation of the layers… (more)

Subjects/Keywords: Longitudinal Muscle; Kinase Cascade; Myosin light chain phosphorylation; MLCK; MLCP; Colonic Muscle; Rho Kinase; ERK1/2; CaMKII; AMPK; CaMKK; Muscarinic Receptors; Life Sciences; Physiology

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APA (6^th Edition):

Anderson, Charles Dudley, J. (2011). Kinase pathways underlying muscarinic activation of colonic longitudinal muscle. (Doctoral Dissertation). Virginia Commonwealth University. Retrieved from https://doi.org/10.25772/G0W4-2V09 ; https://scholarscompass.vcu.edu/etd/2365

Chicago Manual of Style (16^th Edition):

Anderson, Charles Dudley, Jr. “Kinase pathways underlying muscarinic activation of colonic longitudinal muscle.” 2011. Doctoral Dissertation, Virginia Commonwealth University. Accessed March 01, 2021. https://doi.org/10.25772/G0W4-2V09 ; https://scholarscompass.vcu.edu/etd/2365.

MLA Handbook (7^th Edition):

Anderson, Charles Dudley, Jr. “Kinase pathways underlying muscarinic activation of colonic longitudinal muscle.” 2011. Web. 01 Mar 2021.

Vancouver:

Anderson, Charles Dudley J. Kinase pathways underlying muscarinic activation of colonic longitudinal muscle. [Internet] [Doctoral dissertation]. Virginia Commonwealth University; 2011. [cited 2021 Mar 01]. Available from: https://doi.org/10.25772/G0W4-2V09 ; https://scholarscompass.vcu.edu/etd/2365.

Council of Science Editors:

Anderson, Charles Dudley J. Kinase pathways underlying muscarinic activation of colonic longitudinal muscle. [Doctoral Dissertation]. Virginia Commonwealth University; 2011. Available from: https://doi.org/10.25772/G0W4-2V09 ; https://scholarscompass.vcu.edu/etd/2365

5. 王, 志丹. Caffeine inhibits smooth muscle actin-myosin interaction : カフェインは平滑筋ミオシンアクチン相互作用を抑制する.

Degree: 修士（健康科学）, 2017, Tokyo Metropolitan University / 首都大学東京

URL: http://hdl.handle.net/10748/00009635

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Caffeine is known to have inhibitory effects on Ca^<2+>-induced contraction in smooth muscle, and possible mechanisms may contribute the inhibitory effects. Recently, it was found… (more)

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Caffeine is known to have inhibitory effects on Ca^<2+>-induced contraction in smooth muscle, and possible mechanisms may contribute the inhibitory effects. Recently, it was found a caffeine effect on direct inhibition of myosin-actin interaction in smooth muscle. To clarify whether direct inhibition of myosin-actin interaction of caffeine to be dependent on the regulation of myosin light chain phosphorylation, in the present study, the author examined caffeine effects on skinned (cell membrane permeabilized) smooth muscle contraction. At 10 mM, caffeine significantly suppressed Ca^<2+> induced contraction, which was dependent on myosin light chain phosphorylation. On the other hand, caffeine did not affect 15.5 mM Mg^<2+> induced contraction, which was independent of myosin light chain phosphorylation. The present results suggest that caffeine inhibits actin-myosin interaction of smooth muscle through either inhibition of myosin light chain kinase activity or acceleration of myosin phosphatase activity.

カフェインには平滑筋にCaイオンの抑制があることが知られている。様々な機構がこの抑制に関与している。最近、カフェインは平滑筋のミオシンアクチン相互作用を直接的に抑制することが明らかになった。本研究では、細胞膜を破壊したスキンド盲腸紐標本を用いて、カフェインの平滑筋アクチン・ミオシン相互作用の抑制が、ミオシン軽鎖リン酸化の抑制によるものなのかを検討した。10mMのカェインはミオシン軽鎖リン酸化に依存するCaイオン活性化収縮張力を抑制した。一方、カフェインはミオシン軽鎖リン酸化に依存しない15.5mM Mgイオンによる収縮張力を抑制しない。以上から、カフェインはミオシン軽鎖リン酸化酵素の活性阻害、もしくはミオシンボスファターゼの活性を促進することでミオシン軽鎖リン酸化レベルを低下させることで、平滑筋ミオシンアクチン相互作用を抑制し、平滑筋収縮を抑制することが示唆された。

首都大学東京, 2017-03-25, 修士（健康科学）

Subjects/Keywords: caffeine; Ca^<; 2+>; -induced contraction; myosin-actin interaction; myosin light chain phosphorylation; カフェイン; Ca^<; 2+>; 活性化収縮; ミオシン-アクチン相互作用; ミオシン軽鎖リン酸化

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APA (6^th Edition):

王, �. (2017). Caffeine inhibits smooth muscle actin-myosin interaction : カフェインは平滑筋ミオシンアクチン相互作用を抑制する. (Thesis). Tokyo Metropolitan University / 首都大学東京. Retrieved from http://hdl.handle.net/10748/00009635

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):

王, 志丹. “Caffeine inhibits smooth muscle actin-myosin interaction : カフェインは平滑筋ミオシンアクチン相互作用を抑制する.” 2017. Thesis, Tokyo Metropolitan University / 首都大学東京. Accessed March 01, 2021. http://hdl.handle.net/10748/00009635.

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

MLA Handbook (7^th Edition):

王, 志丹. “Caffeine inhibits smooth muscle actin-myosin interaction : カフェインは平滑筋ミオシンアクチン相互作用を抑制する.” 2017. Web. 01 Mar 2021.

Vancouver:

王 �. Caffeine inhibits smooth muscle actin-myosin interaction : カフェインは平滑筋ミオシンアクチン相互作用を抑制する. [Internet] [Thesis]. Tokyo Metropolitan University / 首都大学東京; 2017. [cited 2021 Mar 01]. Available from: http://hdl.handle.net/10748/00009635.

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

Council of Science Editors:

王 �. Caffeine inhibits smooth muscle actin-myosin interaction : カフェインは平滑筋ミオシンアクチン相互作用を抑制する. [Thesis]. Tokyo Metropolitan University / 首都大学東京; 2017. Available from: http://hdl.handle.net/10748/00009635

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

University of Illinois – Urbana-Champaign

6. Shin, Myung Eun. Spatiotemporal organization, regulation and function of traction during neutrophil chemotaxis.

Degree: PhD, 4094, 2012, University of Illinois – Urbana-Champaign

URL: http://hdl.handle.net/2142/29509

► Despite recent advances in our understanding of biochemical regulation of neutrophil chemotaxis, little is known about how mechanical factors control neutrophils’ persistent polarity and rapid… (more)

Subjects/Keywords: Neutrophil Chemotaxis; Traction; Myosin-Light-Chain Kinase; Myosin Type II; Cell Adhesion; Cell Motility; Mechanotransduction

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APA (6^th Edition):

Shin, M. E. (2012). Spatiotemporal organization, regulation and function of traction during neutrophil chemotaxis. (Doctoral Dissertation). University of Illinois – Urbana-Champaign. Retrieved from http://hdl.handle.net/2142/29509

Chicago Manual of Style (16^th Edition):

Shin, Myung Eun. “Spatiotemporal organization, regulation and function of traction during neutrophil chemotaxis.” 2012. Doctoral Dissertation, University of Illinois – Urbana-Champaign. Accessed March 01, 2021. http://hdl.handle.net/2142/29509.

MLA Handbook (7^th Edition):

Shin, Myung Eun. “Spatiotemporal organization, regulation and function of traction during neutrophil chemotaxis.” 2012. Web. 01 Mar 2021.

Vancouver:

Shin ME. Spatiotemporal organization, regulation and function of traction during neutrophil chemotaxis. [Internet] [Doctoral dissertation]. University of Illinois – Urbana-Champaign; 2012. [cited 2021 Mar 01]. Available from: http://hdl.handle.net/2142/29509.

Council of Science Editors:

Shin ME. Spatiotemporal organization, regulation and function of traction during neutrophil chemotaxis. [Doctoral Dissertation]. University of Illinois – Urbana-Champaign; 2012. Available from: http://hdl.handle.net/2142/29509

Iowa State University

7. Anderson, Mark Joseph. Identification of proteins and biological processes associated with tenderness in beef muscles.

Degree: 2011, Iowa State University

URL: https://lib.dr.iastate.edu/etd/12020

► During the postmortem storage there are numerous changes in the protein profile of beef. It is well documented that some of these changes directly affect… (more)

▼ During the postmortem storage there are numerous changes in the protein profile of beef. It is well documented that some of these changes directly affect the structure of the myofibril during postmortem aging. Our hypothesis was that there are alterations to proteins during postmortem storage that affect tenderness development. By identifying these alterations, these proteins can be used as indicators of tenderness and can aid in the identification of consistently tender beef. The first experiment was designed to define the biochemical differences that govern tenderness and palatability of economically important muscles from the beef round using muscles with known tenderness differences. At 24 h postmortem, the longissimus dorsi (LD), gracillus (GR), adductor (AD), semimembranosus (SM), sartorius (SAR), vastus lateralis (VL), and vastus intermedius (VI) muscles were removed from ten market-weight beef cattle. Sensory and biochemical characteristics were determined in each muscle and compared with the LD. This study showed that the AD and VL had poor sensory traits compared to the LD. However, the GR, SAR, and VI had sensory traits similar to the LD. The AD was also an important example of how understanding the biochemical characteristics of a muscle can aid in the utilization of that muscle. The most notable attribute of the AD was its lack of change in protein degradation during aging. The AD had no detectable change in the abundance of the 30 kDa degradation of troponin T from one to 14 days postmortem, and no significant change in tenderness. Postmortem aging of this muscle provided no added benefit as it did in many of the other muscles evaluated. In most beef round muscles, postmortem proteolysis provided a good indication of the postmortem tenderization occurring during aging. Results from our first study suggested that proteolysis is the key process in indicating postmortem tenderness and that the AD had little proteolysis from one to 14 days postmortem. The lack of change in protein degradation in the AD provided a model to determine the changes in protein abundance over time in a muscle with little proteolysis from one to 14 days postmortem. Once these changes were determined, they were then compared to the changes in protein abundance over time in a muscle with greater proteolysis (LD) from one to 14 days postmortem to identify the proteins that may play a role in postmortem tenderization. So, this second experiment was designed to determine the identity of proteins that are altered during the postmortem aging process by using muscles that differ in tenderness and postmortem protein degradation. The AD (n=5) was chosen because it shows very little change in sensory and instrumental tenderness during 14 days of aging and the LD (n=5) was chosen because it showed a large increase in sensory and instrumental tenderness. A highly soluble sarcoplasmic fraction and a less soluble, crude myofibrillar fraction were extracted from each muscle. Two-Dimensional Difference In Gel Electrophoresis (2-D DIGE) was used…

Subjects/Keywords: Beef; DIGE; Myosin light chain; Phosphoglucomutase; Tenderness; Animal Sciences

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

APA (6^th Edition):

Anderson, M. J. (2011). Identification of proteins and biological processes associated with tenderness in beef muscles. (Thesis). Iowa State University. Retrieved from https://lib.dr.iastate.edu/etd/12020

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):

Anderson, Mark Joseph. “Identification of proteins and biological processes associated with tenderness in beef muscles.” 2011. Thesis, Iowa State University. Accessed March 01, 2021. https://lib.dr.iastate.edu/etd/12020.

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

MLA Handbook (7^th Edition):

Anderson, Mark Joseph. “Identification of proteins and biological processes associated with tenderness in beef muscles.” 2011. Web. 01 Mar 2021.

