论文信息:Zhuyun Bian, Yajia Ni, Jin-Rong Xu, Huiquan Liu*.A-to-I mRNA editing in fungi: occurrence, function, and evolution. Cellular and Molecular Life Sciences (2019) 76:329-340.. JCR分区Q1,中科院大类分区二区,IF=6.721. 论文摘要: A-to-I RNA editing is an important post-transcriptional modification that converts adenosine (A) to inosine (I) in RNA molecules via hydrolytic deamination. Although editing of mRNAs catalyzed by adenosine deaminases acting on RNA (ADARs) is an evolutionarily conserved mechanism in metazoans, organisms outside the animal kingdom lacking ADAR orthologs were thought to lack A-to-I mRNA editing. However, recent discoveries of genome-wide A-to-I mRNA editing during the sexual stage of the wheat scab fungus Fusarium graminearum, model filamentous fungus Neurospora crassa, Sordaria macrospora, and an early diverging filamentous ascomycete Pyronema confluens indicated that A-to-I mRNA editing is likely an evolutionarily conserved feature in ...
A tripartite motif located in the centre of the 7.5kb exon 26 of apolipoprotein B (apoB) mRNA directs editosome assembly and site-specific cytidine-to-uridine editing at nucleotide 6666. apoB mRNA editing is a post-transcriptional event, occurring primarily at the time exon 26 is spliced or at a time after splicing, but before nuclear export. We show, through reporter RNA constructs, that RNA splice sites suppress editing of precursor RNAs when placed proximal or distal to the editing site. Processed RNAs were edited more efficiently than precursor RNAs. Mutation of both the splice donor and acceptor sites was necessary for RNAs to be edited efficiently. The results suggested that commitment of pre-mRNA to the splicing and/or nuclear-export pathways may play a role in regulating editing-site utilization. The HIV-1 Rev-Rev response element (RRE) interaction was utilized to uncouple the commitment of precursor RNAs to the spliceosome assembly pathway and associated nuclear-export pathway. Under ...
Ocean Acoustic Tomography requires deep-ocean moorings whose horizontal excursions are either small or accurately measured. The present study rigorously investigates the former case: the design of stiff moorings to meet any particular horizontal excursion goal (e.g., 25 meters) under two typical ocean current-versus-depth profiles. Moorings are considered for tomographic transmitters and receivers at depths ranging from one thousand to four thousand meters. Mooring components considered include steel sphere, glass ball, and syntactic foam buoyancy; jacketed 3 x 19 wire and electromagnetic cable; and a realistic (large) battery pack for the acoustic transmitter. Kevlar mooring line was considered and rejected. The basic tool of this study is a well-verified computer program that simulates mooring motion. Many runs of this program have yielded enough data to make plots showing mooring cost as a function of excursion, depth, and mooring type. It has been found that cost and excursion are very sensitive to
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antibody-antibodies.com is the marketplace for research antibodies. Find the right antibody for your research needs. Mechanism of U insertion RNA editing in trypanosome mitochondria: the bimodal TUTase activity of the core complex.
Line number RuleID ViolationType Message Line #------------ #------------ # Validation for #430725 annotations in 430768 lines #------------ #Line number RuleID ViolationType Message Line #------------ # GO_AR:0000014 Valid GO term ID Error count: 212 3146 GO_AR:0000014 Error The relation has_direct_input in the c16 annotation extension is an obsolete relation MGI MGI:1917115 A1cf GO:0016556 MGI:MGI:4943819,PMID:20541607 IGI MGI:MGI:104663 P APOBEC1 complementation factor 1810073H04Rik,ACF,apobec-1 complementation factor protein taxon:10090 20140709 MGI has_direct_input(MGI:MGI:88052),occurs_in(EMAPA:16900) 9354 GO_AR:0000014 Error The relation has_direct_input in the c16 annotation extension is an obsolete relation MGI MGI:105377 Adam19 GO:0006509 MGI:MGI:3625788,PMID:11116142 IMP P a disintegrin and metallopeptidase domain 19 (meltrin beta) Mltnb protein taxon:10090 20150513 MGI ...
we used RNA-Seq to quantify the RNA editing level at more than 8,000 previously annotated exonic A-to-I RNA editing sites in two brain regions - prefrontal cortex and cerebellum - of humans, chimpanzees and rhesus macaques. We observed substantial conservation of RNA editing levels between the brain regions, as well as among the three primate species. Evolutionary changes in RNA editing were nonetheless evident among the species. Across lifespan, we observed an increase of the RNA editing level with advanced age in both brain regions of all three primate species.
