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Integration of ER stress, oxidative stress and the inflammatory response in health and disease. International journal of clinical and experimental medicine. Stress signaling from the lumen of the endoplasmic reticulum: coordination of gene transcriptional and translational controls. The endoplasmic reticulum is the site of cholesterol induced cytotoxicity in macrophages. Nature cell biology. Saturated fatty acids induce endoplasmic reticulum stress and apoptosis independently of ceramide in liver cells.
American journal of physiology Endocrinology and metabolism. Control of mRNA translation preserves endoplasmic reticulum function in beta cells and maintains glucose homeostasis. Nature medicine. Inflammation and cellular stress: a mechanistic link between immune-mediated and metabolically driven pathologies. European journal of nutrition.
Evidence supporting a role for endoplasmic reticulum stress in the development of atherosclerosis in a hyperglycaemic mouse model. Contributions of hyperhomocysteinemia to atherosclerosis: Causal relationship and potential mechanisms. BioFactors Oxford, England.
TDAG51 is induced by homocysteine, promotes detachment-mediated programmed cell death, and contributes to the cevelopment of atherosclerosis in hyperhomocysteinemia. The Journal of biological chemistry. The role of endoplasmic reticulum stress in the progression of atherosclerosis. Macrophage death and defective inflammation resolution in atherosclerosis. Endoplasmic reticulum stress and atherosclerosis.
Intersection of the unfolded protein response and hepatic lipid metabolism. Cellular and molecular life sciences : CMLS.
Imaging the unfolded protein response in primary tumors reveals microenvironments with metabolic variations that predict tumor growth. Cancer research. Tumor stress inside out: cell-extrinsic effects of the unfolded protein response in tumor cells modulate the immunological landscape of the tumor microenvironment. Journal of immunology Baltimore, Md : Regulation of basal cellular physiology by the homeostatic unfolded protein response.
The Journal of cell biology. The unfolded protein response: controlling cell fate decisions under ER stress and beyond. Nature reviews Molecular cell biology. A novel ER alpha-mannosidase-like protein accelerates ER-associated degradation. Cell death and differentiation. Selective inhibition of a regulatory subunit of protein phosphatase 1 restores proteostasis.
Ppp1r15 gene knockout reveals an essential role for translation initiation factor 2 alpha eIF2alpha dephosphorylation in mammalian development. The unfolded protein response signals through high-order assembly of Ire1. Plasma cell differentiation requires the transcription factor XBP Phosphoregulation of Ire1 RNase splicing activity. Mammalian transcription factor ATF6 is synthesized as a transmembrane protein and activated by proteolysis in response to endoplasmic reticulum stress.
Molecular biology of the cell. Critical reviews in eukaryotic gene expression. J Biol Chem. Mol Biol Cell. Cell death: critical control points. Snapshot: caspases. Acta Biochim Biophys Sin. ER-stress-induced transcriptional regulation increases protein synthesis leading to cell death. ER stress does not cause upregulation and activation of caspase-2 to initiate apoptosis. Opposing unfolded-protein-response signals converge on death receptor 5 to control apoptosis. Two Y genes can replace the entire Y chromosome for assisted reproduction in the mouse. ATF6alpha optimizes long-term endoplasmic reticulum function to protect cells from chronic stress.
Developmental cell. Cell death and endoplasmic reticulum stress: disease relevance and therapeutic opportunities. Nature reviews Drug discovery. Activating transcription factor-6 ATF6 mediates apoptosis with reduction of myeloid cell leukemia sequence 1 Mcl-1 protein via induction of WW domain binding protein 1.
Molecular components of the mammalian circadian clock. Human molecular genetics. Watching the clock: endoplasmic reticulum-mediated control of circadian rhythms in cancer. Ann Med. A wheel of time: the circadian clock, nuclear receptors, and physiology.
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Cognitive performance as a zeitgeber: cognitive oscillators and cholinergic modulation of the SCN entrain circadian rhythms. Circadian topology of metabolism. Nuclear receptors rock around the clock. Transcriptional coactivator PGC-1alpha integrates the mammalian clock and energy metabolism. Nuclear receptor Rev-erbalpha is a critical lithium-sensitive component of the circadian clock.
Nocturnin: at the crossroads of clocks and metabolism. Proceedings of the National Academy of Sciences. Nucleic acids research. Orphan nuclear receptor estrogen-related receptor gamma ERRgamma is key regulator of hepatic gluconeogenesis. Circadian clock-coordinated 12 Hr period rhythmic activation of the IRE1alpha pathway controls lipid metabolism in mouse liver.
Cell metabolism. SIRT1 and energy metabolism. Regulation of unfolded protein response modulator XBP1s by acetylation and deacetylation. The Biochemical journal. Hepatic overexpression of SIRT1 in mice attenuates endoplasmic reticulum stress and insulin resistance in the liver.
Circadian clock-coordinated hepatic lipid metabolism: only transcriptional regulation? Aging Albany NY. Oscillations in NF-kappaB signaling control the dynamics of gene expression. Regulation of apoptosis by the circadian clock through NF-kappaB signaling. NF-kappa B and Rel proteins: evolutionarily conserved mediators of immune responses.
