112 results match your criteria interaction hexanucleotide

-derived arginine-containing dipeptide repeats associate with axonal transport machinery and impede microtubule-based motility.

Sci Adv 2021 Apr 9;7(15). Epub 2021 Apr 9.

KU Leuven-University of Leuven, Department of Neurosciences, Experimental Neurology and Leuven Brain Institute (LBI), Leuven, Belgium.

A hexanucleotide repeat expansion in the gene is the most common genetic cause of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). How this mutation leads to these neurodegenerative diseases remains unclear. Here, we show using patient stem cell-derived motor neurons that the repeat expansion impairs microtubule-based transport, a process critical for neuronal survival. Read More

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Intermediate lengths of the hexanucleotide repeat expansion may synergistically contribute to attention deficit hyperactivity disorder in child and his father: case report.

Neurocase 2021 Mar 18:1-8. Epub 2021 Mar 18.

Biological Psychiatry Unit, IRCCS Istituto Centro San Giovanni Di Dio Fatebenefratelli, Brescia, Italy.

We have summarized the abstract section as follows: "We report a son and his father affected by Attention Deficit Hyperactivity Disorder (ADHD). They belonged to a larger cohort (116 ADHD children, 20 related parents, 77 controls) wholly genotyped forexpansion. Ten ADHD susceptibility genes were further investigated in the family. Read More

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Cryo-EM structure of C9ORF72-SMCR8-WDR41 reveals the role as a GAP for Rab8a and Rab11a.

Proc Natl Acad Sci U S A 2020 05 17;117(18):9876-9883. Epub 2020 Apr 17.

Department of Urology, State Key Laboratory of Biotherapy, West China Hospital, College of Life Sciences, Sichuan University, 610041 Chengdu, China;

A massive intronic hexanucleotide repeat (GGGGCC) expansion in is a genetic origin of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). Recently, C9ORF72, together with SMCR8 and WDR41, has been shown to regulate autophagy and function as Rab GEF. However, the precise function of C9ORF72 remains unclear. Read More

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A synthetic Pur-based peptide binds and alters G-quadruplex secondary structure present in the expanded RNA repeat of C9orf72 ALS/FTD.

Biochim Biophys Acta Mol Cell Res 2020 06 6;1867(6):118674. Epub 2020 Feb 6.

Department of Microbiology and Molecular Cell Biology, Eastern Virginia Medical School, Norfolk, VA 23507, USA. Electronic address:

Increased Pur-alpha (Pura) protein levels in animal models alleviate certain cellular symptoms of the disease spectrum amyotrophic lateral sclerosis/frontotemporal dementia (ALS/FTD). Pura is a member of the Pur family of evolutionarily conserved guanine-rich polynucleotide binding proteins containing a repeated signature PUR domain of 60-80 amino acids. Here we have employed a synthetic peptide, TZIP, similar to a Pur domain, but with sequence alterations based on a consensus of evolutionarily conserved Pur family binding domains and having an added transporter sequence. Read More

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Small Molecule Targeting TDP-43's RNA Recognition Motifs Reduces Locomotor Defects in a Model of Amyotrophic Lateral Sclerosis (ALS).

ACS Chem Biol 2019 09 27;14(9):2006-2013. Epub 2019 Aug 27.

Department of Pharmacology, College of Medicine , University of Arizona , Tucson , Arizona 85724 , United States.

RNA dysregulation likely contributes to disease pathogenesis of amyotrophic lateral sclerosis (ALS) and other neurodegenerative diseases. A pathological form of the transactive response (TAR) DNA binding protein (TDP-43) binds to RNA in stress granules and forms membraneless, amyloid-like TDP-43 aggregates in the cytoplasm of ALS motor neurons. In this study, we hypothesized that by targeting the RNA recognition motif (RRM) domains of TDP-43 that confer a pathogenic interaction between TDP-43 and RNA, motor neuron toxicity could be reduced. Read More

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September 2019

The ALS-FTD-linked gene product, C9orf72, regulates neuronal morphogenesis via autophagy.

Autophagy 2019 05 28;15(5):827-842. Epub 2019 Jan 28.

a Department of Physiology , National University of Singapore , Singapore , Singapore.

Mutations in C9orf72 leading to hexanucleotide expansions are the most common genetic causes for amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). A phenotype resembling ALS and FTD is seen in transgenic mice overexpressing the hexanucleotide expansions, but is absent in C9orf72-deficient mice. Thus, the exact function of C9orf72 in neurons and how loss of C9orf72 may contribute to neuronal dysfunction remains to be clearly defined. Read More

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Unraveling the Role of RNA Mediated Toxicity of Repeats in C9-FTD/ALS.

Front Neurosci 2017 15;11:711. Epub 2017 Dec 15.

Centre for Interdisciplinary Research in Basic Sciences, Jamia Millia Islamia, Jamia Nagar, India.

The most frequent genetic cause of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) is intronic hexanucleotide (G4C2) repeat expansions (HRE) in the gene. The non-exclusive pathogenic mechanisms by which C9orf72 repeat expansions contribute to these neurological disorders include loss of C9orf72 function and gain-of-function determined by toxic RNA molecules and dipeptides repeats protein toxicity. The expanded repeats are transcribed bidirectionally and forms RNA foci in the central nervous system, and sequester key RNA-binding proteins (RBPs) leading to impairment in RNA processing events. Read More

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December 2017

Structural insights into the assembly and polyA signal recognition mechanism of the human CPSF complex.

