Relevant bibliographies by topics / GlycoGag

Academic literature on the topic 'GlycoGag'

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Published: 11 March 2023

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Journal articles on the topic "GlycoGag"

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Fujisawa, Ryuichi, Frank J. McAtee, Cynthia Favara, Stanley F. Hayes, and John L. Portis. "N-Terminal Cleavage Fragment of Glycosylated Gag Is Incorporated into Murine Oncornavirus Particles." Journal of Virology 75, no. 22 (November 15, 2001): 11239–43. http://dx.doi.org/10.1128/jvi.75.22.11239-11243.2001.

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ABSTRACT Glycosylated Gag (Glycogag) is a transmembrane protein encoded by murine and feline oncornaviruses. While the protein is dispensible for virus replication, Glycogag-null mutants of a neurovirulent murine oncornavirus are slow to spread in vivo and exhibit a loss of pathogenicity. The function of this protein in the virus life cycle, however, is not understood. Glycogag is expressed at the plasma membrane of infected cells but has not been detected in virions. In the present study we have reexamined this issue and have found an N-terminal cleavage fragment of Glycogag which was pelleted by high-speed centrifugation and sedimented in sucrose density gradients at the same bouyant density as virus particles. Its association with virions was confirmed by velocity sedimentation through iodixanol, which effectively separated membrane microvesicles from virus particles. Furthermore, the apparent molecular weight of the virion-associated protein was different from that of the protein extracted from the plasma membrane, suggesting some level of specificity or selectivity of incorporation.
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Gonzalez-Enriquez, Gracia Viviana, Martha Escoto-Delgadillo, Eduardo Vazquez-Valls, and Blanca Miriam Torres-Mendoza. "SERINC as a Restriction Factor to Inhibit Viral Infectivity and the Interaction with HIV." Journal of Immunology Research 2017 (2017): 1–9. http://dx.doi.org/10.1155/2017/1548905.

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The serine incorporator 5 (SERINC5) is a recently discovered restriction factor that inhibits viral infectivity by preventing fusion. Retroviruses have developed strategies to counteract the action of SERINC5, such as the expression of proteins like negative regulatory factor (Nef), S2, and glycosylated Gag (glycoGag). These accessory proteins downregulate SERINC5 from the plasma membrane for subsequent degradation in the lysosomes. The observed variability in the action of SERINC5 suggests the participation of other elements like the envelope glycoprotein (Env) that modulates susceptibility of the virus towards SERINC5. The exact mechanism by which SERINC5 inhibits viral fusion has not yet been determined, although it has been proposed that it increases the sensitivity of the Env by exposing regions which are recognized by neutralizing antibodies. More studies are needed to understand the role of SERINC5 and to assess its utility as a therapeutic strategy.
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Firrito, Claudia, Cinzia Bertelli, Teresa Vanzo, Ajit Chande, and Massimo Pizzato. "SERINC5 as a New Restriction Factor for Human Immunodeficiency Virus and Murine Leukemia Virus." Annual Review of Virology 5, no. 1 (September 29, 2018): 323–40. http://dx.doi.org/10.1146/annurev-virology-092917-043308.

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SERINC genes encode for homologous multipass transmembrane proteins with unknown cellular function, despite being highly conserved across eukaryotes. Among the five SERINC genes found in humans, SERINC5 was shown to act as a powerful inhibitor of retroviruses. It is efficiently incorporated into virions and blocks the penetration of the viral core into target cells, by impairing the fusion process with a yet unclear mechanism. SERINC5 was also found to promote human immunodeficiency virus 1 (HIV-1) virion neutralization by antibodies, indicating a pleiotropic activity, which remains mostly unexplored. Counteracting factors have emerged independently in at least three retrovirus lineages, underscoring their fundamental importance during retrovirus evolution. Nef and S2 of primate and equine lentiviruses, and glycoGag of gammaretroviruses, act similarly by targeting SERINC5 to endosomes and excluding it from virions. Here, we discuss the features that distinguish SERINC5 from other known restriction factors, delineating a yet unique class of antiviral inhibitors.
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Cano-Ortiz, Lucía, Qinyong Gu, Patricia de Sousa-Pereira, Zeli Zhang, Catherina Chiapella, Augustin Penda Twizerimana, Chaohui Lin, et al. "Feline Leukemia Virus-B Envelope Together With its GlycoGag and Human Immunodeficiency Virus-1 Nef Mediate Resistance to Feline SERINC5." Journal of Molecular Biology 434, no. 6 (March 2022): 167421. http://dx.doi.org/10.1016/j.jmb.2021.167421.