Vancouver:

Anderson MJ. Identification of proteins and biological processes associated with tenderness in beef muscles. [Internet] [Thesis]. Iowa State University; 2011. [cited 2021 Mar 01]. Available from: https://lib.dr.iastate.edu/etd/12020.

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

Council of Science Editors:

Anderson MJ. Identification of proteins and biological processes associated with tenderness in beef muscles. [Thesis]. Iowa State University; 2011. Available from: https://lib.dr.iastate.edu/etd/12020

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

University of Melbourne

8. Williams, Melanie Joy. Structural and functional analyses of the host cell invasion motor in Toxoplasma parasites.

Degree: 2018, University of Melbourne

URL: http://hdl.handle.net/11343/216517

► Key to the virulence of apicomplexan parasites is their ability move through tissue, invade and subsequently egress from host cells. Apicomplexan motility is initiated in… (more)

Subjects/Keywords: parasites; Toxoplasma; infectious disease; motility; essential light chain; calcium regulation; myosin

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

APA (6^th Edition):

Williams, M. J. (2018). Structural and functional analyses of the host cell invasion motor in Toxoplasma parasites. (Doctoral Dissertation). University of Melbourne. Retrieved from http://hdl.handle.net/11343/216517

Chicago Manual of Style (16^th Edition):

Williams, Melanie Joy. “Structural and functional analyses of the host cell invasion motor in Toxoplasma parasites.” 2018. Doctoral Dissertation, University of Melbourne. Accessed March 01, 2021. http://hdl.handle.net/11343/216517.

MLA Handbook (7^th Edition):

Williams, Melanie Joy. “Structural and functional analyses of the host cell invasion motor in Toxoplasma parasites.” 2018. Web. 01 Mar 2021.

Vancouver:

Williams MJ. Structural and functional analyses of the host cell invasion motor in Toxoplasma parasites. [Internet] [Doctoral dissertation]. University of Melbourne; 2018. [cited 2021 Mar 01]. Available from: http://hdl.handle.net/11343/216517.

Council of Science Editors:

Williams MJ. Structural and functional analyses of the host cell invasion motor in Toxoplasma parasites. [Doctoral Dissertation]. University of Melbourne; 2018. Available from: http://hdl.handle.net/11343/216517

9. Karabina, Anastasia Smaro. Effects of regulatory light chain phosphorylation on mutant and wild-type cardiac muscle myosin mechanochemistry.

Degree: PhD, Physiology & Biophysics, 2015, Boston University

URL: http://hdl.handle.net/2144/13939

► Cardiac muscle contraction is responsible for pumping blood throughout the body. The cyclical, ATP-hydrolysis dependent interaction of the myosin motor protein with filamentous actin drives… (more)

▼ Cardiac muscle contraction is responsible for pumping blood throughout the body. The cyclical, ATP-hydrolysis dependent interaction of the myosin motor protein with filamentous actin drives muscle contraction. During this process the α-helical neck region of myosin acts as a lever arm, transmitting contractile force between thick and thin filaments by amplifying small conformational changes in the myosin motor domain. The resulting relative displacement of thick and thin filaments causes muscle shortening. The regulatory light chain (RLC) of myosin mechanically supports the lever arm by binding to the myosin heavy chain neck region; this is a crucial interaction in maintaining myosin's ability to produce force and motion. We investigated the role of N-terminal modifications of the RLC in modulating actomyosin contractility at the molecular level. Phosphorylation of the RLC is a naturally occurring post-translational modification of the RLC N-terminus that is important for cardiac function and has been shown to enhance contractility at the cellular level. In contrast, genetic mutations of the RLC that lead to familial hypertrophic cardiomyopathy (FHC) disrupt cardiac function and trigger remodeling of the cardiac muscle structure. We studied two FHC-linked mutations, N47K and R58Q, located in the N-terminus of the RLC in close proximity to the phosphorylation site. Using in vitro motility assays we examined how RLC modifications affect the mechanochemical properties of cardiac β-myosin. We found that the FHC mutations reduced myosin force and power generation, in contrast to RLC phosphorylation which increased myosin force and power for WT and mutant myosins. Phosphorylation of mutant RLC resulted in a restoration of the mutation-induced decreases in contractility to WT dephosphorylated levels. These results point to RLC phosphorylation as a general mechanism to increase force production of the individual myosin motor and as a potential target to ameliorate the fundamental contractile FHC-induced phenotype.

Subjects/Keywords: Biophysics; Phosphorylation; Cardiac myosin; Hypertrophic cardiomyopathy; In Vitro motility; Load dependence; Regulatory light chain

…43 2.1.3 Myosin Light Chain Kinase… …ribonucleoside MHC myosin heavy chain MLCK myosin light chain kinase MOPS 3-(N-morpholino… …Myosin subfragment 1 (S1) consists of a motor domain, an essential light chain (… …ELC), and a regulatory light chain (RLC). Myosin subfragment 2 (S2)… …globular head along with the light chain 12 bound neck region constitute the myosin cross…

11 more images…

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APA (6^th Edition):

Karabina, A. S. (2015). Effects of regulatory light chain phosphorylation on mutant and wild-type cardiac muscle myosin mechanochemistry. (Doctoral Dissertation). Boston University. Retrieved from http://hdl.handle.net/2144/13939

Chicago Manual of Style (16^th Edition):

Karabina, Anastasia Smaro. “Effects of regulatory light chain phosphorylation on mutant and wild-type cardiac muscle myosin mechanochemistry.” 2015. Doctoral Dissertation, Boston University. Accessed March 01, 2021. http://hdl.handle.net/2144/13939.

MLA Handbook (7^th Edition):

Karabina, Anastasia Smaro. “Effects of regulatory light chain phosphorylation on mutant and wild-type cardiac muscle myosin mechanochemistry.” 2015. Web. 01 Mar 2021.

Vancouver:

Karabina AS. Effects of regulatory light chain phosphorylation on mutant and wild-type cardiac muscle myosin mechanochemistry. [Internet] [Doctoral dissertation]. Boston University; 2015. [cited 2021 Mar 01]. Available from: http://hdl.handle.net/2144/13939.

Council of Science Editors:

Karabina AS. Effects of regulatory light chain phosphorylation on mutant and wild-type cardiac muscle myosin mechanochemistry. [Doctoral Dissertation]. Boston University; 2015. Available from: http://hdl.handle.net/2144/13939

University of Minnesota

10. Kast, David John Edward. Phosphorylation-induced structural changes in smooth muscle myosin.

Degree: PhD, Biochemistry, Molecular Bio, and Biophysics, 2010, University of Minnesota

URL: http://purl.umn.edu/94937

► Activation of smooth muscle myosin (SMM) requires phosphorylation of the myosin's regulatory light chain (RLC) to relieve autoinhibitory head-head interactions, but the structural basis of… (more)

▼ Activation of smooth muscle myosin (SMM) requires phosphorylation of the myosin's regulatory light chain (RLC) to relieve autoinhibitory head-head interactions, but the structural basis of this mechanism in unknown. There are no crystal structures of any fragment of SMM, and there are no crystal structures of any RLC that contains the N-terminal 24 amino acids required for phosphorylation. Site-directed spin labeling of this N-terminal segment, referred to as the phosphorylation domain (PD), showed that phosphorylation increases α-helicity, mobility and solvent accessibility of the PD. A model emerged, where the unphosphorylated RLC is compact with a disordered PD, and phosphorylation causes the PD extend away from the RLC while inducing helical ordering. The goal of this research is to test the hypothesis that the PD functions as a structural switch that changes the structure of RLC upon phosphorylation, and to define these structural changes in atomic detail. Complementary fluorescence resonance energy transfer (FRET) experiments and molecular dynamics (MD) simulations were performed to elucidate structural changes in the phosphorylation domain (PD) of smooth muscle regulatory light chain (RLC). MD simulations on the isolated PD reveal disorder-to-order transition, where residues K11-Q15 are disordered in the unphosphorylated PD but completely α-helical in the phosphorylated PD. A salt bridge formed between R16 and the phosphorylated S19 promotes ordering by stabilizing α-helicity and reducing conformational fluctuations. Consequently, this disorder-to-order transition is regulated by delicate balance between enthalpy and entropy. To elucidate the structural changes of the PD in context with the RLC bound to smooth muscle myosin, donor-acceptor pairs of probes were attached to three site-directed di-Cys mutants of RLC, each having one Cys at position 129 in the C-terminal lobe and the other at position 2, 3, or 7 in the N-terminal PD. Labeled RLC was reconstituted onto myosin S1. Time-resolved FRET demonstrated two simultaneously resolved structural states of the RLC, closed and open, which are present in both unphosphorylated and phosphorylated biochemical states. All three FRET pairs show that phosphorylation shifts the equilibrium toward the open state, increasing its mole fraction by 23%. Molecular dynamics simulations agree with FRET data in remarkable detail, supporting the coexistence of two structural states, with phosphorylation shifting the system toward a more open and mobile structure. This agreement between experiment and simulation validates the additional structural details provided by the MD simulations: In the closed state, the PD is bent onto the surface of the C-terminal lobe, stabilized by two specific interdomain salt bridges. In the open state, the PD is more helical and straight, resides farther from the C-terminal lobe, and is stabilized by a specific intradomain salt bridge. The closed and open states are also present in phosphorylated HMM, while unphosphorylated HMM…

Subjects/Keywords: Fluorescence Resonance Energy Transfer; Molecular Dynamics Simulations; Myosin; Phosphorylation; Regulatory Light Chain; Smooth Muscle; Biochemistry, Molecular Bio, and Biophysics

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

APA (6^th Edition):

Kast, D. J. E. (2010). Phosphorylation-induced structural changes in smooth muscle myosin. (Doctoral Dissertation). University of Minnesota. Retrieved from http://purl.umn.edu/94937

Chicago Manual of Style (16^th Edition):

Kast, David John Edward. “Phosphorylation-induced structural changes in smooth muscle myosin.” 2010. Doctoral Dissertation, University of Minnesota. Accessed March 01, 2021. http://purl.umn.edu/94937.

MLA Handbook (7^th Edition):

Kast, David John Edward. “Phosphorylation-induced structural changes in smooth muscle myosin.” 2010. Web. 01 Mar 2021.

Vancouver:

Kast DJE. Phosphorylation-induced structural changes in smooth muscle myosin. [Internet] [Doctoral dissertation]. University of Minnesota; 2010. [cited 2021 Mar 01]. Available from: http://purl.umn.edu/94937.

Council of Science Editors:

Kast DJE. Phosphorylation-induced structural changes in smooth muscle myosin. [Doctoral Dissertation]. University of Minnesota; 2010. Available from: http://purl.umn.edu/94937

University of Southern California

11. Cao, Christine. The role of α-catlulin during tumor progression and early mouse development.

Degree: PhD, Genetic, Molecular and Cellular Biology, 2014, University of Southern California

URL: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/57748/rec/7282

► Recently, the merge in developmental biology and cancer biology research fields have begun to be appreciated, as important cellular activities and signaling pathways in embryogenesis… (more)

▼ Recently, the merge in developmental biology and cancer biology research fields have begun to be appreciated, as important cellular activities and signaling pathways in embryogenesis and morphogenesis are also key to cancer progression. For example, factors associated with cellular adhesion and cellular migration are commonly accepted to be critical in embryogenesis and tumor cell invasion and metastasis. In this dissertation, I attempt to gain further insight into the biological role of a member of the cellular adhesion family, α-catulin, focusing on (1) the role of α-catulin in human squamous cell carcinoma and tumor cell metastasis, (2) the role of α-catulin in mouse development, and (3) the molecular mechanism in which α-catulin functions. Here I find α-catulin upregulated in squamous cell carcinomas, where it is expressed at the invasion front in more malignant grade tumors. Additionally, α-catulin seems to contribute to the invasive behavior of metastatic cancer cells. These findings led me to gain a better understanding of the function of α-catulin using an α-catulin knockout mouse model. In doing so, I found α-catulin knockout mice to be embryonic lethal with neural tube closure defects. The α-catulin knockout embryos lacked apically localized actin and intermediate filaments, which typically correlate with proper cell constriction. Additionally, these α-catulin knockout embryos had disrupted integrin-mediated basement membrane assembly in the neuroepithelium. Upon analyses of α-catulin at the cellular level, α-catulin knockout cells lacked proper actin dynamics, focal contacts turnover, and directional migration. The function of α-catulin is only partially understood, but my data presented here strongly suggests that α-catulin is an important mediator of integrin-ECM signaling, by acting as a scaffold for Rho complex distribution, that results in proper spatial activation of downstream ROCK and myosin to influence actin-myosin dynamics and integrin-mediated cell adhesion. Further understanding of the biologic relevance of α-catulin may lead to insight into its value as a prognostic marker and future therapeutic target for cancer patients. Advisors/Committee Members: Maxson, Robert E., Jr. (Committee Chair), Kobielak, Agnieszka (Committee Member), Li, Wei (Committee Member), Goldkorn, Amir (Committee Member).