Sigma-Aldrich offers abstracts and full-text articles by [Zhenqiu Huang, Drahomíra Faktorová, Adéla Křížová, Lucie Kafková, Laurie K Read, Julius Lukeš, Hassan Hashimi].
I have been trying for over 6 months to purchase 5 mooring bits as pictured, to replace my 3 rather small mooring cleats on my CM32 CC Aft Cabin Ketch. First I
Both miRNAs and A-to-I RNA editing, a widespread nucleotide modification mechanism, have recently emerged as key players in cancer pathophysiology. However, the functional impact of RNA editing of miRNAs in cancer remains largely unexplored. Here, we focused on an ADAR2-catalyzed RNA editing site within the miR-379-5p seed region. This site was under-edited in tumors relative to normal tissues, with a high editing level being correlated with better patient survival times across cancer types. We demonstrated that in contrast to wild-type miRNA, edited miR-379-5p inhibited cell proliferation and promoted apoptosis in diverse tumor contexts in vitro, which was due to the ability of edited but not wild-type miR-379-5p to target CD97. Importantly, through nanoliposomal delivery, edited miR-379-5p mimics significantly inhibited tumor growth and extended survival of mice. Our study indicates a role of RNA editing in diversifying miRNA function during cancer progression and highlights the translational ...
Both miRNAs and A-to-I RNA editing, a widespread nucleotide modification mechanism, have recently emerged as key players in cancer pathophysiology. However, the functional impact of RNA editing of miRNAs in cancer remains largely unexplored. Here, we focused on an ADAR2-catalyzed RNA editing site within the miR-379-5p seed region. This site was under-edited in tumors relative to normal tissues, with a high editing level being correlated with better patient survival times across cancer types. We demonstrated that in contrast to wild-type miRNA, edited miR-379-5p inhibited cell proliferation and promoted apoptosis in diverse tumor contexts in vitro, which was due to the ability of edited but not wild-type miR-379-5p to target CD97. Importantly, through nanoliposomal delivery, edited miR-379-5p mimics significantly inhibited tumor growth and extended survival of mice. Our study indicates a role of RNA editing in diversifying miRNA function during cancer progression and highlights the translational ...
This annual meeting is one of a series seeking to improve and where possible standardise QA and QC across the Moorings sub-facilities through common techniques, procedures and tools.
/PRNewswire/ -- Research and Markets has announced the addition of the Global Mooring Systems Market Analysis & Trends - Industry Forecast to 2025 report to...
Plasmid pUC119-gRNA from Dr. Jen Sheens lab contains the insert guide RNA targeting AtPDS3 and is published in Nat Biotechnol. 2013 Aug;31(8):688-91. doi: 10.1038/nbt.2654. This plasmid is available through Addgene.
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Double-stranded RNA-specific adenosine deaminase is an enzyme that in humans is encoded by the ADAR gene (which stands for adenosine deaminase acting on RNA). Adenosine deaminases acting on RNA (ADAR) are enzymes responsible for binding to double stranded RNA (dsRNA) and converting adenosine (A) to inosine (I) by deamination. ADAR protein is a RNA-binding protein, which functions in RNA-editing through post-transcriptional modification of mRNA transcripts by changing the nucleotide content of the RNA. The conversion from A to I in the RNA disrupt the normal A:U pairing which makes the RNA unstable. Inosine is structurally similar to that of guanine (G) which leads to I to cytosine (C) binding. In RNA I functions the same as G in both translation and replication. Codon changes can arise from editing which may lead to changes in the coding sequences for proteins and their functions. Most editing site are found in noncoding regions of RNA such as untranslated regions (UTRs), Alu elements and long ...
