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Cellular Reprogramming

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https://www.readbyqxmd.com/read/28548464/control-of-cell-death-and-mitochondrial-fission-by-erk1-2-map-kinase-signalling
#1
REVIEW
Simon J Cook, Kate Stuart, Rebecca Gilley, Matthew J Sale
The ERK1/2 signalling pathway is best known for its role in connecting activated growth factor receptors to changes in gene expression due to activated ERK1/2 entering the nucleus and phosphorylating transcription factors. However, active ERK1/2 also translocate to a variety of other organelles including the endoplasmic reticulum, endosomes, golgi and mitochondria to access specific substrates and influence cell physiology. In this article we review two aspects of ERK1/2 signalling at the mitochondria that are involved in regulating cell fate decisions...
May 26, 2017: FEBS Journal
https://www.readbyqxmd.com/read/28546511/the-nanci-nkx2-1-gene-duplex-buffers-nkx2-1-expression-to-maintain-lung-development-and-homeostasis
#2
Michael J Herriges, David J Tischfield, Zheng Cui, Michael P Morley, Yumiao Han, Apoorva Babu, Su Li, MinMin Lu, Isis Cendan, Benjamin A Garcia, Stewart A Anderson, Edward E Morrisey
A subset of long noncoding RNAs (lncRNAs) is spatially correlated with transcription factors (TFs) across the genome, but how these lncRNA-TF gene duplexes regulate tissue development and homeostasis is unclear. We identified a feedback loop within the NANCI (Nkx2.1-associated noncoding intergenic RNA)-Nkx2.1 gene duplex that is essential for buffering Nkx2.1 expression, lung epithelial cell identity, and tissue homeostasis. Within this locus, Nkx2.1 directly inhibits NANCI, while NANCI acts in cis to promote Nkx2...
May 25, 2017: Genes & Development
https://www.readbyqxmd.com/read/28544151/the-emt-spectrum-and-therapeutic-opportunities
#3
REVIEW
Dominic Chih-Cheng Voon, Ruby Yun-Ju Huang, Rebecca A Jackson, Jean Paul Thiery
Carcinomas are phenotypically arrayed along an EMT spectrum, a developmental program currently exploited to understand the acquisition of drug resistance through a re-routing of growth factor signalling. This review collates the current approaches employed in developing therapeutics against cancer-associated EMT, and provides an assessment of their respective strengths and drawbacks. We reflect on the close relationship between EMT and chemoresistance against current targeted therapeutics, with a special focus on the epigenetic mechanisms that links these processes...
May 24, 2017: Molecular Oncology
https://www.readbyqxmd.com/read/28538163/metabolic-signatures-of-t-cells-and-macrophages-in-rheumatoid-arthritis
#4
REVIEW
Cornelia M Weyand, Markus Zeisbrich, Jörg J Goronzy
In most autoimmune diseases, a decade-long defect in self-tolerance eventually leads to clinically relevant, tissue-destructive inflammatory disease. The pathogenic potential of chronic persistent immune responses during the pre-clinical and clinical phase is ultimately linked to the bioenergetic fitness of innate and adaptive immune cells. Chronic immune cell stimulation, high cellular turn-over, structural damage to the host tissue and maladaptive wound healing, all require a reliable supply of nutrients, oxygen, and biosynthetic precursors...
May 21, 2017: Current Opinion in Immunology
https://www.readbyqxmd.com/read/28536395/cellular-and-molecular-preconditions-for-retinal-pigment-epithelium-rpe-natural-reprogramming-during-retinal-regeneration-in-urodela
#5
REVIEW
Eleonora N Grigoryan, Yuliya V Markitantova
Many regeneration processes in animals are based on the phenomenon of cell reprogramming followed by proliferation and differentiation in a different specialization direction. An insight into what makes natural (in vivo) cell reprogramming possible can help to solve a number of biomedical problems. In particular, the first problem is to reveal the intrinsic properties of the cells that are necessary and sufficient for reprogramming; the second, to evaluate these properties and, on this basis, to reveal potential endogenous sources for cell substitution in damaged tissues; and the third, to use the acquired data for developing approaches to in vitro cell reprogramming in order to obtain a cell reserve for damaged tissue repair...