Circuitry of nuclear factor kappaB signaling. Immunological reviews. Cold Spring Harbor perspectives in biology. Autocrine tumor necrosis factor alpha links endoplasmic reticulum stress to the membrane death receptor pathway through IRE1alpha-mediated NF-kappaB activation and down-regulation of TRAF2 expression.
In vivo genome-wide profiling reveals a tissue-specific role for 5-formylcytosine. TET is able to oxidise 5-methylcytosine 5mC to 5-hydroxymethylcytosine 5hmC , 5-formylcytosine 5fC and 5-carboxylcytosine 5caC. TDG can excise the oxidative products 5fC and 5caC, initiating base excision repair. These modified bases are stable and detectable in the genome, suggesting that they could have epigenetic functions in their own right. However, functional investigation of the genome-wide distribution of 5fC has been restricted to cell culture-based systems, while its in vivo profile remains unknown.
Capture Hi-C CHi-C is a method for profiling chromosomal interactions involving targeted regions of interest, such as gene promoters, globally and at high resolution. Signal detection in CHi-C data involves a number of statistical challenges that are not observed when using other Hi-C-like techniques.
We present a background model and algorithms for normalisation and multiple testing that are specifically adapted to CHi-C experiments. To date, there are no effective disease-modifying treatments for Alzheimer's disease AD. In order to develop new therapeutics for stages where they are most likely to be effective, it is important to identify the first pathological alterations in the disease cascade.
In this regard, long term organotypic hippocampal slice cultures OHSCs from neonatal amyloid mice offer an excellent compromise between in vivo and primary culture studies, largely retaining the cellular composition and neuronal architecture of the in vivo hippocampus, but with the in vitro advantages of accessibility to live imaging, sampling and intervention.
Sewitz S, Lipkow K. The linear and three-dimensional arrangement and composition of chromatin in eukaryotic genomes underlies the mechanisms directing gene regulation. Understanding this organization requires the integration of many data types and experimental results. Here we describe the approach of integrating genome-wide protein-DNA binding data to determine chromatin states.
To investigate spatial aspects of genome organization, we present a detailed description of how to run stochastic simulations of protein movements within a simulated nucleus in 3D. This systems level approach enables the development of novel questions aimed at understanding the basic mechanisms that regulate genome dynamics. Methods in molecular biology Clifton, N. Understanding how recombination is regulated requires a comprehensive, unbiased readout of V gene usage. We reveal a fold range of recombination efficiency among recombining V genes in the primary mouse Igh repertoire.
We used machine learning to integrate these data with local chromatin profiles to identify combinatorial patterns of epigenetic features that associate with active VH gene recombination. These features localize downstream of VH genes and are excised by recombination, revealing a class of cis-regulatory element that governs recombination, distinct from expression. Thus, local chromatin signatures downstream of VH genes provide an essential layer of regulation that determines recombination efficiency. Global demethylation is part of a conserved program of epigenetic reprogramming to naive pluripotency.
The transition from primed hypermethylated embryonic stem cells ESCs to naive hypomethylated ones serum-to-2i is a valuable model system for epigenetic reprogramming. We present a mathematical model, which accurately predicts global DNA demethylation kinetics. UHRF1 protein, the essential targeting factor for DNMT1, is reduced upon transition to 2i, and so is recruitment of the maintenance methylation machinery to replication foci.
These mechanisms synergistically enforce global DNA hypomethylation in a replication-coupled fashion.
Our observations establish the molecular mechanism for global demethylation in naive ESCs, which has key parallels with those operating in primordial germ cells and early embryos. Immunologic profiles of multiple sclerosis treatments reveal shared early B cell alterations. We undertook a systems immunology approach of the adaptive immune system in multiple sclerosis MS , overcoming tradeoffs between scale and level of detail, in order to identify the immunologic signature of MS and the changes wrought by current immunomodulatory treatments. RNA-binding proteins RBPs facilitate post-transcriptional control of eukaryotic gene expression at multiple levels.
Taken together, our study uncovers a role of TTP as a suppressor of feedback inhibitors of inflammation and highlights the importance of fine-tuned TTP activity-regulation by MK2 in order to control the pro-inflammatory response. Despite the lack of Th1-like ex-Th17 cells, the degree of H. However, ILA Cre -mediated deletion of Tbx21 has only limited effects on disease course in this model and is not compensated by Ag-specific Th1 cells. These results show that neither the single Th17 subset, nor its progeny, is solely responsible for immunopathology or autoimmunity.
Journal of immunology Baltimore, Md. We hypothesized that access of signal-dependent transcription factors TFs to enhancers is dynamically regulated to shape transcriptional responses to TCR signaling. We found that the TF BACH2 restrains terminal differentiation to enable generation of long-lived memory cells and protective immunity after viral infection.
In naive cells, this prevented TCR-driven induction of genes associated with terminal differentiation. Upon effector differentiation, reduced expression of BACH2 and its phosphorylation enabled unrestrained induction of TCR-driven effector programs.