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- Nair, Anu G., et al.
(författare)
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Modeling Intracellular Signaling Underlying Striatal Function in Health and Disease
- 2014
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Ingår i: Computational Neuroscience. - Amsterdam : Elsevier. - 9780123978974 ; 123, s. 277-304
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Bokkapitel (refereegranskat)abstract
- Striatum, which is the input nucleus of the basal ganglia, integrates cortical and thalamic glutamatergic inputs with dopaminergic afferents from the substantia nigra pars cornpacta. The combination of dopamine and glutamate strongly modulates molecular and cellular properties of striatal neurons and the strength of corticostriatal synapses. These actions are performed via intracellular signaling networks, containing several intertwined feedback loops. Understanding the role of dopamine and other neuromodulators requires the development of quantitative dynamical models for describing the intracellular signaling, in order to provide precise unambiguous descriptions and quantitative predictions. Building such models requires integration of data from multiple data sources containing information regarding the molecular interactions, the strength of these interactions, and the subcellular localization of the molecules. Due to the uncertainty, variability, and sparseness of these data, parameter estimation techniques are critical for inferring or constraining the unknown parameters, and sensitivity analysis evaluates which parameters are most critical for a given observed macroscopic behavior. Here, we briefly review the modeling approaches and tools that have been used to investigate biochemical signaling in the striatum, along with some of the models built around striatum. We also suggest a future direction for the development of such models from the, now becoming abundant, high-throughput data.
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- Borggren, Marie, et al.
(författare)
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The Evolution of HIV-1 Interactions with Coreceptors and Mannose C-Type Lectin Receptors.
- 2015
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Ingår i: Progress in Molecular Biology and Translational Science. - : Elsevier. - 1877-1173 .- 1878-0814. ; 129, s. 109-140
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Tidskriftsartikel (refereegranskat)abstract
- The phenotype of human immunodeficiency virus type 1 (HIV-1) commonly evolves between and within infected individuals, at virus transmission, and during disease progression. This evolution includes altered interactions between the virus and its coreceptors, i.e., chemokine receptors, as well as mannose C-type lectin receptors (CLRs). Transmitted/founder viruses are predominantly restricted to CCR5, whereas the subsequent intrapatient evolution of HIV-1 coreceptor use during progressive disease can be subdivided into two distinct pathways. Accordingly, the CCR5-restricted virus population is either gradually replaced by virus variants able to use CXCR4 or evolves toward an altered, more flexible use of CCR5. Despite a strong dependency on these coreceptors for host cell entry, HIV-1 also interacts with other cell surface molecules during target cell attachment, including the CLRs. The virus interaction with the CLRs may result either in the efficient transfer of virus to CD4(+) T cells or in the degradation of the virus in endosomal compartments. The determinants of the diverse outcomes depend on which CLR is engaged and also on the glycan makeup of the envelope glycoproteins, which may evolve with the strength of the immune pressure during the disease course. With the current clinical introduction of CCR5 antagonists and the development of additional entry inhibitors, knowledge on the evolution and baseline characteristics of HIV-1 interactions with coreceptor and CLR interactions may play important roles for individualized and optimized treatment strategies. This review summarizes our current understanding of the evolution of HIV-1 interactions with these receptors.
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- Dahlman, I, et al.
(författare)
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Genetics of adipose tissue biology
- 2010
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Ingår i: Progress in molecular biology and translational science. - 1878-0814. ; 94, s. 39-74
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Tidskriftsartikel (refereegranskat)
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- Renzi, Chiara, et al.
(författare)
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From Epigenetic Associations to Biological and Psychosocial Explanations in Mental Health.
- 2018
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Ingår i: Progress in Molecular Biology and Translational Science. - : Elsevier. - 1877-1173 .- 1878-0814. ; 158, s. 299-323
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Forskningsöversikt (refereegranskat)abstract
- The development of mental disorders constitutes a complex phenomenon driven by unique social, psychological and biological factors such as genetics and epigenetics, throughout an individual's life course. Both environmental and genetic factors have an impact on mental health phenotypes and act simultaneously to induce changes in brain and behavior. Here, we describe and critically evaluate the current literature on gene-environment interactions and epigenetics on mental health by highlighting recent human and animal studies. We furthermore review some of the main ethical and social implications concerning gene-environment interactions and epigenetics and provide explanations and suggestions on how to move from statistical and epigenetic associations to biological and psychological explanations within a multi-disciplinary and integrative approach of understanding mental health.
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