December 1, 2016: Biomedicines
https://www.readbyqxmd.com/read/28531108/regulation-of-metabolic-activity-by-p53
#6
REVIEW
Jessica Flöter, Irem Kaymak, Almut Schulze
Metabolic reprogramming in cancer cells is controlled by the activation of multiple oncogenic signalling pathways in order to promote macromolecule biosynthesis during rapid proliferation. Cancer cells also need to adapt their metabolism to survive and multiply under the metabolically compromised conditions provided by the tumour microenvironment. The tumour suppressor p53 interacts with the metabolic network at multiple nodes, mostly to reduce anabolic metabolism and promote preservation of cellular energy under conditions of nutrient restriction...
May 20, 2017: Metabolites
https://www.readbyqxmd.com/read/28529938/senescence-inflammatory-regulation-of-reparative-cellular-reprogramming-in-aging-and-cancer
#7
Javier A Menendez, Tomás Alarcón
The inability of adult tissues to transitorily generate cells with functional stem cell-like properties is a major obstacle to tissue self-repair. Nuclear reprogramming-like phenomena that induce a transient acquisition of epigenetic plasticity and phenotype malleability may constitute a reparative route through which human tissues respond to injury, stress, and disease. However, tissue rejuvenation should involve not only the transient epigenetic reprogramming of differentiated cells, but also the committed re-acquisition of the original or alternative committed cell fate...
2017: Frontiers in Cell and Developmental Biology
https://www.readbyqxmd.com/read/28528696/reprogramming-of-dermal-fibroblasts-into-osteo-chondrogenic-cells-with-elevated-osteogenic-potency-by-defined-transcription-factors
#8
Yinxiang Wang, Ming-Hoi Wu, May Pui Lai Cheung, Mai Har Sham, Haruhiko Akiyama, Danny Chan, Kathryn S E Cheah, Martin Cheung
Recent studies using defined transcription factors to convert skin fibroblasts into chondrocytes have raised the question of whether osteo-chondroprogenitors expressing SOX9 and RUNX2 could also be generated during the course of the reprogramming process. Here, we demonstrated that doxycycline-inducible expression of reprogramming factors (KLF4 [K] and c-MYC [M]) for 6 days were sufficient to convert murine fibroblasts into SOX9(+)/RUNX2(+) cellular aggregates and together with SOX9 (S) promoted the conversion efficiency when cultured in a defined stem cell medium, mTeSR...
May 15, 2017: Stem Cell Reports
https://www.readbyqxmd.com/read/28526133/metabolic-reprogramming-and-oncogenesis-one-hallmark-many-organelles
#9
A S H Costa, C Frezza
The process of tumorigenesis can be described by a series of molecular features, among which alteration of cellular metabolism has recently emerged. This metabolic rewiring fulfills the energy and biosynthetic demands of fast proliferating cancer cells and amplifies their metabolic repertoire to survive and proliferate in the poorly oxygenated and nutrient-deprived tumor microenvironment. During the last decade, the complex reprogramming of cancer cell metabolism has been widely investigated, revealing cancer-specific metabolic alterations...
2017: International Review of Cell and Molecular Biology
https://www.readbyqxmd.com/read/28521236/targeting-t-cell-metabolism-to-regulate-t-cell-activation-differentiation-and-function-in-disease
#10
REVIEW
Chirag H Patel, Jonathan D Powell
It is becoming increasingly clear that metabolic reprogramming plays a critical role in T cell activation, differentiation and function. To this end, cellular metabolism not only meets the energetic demands of T cells but also provides critical substrates for their growth and function. Furthermore, metabolites themselves are emerging as key regulators of immune responses. As the details of how metabolic reprogramming regulates immune function are revealed, new potential targets for modulating immune responses have emerged...
