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Article ; Online: The structural mechanism of human glycogen synthesis by the GYS1-GYG1 complex.

Fastman, Nathan M / Liu, Yuxi / Ramanan, Vyas / Merritt, Hanne / Ambing, Eileen / DePaoli-Roach, Anna A / Roach, Peter J / Hurley, Thomas D / Mellem, Kevin T / Ullman, Julie C / Green, Eric / Morgans, David / Tzitzilonis, Christos

Cell reports

2022 Volume 40, Issue 1, Page(s) 111041

Abstract: Glycogen is the primary energy reserve in mammals, and dysregulation of glycogen metabolism can result in glycogen storage diseases (GSDs). In muscle, glycogen synthesis is initiated by the enzymes glycogenin-1 (GYG1), which seeds the molecule by ... ...

Abstract	Glycogen is the primary energy reserve in mammals, and dysregulation of glycogen metabolism can result in glycogen storage diseases (GSDs). In muscle, glycogen synthesis is initiated by the enzymes glycogenin-1 (GYG1), which seeds the molecule by autoglucosylation, and glycogen synthase-1 (GYS1), which extends the glycogen chain. Although both enzymes are required for proper glycogen production, the nature of their interaction has been enigmatic. Here, we present the human GYS1:GYG1 complex in multiple conformations representing different functional states. We observe an asymmetric conformation of GYS1 that exposes an interface for close GYG1 association, and propose this state facilitates handoff of the GYG1-associated glycogen chain to a GYS1 subunit for elongation. Full activation of GYS1 widens the GYG1-binding groove, enabling GYG1 release concomitant with glycogen chain growth. This structural mechanism connecting chain nucleation and extension explains the apparent stepwise nature of glycogen synthesis and suggests distinct states to target for GSD-modifying therapeutics.
MeSH term(s)	Glucosyltransferases/metabolism ; Glycogen/metabolism ; Glycogen Synthase/metabolism ; Glycogenolysis ; Glycoproteins/metabolism ; Humans
Chemical Substances	Glycoproteins ; glycogenin ; Glycogen (9005-79-2) ; Glucosyltransferases (EC 2.4.1.-) ; Glycogen Synthase (EC 2.4.1.11)
Language	English
Publishing date	2022-07-03
Publishing country	United States
Document type	Journal Article
ZDB-ID	2649101-1
ISSN	2211-1247 ; 2211-1247
ISSN (online)	2211-1247
ISSN	2211-1247
DOI	10.1016/j.celrep.2022.111041
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Article ; Online: The structural mechanism of human glycogen synthesis by the GYS1-GYG1 complex

Nathan M. Fastman / Yuxi Liu / Vyas Ramanan / Hanne Merritt / Eileen Ambing / Anna A. DePaoli-Roach / Peter J. Roach / Thomas D. Hurley / Kevin T. Mellem / Julie C. Ullman / Eric Green / David Morgans, Jr. / Christos Tzitzilonis

Cell Reports, Vol 40, Iss 1, Pp 111041- (2022)

2022

Abstract: Summary: Glycogen is the primary energy reserve in mammals, and dysregulation of glycogen metabolism can result in glycogen storage diseases (GSDs). In muscle, glycogen synthesis is initiated by the enzymes glycogenin-1 (GYG1), which seeds the molecule ... ...

Abstract	Summary: Glycogen is the primary energy reserve in mammals, and dysregulation of glycogen metabolism can result in glycogen storage diseases (GSDs). In muscle, glycogen synthesis is initiated by the enzymes glycogenin-1 (GYG1), which seeds the molecule by autoglucosylation, and glycogen synthase-1 (GYS1), which extends the glycogen chain. Although both enzymes are required for proper glycogen production, the nature of their interaction has been enigmatic. Here, we present the human GYS1:GYG1 complex in multiple conformations representing different functional states. We observe an asymmetric conformation of GYS1 that exposes an interface for close GYG1 association, and propose this state facilitates handoff of the GYG1-associated glycogen chain to a GYS1 subunit for elongation. Full activation of GYS1 widens the GYG1-binding groove, enabling GYG1 release concomitant with glycogen chain growth. This structural mechanism connecting chain nucleation and extension explains the apparent stepwise nature of glycogen synthesis and suggests distinct states to target for GSD-modifying therapeutics.
Keywords	CP: Molecular biology ; Biology (General) ; QH301-705.5
Language	English
Publishing date	2022-07-01T00:00:00Z
Publisher	Elsevier
Document type	Article ; Online
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Article ; Online: Small-molecule inhibition of glycogen synthase 1 for the treatment of Pompe disease and other glycogen storage disorders.

