| 1. |
- Alm, Kersti, et al.
(författare)
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Cells and polyamines do it cyclically
- 2009
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Ingår i: Essays in Biochemistry. - : Portland Press Ltd.. - 0071-1365 .- 1744-1358. ; 46, s. 63-76
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Tidskriftsartikel (refereegranskat)abstract
- Cell-cycle progression is a one-way journey where the cell grows in size to be able to divide into two equally sized daughter cells. The cell cycle is divided into distinct consecutive phases defined as G(1) (first gap), S (synthesis), G(2) (second gap) and M (mitosis). A non-proliferating cell, which has retained the ability to enter the cell cycle when it receives appropriate signals, is in G(0) phase, and cycling cells that do not receive proper signals leave the cell cycle from G(1) into G(0). One of the major events of the cell cycle is the duplication of DNA during S-phase. A group of molecules that are important for proper cell-cycle progression is the polyamines. Polyamine biosynthesis occurs cyclically during the cell cycle with peaks in activity in conjunction with the G(1)/S transition and at the end of S-phase and during G(2)-phase. The negative regulator of polyamine biosynthesis, antizyme, shows an inverse activity compared with the polyamine biosynthetic activity. The levels of the polyamines, putrescine, spermidine and spermine, double during the cell cycle and show a certain degree of cyclic variation in accordance with the biosynthetic activity. When cells in G(0)/G(1) -phase are seeded in the presence of compounds that prevent the cell-cycle-related increases in the polyamine pools, the S-phase of the first cell cycle is prolonged, whereas the other phases are initially unaffected. The results point to an important role for polyamines with regard to the ability of the cell to attain optimal rates of DNA replication.
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| 2. |
- Ashrafzadeh, Parham, et al.
(författare)
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Methods applicable to membrane nanodomain studies?
- 2015
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Ingår i: Essays in Biochemistry. - London : Portland Press. - 0071-1365 .- 1744-1358. ; 57, s. 57-68
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Forskningsöversikt (refereegranskat)abstract
- Membrane nanodomains are dynamic liquid entities surrounded by another type of dynamic liquid. Diffusion can take place inside, around and in and out of the domains, and membrane components therefore continuously shift between domains and their surroundings. In the plasma membrane, there is the further complexity of links between membrane lipids and proteins both to the extracellular matrix and to intracellular proteins such as actin filaments. In addition, new membrane components are continuously delivered and old ones removed. On top of this, cells move. Taking all of this into account imposes great methodological challenges, and in the present chapter we discuss some methods that are currently used for membrane nanodomain studies, what information they can provide and their weaknesses.
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| 3. |
- Baar, K, et al.
(författare)
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Resistance exercise, muscle loading/unloading and the control of muscle mass
- 2006
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Ingår i: Essays in biochemistry. - : Portland Press Ltd.. - 0071-1365 .- 1744-1358. ; 42, s. 61-74
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Tidskriftsartikel (refereegranskat)abstract
- Muscle mass is determined by the difference between the rate of protein synthesis and degradation. If synthesis is greater than degradation, muscle mass will increase (hypertrophy) and when the reverse is true muscle mass will decrease (atrophy). Following resistance exercise/increased loading there is a transient increase in protein synthesis within muscle. This change in protein synthesis correlates with an increase in the activity of protein kinase B/Akt and mTOR (mammalian target of rapamycin). mTOR increases protein synthesis by increasing translation initiation and by inducing ribosomal biogenesis. By contrast, unloading or inactivity results in a decrease in protein synthesis and a significant increase in muscle protein breakdown. The decrease in synthesis is due in part to the inactivation of mTOR and therefore a decrease in translation initiation, but also to a decrease in the rate of translation elongation. The increase in degradation is the result of a co-ordinated response of the calpains, lysosomal proteases and the ATP-dependent ubiquitin-proteosome. Caspase 3 and the calpains act upstream of the ubiquitin–proteosome system to assist in the complete breakdown of the myofibrillar proteins. Two muscle specific E3 ubiquitin ligases, MuRF1 and MAFbx/atrogen-1, have been identified as key regulators of muscle atrophy. In this chapter, these pathways and how the balance between anabolism and catabolism is affected by loading and unloading will be discussed.