RNA editing by deamination of adenosine to inosine is an evolutionarily conserved process involved in many cellular pathways, from alternative splicing to miRNA targeting. In humans, it is carried out by no less than three major adenosine deaminases acting on RNA (ADARs): ADAR1-p150, ADAR1-p110, and ADAR2. However, the first two derive from alternative splicing, so that it is currently impossible to delete ADAR1-p110 without also knocking out ADAR1-p150 expression. Furthermore, the expression levels of ADARs varies wildly among cell types, and no study has systematically explored the effect of each of these isoforms on the cell transcriptome. In this study, RNA immunoprecipitation (RIP)-sequencing on overexpressed ADAR isoforms tagged with green fluorescent protein (GFP) shows that each ADAR is associated with a specific set of differentially expressed genes, and that they each bind to distinct set of RNA targets. Our results show a good overlap with known edited transcripts, establishing RIP-seq as a
TY - JOUR. T1 - ADAR2 regulates RNA stability by modifying access of decay-promoting RNA-binding proteins. AU - Anantharaman, Aparna. AU - Tripathi, Vidisha. AU - Khan, Abid. AU - Yoon, Je Hyun. AU - Singh, Deepak K.. AU - Gholamalamdari, Omid. AU - Guang, Shuomeng. AU - Ohlson, Johan. AU - Wahlstedt, Helene. AU - Öhman, Marie. AU - Jantsch, Michael F.. AU - Conrad, Nicholas K.. AU - Ma, Jian. AU - Gorospe, Myriam. AU - Prasanth, Supriya G.. AU - Prasanth, Kannanganattu V.. PY - 2017/4/20. Y1 - 2017/4/20. N2 - Adenosine deaminases acting on RNA (ADARs) catalyze the editing of adenosine residues to inosine (A-to-I) within RNA sequences, mostly in the introns and UTRs (un-translated regions). The significance of editing within non-coding regions of RNA is poorly understood. Here, we demonstrate that association of ADAR2 with RNA stabilizes a subset of transcripts. ADAR2 interacts with and edits the 3Î.,UTR of nuclear-retained Cat2 transcribed nuclear RNA (Ctn RNA). In absence of ADAR2, the ...
Background: Adenosine deaminase acting on RNA-2 (ADAR2) enzyme catalyzes adenosine-to-inosine (A-to-I) RNA editing of mRNAs and microRNAs and controls brain development. However, the role of endothelial cell ADAR2 in vascular biology and inflammation has not been described so far.. Methods and Results: ADAR2 is expressed in human and murine endothelial cells and is 2-fold induced by hypoxia or hind limb ischemia in mice (P,0.05 for all). ADAR2 deficiency resulted in 73±12% impairment of leukocyte infiltration, in 53±4% reduced neovascularization, and a 40±6% decreased blood-flow recovery of ischemic muscle tissues in a hindlimb ischemia mouse model (P,0.001 for all). Mechanistically, among the highly ADAR2-regulated transcripts was interleukin-6 signal transducer (IL6ST or gp130), the receptor of interleukin-6 (IL-6). Silencing of ADAR2 resulted in a downregulation of gp130 mRNA and protein expression in endothelial cells by 65±5% and 50±5%, respectively (P,0.001 for both). Similarly, the ...
Abstract: RNA editing by the adenosine deaminase acting on RNA (ADAR) enzymes has been associated with many human neurological diseases including: epilepsy; suicidal depression; autism; pediatric glioblastoma; and ALS (Lou Gehrigs disease). RNA editing is ubiquitous in the animal kingdom. ADAR deaminates the RNA base adenosine (A) to inosine (I) in dsRNA molecules. Inosine is recognized by all cellular machineries as guanosine (G). ADAR specifically edits, recodes, a small number of adenosines in messenger RNA (mRNA) to such "Gs". However, hyper editing acts more generally on perfect or nearly perfect double-stranded RNA (dsRNA). Within long dsRNA (,30bp), over 40% of adenosine residues are modified on both strands, generating numerous I-U mismatch pairs, and structurally destabilizing dsRNA. Dicer is an enzyme that cleaves near perfect long dsRNAs, and thus competes with ADAR. As a consequence, ADARs hyper editing has downstream consequences on Dicer products including gene expression ...
The posttranscriptional modification of messenger RNA precursors (pre-mRNAs) by base deamination can profoundly alter the physiological function of the encoded proteins. The recent identification of tRNA-specific adenosine deaminases (ADATs) has led to the suggestion that these enzymes, as well as the cytidine and adenosine deaminases acting on pre-mRNAs (CDARs and ADARs), belong to a superfamily of RNA-dependent deaminases. This superfamily might have evolved from an ancient cytidine deaminase. This article reviews the reactions catalysed by these enzymes and discusses their evolutionary relationships.. ...