Ullman, Julie C / Mellem, Kevin T / Xi, Yannan / Ramanan, Vyas / Merritt, Hanne / Choy, Rebeca / Gujral, Tarunmeet / Young, Lyndsay E A / Blake, Kerrigan / Tep, Samnang / Homburger, Julian R / O'Regan, Adam / Ganesh, Sandya / Wong, Perryn / Satterfield, Terrence F / Lin, Baiwei / Situ, Eva / Yu, Cecile / Espanol, Bryan /

Sarwaikar, Richa / Fastman, Nathan / Tzitzilonis, Christos / Lee, Patrick / Reiton, Daniel / Morton, Vivian / Santiago, Pam / Won, Walter / Powers, Hannah / Cummings, Beryl B / Hoek, Maarten / Graham, Robert R / Chandriani, Sanjay J / Bainer, Russell / DePaoli-Roach, Anna A / Roach, Peter J / Hurley, Thomas D / Sun, Ramon C / Gentry, Matthew S / Sinz, Christopher / Dick, Ryan A / Noonberg, Sarah B / Beattie, David T / Morgans, David J / Green, Eric M

Science translational medicine

2024 Volume 16, Issue 730, Page(s) eadf1691

Abstract: Glycogen synthase 1 (GYS1), the rate-limiting enzyme in muscle glycogen synthesis, plays a central role in energy homeostasis and has been proposed as a therapeutic target in multiple glycogen storage diseases. Despite decades of investigation, there are ...

Abstract	Glycogen synthase 1 (GYS1), the rate-limiting enzyme in muscle glycogen synthesis, plays a central role in energy homeostasis and has been proposed as a therapeutic target in multiple glycogen storage diseases. Despite decades of investigation, there are no known potent, selective small-molecule inhibitors of this enzyme. Here, we report the preclinical characterization of MZ-101, a small molecule that potently inhibits GYS1 in vitro and in vivo without inhibiting GYS2, a related isoform essential for synthesizing liver glycogen. Chronic treatment with MZ-101 depleted muscle glycogen and was well tolerated in mice. Pompe disease, a glycogen storage disease caused by mutations in acid α glucosidase (GAA), results in pathological accumulation of glycogen and consequent autophagolysosomal abnormalities, metabolic dysregulation, and muscle atrophy. Enzyme replacement therapy (ERT) with recombinant GAA is the only approved treatment for Pompe disease, but it requires frequent infusions, and efficacy is limited by suboptimal skeletal muscle distribution. In a mouse model of Pompe disease, chronic oral administration of MZ-101 alone reduced glycogen buildup in skeletal muscle with comparable efficacy to ERT. In addition, treatment with MZ-101 in combination with ERT had an additive effect and could normalize muscle glycogen concentrations. Biochemical, metabolomic, and transcriptomic analyses of muscle tissue demonstrated that lowering of glycogen concentrations with MZ-101, alone or in combination with ERT, corrected the cellular pathology in this mouse model. These data suggest that substrate reduction therapy with GYS1 inhibition may be a promising therapeutic approach for Pompe disease and other glycogen storage diseases.
MeSH term(s)	Mice ; Animals ; Glycogen Storage Disease Type II/drug therapy ; Glycogen Synthase/metabolism ; Glycogen Synthase/pharmacology ; Mice, Knockout ; Glycogen/metabolism ; Muscle, Skeletal/metabolism ; Enzyme Replacement Therapy/methods
Chemical Substances	Glycogen Synthase (EC 2.4.1.11) ; Glycogen (9005-79-2)
Language	English
Publishing date	2024-01-17
Publishing country	United States
Document type	Journal Article
ZDB-ID	2518854-9
ISSN	1946-6242 ; 1946-6234
ISSN (online)	1946-6242
ISSN	1946-6234
DOI	10.1126/scitranslmed.adf1691
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Article ; Online: New Methods in Tissue Engineering: Improved Models for Viral Infection.