Subjects/Keywords: catulin; squamous cell carcinoma; EMT; migration; invasion; mouse development; myosin light chain; neural tube

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APA (6^th Edition):

Cao, C. (2014). The role of α-catlulin during tumor progression and early mouse development. (Doctoral Dissertation). University of Southern California. Retrieved from http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/57748/rec/7282

Chicago Manual of Style (16^th Edition):

Cao, Christine. “The role of α-catlulin during tumor progression and early mouse development.” 2014. Doctoral Dissertation, University of Southern California. Accessed March 01, 2021. http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/57748/rec/7282.

MLA Handbook (7^th Edition):

Cao, Christine. “The role of α-catlulin during tumor progression and early mouse development.” 2014. Web. 01 Mar 2021.

Vancouver:

Cao C. The role of α-catlulin during tumor progression and early mouse development. [Internet] [Doctoral dissertation]. University of Southern California; 2014. [cited 2021 Mar 01]. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/57748/rec/7282.

Council of Science Editors:

Cao C. The role of α-catlulin during tumor progression and early mouse development. [Doctoral Dissertation]. University of Southern California; 2014. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/57748/rec/7282

Brock University

12. Caterini, Daniel. THE INFLUENCE OF LENGTH CHANGE SPEED AND DIRECTION ON DYNAMIC FUNCTION POTENTIATION IN FAST MOUSE MUSCLE .

Degree: Applied Health Sciences Program, 2011, Brock University

URL: http://hdl.handle.net/10464/3398

► The purpose of this study was to test the hypothesis that the potentiation of dynamic function was dependent upon both length change speed and direction.… (more)

Subjects/Keywords: myosin; phosphorylation; concentric; eccentric

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APA (6^th Edition):

Caterini, D. (2011). THE INFLUENCE OF LENGTH CHANGE SPEED AND DIRECTION ON DYNAMIC FUNCTION POTENTIATION IN FAST MOUSE MUSCLE . (Thesis). Brock University. Retrieved from http://hdl.handle.net/10464/3398

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):

Caterini, Daniel. “THE INFLUENCE OF LENGTH CHANGE SPEED AND DIRECTION ON DYNAMIC FUNCTION POTENTIATION IN FAST MOUSE MUSCLE .” 2011. Thesis, Brock University. Accessed March 01, 2021. http://hdl.handle.net/10464/3398.

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

MLA Handbook (7^th Edition):

Caterini, Daniel. “THE INFLUENCE OF LENGTH CHANGE SPEED AND DIRECTION ON DYNAMIC FUNCTION POTENTIATION IN FAST MOUSE MUSCLE .” 2011. Web. 01 Mar 2021.

Vancouver:

Caterini D. THE INFLUENCE OF LENGTH CHANGE SPEED AND DIRECTION ON DYNAMIC FUNCTION POTENTIATION IN FAST MOUSE MUSCLE . [Internet] [Thesis]. Brock University; 2011. [cited 2021 Mar 01]. Available from: http://hdl.handle.net/10464/3398.

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

Council of Science Editors:

Caterini D. THE INFLUENCE OF LENGTH CHANGE SPEED AND DIRECTION ON DYNAMIC FUNCTION POTENTIATION IN FAST MOUSE MUSCLE . [Thesis]. Brock University; 2011. Available from: http://hdl.handle.net/10464/3398

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

University of Stirling

13. Hunter, David John. An increase in copy number of Myosin Light Chain Kinase 1 associates with increased force production in Lithuanian athletes.

Degree: M. Phil., 2014, University of Stirling

URL: http://hdl.handle.net/1893/21544

► Copy number variation has been linked to the development of various diseases, however copy number variants have not been investigated for associations with athletic performance.… (more)

Subjects/Keywords: Myosin Light Chain Kinase 1; MYLK1; Myosin Light Chain Kinase Antisense 1; MYLK-AS1; Copy number variation; CNV; Genetic variation; Muscle performance; Exercise; Myosin Research Technique; Genetic Research; Genetics Research; Genetic Variation; DNA Analysis; Muscles; Exercise

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APA (6^th Edition):

Hunter, D. J. (2014). An increase in copy number of Myosin Light Chain Kinase 1 associates with increased force production in Lithuanian athletes. (Masters Thesis). University of Stirling. Retrieved from http://hdl.handle.net/1893/21544

Chicago Manual of Style (16^th Edition):

Hunter, David John. “An increase in copy number of Myosin Light Chain Kinase 1 associates with increased force production in Lithuanian athletes.” 2014. Masters Thesis, University of Stirling. Accessed March 01, 2021. http://hdl.handle.net/1893/21544.

MLA Handbook (7^th Edition):

Hunter, David John. “An increase in copy number of Myosin Light Chain Kinase 1 associates with increased force production in Lithuanian athletes.” 2014. Web. 01 Mar 2021.

Vancouver:

Hunter DJ. An increase in copy number of Myosin Light Chain Kinase 1 associates with increased force production in Lithuanian athletes. [Internet] [Masters thesis]. University of Stirling; 2014. [cited 2021 Mar 01]. Available from: http://hdl.handle.net/1893/21544.

Council of Science Editors:

Hunter DJ. An increase in copy number of Myosin Light Chain Kinase 1 associates with increased force production in Lithuanian athletes. [Masters Thesis]. University of Stirling; 2014. Available from: http://hdl.handle.net/1893/21544

Freie Universität Berlin

14. Schanz, Miriam A. Identification and characterisation of Myosin Light Chain 4 and Medium Chain Acyl CoA- Dehydrogenase as novel interaction partners of estrogen receptor alpha.

Degree: 2012, Freie Universität Berlin

URL: http://dx.doi.org/10.17169/refubium-5913

► Estrogens (E2) are key regulators of growth, differentiation and physiological processes in various target tissues, including the human heart. E2 exerts its effects mainly through… (more)

▼ Estrogens (E2) are key regulators of growth, differentiation and physiological processes in various target tissues, including the human heart. E2 exerts its effects mainly through its cognate receptors, e.g.estrogen receptor (ER) α. ERα acts in concert with other interaction partners to mediate estrogenic effects. So far, only few interaction partners of ERα are known in the human myocardium. This project identified Medium Chain Acyl-CoA Dehydrogenase (MCAD) and atrial Myosin Light Chain 4 (MYL4) as novel interaction partners of ERα in the human myocardium. MCAD is catalyzing the initial step of mitochondrial ß-fatty acid oxidation and therefore takes an important role in the energy supply of the heart. It is known that in the diseased heart, the MCAD expression is down regulated due to switching myocardial energy substrate from fatty acids to glucose. MYL4, as part of the contractile apparatus, is expressed in the fetal heart and in the adult heart becomes restricted to the atria under physiological conditions. It is re-expressed in the adult hypertrophic ventricle and this switch is accompanied by alteration of contractile performance, thus improving global heart function. Yeast-Two- Hybrid (YTH) retransformation experiments showed the estrogen dependent interaction of ERα with MCAD and MYL4, respectively. Our data show the N-terminal region of MYL4 protein as location of the interaction with ERα, the area of the protein which is responsible for modulating contractile properties. Results of the co-immunoprecipitation (IP) confirmed the interaction of ERa with MCAD and MYL4 in the human myocardium. By immunofluorescence we could show the co-localisation of ERα and MCAD in the Mitochondria of AC16 cells. Co-localization experiments could localize the interaction of ERα and MYL4 within the sarcomeres of cardiomyocytes. Amplified signals for MYL4 in the nucleus of AC16 cells after estrogen stimulation indicated a regulation of expression of MYL4. With present work new knowledge about hormone effects specific for heart was achieved by investigating new interaction partners of ERα in the human myocardium which in future times could lead to new therapeutic attempts for cardiovascular diseases. Advisors/Committee Members: [email protected] (contact), w (gender), Prof. Dr. med. Regitz-Zagrosek (firstReferee), Prof. Dr. med. C. Grohé (furtherReferee), Prof. Dr. med. Geibel-Zehender (furtherReferee).

Subjects/Keywords: estrogenreceptor alpha; interaction partners; human heart; MCAD; Myosin Light Chain; atrial light chain; estrogen; 600 Technik, Medizin, angewandte Wissenschaften::610 Medizin und Gesundheit

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APA (6^th Edition):

Schanz, M. A. (2012). Identification and characterisation of Myosin Light Chain 4 and Medium Chain Acyl CoA- Dehydrogenase as novel interaction partners of estrogen receptor alpha. (Thesis). Freie Universität Berlin. Retrieved from http://dx.doi.org/10.17169/refubium-5913

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):

Schanz, Miriam A. “Identification and characterisation of Myosin Light Chain 4 and Medium Chain Acyl CoA- Dehydrogenase as novel interaction partners of estrogen receptor alpha.” 2012. Thesis, Freie Universität Berlin. Accessed March 01, 2021. http://dx.doi.org/10.17169/refubium-5913.

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

MLA Handbook (7^th Edition):

Schanz, Miriam A. “Identification and characterisation of Myosin Light Chain 4 and Medium Chain Acyl CoA- Dehydrogenase as novel interaction partners of estrogen receptor alpha.” 2012. Web. 01 Mar 2021.

Vancouver:

Schanz MA. Identification and characterisation of Myosin Light Chain 4 and Medium Chain Acyl CoA- Dehydrogenase as novel interaction partners of estrogen receptor alpha. [Internet] [Thesis]. Freie Universität Berlin; 2012. [cited 2021 Mar 01]. Available from: http://dx.doi.org/10.17169/refubium-5913.

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

Council of Science Editors:

Schanz MA. Identification and characterisation of Myosin Light Chain 4 and Medium Chain Acyl CoA- Dehydrogenase as novel interaction partners of estrogen receptor alpha. [Thesis]. Freie Universität Berlin; 2012. Available from: http://dx.doi.org/10.17169/refubium-5913

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

University of Illinois – Chicago

15. Ryba, David M. Modulation of Sarcomere Function via Seven-Transmembrane Receptor Signaling to Ameliorate Cardiomyopathy.