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| 4. |
- Falkenberg, Maria, 1968
(författare)
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Mitochondrial DNA replication in mammalian cells: overview of the pathway
- 2018
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Ingår i: Essays in Biochemistry. - : Portland Press Ltd.. - 0071-1365 .- 1744-1358. ; 62:3, s. 287-296
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Forskningsöversikt (refereegranskat)abstract
- Mammalian mitochondria contain multiple copies of a circular, double-stranded DNA genome and a dedicated DNA replication machinery is required for its maintenance. Many disease-causing mutations affect mitochondrial replication factors and a detailed understanding of the replication process may help to explain the pathogenic mechanisms underlying a number of mitochondrial diseases. We here give a brief overview of DNA replication in mammalian mitochondria, describing our current understanding of this process and some unanswered questions remaining.
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| 5. |
- Frayn, KN, et al.
(författare)
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Fatty acid metabolism in adipose tissue, muscle and liver in health and disease
- 2006
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Ingår i: Essays in biochemistry. - : Portland Press Ltd.. - 0071-1365 .- 1744-1358. ; 42, s. 89-103
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Tidskriftsartikel (refereegranskat)abstract
- Fat is the largest energy reserve in mammals. Most tissues are involved in fatty acid metabolism, but three are quantitatively more important than others: adipose tissue, skeletal muscle and liver. Each of these tissues has a store of triacylglycerol that can be hydrolysed (mobilized) in a regulated way to release fatty acids. In the case of adipose tissue, these fatty acids may be released into the circulation for delivery to other tissues, whereas in muscle they are a substrate for oxidation and in liver they are a substrate for re-esterification within the endoplasmic reticulum to make triacylglycerol that will be secreted as very-low-density lipoprotein. These pathways are regulated, most clearly in the case of adipose tissue. Adipose tissue fat storage is stimulated, and fat mobilization suppressed, by insulin, leading to a drive to store energy in the fed state. Muscle fatty acid metabolism is more sensitive to physical activity, during which fatty acid utilization from extracellular and intracellular sources may increase enormously. The uptake of fat by the liver seems to depend mainly upon delivery in the plasma, but the secretion of very-low-density lipoprotein triacylglycerol is suppressed by insulin. There is clearly cooperation amongst the tissues, so that, for instance, adipose tissue fat mobilization increases to meet the demands of skeletal muscle during exercise. When triacylglycerol accumulates excessively in skeletal muscle and liver, sometimes called ectopic fat deposition, then the condition of insulin resistance arises. This may reflect a lack of exercise and an excess of fat intake.
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| 6. |
- Hajji, N, et al.
(författare)
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Epigenetic regulation of cell life and death decisions and deregulation in cancer
- 2010
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Ingår i: Essays in biochemistry. - : Portland Press Ltd.. - 1744-1358 .- 0071-1365. ; 48:1, s. 121-146
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Tidskriftsartikel (refereegranskat)abstract
- For every cell, there is a time to live and a time to die. It is apparent that cell life and death decisions are taken by individual cells based on their interpretation of physiological or non-physiological stimuli, or their own self-assessment of internal damage or changes in their environment. Apoptosis or programmed cell death is a key regulator of physiological growth control and regulation of tissue homoeostasis. One of the most important advances in cancer research in recent years is the recognition that cell death, mostly by apoptosis, is crucially involved in the regulation of tumour formation and also critically determines treatment response. The initiation and progression of cancer, traditionally seen as a genetic disease, is now realized to involve epigenetic abnormalities along with genetic alterations. The study of epigenetic mechanisms in cancer, such as DNA methylation, histone modifications and microRNA expression, has revealed a plethora of events that contribute to the neoplastic phenotype through stable changes in the expression of genes critical to cell death pathways. A better understanding of the epigenetic molecular events that regulate apoptosis, together with the reversible nature of epigenetic aberrations, should contribute to the emergence of the promising field of epigenetic therapy.