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Diehl, William E., Mehmet H. Guney, Teresa Vanzo, Pyae P. Kyawe, Judith M. White, Massimo Pizzato, and Jeremy Luban. "Influence of Different Glycoproteins and of the Virion Core on SERINC5 Antiviral Activity." Viruses 13, no. 7 (June 30, 2021): 1279. http://dx.doi.org/10.3390/v13071279.

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Host plasma membrane protein SERINC5 is incorporated into budding retrovirus particles where it blocks subsequent entry into susceptible target cells. Three structurally unrelated proteins encoded by diverse retroviruses, human immunodeficiency virus type 1 (HIV-1) Nef, equine infectious anemia virus (EIAV) S2, and ecotropic murine leukemia virus (MLV) GlycoGag, disrupt SERINC5 antiviral activity by redirecting SERINC5 from the site of virion assembly on the plasma membrane to an internal RAB7+ endosomal compartment. Pseudotyping retroviruses with particular glycoproteins, e.g., vesicular stomatitis virus glycoprotein (VSV G), renders the infectivity of particles resistant to inhibition by virion-associated SERINC5. To better understand viral determinants for SERINC5-sensitivity, the effect of SERINC5 was assessed using HIV-1, MLV, and Mason-Pfizer monkey virus (M-PMV) virion cores, pseudotyped with glycoproteins from Arenavirus, Coronavirus, Filovirus, Rhabdovirus, Paramyxovirus, and Orthomyxovirus genera. SERINC5 restricted virions pseudotyped with glycoproteins from several retroviruses, an orthomyxovirus, a rhabdovirus, a paramyxovirus, and an arenavirus. Infectivity of particles pseudotyped with HIV-1, amphotropic-MLV (A-MLV), or influenza A virus (IAV) glycoproteins, was decreased by SERINC5, whether the core was provided by HIV-1, MLV, or M-PMV. In contrast, particles pseudotyped with glycoproteins from M-PMV, parainfluenza virus 5 (PIV5), or rabies virus (RABV) were sensitive to SERINC5, but only with particular retroviral cores. Resistance to SERINC5 did not correlate with reduced SERINC5 incorporation into particles, route of viral entry, or absolute infectivity of the pseudotyped virions. These findings indicate that some non-retroviruses may be sensitive to SERINC5 and that, in addition to the viral glycoprotein, the retroviral core influences sensitivity to SERINC5.
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Li, Minghua, Abdul A. Waheed, Jingyou Yu, Cong Zeng, Hui-Yu Chen, Yi-Min Zheng, Amin Feizpour, et al. "TIM-mediated inhibition of HIV-1 release is antagonized by Nef but potentiated by SERINC proteins." Proceedings of the National Academy of Sciences 116, no. 12 (March 6, 2019): 5705–14. http://dx.doi.org/10.1073/pnas.1819475116.

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The T cell Ig and mucin domain (TIM) proteins inhibit release of HIV-1 and other enveloped viruses by interacting with cell- and virion-associated phosphatidylserine (PS). Here, we show that the Nef proteins of HIV-1 and other lentiviruses antagonize TIM-mediated restriction. TIM-1 more potently inhibits the release of Nef-deficient relative to Nef-expressing HIV-1, and ectopic expression of Nef relieves restriction. HIV-1 Nef does not down-regulate the overall level of TIM-1 expression, but promotes its internalization from the plasma membrane and sequesters its expression in intracellular compartments. Notably, Nef mutants defective in modulating membrane protein endocytic trafficking are incapable of antagonizing TIM-mediated inhibition of HIV-1 release. Intriguingly, depletion of SERINC3 or SERINC5 proteins in human peripheral blood mononuclear cells (PBMCs) attenuates TIM-1 restriction of HIV-1 release, in particular that of Nef-deficient viruses. In contrast, coexpression of SERINC3 or SERINC5 increases the expression of TIM-1 on the plasma membrane and potentiates TIM-mediated inhibition of HIV-1 production. Pulse-chase metabolic labeling reveals that the half-life of TIM-1 is extended by SERINC5 from <2 to ∼6 hours, suggesting that SERINC5 stabilizes the expression of TIM-1. Consistent with a role for SERINC protein in potentiating TIM-1 restriction, we find that MLV glycoGag and EIAV S2 proteins, which, like Nef, antagonize SERINC-mediated diminishment of HIV-1 infectivity, also effectively counteract TIM-mediated inhibition of HIV-1 release. Collectively, our work reveals a role of Nef in antagonizing TIM-1 and highlights the complex interplay between Nef and HIV-1 restriction by TIMs and SERINCs.
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Chande, Ajit, Emilia Cristiana Cuccurullo, Annachiara Rosa, Serena Ziglio, Susan Carpenter, and Massimo Pizzato. "S2 from equine infectious anemia virus is an infectivity factor which counteracts the retroviral inhibitors SERINC5 and SERINC3." Proceedings of the National Academy of Sciences 113, no. 46 (November 1, 2016): 13197–202. http://dx.doi.org/10.1073/pnas.1612044113.