Both TAR DNA binding protein of 43kDa (TDP-43) pathology and failure of RNA editing at the glutamine/arginine (Q/R) site of GluA2, a subunit of the α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) receptor, are the characteristic etiology-linked molecular abnormalities that concomitantly occur in the motor neurons of the majority of patients with amyotrophic lateral sclerosis (ALS), the most common adult-onset fatal motor neuron disease. Adenosine deaminase acting on RNA 2 (ADAR2) specifically catalyzes RNA editing at the Q/R site of GluA2, and conditional ADAR2 knockout mice (ADAR2flox/flox/VAChT-Cre.Fast ; AR2 mice) exhibit a progressive ALS phenotype with TDP-43 pathology-like TDP-43 mislocalization in the ADAR2-lacking motor neurons. Because Ca2+-permeable AMPA receptor-mediated mechanism underlies death of motor neurons in the AR2 mice, amelioration of exaggerated Ca2+ influx by AMPA receptor antagonists may be a potential ALS therapy. Here we showed that oral perampanel, a selective
8-Azaadenosine is a potent ADAR1 (adenosine deaminases acting on double-stranded RNA) inhibitor. 8-Azaadenosine reduces A-to-I editing activity in a leukemia cell line, restores let-7 and inhibits leukemia stem cells self-renewal in vitro. - Mechanism of Action & Protocol.
BACKGROUND: Adenosine-to-inosine (A-to-I) editing is a site-selective post-transcriptional alteration of double-stranded RNA by ADAR deaminases that is crucial for homeostasis and development. Recently the Mouse Genomes Project generated genome sequences for 17 laboratory mouse strains and rich catalogues of variants. We also generated RNA-seq data from whole brain RNA from 15 of the sequenced strains. RESULTS: Here we present a computational approach that takes an initial set of transcriptome/genome mismatch sites and filters these calls taking into account systematic biases in alignment, single nucleotide variant calling, and sequencing depth to identify RNA editing sites with high accuracy. We applied this approach to our panel of mouse strain transcriptomes identifying 7,389 editing sites with an estimated false-discovery rate of between 2.9 and 10.5%. The overwhelming majority of these edits were of the A-to-I type, with less than 2.4% not of this class, and only three of these edits could not be
BACKGROUND: Adenosine-to-inosine (A-to-I) editing is a site-selective post-transcriptional alteration of double-stranded RNA by ADAR deaminases that is crucial for homeostasis and development. Recently the Mouse Genomes Project generated genome sequences for 17 laboratory mouse strains and rich catalogues of variants. We also generated RNA-seq data from whole brain RNA from 15 of the sequenced strains. RESULTS: Here we present a computational approach that takes an initial set of transcriptome/genome mismatch sites and filters these calls taking into account systematic biases in alignment, single nucleotide variant calling, and sequencing depth to identify RNA editing sites with high accuracy. We applied this approach to our panel of mouse strain transcriptomes identifying 7,389 editing sites with an estimated false-discovery rate of between 2.9 and 10.5%. The overwhelming majority of these edits were of the A-to-I type, with less than 2.4% not of this class, and only three of these edits could not be
Array ( [0] => 30 [1] => 31 [2] => 32 [3] => 34 [4] => 33 [5] => 49 ) Array ( [1513164984] => Array ( [timeid] => 1513164984 [id] => 14978 [title] => Applications of stimuli-responsive nanoscale drug delivery systems in translational research. (Drug Discov Today, Nov 2017) [time] => 13 December 2017 11:36:24 [postcat] => 30 ) [1511955285] => Array ( [timeid] => 1511955285 [id] => 14880 [title] => CSI Deputy Director, Prof Chng Wee Joo, Appointed Provosts Chair at NUSMed [time] => 29 November 2017 11:34:45 [postcat] => 31 ) [1511286152] => Array ( [timeid] => 1511286152 [id] => 14843 [title] => Triple negative breast cancer in Asia: An insiders view. (Cancer Treat Rev, Nov 2017) [time] => 21 November 2017 17:42:32 [postcat] => 30 ) [1510763331] => Array ( [timeid] => 1510763331 [id] => 14808 [title] => CSI Research Scientist Awarded the ASH Abstract Achievement Award! [time] => 15 November 2017 16:28:51 [postcat] => 31 ) [1510588491] => Array ( [timeid] => 1510588491 [id] => 14803 [title] => ...