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| 7. |
- Hawley, JA, et al.
(författare)
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Signalling mechanisms in skeletal muscle: role in substrate selection and muscle adaptation
- 2006
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Ingår i: Essays in biochemistry. - : Portland Press Ltd.. - 0071-1365 .- 1744-1358. ; 42, s. 1-12
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Tidskriftsartikel (refereegranskat)abstract
- Exercise produces a multitude of time- and intensity-dependent physiological, biochemical and molecular changes within skeletal muscle. With the onset of contractile activity, cytosolic and mitochondrial [Ca2+] levels are rapidly increased and, depending on the relative intensity of the exercise, metabolite concentrations change (i.e. increases in [ADP] and [AMP], decreases in muscle creatine phosphate and glycogen). These contraction-induced metabolic disturbances activate several key kinases and phosphatases involved in signal transduction. Important among these are the calcium dependent signalling pathways that respond to elevated Ca2+ concentrations (including Ca2+/calmodulin-dependent kinase, Ca2+-dependent protein kinase C and the Ca2+/calmodulin-dependent phosphatase calcineurin), the 5′-adenosine monophosphate-activated protein kinase, several of the mitogen-activated protein kinases and protein kinase B/Akt. The role of these signal transducers in the regulation of carbohydrate and fat metabolism in response to increased contractile activity has been the focus of intense research efforts during the past decade.
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| 8. |
- Madhu, Priyanka, et al.
(författare)
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How viral proteins bind short linear motifs and intrinsically disordered domains
- 2022
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Ingår i: Essays in Biochemistry. - : Portland Press. - 0071-1365 .- 1744-1358. ; 66:7, s. 935-944
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Forskningsöversikt (refereegranskat)abstract
- Viruses are the obligate intracellular parasites that exploit the host cellular machinery to repli-cate their genome. During the viral life cycle viruses manipulate the host cell through inter-actions with host proteins. Many of these protein-protein interactions are mediated through the recognition of host globular domains by short linear motifs (SLiMs), or longer intrinsically disordered domains (IDD), in the disordered regions of viral proteins. However, viruses also employ their own globular domains for binding to SLiMs and IDDs present in host proteins or virus proteins. In this review, we focus on the different strategies adopted by viruses to utilize proteins or protein domains for binding to the disordered regions of human or/and viral ligands. With a set of examples, we describe viral domains that bind human SLiMs. We also provide examples of viral proteins that bind to SLiMs, or IDDs, of viral proteins as a part of complex assembly and regulation of protein functions. The protein-protein interactions are often crucial for viral replication, and may thus offer possibilities for innovative inhibitor design.
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| 9. |
- Newman, Jeffrey D., et al.
(författare)
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Biosensors : principles and practice
- 1992
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Ingår i: Essays in Biochemistry. - : Portland Press. - 0071-1365 .- 1744-1358. ; 27, s. 147-159
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Forskningsöversikt (refereegranskat)
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| 10. |
- Nicholls, David
(författare)
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Mitochondrial ion circuits.
- 2010
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Ingår i: Essays in Biochemistry. - : Portland Press Ltd.. - 0071-1365 .- 1744-1358. ; 47, s. 25-35
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Tidskriftsartikel (refereegranskat)abstract
- Proton circuits across the inner mitochondrial membrane link the primary energy generators, namely the complexes of the electron transport chain, to multiple energy utilizing processes, including the ATP synthase, inherent proton leak pathways, metabolite transport and linked circuits of sodium and calcium. These mitochondrial circuits can be monitored in both isolated preparations and intact cells and, for the primary proton circuit techniques, exist to follow both the proton current and proton electrochemical potential components of the circuit in parallel experiments, providing a quantitative means of assessing mitochondrial function and, equally importantly, dysfunction.
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