Degree: 2018, University of Illinois – Chicago

URL: http://hdl.handle.net/10027/22610

► Work presented in this thesis describes efforts to investigate mechanisms of improving cardiac function via cellular signaling downstream of seven-transmembrane receptors (7TMRs), also known as… (more)

▼ Work presented in this thesis describes efforts to investigate mechanisms of improving cardiac function via cellular signaling downstream of seven-transmembrane receptors (7TMRs), also known as G-protein coupled receptors. In the cardiomyocyte, agonism of 7TMRs can have a profound functional effect. This can be mediated through multiple mechanisms, such as altering the post-translational modification status or expression of proteins involved in calcium homeostasis or sarcomere and sarcomere-associated proteins. Because alterations in myofilament-Ca-responsiveness are commonly seen in cardiomyopathy, we hypothesized that normalizing the myofilament-Ca-response via 7TMRs might ameliorate disease. A dilated cardiomyopathy–linked mouse model expressing a mutant tropomyosin (Tm-E54K) was studied using an angiotensin II type 1 receptor (AT1R) antagonist, losartan, and a novel compound, TRV120067, able to selectively engage beta-arrestin 2 signaling pathways downstream of the AT1R. TRV120067-treated Tm-E54K mice showed improved cardiac structure and function, whereas losartan-treated mice had no improvement. Myofilaments of TRV120067-treated Tm-E54K mice had significantly improved myofilament-Ca-responsiveness, which was depressed in untreated Tm-E54K mice. We attributed these functional changes observed in Tm-E54K mice treated with TRV120067 to increased myosin light chain phosphorylation. In a second line of experiments we employed a hypertrophic cardiomyopathy–linked mouse model expressing a mutant tropomyosin (Tm-E180G) and investigated the impact of sphingosine-1-phosphate receptor (S1PR) signaling on cardiac function and structure. We found that S1PR modulation with the immunomodulatory drug, FTY720, has profound effects on cardiac hypertrophy and improved diastolic function in the Tm-E180G mice. We attributed the functional effects to modification of the cross-bridge kinetic due to reversal of oxidative modification of cardiac myosin-binding protein C. These data suggest that modulating novel signaling pathways via 7TMRs to target sarcomere function may be promising therapeutic approach for the treatment of cardiomyopathy and heart failure. Advisors/Committee Members: Solaro, R. John (advisor), Wolska, Beata M (advisor), de Tombe, Pieter (committee member), Rasenick, Mark M (committee member), McCauley, Mark D (committee member), Russell, Brenda (chair).

Subjects/Keywords: Heart Failure; Dilated Cardiomyopathy; Hypertrophic Cardiomyopathy; Biased Ligand; Beta-arrestin; Diastolic Dysfunction; Myosin Light Chain; Myosin Binding Protein C; Sphingosine-1-Phosphate Receptor; Angiotensin II Type 1 Receptor

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APA (6^th Edition):

Ryba, D. M. (2018). Modulation of Sarcomere Function via Seven-Transmembrane Receptor Signaling to Ameliorate Cardiomyopathy. (Thesis). University of Illinois – Chicago. Retrieved from http://hdl.handle.net/10027/22610

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):

Ryba, David M. “Modulation of Sarcomere Function via Seven-Transmembrane Receptor Signaling to Ameliorate Cardiomyopathy.” 2018. Thesis, University of Illinois – Chicago. Accessed March 01, 2021. http://hdl.handle.net/10027/22610.

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

MLA Handbook (7^th Edition):

Ryba, David M. “Modulation of Sarcomere Function via Seven-Transmembrane Receptor Signaling to Ameliorate Cardiomyopathy.” 2018. Web. 01 Mar 2021.

Vancouver:

Ryba DM. Modulation of Sarcomere Function via Seven-Transmembrane Receptor Signaling to Ameliorate Cardiomyopathy. [Internet] [Thesis]. University of Illinois – Chicago; 2018. [cited 2021 Mar 01]. Available from: http://hdl.handle.net/10027/22610.

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

Council of Science Editors:

Ryba DM. Modulation of Sarcomere Function via Seven-Transmembrane Receptor Signaling to Ameliorate Cardiomyopathy. [Thesis]. University of Illinois – Chicago; 2018. Available from: http://hdl.handle.net/10027/22610

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

The Ohio State University

16. Rodriguez, Deyra Marie. Isolation and characterization of stretchin-myosin light chain kinase mutants in drosophila melanogaster.

Degree: PhD, Molecular, Cellular, and Developmental Biology, 2004, The Ohio State University

URL: http://rave.ohiolink.edu/etdc/view?acc_num=osu1079994503

► Muscle function depends upon the molecular interaction of myosin and actin. This interaction and the function of each molecule are tightly regulated and have… (more)

▼ Muscle function depends upon the molecular interaction of myosin and actin. This interaction and the function of each molecule are tightly regulated and have been extensively studied. In Drosophila , the indirect flight musculature (IFM) is a powerful model to study muscle structure and function as these muscles are dispensable for life under laboratory conditions. Furthermore, disruption of these muscles leads to a flightless behavior. Flies with mutations in the muscle regulatory light chain (MLC2) that cannot be phosphorylated at the conserved Myosin light chain kinase (Mlck) target sites are flightless, but the IFM is normal. Flight impairment is due to an altered stretch activation response, thus phosphorylation of MLC2 at the Mlck target sites is important for flight. In Drosophila , the Stretchin-Mlck (Strn-Mlck) gene encodes several Mlck-like isoforms with kinase activity as well as other isoforms lacking this domain. This work has shown that the gene is expressed in both muscle and nonmuscle cells and that some isoforms show tissue specific expression patterns. In order to understand what role Strn-Mlck plays in MLC2 regulation, mutants were isolated. Three new mutants were identified and were shown to be new alleles of the previously identified mutant curved . Strikingly, Strn-Mlck mutants lacking kinase activity are viable. However, the mutants show a recessive flightless phenotype and defects in wing position. Electron micrographs demonstrated the flight musculature is intact, therefore, the flightless phenotype is most likely due to the wing position defect. As mentioned, Strn-Mlck is expressed in nonmuscle cells. The myosin nonmuscle regulatory light chain is encoded by spaghetti squash (sqh) . Mutations in nonmuscle RLC at the conserved Mlck target sites are lethal. Finding that mutants lacking Strn-Mlck kinase activity are viable suggests other Mlcks exist in flies and function redundantly. Preliminary genetic studies have linked Strn-Mlck with another Mlck, CG1776 (also known as Mlck-2 ). This Mlck-like kinase has been implicated in morphogenesis in nonmuscle tissue culture cells. In the future, it will be important to analyze these two Mlcks in depth at the genetic level. Double mutants may reveal functions for these enzymes that are masked in the single mutants analyzed to date. Advisors/Committee Members: Simcox, Amanda (Advisor).

Subjects/Keywords: myosin light chain kinase; curved; muscle and nonmuscle function

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APA (6^th Edition):

Rodriguez, D. M. (2004). Isolation and characterization of stretchin-myosin light chain kinase mutants in drosophila melanogaster. (Doctoral Dissertation). The Ohio State University. Retrieved from http://rave.ohiolink.edu/etdc/view?acc_num=osu1079994503

Chicago Manual of Style (16^th Edition):

Rodriguez, Deyra Marie. “Isolation and characterization of stretchin-myosin light chain kinase mutants in drosophila melanogaster.” 2004. Doctoral Dissertation, The Ohio State University. Accessed March 01, 2021. http://rave.ohiolink.edu/etdc/view?acc_num=osu1079994503.

MLA Handbook (7^th Edition):

Rodriguez, Deyra Marie. “Isolation and characterization of stretchin-myosin light chain kinase mutants in drosophila melanogaster.” 2004. Web. 01 Mar 2021.

Vancouver:

Rodriguez DM. Isolation and characterization of stretchin-myosin light chain kinase mutants in drosophila melanogaster. [Internet] [Doctoral dissertation]. The Ohio State University; 2004. [cited 2021 Mar 01]. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=osu1079994503.

Council of Science Editors:

Rodriguez DM. Isolation and characterization of stretchin-myosin light chain kinase mutants in drosophila melanogaster. [Doctoral Dissertation]. The Ohio State University; 2004. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=osu1079994503

17. VIVEKA GAJENDIRAN. MATHEMATICAL MODELLING OF CALCIUM DEPENDENT ACTIVE CONTRACTION IN A GASTROINTESTINAL SMOOTH MUSCLE CELL.

Degree: 2011, National University of Singapore

URL: http://scholarbank.nus.edu.sg/handle/10635/34506

Subjects/Keywords: Smooth Muscle; Phasic Contraction; Electro-mechanical coupling; Myosin light chain kinase; Myosin light chain phosphatase; Mathematical model.

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APA (6^th Edition):

GAJENDIRAN, V. (2011). MATHEMATICAL MODELLING OF CALCIUM DEPENDENT ACTIVE CONTRACTION IN A GASTROINTESTINAL SMOOTH MUSCLE CELL. (Thesis). National University of Singapore. Retrieved from http://scholarbank.nus.edu.sg/handle/10635/34506

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):

GAJENDIRAN, VIVEKA. “MATHEMATICAL MODELLING OF CALCIUM DEPENDENT ACTIVE CONTRACTION IN A GASTROINTESTINAL SMOOTH MUSCLE CELL.” 2011. Thesis, National University of Singapore. Accessed March 01, 2021. http://scholarbank.nus.edu.sg/handle/10635/34506.

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

MLA Handbook (7^th Edition):

GAJENDIRAN, VIVEKA. “MATHEMATICAL MODELLING OF CALCIUM DEPENDENT ACTIVE CONTRACTION IN A GASTROINTESTINAL SMOOTH MUSCLE CELL.” 2011. Web. 01 Mar 2021.

Vancouver:

GAJENDIRAN V. MATHEMATICAL MODELLING OF CALCIUM DEPENDENT ACTIVE CONTRACTION IN A GASTROINTESTINAL SMOOTH MUSCLE CELL. [Internet] [Thesis]. National University of Singapore; 2011. [cited 2021 Mar 01]. Available from: http://scholarbank.nus.edu.sg/handle/10635/34506.

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

Council of Science Editors:

GAJENDIRAN V. MATHEMATICAL MODELLING OF CALCIUM DEPENDENT ACTIVE CONTRACTION IN A GASTROINTESTINAL SMOOTH MUSCLE CELL. [Thesis]. National University of Singapore; 2011. Available from: http://scholarbank.nus.edu.sg/handle/10635/34506

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

18. Bunda, Jordan. Myosin Regulatory Light Chain Phosphorylation and Its Effect on the Contractile Economy of Mouse Fast Muscle .

Degree: Applied Health Sciences Program, Brock University

URL: http://hdl.handle.net/10464/7234

► Activated by elevations in myoplasmic calcium concentration, myosin light chain kinase (skMLCK) phosphorylates the regulatory light chains (RLCs) of fast muscle myosin. This covalent modification… (more)

Subjects/Keywords: Skeletal muscle; Potentiation; Myosin light chain kinase; Economy; Myosin regulatory light chain

…106 Appendix II: Measurement of Myosin Regulatory Light Chain Phosphorylation by Urea… …light chain kinase (skMLCK) which catalyzes the phosphorylation of the myosin RLC… …Myosin Regulatory Light Chain Phosphorylation. Here, focus is given to the enzymes that… …between actin and myosin. 16 2.4. Myosin Regulatory Light Chain Phosphorylation The myosin… …light chain of myosin FTI Force-time integral G-6-P-DH Glucose-6-phosphate dehydrogenase…

2 more images…

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

APA (6^th Edition):

Bunda, J. (n.d.). Myosin Regulatory Light Chain Phosphorylation and Its Effect on the Contractile Economy of Mouse Fast Muscle . (Thesis). Brock University. Retrieved from http://hdl.handle.net/10464/7234

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):

Bunda, Jordan. “Myosin Regulatory Light Chain Phosphorylation and Its Effect on the Contractile Economy of Mouse Fast Muscle .” Thesis, Brock University. Accessed March 01, 2021. http://hdl.handle.net/10464/7234.