Abstract: Mitochondrial mRNAs in kinetoplastids require extensive U-insertion/deletion editing that progresses 3-to-5 in small blocks, each directed by a guide RNA (gRNA), and exhibits substrate and developmental stage-specificity by unsolved mechanisms. Here, we address compositionally related factors, collectively known as the mitochondrial RNA-binding complex 1 (MRB1) or gRNA-binding complex (GRBC), that contain gRNA, have a dynamic protein composition, and transiently associate with several mitochondrial factors including RNA editing core complexes (RECC) and ribosomes. MRB1 controls editing by still unknown mechanisms. We performed the first next-generation sequencing study of native subcomplexes of MRB1, immunoselected via either RNA helicase 2 (REH2), that binds RNA and associates with unwinding activity, or MRB3010, that affects an early editing step. The particles contain either REH2 or MRB3010 but share the core GAP1 and other proteins detected by RNA photo-crosslinking. Analyses of ...
Background The post-transcriptional processing of pre-mRNAs by RNA editing contributes significantly to the complexity of the mammalian transcriptome. RNA editing by site-selective A-to-I modification also regulates protein function through recoding of genomically specified sequences. The adenosine deaminase ADAR2 is the main enzyme responsible for recoding editing and loss of ADAR2 function in mice leads to a phenotype of epilepsy and premature death. Although A-to-I RNA editing is known to be subject to developmental and cell-type specific regulation, there is little knowledge regarding the mechanisms that regulate RNA editing in vivo. Therefore, the characterization of ADAR expression and identification of alternative ADAR variants is an important prerequisite for understanding the mechanisms for regulation of RNA editing and the causes for deregulation in disease. Methodology/Principal Findings Here we present evidence for a new ADAR2 splice variant that extends the open reading frame of ADAR2 by
abstract = {Adenosine-to-inosine (A-to-I) RNA editing is a conserved post-transcriptional mechanism mediated by ADAR enzymes that diversifies the transcriptome by altering selected nucleotides in RNA molecules1. Although many editing sites have recently been discovered2,3,4,5,6,7, the extent to which most sites are edited and how the editing is regulated in different biological contexts are not fully understood8,9,10. Here we report dynamic spatiotemporal patterns and new regulators of RNA editing, discovered through an extensive profiling of A-to-I RNA editing in 8,551 human samples (representing 53 body sites from 552 individuals) from the Genotype-Tissue Expression (GTEx) project and in hundreds of other primate and mouse samples. We show that editing levels in non-repetitive coding regions vary more between tissues than editing levels in repetitive regions. Globally, ADAR1 is the primary editor of repetitive sites and ADAR2 is the primary editor of non-repetitive coding sites, whereas the ...
Double-stranded RNA adenosine deaminase (ADAR1) is an ubiquitous enzyme in metazoa that edits pre-mRNA changing adenosine to inosine in regions of double-stranded RNA. Zalpha, an N-terminal domain of human ADAR1 encompassing 76 amino acid residues, shows apparent specificity for the left-handed Z-DN …
Source: NIH.gov. A set of proteins involved in the bodys natural defences produces a large number of mutations in human DNA, according to a study led by researchers at the National Institutes of Health. The findings suggest that these naturally produced mutations are just as powerful as known cancer-causing agents in producing tumors.. The proteins are part of a group called apolipoprotein B mRNA-editing enzyme catalytic polypeptide-like (APOBEC) cytidine deaminases. The investigators found that APOBEC mutations can outnumber all other mutations in some cancers, accounting for over two-thirds in some bladder, cervical, breast, head and neck, and lung tumours.. The scientists published their findings online July 14 in the journal Nature Genetics. Dmitry Gordenin, Ph.D., is corresponding author of the paper and a senior associate scientist at the National Institute of Environmental Health Sciences (NIEHS), part of NIH. He said scientists knew the main functions of APOBEC cytosine deaminases were ...
Has A-to-I RNA editing activity on extended dsRNA: edits RNA-binding protein Rnp4F. A-to-I editing of pre-mRNAs acts predominantly through nervous system targets to affect adult nervous system integrity, function and behavior. Essential for adaptation to environmental stresses, such as oxygen deprivation, and for the prevention of premature neuronal degeneration, through the editing of ion channels as targets.