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The lentivirus equine infectious anemia virus (EIAV) encodes the small protein S2, a pathogenic determinant that is important for virus replication and disease progression in horses. No molecular function had been linked to this accessory protein. We report that S2 can replace the activity of Negative factor (Nef) in HIV-1 infectivity, being required to antagonize the inhibitory activity of Serine incorporator (SERINC) proteins on Nef-defective HIV-1. Like Nef, S2 excludes SERINC5 from virus particles and requires an ExxxLL motif predicted to recruit the clathrin adaptor, Adaptor protein 2 (AP2). Accordingly, functional endocytic machinery is essential for S2-mediated infectivity enhancement, and S2-mediated enhancement is impaired by inhibitors of clathrin-mediated endocytosis. In addition to retargeting SERINC5 to a late endosomal compartment, S2 promotes host factor degradation. Emphasizing the similarity with Nef, we show that S2 is myristoylated, and, as is compatible with a crucial role in posttranslational modification, its N-terminal glycine is required for anti-SERINC5 activity. EIAV-derived vectors devoid of S2 are less susceptible than HIV-1 to the inhibitory effect of both human and equine SERINC5. We then identified the envelope glycoprotein of EIAV as a determinant that also modulates retroviral susceptibility to SERINC5, indicating that EIAV has a bimodal ability to counteract the host factor. S2 shares no sequence homology with other retroviral factors known to counteract SERINC5. Like the primate lentivirus Nef and the gammaretrovirus glycoGag, the accessory protein from EIAV is an example of a retroviral virulence determinant that independently evolved SERINC5-antagonizing activity. SERINC5 therefore plays a critical role in the interaction of the host with diverse retrovirus pathogens.
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Ma, Yulong, Yanhui Cai, Doutong Yu, Yuting Qiao, Haiyun Guo, Zejun Gao, and Li Guo. "Astrocytic Glycogen Mobilization in Cerebral Ischemia/Reperfusion Injury." Neuroscience and Neurological Surgery 11, no. 3 (February 21, 2022): 01–05. http://dx.doi.org/10.31579/2578-8868/228.

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Glycogen is an important energy reserve in the brain and can be rapidly degraded to maintain metabolic homeostasis during cerebral blood vessel occlusion. Recent studies have pointed out the alterations in glycogen and its underlying mechanism during reperfusion after ischemic stroke. In addition, glycogen metabolism may work as a promising therapeutic target to relieve reperfusion injury. Here, we summarize the progress of glycogen metabolism during reperfusion injury and its corresponding application in patients suffering from ischemic stroke.
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Nanware, Sanjay Shamrao, Habib Mohammed Hasmi, and Dhanraj Balbhim Bhure. "Glycogen Content in Moniezia Expansa and its Host Intestine." Indian Journal of Applied Research 4, no. 5 (October 1, 2011): 651–52. http://dx.doi.org/10.15373/2249555x/may2014/206.

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Kanungo, Shibani, Kimberly Wells, Taylor Tribett, and Areeg El-Gharbawy. "Glycogen metabolism and glycogen storage disorders." Annals of Translational Medicine 6, no. 24 (December 2018): 474. http://dx.doi.org/10.21037/atm.2018.10.59.

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Dissertations / Theses on the topic "GlycoGag"

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Bertelli, Cinzia. "Antiviral activity and retroviral counteraction of SERINC genes." Doctoral thesis, Università degli studi di Trento, 2021. http://hdl.handle.net/11572/321392.