May 15, 2017: Current Opinion in Immunology
https://www.readbyqxmd.com/read/28516914/adenylate-kinase-hcinap-determines-self-renewal-of-colorectal-cancer-stem-cells-by-facilitating-ldha-phosphorylation
#11
Yapeng Ji, Chuanzhen Yang, Zefang Tang, Yongfeng Yang, Yonglu Tian, Hongwei Yao, Xi Zhu, Zeming Zhang, Jiafu Ji, Xiaofeng Zheng
Targeting the specific metabolic phenotypes of colorectal cancer stem cells (CRCSCs) is an innovative therapeutic strategy for colorectal cancer (CRC) patients with poor prognosis and relapse. However, the context-dependent metabolic traits of CRCSCs remain poorly elucidated. Here we report that adenylate kinase hCINAP is overexpressed in CRC tissues. Depletion of hCINAP inhibits invasion, self-renewal, tumorigenesis and chemoresistance of CRCSCs with a loss of mesenchymal signature. Mechanistically, hCINAP binds to the C-terminal domain of LDHA, the key regulator of glycolysis, and depends on its adenylate kinase activity to promote LDHA phosphorylation at tyrosine 10, resulting in the hyperactive Warburg effect and the lower cellular ROS level and conferring metabolic advantage to CRCSC invasion...
May 18, 2017: Nature Communications
https://www.readbyqxmd.com/read/28515784/improving-saccharomyces-cerevisiae-ethanol-production-and-tolerance-via-rna-polymerase-ii-subunit-rpb7
#12
Zilong Qiu, Rongrong Jiang
BACKGROUND: Classical strain engineering methods often have limitations in altering multigenetic cellular phenotypes. Here we try to improve Saccharomyces cerevisiae ethanol tolerance and productivity by reprogramming its transcription profile through rewiring its key transcription component RNA polymerase II (RNAP II), which plays a central role in synthesizing mRNAs. This is the first report on using directed evolution method to engineer RNAP II to alter S. cerevisiae strain phenotypes...
2017: Biotechnology for Biofuels
https://www.readbyqxmd.com/read/28515364/nicotinamide-metabolism-regulates-glioblastoma-stem-cell-maintenance
#13
Jinkyu Jung, Leo J Y Kim, Xiuxing Wang, Qiulian Wu, Tanwarat Sanvoranart, Christopher G Hubert, Briana C Prager, Lisa C Wallace, Xun Jin, Stephen C Mack, Jeremy N Rich
Metabolic dysregulation promotes cancer growth through not only energy production, but also epigenetic reprogramming. Here, we report that a critical node in methyl donor metabolism, nicotinamide N-methyltransferase (NNMT), ranked among the most consistently overexpressed metabolism genes in glioblastoma relative to normal brain. NNMT was preferentially expressed by mesenchymal glioblastoma stem cells (GSCs). NNMT depletes S-adenosyl methionine (SAM), a methyl donor generated from methionine. GSCs contained lower levels of methionine, SAM, and nicotinamide, but they contained higher levels of oxidized nicotinamide adenine dinucleotide (NAD+) than differentiated tumor cells...
May 18, 2017: JCI Insight
https://www.readbyqxmd.com/read/28515225/energy-metabolic-pathways-control-the-fate-and-function-of-myeloid-immune-cells
#14
REVIEW
Amir A Al-Khami, Paulo C Rodriguez, Augusto C Ochoa
The past decade has seen a significant interest in investigating the intracellular metabolism of cells of the immune system. This has increased the realization that immune cells endure metabolic reprogramming upon responding to pathogen-derived or inflammatory signals. More importantly, not only does this metabolic switch provide for the bioenergetic and biosynthetic demands but also it, in a highly specific manner, determines the cellular fate and function. In this review, we discuss the metabolic aspects that regulate the differentiation and function of myeloid cells, pivotal for both innate and adaptive immunity...
May 17, 2017: Journal of Leukocyte Biology
https://www.readbyqxmd.com/read/28514713/pattern-recognition-receptors-and-coordinated-cellular-pathways-involved-in-tuberculosis-immunopathogenesis-emerging-concepts-and-perspectives
#15
REVIEW
Abhishek Mishra, Shamim Akhtar, Chinnaswamy Jagannath, Arshad Khan
Pattern Recognition Receptors (PRRs) play a central role in the recognition of numerous pathogens, including Mycobacterium tuberculosis, resulting in activation of innate and adaptive immune responses. Besides Toll Like Receptors, C-type Lectin Receptors and Nod Like Receptors are now being recognized for their involvement in inducing immune response against M. tuberculosis infection. Although, a functional redundancy of the PRRs has also been reported in many studies, emerging evidences support the notion that a cooperative and coordinated response generated by these receptors is critical to sustain the full immune control of M...