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):

Bunda, Jordan. “Myosin Regulatory Light Chain Phosphorylation and Its Effect on the Contractile Economy of Mouse Fast Muscle .” Web. 01 Mar 2021.

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

Vancouver:

Bunda J. Myosin Regulatory Light Chain Phosphorylation and Its Effect on the Contractile Economy of Mouse Fast Muscle . [Internet] [Thesis]. Brock University; [cited 2021 Mar 01]. Available from: http://hdl.handle.net/10464/7234.

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:

Bunda J. Myosin Regulatory Light Chain Phosphorylation and Its Effect on the Contractile Economy of Mouse Fast Muscle . [Thesis]. Brock University; Available from: http://hdl.handle.net/10464/7234

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

19. Κωνσταντινίδης, Γεώργιος. Θετική και αρνητική ρύθμιση των μικρών GTPασών Rho και του κυτταροσκελετού ακτίνης από τις BMP και TGF-β.

Degree: 2011, University of Crete (UOC); Πανεπιστήμιο Κρήτης

URL: http://hdl.handle.net/10442/hedi/25836

► Actin cytoskeleton dynamics support and coordinate a large number of signaling events that control cell proliferation, differentiation and migration. Cytoskeletal plasticity is based on multi-??protein… (more)

▼ Actin cytoskeleton dynamics support and coordinate a large number of signaling events that control cell proliferation, differentiation and migration. Cytoskeletal plasticity is based on multi-??protein complexes that regulate actin polymerization, stability and assembly with myosin. Growth factors provide essential signals that govern cytoskeletal dynamics. One such growth factor network is the transforming growth factor β (TGF-??β) that includes secreted polypeptides such as bone morphogenetic proteins (BMP) and activins. Here, it is demonstrated that BMP-??7 signals through Smad1, p38 and p44/42 (Erk1/2) MAPKs and induces actin polymerization and focal adhesion remodeling in starved fibroblasts and various other cell lines as potently as TGF-??β. Moreover, BMP-??7 induces migration of Swiss3T3 fibroblasts letting at the same time proliferation and apoptosis unaffected. An important regulator of actin remodeling, the kinase ROCK1 mediates changes of actin dynamics by BMP-??7, while this growth factor induces rapid activation of RhoA and RhoB GTPases with concomitant inactivation of Cdc42. In parallel, BMP-??7 induces RhoB and Smad6 expression providing with a positive and a negative signalling feedback simultaneously. Activation of Rho GTPases and the downstream ROCK1 kinase by BMP-??7 correlate well with induction of phosphorylation on Ser19 of the myosin light chain, but not with LIMK1 kinase activation. ROCK inhibitor Y-??27632 blocks actin polymerization and reduces migration capacity induced by BMP-??7. Furthermore, the same ROCK inhibitor blocks the myosin light chain phosphorylation of Ser19 during BMP-??7 signalling. Depletion of endogenous myosin light chain also inhibits the actin remodeling induced by BMP-??7. Thus, in a next step, this novel pathway regulates fibroblast migration without affecting cell proliferation. Taking everything into consideration, here it is established not only that BMP signals through Smad and, the so-??called, non-??Smad pathway of MAPKs, but also through Rho/ROCK pathway which targets myosin light chain during actin remodeling and migration of Swiss3T3 fibroblasts.

Subjects/Keywords: Ακτίνη; Πρωτεϊνη μορφογένεσης οστών; Κυτταροσκελετός; Ελαφριά αλυσίδα μυοσίνης; Κινάση της ελαφριάς αλυσίδας μυοσίνης; RHO κινάση 1; Μετασχηματίζων αυξητικός παράγοντας β; Actin; Bone morphogenetic proteins; Cytoskeleton; Myosin light chain; Myosin light chain kinase; RHO coiled-coil kinase 1; Transforming growth factor β

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APA (6^th Edition):

Κωνσταντινίδης, . �. (2011). Θετική και αρνητική ρύθμιση των μικρών GTPασών Rho και του κυτταροσκελετού ακτίνης από τις BMP και TGF-β. (Thesis). University of Crete (UOC); Πανεπιστήμιο Κρήτης. Retrieved from http://hdl.handle.net/10442/hedi/25836

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):

Κωνσταντινίδης, Γεώργιος. “Θετική και αρνητική ρύθμιση των μικρών GTPασών Rho και του κυτταροσκελετού ακτίνης από τις BMP και TGF-β.” 2011. Thesis, University of Crete (UOC); Πανεπιστήμιο Κρήτης. Accessed March 01, 2021. http://hdl.handle.net/10442/hedi/25836.

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

MLA Handbook (7^th Edition):

Κωνσταντινίδης, Γεώργιος. “Θετική και αρνητική ρύθμιση των μικρών GTPασών Rho και του κυτταροσκελετού ακτίνης από τις BMP και TGF-β.” 2011. Web. 01 Mar 2021.

Vancouver:

Κωνσταντινίδης �. Θετική και αρνητική ρύθμιση των μικρών GTPασών Rho και του κυτταροσκελετού ακτίνης από τις BMP και TGF-β. [Internet] [Thesis]. University of Crete (UOC); Πανεπιστήμιο Κρήτης; 2011. [cited 2021 Mar 01]. Available from: http://hdl.handle.net/10442/hedi/25836.

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

Council of Science Editors:

Κωνσταντινίδης �. Θετική και αρνητική ρύθμιση των μικρών GTPασών Rho και του κυτταροσκελετού ακτίνης από τις BMP και TGF-β. [Thesis]. University of Crete (UOC); Πανεπιστήμιο Κρήτης; 2011. Available from: http://hdl.handle.net/10442/hedi/25836

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

Youngstown State University

20. Cosper, Marcus S. Identification of Myosin Light Chain, Myosin Light Chain Phosphatase, and Rho Kinase in the Corpus Cavernosum of the Rat.

Degree: MSin Biological Sciences, Department of Biological Sciences and Chemistry, 2009, Youngstown State University

URL: http://rave.ohiolink.edu/etdc/view?acc_num=ysu1244735791

► Myosin light chain kinase, Myosin light chain phosphatase, and Rho kinase are three important regulatory proteins that are involved in regulating penile erection. This study… (more)

Subjects/Keywords: Biology; Health Education; Molecular Biology; corpus cavernosum; myosin light chain kinase; myosin light chain phosphatase; rho kinase

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APA (6^th Edition):

Cosper, M. S. (2009). Identification of Myosin Light Chain, Myosin Light Chain Phosphatase, and Rho Kinase in the Corpus Cavernosum of the Rat. (Masters Thesis). Youngstown State University. Retrieved from http://rave.ohiolink.edu/etdc/view?acc_num=ysu1244735791

Chicago Manual of Style (16^th Edition):

Cosper, Marcus S. “Identification of Myosin Light Chain, Myosin Light Chain Phosphatase, and Rho Kinase in the Corpus Cavernosum of the Rat.” 2009. Masters Thesis, Youngstown State University. Accessed March 01, 2021. http://rave.ohiolink.edu/etdc/view?acc_num=ysu1244735791.

MLA Handbook (7^th Edition):

Cosper, Marcus S. “Identification of Myosin Light Chain, Myosin Light Chain Phosphatase, and Rho Kinase in the Corpus Cavernosum of the Rat.” 2009. Web. 01 Mar 2021.

Vancouver:

Cosper MS. Identification of Myosin Light Chain, Myosin Light Chain Phosphatase, and Rho Kinase in the Corpus Cavernosum of the Rat. [Internet] [Masters thesis]. Youngstown State University; 2009. [cited 2021 Mar 01]. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=ysu1244735791.

Council of Science Editors:

Cosper MS. Identification of Myosin Light Chain, Myosin Light Chain Phosphatase, and Rho Kinase in the Corpus Cavernosum of the Rat. [Masters Thesis]. Youngstown State University; 2009. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=ysu1244735791

21. Pillet, Laure-Elise. Interactions neurogliales dans la déficience intellectuelle : étude du modèle oligophrénine-1 : Astroglial contribution to synaptophaties : the oligophrenin1 gene model.

Degree: Docteur es, Neurobiologie, 2018, Sorbonne Paris Cité

URL: http://www.theses.fr/2018USPCB246

►

La synapse est le lieu de communication entre les neurones à l'origine de nos capacités cognitives. Les mutations des gènes codant pour des protéines synaptiques… (more)

▼

La synapse est le lieu de communication entre les neurones à l'origine de nos capacités cognitives. Les mutations des gènes codant pour des protéines synaptiques sont responsables des maladies neurodéveloppementales appelées synaptopathies, recouvrant un large spectre de pathologies, de la déficience intellectuelle aux troubles du spectre autistique. Cependant, il est actuellement établi que les neurones ne sont pas les seuls acteurs au niveau de la synapse. Les astrocytes jouent également un rôle essentiel dans la mise en place du réseau neuronal et le fonctionnement de la synapse. Ils assurent aussi l'homéostasie ionique synaptique et sont capables de sécréter des glio-transmetteurs qui modulent l'activité synaptique. Oligophrénine-1 (OPHN1) est un gène associé à la déficience intellectuelle liée à l'X chez l'Homme. OPHN1 est une protéine synaptique dont les fonctions neuronales sont bien connues. La protéine peut directement interagir avec le cytosquelette d'actine et joue un rôle dans la formation et la maturation des épines dendritiques. Cette protéine est aussi exprimée dans les astrocytes mais sa fonction astrocytaire n'est pas connue. A l'aide d'un modèle KO de souris pour Ophn1, nous avons mis en évidence les conséquences de l'absence d'Ophn1 dans les astrocytes. Nous avons démontré que la délétion d'OPHN1 altère la migration et la morphologie des astrocytes in vitro. Sachant qu'Ophn1 est capable d'inactiver la GTPase RhoA, nous avons utilisé un inhibiteur de la voie RhoA/ROCK pour retrouver un phénotype de migration normal. In vivo nous avons choisi un modèle de cicatrisation gliale cortical afin de pouvoir observer la migration et la morphologie des astrocytes au niveau de la cicatrice. Nous avons observé que la délétion d'Ophn1 altérait la cicatrisation gliale et que les astrocytes à proximité de la cicatrice était moins ramifiés. L'ensemble de ces résultats nous permet de constater que les astrocytes sont altérés dans notre modèle murin de déficience intellectuelle liée à l'X. De plus, le KO conditionel astrocytaire mis en place nous permettra à l'avenir d'étudier les conséquences de la perte d'OPHN1 uniquement dans les astrocytes, et de comprendre la contribution astrocytaire dans la physiopathologie de cette maladie neuro-développementale.

The synapse mediates the inter-neuron communication that forms the basis of all cognitive activity. Mutations in genes encoding for synaptic proteins are responsible for neurodevelopmental disorders called synaptopathies, covering a large clinical spectrum from intellectual disability (ID) to autism spectrum disorders. However it is currently established that neurons are not the only active cells at the synapse. Astrocytes play as well an essential role for its development and functioning. They maintain synaptic ionic homeostasis and are capable of secreting gliotransmitters, which can modulate synaptic activity. Oligophrenin-1 gene (OPHN1) was identified and associated with X-linked human ID. OPHN1 is a synaptic protein, which neuronal function is well known. It…

Advisors/Committee Members: Billuart, Pierre (thesis director), Rouach-Holcman, Nathalie (thesis director).