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SERINC5 is a restriction factor for retroviruses, antagonized by Nef of primate lentiviruses, by glycoGag of Moloney Murine Leukaemia Virus (MoMLV) and by S2 of Equine Infectious Anaemia virus (EIAV). In addition, SERINC5 sensitizes HIV-1 to neutralizing antibodies (nAbs) targeting the MPER in gp41. However, since the identification of SERINC5 as an inhibitor of retrovirus infectivity, many features of the host factor await clarification, notably the molecular mechanisms of restriction and viral counteraction. Furthermore, SERINC5 cellular role beyond restriction is still obscure. This thesis explores multiple aspects of the mutual antagonism governing the SERINC5 interplay with retroviruses. We first describe a contribution towards the determination of the structure of SERINC5 and the identification of the determinants crucial for antiviral activity, virus sensitization to neutralization and counteraction by retroviruses. By performing a structure-based mutagenesis screening, we identified SERINC5 ECL3, ECL5 and the interface between subdomains as regions essential for inhibition of HIV-1 infectivity and virus sensitization to 4E10 and 2F5 nAbs. The simultaneous impairment of both SERINC5 antiviral effects indicates that they are mechanistically related and support the hypothesis of a SERINC5-mediated impairment of the envelope glycoproteins. We included a comparative analysis of the antiviral activity of human SERINC paralogs and their sensitivity to retroviral counteraction. It has been previously established that SERINC3 inhibits HIV-1 infectivity less potently than SERINC5, while SERINC2 has no antiviral effects. We report here that similarly to SERINC3, SERINC1 is endowed with a modest antiviral activity; in contrast, SERINC4 severely inhibits HIV-1 infectivity, despite being poorly expressed. Irrespectively of their antiretroviral potency, all SERINC proteins are incorporated into virus particles. Interestingly, we observed that virion-associated SERINC2 is specifically cleaved by the viral protease, but proteolysis does not explain the lack of antiretroviral effects. Furthermore, SERINC5 and SERINC2 have different glycomic profiles, but diverse post-translational modification is irrelevant for their opposite activity against HIV-1. In addition, we reported that human SERINCs are differently targeted by retroviral counteracting factors, with SERINC5 being the paralog most efficiently downregulated, while SERINC1 being completely resistant. A cysteines cluster within ICL4 emerged as the major determinant of SERINC5 responsiveness to different nef alleles, while it proved irrelevant for internalization by MoMLV glycoGag and EIAV S2, indicating that diverse retroviral counteractors likely target the host factor differently. Though SERINC5 ICL4 harbours multiple motifs governing SERINC5 sensitivity to antagonization, insertion of this loop within SERINC2 was not enough to transfer susceptibility to Nef activity, suggesting that the overall conformation of the protein is essential for downregulation by Nef. Importantly, the cysteine stretch within ICL4 is palmitoylated, suggesting that this modification may be important for counteraction by the lentiviral factor. SERINC5 and CD4 downregulation by Nef are functionally related, as they both require AP-2 mediated endocytosis. However, regions in Nef selectively governing SERINC5 internalization are unknown. We reported here that Phe90 within Nef αA-helix genetically uncouples the activities on SERINC5 and CD4, being selectively involved in SERINC5 downregulation. In parallel, we explored SERINC5 antagonization by different glycoGag alleles and observed that the ability to target the host factor is not conserved across divergent γ-retroviruses. Finally, we observed that HIV-1 may evade SERINC5 restriction by direct cell-to-cell infection, suggesting that the host factor may have a broader role in retroviral spreading, requiring the evolution and the conservation of active viral counteraction. To this end, we preliminary investigated a positive contribution of SERINC5 to intracellular signalling.
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Syed, Noor Afshan. "Regulation of glycogen synthase and glycogen phosphorylase by insulin in HepG2 cells." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2001. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp05/NQ63926.pdf.

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Martin, Jennifer Louise. "Molecular interactions involving glycogen phosphorylase." Thesis, University of Oxford, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.253306.

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Ghosh, Paritosh. "De Novo Glycogen Biosynthesis by a Glycogen Primer Complex in the Obliquely Striated Skeletal Muscle of Ascaris suum." Thesis, North Texas State University, 1987. https://digital.library.unt.edu/ark:/67531/metadc935639/.