To investigate whether the JAK-STAT (Janus kinase-signal transducers and activators of transcription) pathway participates in the regulation of APOBEC3G (Apolipoprotein B mRNA-editing enzyme, catalytic polypeptide-like 3G) gene transcription and to study the molecular mechanisms of interferon resistance in patients with chronic hepatitis B (CHB), changes in APOBEC3G and STAT-1 expression levels in HepG2.2.15 cells after treatment with various concentrations of IFN-a, were detected using real-time RT-PCR and Western-blot. In addition, the differences in STAT-1 and APOBEC3G expression in liver tissues were also observed in patients with different anti-viral responses to IFN-a. It is found that IFN-a suppressed HBV replication and expression markedly in HepG2.2.15 cells, and simultaneously enhanced APOBEC3G expression in a dose- or time-dependent manner within a certain range. Moreover, a corresponding gradual increase in STAT-1 expression levels was also observed. The expression levels of STAT-1 and
The most significant finding of this study is that the expression and activity of the RNA editase ADAR1 is upregulated in lungs subjected to endotoxin-induced microvascular injury and in alveolar macrophages stimulated with endotoxin, live bacteria, or IFN. These findings implicate for the first time RNA editing as a possible inflammatory event. Specifically, the data suggest that A-to-I RNA editing is involved in the pathogenic mechanisms that lead to acute lung injury. Another significant finding is that ADAR1 is expressed in sham mouse lungs, which was previously demonstrated only in the rat.8 The sequence of early production of IFN, a known inducer of ADAR1,12 followed by ADAR1 expression and development of microvascular lung injury, suggests that A-to-I RNA editing may be a proximal event in the inflammatory cascade involved in the pathogenesis of microvascular lung injury. Furthermore, it is conceivable that early induction of pulmonary IFN during the inflammatory process could be the ...
RNA editing is a regulatory mechanism in which nucleotides are altered posttranscriptionally and most frequently involves conversion of adenosine to inosine, which is recognized as a guanosine during translation. Chen and colleagues performed RNA sequencing analysis to identify molecular changes in hepatocellular carcinoma (HCC) samples that might contribute to disease progression, and they detected elevated adenosine-to-inosine RNA editing of antizyme inhibitor 1 (AZIN1) in HCC samples compared with adjacent normal tissues. The frequency of AZIN1 editing increased during HCC progression and was correlated with liver cirrhosis, tumor recurrence, and poor prognosis, suggesting that this recoding event may promote HCC pathogenesis. AZIN1 RNA modification was mediated by the p110 isoform of adenosine deaminase, RNA-specific (ADAR1), but not by other ADAR family members, and resulted in substitution of glycine for serine at residue 367 in the AZIN1 protein, which was predicted to induce a ...
The current research, which involved 13 patients with lupus and eight healthy participants, was based on Laxminarayanas earlier findings that 150-kDa ADAR1, one of the three enzymes involved in editing gene messages, is higher in the T cells of lupus patients compared to those without lupus. ADARs are ademosine deaminases that act on RNA.. Laxminarayana made the initial finding about 150-kDa ADAR1 levels in 2002 and has been working to solve the mystery of how it is related to the development of lupus. In the current study, Laxminarayana found that the higher levels of 150-kDa ADAR1 alters the editing induced by two other ADAR enzymes and may cause an imbalance of proteins. Editing by the two other ADAR enzymes is a normal cellular process; it is 150-kDa ADAR1 that causes normal editing to go awry.. The process is complicated and took Laxminarayana years to uncover. The current studies demonstrate that, essentially, too much 150-kDa ADAR1 results in an increase in the gene message of ...
While most discussions about big data typically focus on the massive size of data, a better discussion might be about what big data is really providing: objective information about peoples behavior - uncensored, unfiltered, unedited. This Harvard Business Review paper, Predicting Customers (Unedited) Behavior explores how the analysis of big data is increasingly about finding the connections between peoples behavior and outcomes. ...
While most discussions about big data typically focus on the massive size of data, a better discussion might be about what big data is really providing: objective information about peoples behavior - uncensored, unfiltered, unedited. This Harvard Business Review paper, Predicting Customers (Unedited) Behavior explores how the analysis of big data is increasingly about finding the connections between peoples behavior and outcomes. ...