Subjects/Keywords: Déficience intellectuelle; Oligophrénine-1; RhoGAP; Myosin light chain; Astrocytes; Cicarisation gliale corticale; Migration; Morphologie; KO conditionnel astrocytaire; Intellectual disability; Oligophrenin-1; RhoGAP; Myosin light chain; Astrocytes; Cotical glial scar; Migration; Morphology; Astrocytic conditional KO; 616.858 8

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

APA (6^th Edition):

Pillet, L. (2018). Interactions neurogliales dans la déficience intellectuelle : étude du modèle oligophrénine-1 : Astroglial contribution to synaptophaties : the oligophrenin1 gene model. (Doctoral Dissertation). Sorbonne Paris Cité. Retrieved from http://www.theses.fr/2018USPCB246

Chicago Manual of Style (16^th Edition):

Pillet, Laure-Elise. “Interactions neurogliales dans la déficience intellectuelle : étude du modèle oligophrénine-1 : Astroglial contribution to synaptophaties : the oligophrenin1 gene model.” 2018. Doctoral Dissertation, Sorbonne Paris Cité. Accessed March 01, 2021. http://www.theses.fr/2018USPCB246.

MLA Handbook (7^th Edition):

Pillet, Laure-Elise. “Interactions neurogliales dans la déficience intellectuelle : étude du modèle oligophrénine-1 : Astroglial contribution to synaptophaties : the oligophrenin1 gene model.” 2018. Web. 01 Mar 2021.

Vancouver:

Pillet L. Interactions neurogliales dans la déficience intellectuelle : étude du modèle oligophrénine-1 : Astroglial contribution to synaptophaties : the oligophrenin1 gene model. [Internet] [Doctoral dissertation]. Sorbonne Paris Cité; 2018. [cited 2021 Mar 01]. Available from: http://www.theses.fr/2018USPCB246.

Council of Science Editors:

Pillet L. Interactions neurogliales dans la déficience intellectuelle : étude du modèle oligophrénine-1 : Astroglial contribution to synaptophaties : the oligophrenin1 gene model. [Doctoral Dissertation]. Sorbonne Paris Cité; 2018. Available from: http://www.theses.fr/2018USPCB246

22. Huang, Wenrui. Molecular Mechanisms of Myosin Light Chain Mutation-Induced Cardiomyopathies.

Degree: PhD, Molecular and Cellular Pharmacology (Medicine), 2015, University of Miami

URL: https://scholarlyrepository.miami.edu/oa_dissertations/1373

► In this proposal, I have studied the HCM (hypertrophic cardiomyopathy) and DCM (dilated cardiomyopathy) disease causing mechanisms associated with mutations in the myosin regulatory (RLC)… (more)

▼ In this proposal, I have studied the HCM (hypertrophic cardiomyopathy) and DCM (dilated cardiomyopathy) disease causing mechanisms associated with mutations in the myosin regulatory (RLC) and essential (ELC) light chains. Specifically, four HCM mutations, RLC-A13T, RLC-K104E, ELC-A57G and ELC-M173V and one DCM mutation, RLC-D94A were studied. The RLC-A13T, RLC-K104E and ELC-A57G mutations were primarily investigated in transgenic (Tg) mice using in vitro and in vivo approaches, while RLC-D94A and ELC-M173V were studied in reconstituted system because of no Tg mice available in the laboratory (Specific Aims 1&2). In addition, the effects of RLC/ELC serine phosphorylation on the structure and function of the heart were examined (Specific Aim 3). Our studies indicated that RLC and ELC mutations lead to cardiomyopathy disease through different mechanisms and therefore resulted in different disease phenotypes. Specially, RLC mutations (exclude D94A) resulted in a classic HCM phenotype as left ventricular (LV) / septum hypertrophy and diastolic dysfunction. RLC mutations caused HCM or DCM through altering the secondary structure of the RLC, which further affected the structure (and function) of the lever arm domain imposing changes in the cross bridge cycling rate, myosin force generation ability and muscle relaxation. On the other hand, ELC mutations (e.g. A57G) caused a rare HCM phenotype as eccentric hypertrophy and systolic dysfunction. As for the RLC, ELC mutations also exert their detrimental effects through altering the structure (and function) of the ELC, especially its N-terminus. These changes further affect the N-ELC-actin interactions and the cross talk between the thin and thick filaments resulting in altered force generation and the calcium sensitivity of force (Special Aim 1&2). In Specific Aim 3, we have examined the rescue effects of Serine15 phosphorylation in the RLC and Serine 195 phosphorylation in the ELC. For RLC, we observed a myosin light chain kinase (MLCK)-induced phosphorylation was able to rescue the abnormally high IFS observed in the K104E fibers. However, compromised force generation observed in K104E myocardium was not restored upon K104E phosphorylation. The effects of phosphorylation on the A13T and D94A RLC mutants are still to be studied. For ELC, since no ELC specific kinase exists, Serine195 was mutated to Aspartic Acid (S195D) to mimic ELC phosphorylation. The S195D-ELC protein partially restored the reduced Vmax observed in M173V-ELC exchanged myosin and “corrected” the abnormally high calcium sensitivity of force in A57G-S195D and M173V-S195D exchanged porcine cardiac muscle fibers, to the level near WT. However, no effect of S195D on force generation was observed in ELC-exchanged fibers, presumably due to a harsh treatment with chemicals during ELC exchange. Thus, despite of some promising results, the effects of MLCs phosphorylation on the rescue of abnormal RLC and ELC function are still inconclusive. New strategies need to be applied to further investigate this MLC… Advisors/Committee Members: Danuta Szczesna-Cordary, Keith Webster, Justin Percival, Arun Malhotra, Xupei Huang.

Subjects/Keywords: cardiomyopathy; transgenic mice; mutation; myosin light chains; phosphorylation; rescue mechanism

…86 Myosin light chain phosphorylation mediated rescue mechanisms… …cardiomyopathy ECG-echocardiography EF-ejection fraction ELC –essential light chain of myosin EM… …heavy chain MT-mitochondria MLCs- myosin light chains MLCK-myosin light chain kinase MyBP-C… …ATPase smMLCK: smooth muscle myosin light chain kinase SR: sarcoplasmic reticulum TFP: 10-[… …studies from our group have suggested that myosin light chain kinase (MLCK)-dependent…

10 more images…

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APA (6^th Edition):

Huang, W. (2015). Molecular Mechanisms of Myosin Light Chain Mutation-Induced Cardiomyopathies. (Doctoral Dissertation). University of Miami. Retrieved from https://scholarlyrepository.miami.edu/oa_dissertations/1373

Chicago Manual of Style (16^th Edition):

Huang, Wenrui. “Molecular Mechanisms of Myosin Light Chain Mutation-Induced Cardiomyopathies.” 2015. Doctoral Dissertation, University of Miami. Accessed March 01, 2021. https://scholarlyrepository.miami.edu/oa_dissertations/1373.

MLA Handbook (7^th Edition):

Huang, Wenrui. “Molecular Mechanisms of Myosin Light Chain Mutation-Induced Cardiomyopathies.” 2015. Web. 01 Mar 2021.

Vancouver:

Huang W. Molecular Mechanisms of Myosin Light Chain Mutation-Induced Cardiomyopathies. [Internet] [Doctoral dissertation]. University of Miami; 2015. [cited 2021 Mar 01]. Available from: https://scholarlyrepository.miami.edu/oa_dissertations/1373.

Council of Science Editors:

Huang W. Molecular Mechanisms of Myosin Light Chain Mutation-Induced Cardiomyopathies. [Doctoral Dissertation]. University of Miami; 2015. Available from: https://scholarlyrepository.miami.edu/oa_dissertations/1373

NSYSU

23. LIN, YU-HO. Development of Transgenic Fish for Ornamental Applications.

Degree: PhD, Marine Biotechnology and Resources, 2014, NSYSU

URL: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0801114-100452

► In this study, we first examined the feasibility of establishing various lines of transgenic fluorescent zebrafish by combining the Tol2 transposon system with our newly-constructed… (more)

▼ In this study, we first examined the feasibility of establishing various lines of transgenic fluorescent zebrafish by combining the Tol2 transposon system with our newly-constructed fluorescent protein expression plasmids, in which EGPF or DsRed are expressed under the control of a 2.5 kb mylz2promoter. Of these plasmids, the construct containing the fluorescent EGFP gene was subsequently used to investigate the suitability of in vivoelectroporation for gene transfer directly into the gonads of Pterophyllum scalare. We injected gonads with plasmid DNA expressing zebrafish mylz2 promoter-driven EGFP, and electric pulses were thenapplied to both sides of the gonad with a pair of electrode needles. The fish were allowed to mate and spawn, and PCR was used to confirm the presence of the transferred gene in the next generation fry. Despite a low gene transfer rate (about 1.33%), the presence of the GFP gene in certain hatched offspring indicates that in vivo electroporation is an alternative and relatively simple transgenic tool with which to establish transgenic founders for ornamental fish with a low availability of sperm or fertilized eggs. However, only a small proportion of the transgenic fish exhibited green fluorescencevisible to the naked eye. In an attempt to increase the proportion of fluorescent transgenic fish, we first isolated and characterized a tilapia (Oreochromis niloticus) myosin light chain 3promoter region (~4.3 kb). Sequence analysis of the clone revealed high similarity with a tilapia gene encoding the promoter region, exon 1, and intron 1 of mlc3. This clone contained several putative binding sequences for transcription factors, including MEF-2, MYOG, MyoD, PKNOX1, and AREB6. A genomicfragment (-4314-3882/-800-1/i1) encompassing the tilapia mlc3promoter region but with a deletion from -801 to -3881 bp exhibited promoter activity, as evidencedby luciferase reporter activity following direct intramuscular injection of plasmid DNA into the skeletal muscle of Amatitlania nigrofasciatus var. (convict cichlid); luciferase activity was 32-fold greater than that observed using constructs containing the zebrafish mylz2promoter. Stable transgenic germlines carrying the gene encoding Taiwan coral red fluorescent protein (TcRFP) under the control of the mlc3promoter were established in the ornamental fish species, A. nigrofasciatusvar. F1 adult transgenic A. nigrofasciatusvar. exhibited brilliant-pink fluorescence in skeletal muscles under visible light, and as such, may be suitable for ornamental exhibition. Overall,these findings demonstrate the feasibility of employing in vivoelectroporation and the tilapia mlc3promoter to produce novel, medium-sized, ornamental fish species (such as Cichlidae). Advisors/Committee Members: Ming-Hong Tai (chair), Zhi-Hong Wen (committee member), Hong-Yi Gong (chair), Shao-Yang Hu (chair), Jyh-Yih Chen (chair).

Subjects/Keywords: Danio rerio; Fluorescent ornamental fish; Transgenic fish; Myosin light chain 3 promoter; Amatitlania nigrofasciatus var.; In vivo electroporation; Pterophyllum scalare; Oreochromis niloticus; Tol2 transposon

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

APA (6^th Edition):

LIN, Y. (2014). Development of Transgenic Fish for Ornamental Applications. (Doctoral Dissertation). NSYSU. Retrieved from http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0801114-100452

Chicago Manual of Style (16^th Edition):

LIN, YU-HO. “Development of Transgenic Fish for Ornamental Applications.” 2014. Doctoral Dissertation, NSYSU. Accessed March 01, 2021. http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0801114-100452.

MLA Handbook (7^th Edition):

LIN, YU-HO. “Development of Transgenic Fish for Ornamental Applications.” 2014. Web. 01 Mar 2021.

Vancouver:

LIN Y. Development of Transgenic Fish for Ornamental Applications. [Internet] [Doctoral dissertation]. NSYSU; 2014. [cited 2021 Mar 01]. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0801114-100452.