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During the purification of the enzyme glycogen synthase from the muscle of the nematode Ascaris suum, approximately 70% of the glycogen synthase activity can be separated from the bulk of cellular glycogen by centrifugation for 60 min at 105,000 x . The glycogen synthase in the supernatant fraction has an Mr of 1.2 x 106 as determined by Sepharose 4B gel filtration chromatography. The glycogen synthase in this high molecular weight complex (glycogen primer complex) can be further purified by ConA-Sepharose affinity chromatography; the enzyme activity was eluted with 100 .mM a-methylmannoside. The glycogen synthase in glycogen'primer complex is predominately in the glucose 6-phosphatedependent form. The glycogen primer complex can catalyze the transfer of glucosyl units from UDP-glucose to an endogenous acceptor in the absence of exogenous glycogen. Analysis by SDS-PAGE showed three proteins (Mr 140,000, 78,000 and 34,000) and a carbohydrate polymer. The carbohydrate polymer can be partially digested with a-amylase. The glycogen primer complex was further digested by acid hydrolysis, and upon descending paper chromatography analysis, eight different carbohydrates were isolated, two of which were tentatively identified as glucose and sialic acid. The [14 C]-autoradiograph showed that in vitro synthesis of a glycogen-like polysaccharide occurred on this carbohydrate polymer. Polyclonal antibodies have been made to the glycogen primer complex, and Western Blot analysis indicated that all three proteins of the glycogen primer complex were antigenic. Collectively, the data indicate that a glycogen-like polysaccharide is synthesized from a carbohydrate-associated protein primer in the muscle of this worm.
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Karis, Nils David. "Design and Synthesis of 1,3-Disubstitiuted-2-Pyridones as a New Class of Glycogen Phosphorylase Inhibitors." Thesis, Griffith University, 2009. http://hdl.handle.net/10072/365791.

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Glycogen Phosphorylase (GP) is the regulatory enzyme that catalyses the first step in glycogen degradation and is a potential enzyme target for therapeutic intervention in the treatment of diabetes. The 16 amino acid C-terminal sequence of human Gl is the only known targeting subunit that binds to GPa. Blocking the interactions between Gl and GPa should reduce high blood glucose levels in a diabetic person. A segment of the 16 amino acid segment was chosen for a small molecule peptidomimetric approach, and de nova design from this segment identified the pyridone ring as apotential scaffold. This thesis reports the design and synthesis of 1.3-disubstituted pyridones as new class of GPa inhibitors.
Thesis (PhD Doctorate)
Doctor of Philosophy (PhD)
Eskitis Institute for Cell and Molecular Therapies
Science, Environment, Engineering and Technology
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Street, Ian Philip. "Protein - carbohydrate interactions in glycogen phosphorylase." Thesis, University of British Columbia, 1985. http://hdl.handle.net/2429/25049.

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It has long been observed that some organo-fluorine compounds exhibit enhanced biological activity over their non-fluorinated precursors, however reasons for these unusual properties still remain poorly understood. An explanation which has been widely used relates to the ability of the C-F fragment of the analog to participate in hydrogen-bonding interactions with its protein receptor. For this reason, fluorinated carbohydrates have been used as hydrogen-bonding probes with a number of proteins. Thus there exists a need for a systematic investigation into the hydrogen-bonding ability of the C-F fragment, and the enzyme glycogen phosphorylase provides an excellent subject for such a study. The glucopyranose binding site in the inactive (T-state) conformation of the enzyme has been well characterised and high resolution crystallographic data is available. Thus by comparison of kinetic and crystallographic data for the natural effectors and the fluorinated substrate analogs considerable insight into the hydrogen bonding ability of the C-F fragment and the nature of carbohydrate-protein interactions should be gained. Little is known about the active (R-state) conformation of the enzyme and about the T-state to R-state transition. Use of fluorinated analogs of the enzymes natural substrate, glucose-l-phosphate, could also shed light on these questions. With these aims in mind, all of the isomeric mono-fluorinated derivatives of glucose and glucose-l-phosphate have been synthesised. Some deoxy and difluorinated analogs of glucose and mannose have also been prepared. Kinetic results obtained using the analogs of glucose indicate that the 3 and 6 positions of the sugar participate in strong hydrogen-bonding interactions with the protein while the other positions are only involved in relatively weak interactions. These results agree well with recent X-ray crystallographic data. None of the analogs of glucose-l-phosphate exhibited any substrate activity. The 2-deoxyfluoro analog had a similar affinity to glucose-1-phosphate and therefore probably binds in the same mode. The lack of substrate activity in this case can be explained by the destabi1isation of the putative oxo-carbonium ion intermediate at C(l), by the adjacent fluorine substituent. The other analogs of glucose-l-phosphate showed lower affinity for the enzyme. The similar inhibition constants obtained for these compounds suggested a binding mode in which the glucopyranose ring contributes little to the overall binding energy. This has led to the proposal of a molecular mechanism for the T-state to R-state transition.
Science, Faculty of
Chemistry, Department of
Graduate
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Stambolic, Vuk. "Regulation of glycogen synthase kinase-3." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/tape16/PQDD_0003/NQ27730.pdf.