Ramanan, Vyas / Scull, Margaret A / Sheahan, Timothy P / Rice, Charles M / Bhatia, Sangeeta N

Annual review of virology

2015 Volume 1, Page(s) 475–499

Abstract: New insights in the study of virus and host biology in the context of viral infection are made possible by the development of model systems that faithfully recapitulate the in vivo viral life cycle. Standard tissue culture models lack critical emergent ... ...

Abstract	New insights in the study of virus and host biology in the context of viral infection are made possible by the development of model systems that faithfully recapitulate the in vivo viral life cycle. Standard tissue culture models lack critical emergent properties driven by cellular organization and in vivo-like function, whereas animal models suffer from limited susceptibility to relevant human viruses and make it difficult to perform detailed molecular manipulation and analysis. Tissue engineering techniques may enable virologists to create infection models that combine the facile manipulation and readouts of tissue culture with the virus-relevant complexity of animal models. Here, we review the state of the art in tissue engineering and describe how tissue engineering techniques may alleviate some common shortcomings of existing models of viral infection, with a particular emphasis on hepatotropic viruses. We then discuss possible future applications of tissue engineering to virology, including current challenges and potential solutions.
Keywords	covid19
Language	English
Publishing date	2015-05-06
Publishing country	United States
Document type	Journal Article
ZDB-ID	2764224-0
ISSN	2327-0578 ; 2327-056X
ISSN (online)	2327-0578
ISSN	2327-056X
DOI	10.1146/annurev-virology-031413-085437
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Article ; Online: Development of Light-Activated CRISPR Using Guide RNAs with Photocleavable Protectors.

Jain, Piyush K / Ramanan, Vyas / Schepers, Arnout G / Dalvie, Nisha S / Panda, Apekshya / Fleming, Heather E / Bhatia, Sangeeta N

Angewandte Chemie (International ed. in English)

2016 Volume 55, Issue 40, Page(s) 12440–12444

Abstract: The ability to remotely trigger CRISPR/Cas9 activity would enable new strategies to study cellular events with greater precision and complexity. In this work, we have developed a method to photocage the activity of the guide RNA called "CRISPR-plus" ( ... ...

Abstract	The ability to remotely trigger CRISPR/Cas9 activity would enable new strategies to study cellular events with greater precision and complexity. In this work, we have developed a method to photocage the activity of the guide RNA called "CRISPR-plus" (CRISPR-precise light-mediated unveiling of sgRNAs). The photoactivation capability of our CRISPR-plus method is compatible with the simultaneous targeting of multiple DNA sequences and supports numerous modifications that can enable guide RNA labeling for use in imaging and mechanistic investigations.
MeSH term(s)	Base Sequence ; CRISPR-Cas Systems/genetics ; Green Fluorescent Proteins/genetics ; HeLa Cells ; Humans ; Light ; Nucleic Acid Hybridization ; Photolysis/radiation effects ; RNA, Guide, CRISPR-Cas Systems/chemistry ; RNA, Guide, CRISPR-Cas Systems/metabolism
Chemical Substances	RNA, Guide, CRISPR-Cas Systems ; Green Fluorescent Proteins (147336-22-9)
Language	English
Publishing date	2016-08-24
Publishing country	Germany
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2011836-3
ISSN	1521-3773 ; 1433-7851
ISSN (online)	1521-3773
ISSN	1433-7851
DOI	10.1002/anie.201606123
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Article ; Online: Nanofiber-nanorod composites exhibiting light-induced reversible lower critical solution temperature transitions.