Council of Science Editors:

LIN Y. Development of Transgenic Fish for Ornamental Applications. [Doctoral Dissertation]. NSYSU; 2014. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0801114-100452

University of Louisville

24. Nevitt, Christopher David. Alpha-amino methylation and acetylation are novel regulators of MYL9 function.

Degree: PhD, 2018, University of Louisville

URL: 10.18297/etd/3032 ; https://ir.library.louisville.edu/etd/3032

► Dysregulation of alpha-amino post-translational modifications (Nα-PTMs) is found in multiple cancers and developmental disorders. However, the exact roles Nα-PTMs play in regulating protein function… (more)

▼ Dysregulation of alpha-amino post-translational modifications (Nα-PTMs) is found in multiple cancers and developmental disorders. However, the exact roles Nα-PTMs play in regulating protein function remain poorly understood. I sought to clarify the role of Nα-methylation and Nα-acetylation in the regulation of Myosin Regulatory Light Chain 9 (MYL9). MYL9 is a key cytoskeletal regulator and transcription factor and is the first protein confirmed to undergo both Nα-methylation and Nα-acetylation. Through this work I revealed novel regulatory features of MYL9, while also presenting a framework by which to understand the coordinated regulation of proteins by Nα-methylation and Nα-acetylation. Nα-PTM selective mutants of MYL9 were generated by modifying the consensus sequence targeted by Nα-methyltransferases and Nα-acetyltransferases. These mutants were assayed alongside wildtype (WT) protein for effects on MYL9 stability and function in mammalian cell lines. Offering a counterpoint to the dogmatic perspective of Nα-PTMs as modifiers of protein stability, loss of either Nα-methylation or Nα-acetylation did not alter MYL9 half-life. Instead, distinct functionality of Nα-methylated and Nα-acetylated MYL9 was observed. MYL9 is known primarily as a regulator of cytoskeletal dynamics through its regulation of non-muscle myosin II (NMII) activity. A specialized nuclear role for MYL9 has been described in which it binds at select gene promoters and activates transcription. My results show that Nα-methylation promotes this nuclear function of MYL9. The Nα-methylation selective mutant of MYL9 increased TNFα stimulated transcription of intercellular adhesion molecule 1 (ICAM1) as compared to all other variants of MYL9. In addition, this MYL9 mutant showed increased binding at the ICAM1 promoter. Nα-methylation has been shown to increase protein-DNA interactions, implicating this mechanism in the regulation of MYL9 nuclear function. Phosphorylation of MYL9 at serine 19 (pS19) is required for NMII activity. Expression of a Nα-methylation deficient mutant of MYL9 increased the occurrence of pS19 after stimulation as compared to all other variants of MYL9. This mutant of MYL9 also displayed increased cell migration and cell spreading on fibronectin, measures of NMII activity. As such, I propose a model in which Nα-methylation of MYL9 favors nuclear activity while blocking cytoplasmic activity. Advisors/Committee Members: Schaner Tooley, Christine, Klinge, Carolyn, Klinge, Carolyn, Clark, Barbara, Cheng, Alan, Ceresa, Brian.

Subjects/Keywords: alpha-amino PTM; protein methylation; acetylation; regulatory light chain; non-muscle myosin; compartmentalization; Amino Acids, Peptides, and Proteins; Biochemical Phenomena, Metabolism, and Nutrition; Biological Factors; Medical Biochemistry

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APA (6^th Edition):

Nevitt, C. D. (2018). Alpha-amino methylation and acetylation are novel regulators of MYL9 function. (Doctoral Dissertation). University of Louisville. Retrieved from 10.18297/etd/3032 ; https://ir.library.louisville.edu/etd/3032

Chicago Manual of Style (16^th Edition):

Nevitt, Christopher David. “Alpha-amino methylation and acetylation are novel regulators of MYL9 function.” 2018. Doctoral Dissertation, University of Louisville. Accessed March 01, 2021. 10.18297/etd/3032 ; https://ir.library.louisville.edu/etd/3032.

MLA Handbook (7^th Edition):

Nevitt, Christopher David. “Alpha-amino methylation and acetylation are novel regulators of MYL9 function.” 2018. Web. 01 Mar 2021.

Vancouver:

Nevitt CD. Alpha-amino methylation and acetylation are novel regulators of MYL9 function. [Internet] [Doctoral dissertation]. University of Louisville; 2018. [cited 2021 Mar 01]. Available from: 10.18297/etd/3032 ; https://ir.library.louisville.edu/etd/3032.

Council of Science Editors:

Nevitt CD. Alpha-amino methylation and acetylation are novel regulators of MYL9 function. [Doctoral Dissertation]. University of Louisville; 2018. Available from: 10.18297/etd/3032 ; https://ir.library.louisville.edu/etd/3032

University of Saskatchewan

25. Steinbach, Sarah Katherina. Pik1p, a phosphatidylinositol 4-kinase, interacts with Cdc4p : a contractile ring protein essential for cytokinesis in fission yeast.

Degree: 2008, University of Saskatchewan

URL: http://hdl.handle.net/10388/etd-06212008-112617

► A yeast two-hybrid assay suggested the possibility of an interaction between Cdc4p, a small EF-hand protein essential for cytokinesis, and Pik1p in S. pombe. This… (more)

▼ A yeast two-hybrid assay suggested the possibility of an interaction between Cdc4p, a small EF-hand protein essential for cytokinesis, and Pik1p in S. pombe. This interaction was unexpected, as one function of Cdc4p is that of an essential light chain, bound to the first IQ-motif of type II myosins, whereas Pik1p is a phosphatidylinositol 4-kinase. The objective of this work was to analyze the effects of Pik1p lipid kinase activity on the cell cycle of S. pombe. Another goal of this study was to evaluate the functional significance of the interaction between Cdc4p and Pik1p. This was performed by generating two mutants of pik1: one that abolished lipid kinase activity (pik1-D709A) and one that abolished Pik1p Cdc4p-binding activity (pik1-R838A). Pik1p has a conserved IQ-motif in its C-terminal region. A mutation in this site (R838A), homologous to a residue which was mutated in myosin and abrogated the interaction with Cdc4p, prevented the interaction with Cdc4p in a yeast two-hybrid assay and ELISA. An increase in lipid kinase activity was observed in cell extracts upon ectopic expression of pik1-wt from an episome, which was abolished by a mutation in the lipid kinase domain of Pik1p (D709A), but not by the R838A mutation. However, little to no increase in lipid kinase activity was observed upon ectopic expression of pik1-wt and pik1-R838A in a strain carrying a conditionally lethal allele of cdc4 (cdc4-G107S). This mutation in Cdc4p was shown previously to prevent the interaction with Pik1p in yeast two-hybrid assays. Ectopic expression of pik1-wt suppressed cell proliferation, with disruption of actin cytoskeletal structures and contractile ring formation. These results were not observed with the ectopic expression of the pik1-R838A mutant or when pik1-wt was expressed in the cdc4-G107S strain. Ectopic expression of pik1-R838A resulted in cell shortening, likely through inhibition of growth, and many of the short cells showed an accumulation of the expressed Pik1p protein at the cell tips. Formation of the contractile ring appeared unaffected in cells with ectopic expression of the pik1-D709A mutant, but many of these cells had thick or more than one septum, characteristic of a septation defect. The ectopic expression phenotypes were dosage dependent since lower levels of expression greatly reduced the severity of the ectopic phenotypes. Pik1p lipid kinase activity is essential and, based on ectopic expression studies, is required for septation. There is a physical and functional interaction between Cdc4p and Pik1p which is not essential for cell viability, but suggests a role for Cdc4p in phosphoinositide metabolism. Advisors/Committee Members: Hemmingsen, Sean M..

Subjects/Keywords: phosphoinositides; myosin essential light chain; fission yeast genetics; molecular biology

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APA (6^th Edition):

Steinbach, S. K. (2008). Pik1p, a phosphatidylinositol 4-kinase, interacts with Cdc4p : a contractile ring protein essential for cytokinesis in fission yeast. (Thesis). University of Saskatchewan. Retrieved from http://hdl.handle.net/10388/etd-06212008-112617

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):

Steinbach, Sarah Katherina. “Pik1p, a phosphatidylinositol 4-kinase, interacts with Cdc4p : a contractile ring protein essential for cytokinesis in fission yeast.” 2008. Thesis, University of Saskatchewan. Accessed March 01, 2021. http://hdl.handle.net/10388/etd-06212008-112617.

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

MLA Handbook (7^th Edition):

Steinbach, Sarah Katherina. “Pik1p, a phosphatidylinositol 4-kinase, interacts with Cdc4p : a contractile ring protein essential for cytokinesis in fission yeast.” 2008. Web. 01 Mar 2021.

Vancouver:

Steinbach SK. Pik1p, a phosphatidylinositol 4-kinase, interacts with Cdc4p : a contractile ring protein essential for cytokinesis in fission yeast. [Internet] [Thesis]. University of Saskatchewan; 2008. [cited 2021 Mar 01]. Available from: http://hdl.handle.net/10388/etd-06212008-112617.

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

Council of Science Editors:

Steinbach SK. Pik1p, a phosphatidylinositol 4-kinase, interacts with Cdc4p : a contractile ring protein essential for cytokinesis in fission yeast. [Thesis]. University of Saskatchewan; 2008. Available from: http://hdl.handle.net/10388/etd-06212008-112617

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

University of Debrecen

26. Kola, Job Baffin. Determination of effects of Raf-1 on the regulation of MLC phosphorylation in the primary human intestinal smooth cell .

Degree: DE – Általános Orvostudományi Kar, University of Debrecen

URL: http://hdl.handle.net/2437/270011

► Postoperative ileus arises when normal propulsion of food in the small intestine, is obstructed due to problems with smooth muscle contractility or enteric nervous system… (more)

Subjects/Keywords: POI (Post-operative ileus); CXCL1/CXCR2 signaling; MLC (myosin light chain); MYPT1 (myosin light chain phosphatase targeting subunit 1); PAK (p21 activated kinase); ROCK (Rho-kinase); MLCP (myosin light chain phosphatase); MLCK (myosin light chain kinase); IL8 (interleukin 8); NSAID (Nonsteroidal anti-inflammatory drugs)

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APA (6^th Edition):

Kola, J. B. (n.d.). Determination of effects of Raf-1 on the regulation of MLC phosphorylation in the primary human intestinal smooth cell . (Thesis). University of Debrecen. Retrieved from http://hdl.handle.net/2437/270011

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):

Kola, Job Baffin. “Determination of effects of Raf-1 on the regulation of MLC phosphorylation in the primary human intestinal smooth cell .” Thesis, University of Debrecen. Accessed March 01, 2021. http://hdl.handle.net/2437/270011.

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):

Kola, Job Baffin. “Determination of effects of Raf-1 on the regulation of MLC phosphorylation in the primary human intestinal smooth cell .” Web. 01 Mar 2021.

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

Vancouver:

Kola JB. Determination of effects of Raf-1 on the regulation of MLC phosphorylation in the primary human intestinal smooth cell . [Internet] [Thesis]. University of Debrecen; [cited 2021 Mar 01]. Available from: http://hdl.handle.net/2437/270011.