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Fraser, Bernadine Heather. "Glycogen and glucose metabolism in cardioprotection." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk2/tape17/PQDD_0028/NQ34764.pdf.

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Henning, Sarah Louise. "Myocardial glycogen metabolism and its regulation." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2001. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/NQ61107.pdf.

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Barford, D. "Crystallographic studies on glycogen phosphorylase b." Thesis, University of Oxford, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.233473.

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Books on the topic "GlycoGag"

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DiNuzzo, Mauro, and Arne Schousboe, eds. Brain Glycogen Metabolism. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-27480-1.

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Savage, Madelyn. The Avian Glycogen body. Salford: University of Salford, 1986.

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R, Acharya K., ed. Glycogen phosphorylase b: Description of the protein structure. Singapore: World Scientific, 1991.

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Martinez, Ana, Ana Castro, and Miguel Medina, eds. Glycogen Synthase Kinase 3 (GSK-3) and Its Inhibitors. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2006. http://dx.doi.org/10.1002/0470052171.

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Patel, Mona D. Abnormalities in glycogen storage and metabolism in patients with liver-related diseases. Roehampton: University of Surrey Roehampton, 2002.

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library, Wiley online, ed. Glycogen synthase kinase 3 (GSK-3) and its inhibitors: Drug discovery and development. Hoboken, N.J: Wiley-Interscience, 2006.

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Seal, Leonard Henry. Studies on glycogen in the nervous systems of Haemopis Sanguisuga and Planorbis Corneus. Salford: University of Salford, 1986.

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Clement, Nichole S. The effects of the neurotoxin tetrodotoxin on glycogen content in rat soleus muscles. Sudbury, Ont: Laurentian University, 1993.

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Wender, Regina. Astrocytic glycogen influences axon function and survival during glucose deprivation in central white matter. [Baltimore, MD]: Society for Neuroscience, 2000.

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1863-1902, Johnston Wyatt, ed. The medico-legal significance of the presence of sugar and glycogen in the liver post mortem. [S.l: s.n., 1985.

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Book chapters on the topic "GlycoGag"

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Peck, Stewart B., Carol C. Mapes, Netta Dorchin, John B. Heppner, Eileen A. Buss, Gustavo Moya-Raygoza, Marjorie A. Hoy, et al. "Glycogen." In Encyclopedia of Entomology, 1630. Dordrecht: Springer Netherlands, 2008. http://dx.doi.org/10.1007/978-1-4020-6359-6_1122.

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Pavelka, Margit, and Jürgen Roth. "Glycogen." In Functional Ultrastructure, 140. Vienna: Springer Vienna, 2010. http://dx.doi.org/10.1007/978-3-211-99390-3_73.

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Wagner, Peter, Frank C. Mooren, Hidde J. Haisma, Stephen H. Day, Alun G. Williams, Julius Bogomolovas, Henk Granzier, et al. "Glycogen." In Encyclopedia of Exercise Medicine in Health and Disease, 374. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-540-29807-6_2449.

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Bährle-Rapp, Marina. "Glycogen." In Springer Lexikon Kosmetik und Körperpflege, 230. Berlin, Heidelberg: Springer Berlin Heidelberg, 2007. http://dx.doi.org/10.1007/978-3-540-71095-0_4411.

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Wagner, Peter, Frank C. Mooren, Hidde J. Haisma, Stephen H. Day, Alun G. Williams, Julius Bogomolovas, Henk Granzier, et al. "Glycogen Depletion." In Encyclopedia of Exercise Medicine in Health and Disease, 375. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-540-29807-6_2447.

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Wagner, Peter, Frank C. Mooren, Hidde J. Haisma, Stephen H. Day, Alun G. Williams, Julius Bogomolovas, Henk Granzier, et al. "Glycogen Synthase." In Encyclopedia of Exercise Medicine in Health and Disease, 375. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-540-29807-6_2448.

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Meigs, Thomas E., Alex Lyakhovich, Hoon Shim, Ching-Kang Chen, Denis J. Dupré, Terence E. Hébert, Joe B. Blumer, et al. "Glycogen Synthase." In Encyclopedia of Signaling Molecules, 799. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_100544.