Ramanan, Vyas V / Hribar, Kolin C / Katz, Joshua S / Burdick, Jason A

Nanotechnology

2011 Volume 22, Issue 49, Page(s) 494009

Abstract: Stimuli-responsive materials are promising as smart materials for a range of applications. In this work, a photo-crosslinkable, thermoresponsive macromer was electrospun into fibrous scaffolds containing gold nanorods (AuNRs). The resulting fibrous ... ...

Abstract	Stimuli-responsive materials are promising as smart materials for a range of applications. In this work, a photo-crosslinkable, thermoresponsive macromer was electrospun into fibrous scaffolds containing gold nanorods (AuNRs). The resulting fibrous nanocomposites composed of poly(N-isopropylacrylamide-co-polyethylene glycol acrylate) (PNPA) and PEGylated AuNRs were crosslinked and swollen in water. AuNRs strongly absorb in the near-infrared (NIR) region to generate heat, which triggered the fiber thermal transition upon NIR light exposure. During the thermal transition, scaffolds collapsed both macroscopically and microscopically, with individual fibers deswelling and pulling together. Exposure to a 1.1 W NIR laser decreased the diameter of swollen fibers by 34.7% from 1332 ± 193.3 to 868.9 ± 168.3 nm, and increased fiber density 116% from 209.5 ± 26.34 to 451.9 ± 23.68 fibers mm( - 1). This transition was dependent on the incorporation of the AuNRs, and was utilized to trigger the release of encapsulated proteins from the nanocomposite fiber mats. The expulsion of water from fibers upon NIR exposure caused the release rate of incorporated protein to increase greater than tenfold, from 0.038 ± 0.052 without external stimulus to 0.462 ± 0.227 µg protein/mg polymer/min with NIR exposure. These results suggest that light-responsive fibrous nanocomposites can be utilized in applications such as drug delivery.
MeSH term(s)	Acrylamides/chemistry ; Acrylates/chemistry ; Animals ; Calmodulin/administration & dosage ; Cattle ; Cross-Linking Reagents ; Delayed-Action Preparations/chemistry ; Fluorescein-5-isothiocyanate/administration & dosage ; Gold/chemistry ; Light ; Nanofibers/chemistry ; Nanofibers/ultrastructure ; Nanotubes/chemistry ; Nanotubes/ultrastructure ; Polyethylene Glycols/chemistry ; Tissue Scaffolds/chemistry ; Transition Temperature
Chemical Substances	Acrylamides ; Acrylates ; Calmodulin ; Cross-Linking Reagents ; Delayed-Action Preparations ; Polyethylene Glycols (3WJQ0SDW1A) ; Gold (7440-57-5) ; N-isopropylacrylamide (B7GFF17L9U) ; Fluorescein-5-isothiocyanate (I223NX31W9)
Language	English
Publishing date	2011-11-21
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	1362365-5
ISSN	1361-6528 ; 0957-4484
ISSN (online)	1361-6528
ISSN	0957-4484
DOI	10.1088/0957-4484/22/49/494009
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Article ; Online: Hepatitis B virus induces RNR-R2 expression via DNA damage response activation.

Ricardo-Lax, Inna / Ramanan, Vyas / Michailidis, Eleftherios / Shamia, Tal / Reuven, Nina / Rice, Charles M / Shlomai, Amir / Shaul, Yosef

Journal of hepatology

2015 Volume 63, Issue 4, Page(s) 789–796

Abstract: Background & aims: Hepatitis B virus (HBV) infects and replicates in quiescent hepatocytes, which are deficient in dNTPs, the critical precursors of HBV replication. Most tumor viruses promote dNTP production in host cells by inducing cell proliferation. ...