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:

Kola JB. Determination of effects of Raf-1 on the regulation of MLC phosphorylation in the primary human intestinal smooth cell . [Thesis]. University of Debrecen; Available from: http://hdl.handle.net/2437/270011

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

Queens University

27. Liburd, Janine. Structural Insights Into Dictyostelium Discoideum Myosin Light Chain Specificity .

Degree: Biochemistry, 2013, Queens University

URL: http://hdl.handle.net/1974/7776

► Myosins are molecular motor proteins involved in cell movement, vesicle and organelle transport by moving along the cytoskeletal actin filaments. They include a myosin heavy… (more)

▼ Myosins are molecular motor proteins involved in cell movement, vesicle and organelle transport by moving along the cytoskeletal actin filaments. They include a myosin heavy chain and at least one myosin light chain (LC). The latter are typically bilobal proteins like calmodulin, where each lobe comprises a pair of EF-hand Ca2+-binding motifs. The LCs bind to ~25-residue IQ motifs that loosely conform to an IQXXXRGXXXR consensus sequence, and impart rigidity that is crucial for myosin function. The highly motile amoeba Dictyostelium discoideum expresses seven class I myosins, two of which (MyoD and MyoB) recruit the specific LCs MlcD and MlcB, with MlcB being the first observed single-lobe LC. However, the LCs for the remaining D. discoideum class I myosins are unknown. Identifying and characterizing these LCs is one focus of this thesis, with an overall goal of understanding their role in myosin function and regulation. Nuclear magnetic resonance spectroscopy, site-directed mutagenesis, and computational modeling were used to determine the solution structure of apo-MlcB and identify the MyoB IQ motif-binding site. Apo-MlcB differs from the typical closed conformation of an EF-hand Ca2+-binding protein in the apo-state as helix 1 in its structure is splayed from the remaining helices. The MyoB IQ motif-binding surface is not altered by Ca2+, involves residues from helices 1 and 4, and from residues in the N-terminal canonical EF-hand Ca2+-binding loop, and represents a unique mode of IQ recognition by a myosin LC. Calmodulin was identified as the LC for MyoA and MyoE while another single-lobe LC, MlcC, bound to two of three IQ motifs in MyoC. The solution structure of MlcC was more similar to the C-terminal lobe of apo-calmodulin than to apo-MlcB. Chemical shift perturbation studies suggest that like apo-CaM, MlcC undergoes a global MyoC IQ motif-induced conformational change. Computational modeling of the MlcC-MyoC IQ complex indicates that this is a feasible mode of IQ recognition. The structures of MlcB and MlcC, with their different modes of IQ motif binding, provide novel insights into IQ motif binding specificity and begin to illustrate their role in myosin function and regulation.

Subjects/Keywords: Myosin Light Chains ; IQ Motifs ; NMR Spectroscopy

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APA (6^th Edition):

Liburd, J. (2013). Structural Insights Into Dictyostelium Discoideum Myosin Light Chain Specificity . (Thesis). Queens University. Retrieved from http://hdl.handle.net/1974/7776

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):

Liburd, Janine. “Structural Insights Into Dictyostelium Discoideum Myosin Light Chain Specificity .” 2013. Thesis, Queens University. Accessed March 01, 2021. http://hdl.handle.net/1974/7776.

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

MLA Handbook (7^th Edition):

Liburd, Janine. “Structural Insights Into Dictyostelium Discoideum Myosin Light Chain Specificity .” 2013. Web. 01 Mar 2021.

Vancouver:

Liburd J. Structural Insights Into Dictyostelium Discoideum Myosin Light Chain Specificity . [Internet] [Thesis]. Queens University; 2013. [cited 2021 Mar 01]. Available from: http://hdl.handle.net/1974/7776.

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

Council of Science Editors:

Liburd J. Structural Insights Into Dictyostelium Discoideum Myosin Light Chain Specificity . [Thesis]. Queens University; 2013. Available from: http://hdl.handle.net/1974/7776

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

University of Lund

28. Ekman, Mari. Developmental regulation of smooth muscle contraction in the urinary bladder.

Degree: 2008, University of Lund

URL: https://lup.lub.lu.se/record/1259999 ; https://portal.research.lu.se/ws/files/4097657/1260000.pdf

► Smooth muscle cells in the urinary bladder are involved in the control of urine filling and emptying. We have used mice to study the contractile… (more)

Subjects/Keywords: Basic Medicine; newborn; Rho-kinase; cellular signaling; muscarinic receptors; calcium sensitivity; protein kinase C; non-muscle myosin; myosin light chain phosphatase

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APA (6^th Edition):

Ekman, M. (2008). Developmental regulation of smooth muscle contraction in the urinary bladder. (Doctoral Dissertation). University of Lund. Retrieved from https://lup.lub.lu.se/record/1259999 ; https://portal.research.lu.se/ws/files/4097657/1260000.pdf

Chicago Manual of Style (16^th Edition):

Ekman, Mari. “Developmental regulation of smooth muscle contraction in the urinary bladder.” 2008. Doctoral Dissertation, University of Lund. Accessed March 01, 2021. https://lup.lub.lu.se/record/1259999 ; https://portal.research.lu.se/ws/files/4097657/1260000.pdf.

MLA Handbook (7^th Edition):

Ekman, Mari. “Developmental regulation of smooth muscle contraction in the urinary bladder.” 2008. Web. 01 Mar 2021.

Vancouver:

Ekman M. Developmental regulation of smooth muscle contraction in the urinary bladder. [Internet] [Doctoral dissertation]. University of Lund; 2008. [cited 2021 Mar 01]. Available from: https://lup.lub.lu.se/record/1259999 ; https://portal.research.lu.se/ws/files/4097657/1260000.pdf.

Council of Science Editors:

Ekman M. Developmental regulation of smooth muscle contraction in the urinary bladder. [Doctoral Dissertation]. University of Lund; 2008. Available from: https://lup.lub.lu.se/record/1259999 ; https://portal.research.lu.se/ws/files/4097657/1260000.pdf

29. Hassell, Tommy C. (Tommy Clarence). Phosphorylation of nonmuscle myosin by calcium-dependent and independent protein kinases.

Degree: 1987, North Texas State University

URL: https://digital.library.unt.edu/ark:/67531/metadc798346/

Nonmuscle myosin from bovine thymus was purified, characterized , and phosphorylated with MLCK, H4PK, and Protein Kinase C. Phosphorylation occured exclusively on the myosin regulatory light chain. Phosphorylation by MLCK and H4PK resulted in the activation of the MgATPase activity as well as filament assembly of nonmuscle myosin.

Subjects/Keywords: phosphorylation; myosin; protein kinases

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APA (6^th Edition):

Hassell, T. C. (. C. (1987). Phosphorylation of nonmuscle myosin by calcium-dependent and independent protein kinases. (Thesis). North Texas State University. Retrieved from https://digital.library.unt.edu/ark:/67531/metadc798346/

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):

Hassell, Tommy C (Tommy Clarence). “Phosphorylation of nonmuscle myosin by calcium-dependent and independent protein kinases.” 1987. Thesis, North Texas State University. Accessed March 01, 2021. https://digital.library.unt.edu/ark:/67531/metadc798346/.

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

MLA Handbook (7^th Edition):

Hassell, Tommy C (Tommy Clarence). “Phosphorylation of nonmuscle myosin by calcium-dependent and independent protein kinases.” 1987. Web. 01 Mar 2021.

Vancouver:

Hassell TC(C. Phosphorylation of nonmuscle myosin by calcium-dependent and independent protein kinases. [Internet] [Thesis]. North Texas State University; 1987. [cited 2021 Mar 01]. Available from: https://digital.library.unt.edu/ark:/67531/metadc798346/.

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

Council of Science Editors:

Hassell TC(C. Phosphorylation of nonmuscle myosin by calcium-dependent and independent protein kinases. [Thesis]. North Texas State University; 1987. Available from: https://digital.library.unt.edu/ark:/67531/metadc798346/

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

The Ohio State University

30. Fuller, Geraldine Anne. ALTERATIONS IN MYOSIN AND MYOCYTE STRUCTURE IN AN EXTREMLY LONG TERM PACING MODEL OF CANINE DILATED CARDIOMYOPATHY.

Degree: PhD, Veterinary Biosciences, 2002, The Ohio State University

URL: http://rave.ohiolink.edu/etdc/view?acc_num=osu1038932067

► Canine dilated cardiomyopathy (DCM) induced by rapid pacing produces low cardiac output failure, mimicking naturally occurring human DCM. We studied long-range (>6 months) rapid right… (more)

▼ Canine dilated cardiomyopathy (DCM) induced by rapid pacing produces low cardiac output failure, mimicking naturally occurring human DCM. We studied long-range (>6 months) rapid right ventricular pacing to evaluate similarities to end-stage human DCM and determine differences from previously reported canine pacing studies. Samples were obtained from the right and left auricles (RAU, LAU), right and left atria (RA, LA), right and left ventricles (RV, LV), and LV subauricular and subatrial papillary muscles (PM) from 12 pacing and 11 control dogs. Since both beagle and mongrel hounds commonly are used in models of human DCM, we also investigated levels of cardiac myosin heavy chain (MHC) isoforms from 6 beagle and 6 mongrel controls. Distinct differences were observed, compared to previously reported, shorter-range studies, in numbers of apoptotic myocytes, cross-sectional myocyte size, and Bcl-2 protein levels. Myocyte degeneration and mitochondrial degradation were apparently more severe than previous reports. Rod body formation, indicative of severe myocyte degeneration, was observed. In addition, lower numbers of apoptotic myocytes, increased cross-sectional area with apparent wider size distribution and comparable levels of both Bcl-2 and Bcl-xL on western blot were observed in this study, different from previous pacing studies, but similar to end stage human heart failure. Differences in amounts of apoptosis and type II myocyte nuclei were observed based on sampling location, suggesting variation in cellular response to injury. Significant increases in levels of Beta MHC were observed in the RAU, RA, LAU, LA, and RV of pacing dogs compared to control. In addition, significant levels of ventricular light chain 2 (VLC2) were observed in the RA of pacing dogs, suggesting a compensatory switch in response to prolonged elevated RA pressure. Distinct differences were observed based on breed with levels of Beta MHC approximately 2 fold higher in the RAU, RA, LAU and LA of mongrels. The results of our study suggest that extremely long range rapid ventricular pacing is a relevant model for studying end stage human heart failure. In addition, breed and sampling sites appear to be factors that should be considered when canine models are used for studying human heart failure. Advisors/Committee Members: Yamaguchi, Mamoru (Advisor).

Subjects/Keywords: dilated cardiomyopathy; long-range right ventricular pacing myosin heavy chain isoforms myosin light chain isoforms mitochondrial degradation myocyte size apoptosis bcl-2 TUNEL type II myocyte nuclei

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

APA (6^th Edition):

Fuller, G. A. (2002). ALTERATIONS IN MYOSIN AND MYOCYTE STRUCTURE IN AN EXTREMLY LONG TERM PACING MODEL OF CANINE DILATED CARDIOMYOPATHY. (Doctoral Dissertation). The Ohio State University. Retrieved from http://rave.ohiolink.edu/etdc/view?acc_num=osu1038932067

Chicago Manual of Style (16^th Edition):

Fuller, Geraldine Anne. “ALTERATIONS IN MYOSIN AND MYOCYTE STRUCTURE IN AN EXTREMLY LONG TERM PACING MODEL OF CANINE DILATED CARDIOMYOPATHY.” 2002. Doctoral Dissertation, The Ohio State University. Accessed March 01, 2021. http://rave.ohiolink.edu/etdc/view?acc_num=osu1038932067.

MLA Handbook (7^th Edition):

Fuller, Geraldine Anne. “ALTERATIONS IN MYOSIN AND MYOCYTE STRUCTURE IN AN EXTREMLY LONG TERM PACING MODEL OF CANINE DILATED CARDIOMYOPATHY.” 2002. Web. 01 Mar 2021.

Vancouver:

Fuller GA. ALTERATIONS IN MYOSIN AND MYOCYTE STRUCTURE IN AN EXTREMLY LONG TERM PACING MODEL OF CANINE DILATED CARDIOMYOPATHY. [Internet] [Doctoral dissertation]. The Ohio State University; 2002. [cited 2021 Mar 01]. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=osu1038932067.

Council of Science Editors:

Fuller GA. ALTERATIONS IN MYOSIN AND MYOCYTE STRUCTURE IN AN EXTREMLY LONG TERM PACING MODEL OF CANINE DILATED CARDIOMYOPATHY. [Doctoral Dissertation]. The Ohio State University; 2002. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=osu1038932067

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Open Access Theses and Dissertations