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Wagner, Peter, Frank C. Mooren, Hidde J. Haisma, Stephen H. Day, Alun G. Williams, Julius Bogomolovas, Henk Granzier, et al. "Glycogen Loading." In Encyclopedia of Exercise Medicine in Health and Disease, 375. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-540-29807-6_4246.

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Cavaglieri, Cláudia Regina, Carlos Alberto da Silva, and Celene Fernandes Bernardes. "Glycogen Measurement." In Basic Protocols in Foods and Nutrition, 129–43. New York, NY: Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-2345-9_9.

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Van Hove, Johan L. K. "Glycogen Storage Diseases." In Nutrition Management of Inherited Metabolic Diseases, 295–305. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-14621-8_26.

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Conference papers on the topic "GlycoGag"

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Tretyakova, A. M., and N. A. Vakhnina. "Application of the phenol-sulfuric acid method for the determination of glycogen in skeletal muscles and liver of rats." In VIII Vserossijskaja konferencija s mezhdunarodnym uchastiem «Mediko-fiziologicheskie problemy jekologii cheloveka». Publishing center of Ulyanovsk State University, 2021. http://dx.doi.org/10.34014/mpphe.2021-189-191.

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The possibility of using the phenol-sulfuric acid method for the determination of total glycogen, its acid-soluble and acid-insoluble fractions in the liver and skeletal muscles of rats was studied. It was found that the use of a precipitant in the isolation of total glycogen and its fractions increases the yield of the investigated substances. Key words: phenol-sulfate method, rats, liver, muscles, total glycogen, acid-soluble glycogen, acid-insoluble glycogen.
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Alvarenga, F. A. P., I. J. Lean, and P. McGilchrist. "Impact of dietary potassium levels on muscle glycogen concentration." In 6th EAAP International Symposium on Energy and Protein Metabolism and Nutrition. The Netherlands: Wageningen Academic Publishers, 2019. http://dx.doi.org/10.3920/978-90-8686-891-9_117.

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Schumacher, A., C. Metzendorf, S. Ribback, and F. Dombrowski. "Investigation of the glycogen-associated proteome via proximity-biotinylation." In 36. Jahrestagung der Deutschen Arbeitsgemeinschaft zum Studium der Leber. Georg Thieme Verlag KG, 2020. http://dx.doi.org/10.1055/s-0039-3402193.

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"Expression of glycogen synthase kinase 3β in nephrotic syndrome." In Bioinformatics of Genome Regulation and Structure/ Systems Biology. institute of cytology and genetics siberian branch of the russian academy of science, Novosibirsk State University, 2020. http://dx.doi.org/10.18699/bgrs/sb-2020-343.

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Parker, K. J., T. A. Tuthill, and R. B. Baggs. "Ultrasound Attenuation of Glycogen: In Vitro and In Vivo Results." In IEEE 1987 Ultrasonics Symposium. IEEE, 1987. http://dx.doi.org/10.1109/ultsym.1987.199107.

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Altemus, Megan Ann, Joel A. Yates, ZhiFen Wu, LiWei Bao, and Sofia D. Merajver. "Abstract 1446: Glycogen accumulation in aggressive breast cancers under hypoxia." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-1446.

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Wieloch, Judith, Mandy Lemme, Janin Henkel, and GerhardP Püschel. "Direct impact of fructose on hepatic lipid and glycogen metabolism." In 38. Jahrestagung der Deutsche Arbeitsgemeinschaft zum Studium der Leber. Georg Thieme Verlag, 2022. http://dx.doi.org/10.1055/s-0041-1740655.

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Altemus, Megan, Joel Yates, ZhiFen Wu, LiWei Bao, and Sofia Merajver. "Abstract 433: Glycogen accumulation in aggressive breast cancers during hypoxic exposure." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-433.

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Álvarez-Santos, Mayra D., Marisol Alvarez-González, Elizabeth Eslava-De Jesus, Yazmín Pérez-Del Valle, Javier R. Ambrosio, Olivia Reynoso-Ducoing, Patricia Ramos-Ramirez, and Blanca Margarita Bazan-Perkins. "Role of protein phosphatase 1 glycogen-associated regulatory subunit in asthma." In ERS International Congress 2018 abstracts. European Respiratory Society, 2018. http://dx.doi.org/10.1183/13993003.congress-2018.pa974.

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Melnic, Maria, and Olesea Gliga. "About chemical composition of the nematode Ditylenchus Dipsaci." In Xth International Conference of Zoologists. Institute of Zoology, Republic of Moldova, 2021. http://dx.doi.org/10.53937/icz10.2021.40.