Abstract	Background & aims: Hepatitis B virus (HBV) infects and replicates in quiescent hepatocytes, which are deficient in dNTPs, the critical precursors of HBV replication. Most tumor viruses promote dNTP production in host cells by inducing cell proliferation. Although HBV is known as a major cause of hepatocellular carcinoma, it does not lead to cellular proliferation. Instead, HBV acquires dNTPs by activating the expression of the R2 subunit of the Ribonucleotide Reductase (RNR) holoenzyme, the cell cycle gene that is rate-limiting for generation of dNTPs, without inducing the cell cycle. We wished to elucidate the molecular basis of HBV-dependent R2 expression in quiescent cells. Methods: Quiescent HepG2 cells were transduced with an HBV-containing lentiviral vector, and primary human hepatocytes were infected with HBV. DNA damage response and RNR-R2 gene expression were monitored under this condition. Results: We report here that HBV-induced R2 expression is mediated by the E2F1 transcription factor, and that HBV induces E2F1 accumulation, modification and binding to the R2 promoter. We found that Chk1, a known E2F1 kinase that functions in response to DNA damage, was activated by HBV. In cells where Chk1 was pharmacologically inhibited, or depleted by shRNA-mediated knockdown, HBV-mediated R2 expression was severely attenuated. Furthermore, we found that HBV attenuates DNA repair, thus reducing cellular dNTP consumption. Conclusions: Our findings demonstrate that HBV exploits the Chk1-E2F1 axis of the DNA damage response pathway to induce R2 expression in a cell cycle-independent manner. This suggests that inhibition of this pathway may have a therapeutic value for HBV carriers.
MeSH term(s)	Apoptosis ; Blotting, Southern ; Blotting, Western ; Cell Cycle ; Cell Division ; Cell Proliferation ; DNA Damage/genetics ; Electrophoresis, Gel, Pulsed-Field ; Gene Expression Regulation, Viral ; Hepatitis B virus/genetics ; Hepatitis B virus/metabolism ; Hepatitis C/metabolism ; Hepatitis C/pathology ; Hepatitis C/virology ; Hepatocytes/metabolism ; Hepatocytes/pathology ; Humans ; Immunoprecipitation ; Polymerase Chain Reaction ; RNA, Viral/genetics ; Ribonucleotide Reductases/biosynthesis ; Ribonucleotide Reductases/genetics ; Virus Activation/genetics
Chemical Substances	RNA, Viral ; Ribonucleotide Reductases (EC 1.17.4.-) ; ribonucleotide reductase R2 subunit (EC 1.17.4.-)
Language	English
Publishing date	2015-10
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	605953-3
ISSN	1600-0641 ; 0168-8278
ISSN (online)	1600-0641
ISSN	0168-8278
DOI	10.1016/j.jhep.2015.05.017
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Article: Mesoscale simulations of curvature-inducing protein partitioning on lipid bilayer membranes in the presence of mean curvature fields.

Liu, Jin / Tourdot, Richard / Ramanan, Vyas / Agrawal, Neeraj J / Radhakrishanan, Ravi

Molecular physics

2012 Volume 110, Issue 11-12, Page(s) 1127–1137

Abstract: The membrane-surface migration of curvature-inducing proteins in response to membrane curvature gradients has been investigated using Monte Carlo simulations of a curvilinear membrane model based on the Helfrich Hamiltonian. Consistent with theoretical ... ...

Abstract	The membrane-surface migration of curvature-inducing proteins in response to membrane curvature gradients has been investigated using Monte Carlo simulations of a curvilinear membrane model based on the Helfrich Hamiltonian. Consistent with theoretical and experimental data, we find the proteins that generate curvature can also sense the background membrane curvature, wherein they preferentially partition to the high curvature regions. The partitioning strength depends linearly on local membrane curvature and the slope (or the coupling constant) of the partitioning probability versus mean curvature depends on the membrane bending rigidity and instantaneous curvature field caused by different proteins. Our simulation study allows us to quantitatively characterize and identify the important factors affecting the coupling constant (slope), which may be difficult to determine in experiments. Furthermore, the membrane model is used to study budding of vesicles where it is found that in order to stabilize a mature vesicle with a stable 'neck-region' (or stable membrane overhangs), the area (extent) of the intrinsic curvature region needs to exceed a threshold-critical value. The migration and partitioning of curvature-inducing proteins in a budding vesicle with a stable neck (with a characteristic negative value of the Gaussian curvature) is investigated.
Language	English
Publishing date	2012-03-01
Publishing country	England
Document type	Journal Article
ZDB-ID	1491083-4
ISSN	1362-3028 ; 0026-8976
ISSN (online)	1362-3028
ISSN	0026-8976
DOI	10.1080/00268976.2012.664661
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Article ; Online: A robust cell culture system supporting the complete life cycle of hepatitis B virus.