May 14, 2017: Molecular Immunology
https://www.readbyqxmd.com/read/28514443/cancer-progression-by-reprogrammed-bcaa-metabolism-in-myeloid-leukaemia
#16
Ayuna Hattori, Makoto Tsunoda, Takaaki Konuma, Masayuki Kobayashi, Tamas Nagy, John Glushka, Fariba Tayyari, Daniel McSkimming, Natarajan Kannan, Arinobu Tojo, Arthur S Edison, Takahiro Ito
Reprogrammed cellular metabolism is a common characteristic observed in various cancers. However, whether metabolic changes directly regulate cancer development and progression remains poorly understood. Here we show that BCAT1, a cytosolic aminotransferase for branched-chain amino acids (BCAAs), is aberrantly activated and functionally required for chronic myeloid leukaemia (CML) in humans and in mouse models of CML. BCAT1 is upregulated during progression of CML and promotes BCAA production in leukaemia cells by aminating the branched-chain keto acids...
May 17, 2017: Nature
https://www.readbyqxmd.com/read/28514187/diphenhydramine-inhibits-voltage-gated-proton-channels-hv1-and-induces-acidification-in-leukemic-jurkat-t-cells-new-insights-into-the-pro-apoptotic-effects-of-antihistaminic-drugs
#17
Agustín Asuaje, Pedro Martín, Nicolás Enrique, Leandro Agustín Díaz Zegarra, Paola Smaldini, Guillermo Docena, Verónica Milesi
An established characteristic of neoplastic cells is their metabolic reprogramming, known as the Warburg effect, with greater reliance on energetically less efficient pathways (such as glycolysis and pentose phosphate shunt) compared with oxidative phosphorylation. This results in an overproduction of acidic species that must be extruded to maintain intracellular homeostasis. We recently described that blocking the proton currents in leukemic cells mediated by Hv1 ion channels triggers a marked intracellular acidification and apoptosis induction...
May 17, 2017: Channels
https://www.readbyqxmd.com/read/28512237/regulation-of-dna-demethylation-by-the-xpc-dna-repair-complex-in-somatic-and-pluripotent-stem-cells
#18
Jaclyn J Ho, Claudia Cattoglio, David T McSwiggen, Robert Tjian, Yick W Fong
Faithful resetting of the epigenetic memory of a somatic cell to a pluripotent state during cellular reprogramming requires DNA methylation to silence somatic gene expression and dynamic DNA demethylation to activate pluripotency gene transcription. The removal of methylated cytosines requires the base excision repair enzyme TDG, but the mechanism by which TDG-dependent DNA demethylation occurs in a rapid and site-specific manner remains unclear. Here we show that the XPC DNA repair complex is a potent accelerator of global and locus-specific DNA demethylation in somatic and pluripotent stem cells...
April 15, 2017: Genes & Development
https://www.readbyqxmd.com/read/28512179/cooperative-regulatory-functions-of-mir858-and-myb83-during-cyst-nematode-parasitism
#19
Sarbottam Piya, Christina Kihm, J Hollis Rice, Thomas J Baum, Tarek Hewezi
microRNAs (miRNAs) recently have been established as key regulators of transcriptome reprogramming that defines cell function and identity. Nevertheless, the molecular functions of the greatest number of miRNA genes remain to be determined. Here, we report cooperative regulatory functions of miR858 and its MYB83 transcription factor target gene in transcriptome reprogramming during Heterodera cyst nematode parasitism of Arabidopsis. Gene expression analyses and promoter-GUS fusion assays documented a role of miR858 in post-transcriptional regulation of MYB83 in the Heterodera schachtii-induced feeding sites, the syncytia...
May 16, 2017: Plant Physiology
https://www.readbyqxmd.com/read/28508407/structural-conservation-of-the-pin-domain-active-site-across-all-domains-of-life
#20
REVIEW
M Senissar, M C Manav, D E Brodersen
The PIN (PilT N-terminus) domain is a compact RNA-binding protein domain present in all domains of life. This 120-residue domain consists of a central and parallel β sheet surrounded by α helices, which together organize 4-5 acidic residues in an active site that binds one or more divalent metal ions and in many cases has endoribonuclease activity. In bacteria and archaea, the PIN domain is primarily associated with toxin-antitoxin loci, consisting of a toxin (the PIN domain nuclease) and an antitoxin that inhibits the function of the toxin under normal growth conditions...
May 15, 2017: Protein Science: a Publication of the Protein Society
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