The moorings are in a well-sheltered anchorage.. Farmers Cay Yacht Club announced in January 2016 that its nine moorings in the Harbour have been redone with all new stainless steel chain and line.. Also, the dock has been re-planked and braced. The restaurant is open from 9 am to midnight.. Other moorings close to the Little Harbour are owned by other businesses on the Cay and it can be tricky to find out which one to pay as the mooring balls are poorly marked.. The tidal current is swift and the bottom well scoured, so unless your draft allows anchoring in the sand to the east of the channel, it is best to use a mooring.. See comments from cruisers at bottom of page re. condition of moorings.. Last updated July 2017.. Note that Guana Hideaways Marina on Great Guana Cay is not operational (February 2017) and has been removed from Noonsite listings.. ...
This gene encodes a member of the AID/APOBEC family of polynucleotide (deoxy)cytidine deaminases, which convert cytidine to uridine. Other AID/APOBEC family members are involved in mRNA editing, somatic hypermutation and recombination of immunoglobulin genes, and innate immunity to retroviral infection. [provided by RefSeq, Jul 2008 ...
stability and fatigue of analysis mooring system and which software is better for solve it?Sorry i dont know dat but i wanna know the th emooring te...
Kegunaan tali mooring kapal memang sangat bermanfaat bagi semua pihak di areal dermaga. Tidak hanya akan mempermudah dalam segi penambat yang aman dan
CSA-dependent degradation of CSB by the ubiquitin-proteasome pathway establishes a link between complementation factors of the Cockayne syndrome ...
Upon binding with guide RNA, the two structural lobes of Cas9 reorient so that the two nucleic acid binding clefts face each other, forming a central DNA binding channel that interfaces with target DNA.
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Happy Monday!!! Tomorrow is my birthday!!! WOoHoO- for those who care Ill be 25 years old. Go Me. Last week I had my query critique. It went better than I could ever expected. It has since then been revised and Ive tested the waters now. Thats right Ive dived into the querying world. And Ive been cupcaked (also known as rejected but those are hurtful and harsh words and arent used here. I was given the word my fabulous blogger friend Karen Amanda Hooper). Its not always a negative (its a cupcake for junk sake, cupcakes rock). When I received my first one I was actually excited. My husband and I celebrated. Its like a rite of passage. Something you have to do to realize youre one step closer to that agent. There is an agent out for you. YOUR work is good enough. Dont give up. Just take each rejection with a grain of salt. Appreciate each company for even bothering to take a look. They dont have too. They look at thousands. So the next time you get a cupcake look at it as a positive. ...
This is the non-edited Straight Out Of the Camera (SOOC) shot that I took on a dreary overcast day when Jocelyn was already getting sick. It took me, Jaina, and Jayces therapist to get her to smile even this 1/2 smile. The newly put up Christmas tree was totally blocking my light (what little light I had at 4 PM on an overcast day) from the window. I am hoping to salvage this picture in GIMP and make it match the other 11 monthly pictures so I can print them in a collage frame next month ...
Methods. int :: Int -, repr h IntSource. add :: repr h Int -, repr h Int -, repr h IntSource. z :: repr (a, h) aSource. s :: repr h a -, repr (any, h) aSource. lam :: repr (a, h) b -, repr h (a -, b)Source. app :: repr h (a -, b) -, repr h a -, repr h bSource ...
Plasmid pSpCas9_BB_2A-GFP_MAPRE1-gRNA#2 from Dr. Torsten Wittmanns lab contains the insert MAPRE1 gRNA #1 (targets Exon 1) and is published in Nat Cell Biol. 2018 Jan 29. pii: 10.1038/s41556-017-0028-5. doi: 10.1038/s41556-017-0028-5. This plasmid is available through Addgene.
利用CRISPER系統編輯基因,為您提供基因敲除(CRISPER)或激活本底基因表達(CRISPERa)的文庫篩選工具Guide RNA,不同Guide RNA工具形式可支持瞬轉、穩轉包病毒體系,亦或提供慢病毒顆粒。從各類小基因家族到全基因組范圍,為您提供靈活、方便和高可信度的篩選結果。. 我們的優勢 ...