Michailidis, Eleftherios / Pabon, Jonathan / Xiang, Kuanhui / Park, Paul / Ramanan, Vyas / Hoffmann, Hans-Heinrich / Schneider, William M / Bhatia, Sangeeta N / de Jong, Ype P / Shlomai, Amir / Rice, Charles M

Scientific reports

2017 Volume 7, Issue 1, Page(s) 16616

Abstract: The discovery of sodium taurocholate cotransporting polypeptide (NTCP) as the hepatitis B virus (HBV) receptor enabled researchers to create hepatoma cell lines susceptible to HBV infection. Infection in current systems, however, is inefficient and virus ...

Abstract	The discovery of sodium taurocholate cotransporting polypeptide (NTCP) as the hepatitis B virus (HBV) receptor enabled researchers to create hepatoma cell lines susceptible to HBV infection. Infection in current systems, however, is inefficient and virus fails to spread. Infection efficiency is enhanced by treating cells with polyethylene glycol 8000 (PEG) during infection. However, this alone does not promote virus spread. Here we show that maintaining PEG in culture medium increases the rate of infection by at least one order of magnitude, and, most importantly, promotes virus spread. To demonstrate the utility of this system, we show that two interferon-stimulated genes (ISGs), ISG20 and tetherin, restrict HBV spread in NTCP-expressing hepatoma cells. Thus, this protocol can be easily applied to existing cell culture systems to study the complete HBV life cycle, including virus spread.
MeSH term(s)	Analysis of Variance ; Cell Culture Techniques ; Cell Line ; Coculture Techniques ; Fluorescent Antibody Technique ; Hep G2 Cells ; Hepatitis B/virology ; Hepatitis B virus/metabolism ; Hepatitis B virus/physiology ; Humans ; In Vitro Techniques ; Virus Replication
Language	English
Publishing date	2017-11-30
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-017-16882-5
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Article: Systems biology and physical biology of clathrin-mediated endocytosis

Ramanan, Vyas / Agrawal, Neeraj J / Liu, Jin / Engles, Sean / Toy, Randall / Radhakrishnan, Ravi

Integrative biology. 2011 Aug. 2, v. 3, no. 8

2011

Abstract: In this review, we describe the application of experimental data and modeling of intracellular endocytic trafficking mechanisms with a focus on the process of clathrin-mediated endocytosis. A detailed parts-list for the protein–protein interactions in ... ...

Abstract	In this review, we describe the application of experimental data and modeling of intracellular endocytic trafficking mechanisms with a focus on the process of clathrin-mediated endocytosis. A detailed parts-list for the protein–protein interactions in clathrin-mediated endocytosis has been available for some time. However, recent experimental, theoretical, and computational tools have proved to be critical in establishing a sequence of events, cooperative dynamics, and energetics of the intracellular process. On the experimental front, total internal reflection fluorescence microscopy, photo-activated localization microscopy, and spinning-disk confocal microscopy have focused on assembly and patterning of endocytic proteins at the membrane, while on the theory front, minimal theoretical models for clathrin nucleation, biophysical models for membrane curvature and bending elasticity, as well as methods from computational structural and systems biology, have proved insightful in describing membrane topologies, curvature mechanisms, and energetics.
Keywords	clathrin ; endocytosis ; fluorescence microscopy ; protein-protein interactions ; spinning disk confocal microscopy ; systems biology ; theoretical models
Language	English
Dates of publication	2011-0802
Size	p. 803-815.
Publishing place	The Royal Society of Chemistry
Document type	Article
ZDB-ID	2480063-6
ISSN	1757-9708 ; 1757-9694
ISSN (online)	1757-9708
ISSN	1757-9694
DOI	10.1039/c1ib00036e
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