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In the article are presented data on the quantitative variations of bound amino acids in the tissue protein of the nematode Ditylenchus dipsaci Kuhn, 1857, parasite of Allium sativum crops. It was revealed that the largest share is: glutamic acid + glutamine -21.0% of the total amount, aspartic acid + asparagine - 11.0%, glycine -12.6% and alanine -10.5. In smaller quantities was evidenced: tryptophan (0.8%), histidine (0.8%) and methionine (0.1%). According to the distribution by groups, it was determined that non-essential amino acids have the highest percentage of the total -31.9%, followed by immunoactive amino acids - 25.7% and glycogen - 21.5%.
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Reports on the topic "GlycoGag"

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Wolgamott, D. Storage and use of glycogen by juvenile Carcinonemertes errans. Portland State University Library, January 2000. http://dx.doi.org/10.15760/etd.2966.

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Uni, Zehava, and Peter Ferket. Enhancement of development of broilers and poults by in ovo feeding. United States Department of Agriculture, May 2006. http://dx.doi.org/10.32747/2006.7695878.bard.

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The specific objectives of this research were the study of the physical and nutritional properties of the In Ovo Feeding (IOF) solution (i.e. theosmostic properties and the carbohydrate: protein ratio composition). Then, using the optimal solution for determining its effect on hatchability, early nutritional status and intestinal development of broilers and turkey during the last quarter of incubation through to 7 days post-hatch (i.e. pre-post hatch period) by using molecular, biochemical and histological tools. The objective for the last research phase was the determination of the effect of in ovo feeding on growth performance and economically valuable production traits of broiler and turkey flocks reared under practical commercial conditions. The few days before- and- after hatch is a critical period for the development and survival of commercial broilers and turkeys. During this period chicks make the metabolic and physiological transition from egg nutriture (i.e. yolk) to exogenous feed. Late-term embryos and hatchlings may suffer a low glycogen status, especially when oxygen availability to the embryo is limited by low egg conductance or poor incubator ventilation. Much of the glycogen reserve in the late-term chicken embryo is utilized for hatching. Subsequently, the chick must rebuild that glycogen reserve by gluconeogenesis from body protein (mostly from the breast muscle) to support post-hatch thermoregulation and survival until the chicks are able to consume and utilize dietary nutrients. Immediately post-hatch, the chick draws from its limited body reserves and undergoes rapid physical and functional development of the gastrointestinal tract (GIT) in order to digest feed and assimilate nutrients. Because the intestine is the nutrient primary supply organ, the sooner it achieves this functional capacity, the sooner the young bird can utilize dietary nutrients and efficiently grow at its genetic potential and resist infectious and metabolic disease. Feeding the embryo when they consume the amniotic fluid (IOF idea and method) showed accelerated enteric development and elevated capacity to digest nutrients. By injecting a feeding solution into the embryonic amnion, the embryo naturally consume supplemental nutrients orally before hatching. This stimulates intestinal development to start earlier as was exhibited by elevated gene expression of several functional genes (brush border enzymes an transporters , elvated surface area, elevated mucin production . Moreover, supplying supplemental nutrients at a critical developmental stage by this in ovo feeding technology improves the hatchling’s nutritional status. In comparison to controls, administration of 1 ml of in ovo feeding solution, containing dextrin, maltose, sucrose and amino acids, into the amnion of the broiler embryo increased dramatically total liver glycogen in broilers and in turkeys in the pre-hatch period. In addition, an elevated relative breast muscle size (% of broiler BW) was observed in IOF chicks to be 6.5% greater at hatch and 7 days post-hatch in comparison to controls. Experiment have shown that IOF broilers and turkeys increased hatchling weights by 3% to 7% (P<0.05) over non injected controls. These responses depend upon the strain, the breeder hen age and in ovo feed composition. The weight advantage observed during the first week after hatch was found to be sustained at least through 35 days of age. Currently, research is done in order to adopt the knowledge for commercial practice.
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Osman, Mohamed, Portia Allen, Nimer Mehyar, Gerd Bobe, Johann Coetzee, and Donald C. Beitz. Acute Effects of Postpartal Subcutaneous Injection of Glucagon and/or Oral Administration of Glycerol on Blood Metabolites and Hormones and Liver Lipids and Glycogen of Holstein Dairy Cows Induced with Fatty Liver Disease. Ames (Iowa): Iowa State University, January 2007. http://dx.doi.org/10.31274/ans_air-180814-754.

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