Elife 2017 12 23;6. Epub 2017 Dec 23.

Department of Biochemistry, University of Zurich, Zurich, Switzerland.

3' polyadenylation is a key step in eukaryotic mRNA biogenesis. In mammalian cells, this process is dependent on the recognition of the hexanucleotide AAUAAA motif in the pre-mRNA polyadenylation signal by the cleavage and polyadenylation specificity factor (CPSF) complex. A core CPSF complex comprising CPSF160, WDR33, CPSF30 and Fip1 is sufficient for AAUAAA motif recognition, yet the molecular interactions underpinning its assembly and mechanism of PAS recognition are not understood. Read More

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December 2017

Structural insights into the specific recognition of DSR by the YTH domain containing protein Mmi1.

Biochem Biophys Res Commun 2017 09 20;491(2):310-316. Epub 2017 Jul 20.

State Key Laboratory of Genetic Engineering, Collaborative Innovation Center of Genetics and Development, Department of Biochemistry, Institute of Plant Biology, School of Life Sciences, Fudan University, Shanghai, China. Electronic address:

Meiosis is one of the most dramatic differentiation programs accompanied by a striking change in gene expression profiles in fission yeast Schizosaccharomyces pombe. Whereas a number of meiosis-specific transcripts are expressed untimely in mitotic cells, and the entry of meiosis will be blocked as the accumulation of meiosis-specific mRNAs in the mitotic cells. A YTH domain containing protein Mmi1 was identified as a pivotal effector in a post-transcriptional event termed selective elimination of meiosis-specific mRNAs. Read More

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September 2017

SRSF1-dependent nuclear export inhibition of C9ORF72 repeat transcripts prevents neurodegeneration and associated motor deficits.

Nat Commun 2017 07 5;8:16063. Epub 2017 Jul 5.

Sheffield Institute for Translational Neuroscience, Department of Neuroscience, University of Sheffield, 385a Glossop Road, Sheffield S10 2HQ, UK.

Hexanucleotide repeat expansions in the C9ORF72 gene are the commonest known genetic cause of amyotrophic lateral sclerosis and frontotemporal dementia. Expression of repeat transcripts and dipeptide repeat proteins trigger multiple mechanisms of neurotoxicity. How repeat transcripts get exported from the nucleus is unknown. Read More

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C9orf72 and RAB7L1 regulate vesicle trafficking in amyotrophic lateral sclerosis and frontotemporal dementia.

Brain 2017 04;140(4):887-897

Department of Physiology, Anatomy and Genetics, University of Oxford, South Parks Road, Oxford, OX1 3QX, UK.

A non-coding hexanucleotide repeat expansion in intron 1 of the C9orf72 gene is the most common cause of amyotrophic lateral sclerosis and frontotemporal dementia (C9ALS/FTD), however, the precise molecular mechanism by which the C9orf72 hexanucleotide repeat expansion directs C9ALS/FTD pathogenesis remains unclear. Here, we report a novel disease mechanism arising due to the interaction of C9ORF72 with the RAB7L1 GTPase to regulate vesicle trafficking. Endogenous interaction between C9ORF72 and RAB7L1 was confirmed in human SH-SY5Y neuroblastoma cells. Read More

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Characterization of the interaction between heme and a parallel G-quadruplex DNA formed from d(TTGAGG).

Biochim Biophys Acta Gen Subj 2017 May 9;1861(5 Pt B):1264-1270. Epub 2016 Nov 9.

Department of Chemistry, University of Tsukuba, Tsukuba 305-8571, Japan; Life Science Center of Tsukuba Advanced Research Alliance, University of Tsukuba, Tsukuba 305-8577, Japan. Electronic address:

Structure-function relationships of complexes between heme and G-quadruplex DNAs have attracted interest from researchers in related fields. A carbon monoxide adduct of a complex between heme and a parallel G-quadruplex DNA formed from hexanucleotide d(TTGAGG) (heme-[d(TTGAGG)] complex) has been characterized using H NMR spectroscopy, and the obtained results were compared with those for the heme-[d(TTAGGG)] complex previously studied in order to elucidate the effect of the incorporation of an A-quartet into stacked G-quartets in the 3'-terminal region of the DNA on the structure of the heme-DNA complex. We found that a π-π stacking interaction between the porphyrin moiety of the heme and the 3'-terminal G-quartet of the DNA is affected by the nature of the stacked G-quartets. Read More

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Identification of a GUAAY Pentaloop Sequence Involved in a Novel RNA Loop-Helix Interaction.

J Mol Biol 2016 12 19;428(24 Pt B):4882-4889. Epub 2016 Oct 19.

Department of Chemistry and Biochemistry, University of California, San Diego, La Jolla, CA, 92093, USA. Electronic address:

Large RNAs often utilize GNRA tetraloops as structural elements to stabilize the overall tertiary fold. These tetraloop-receptor (TR) interactions have a conserved geometry in which the tetraloop docks into the receptor at an angle of ~15° from the helix containing the receptor. Here, we show that the conserved GUAAY pentaloop found in domain III of group IIB1 introns participates in a novel class of RNA tertiary interaction with a geometry and mode of binding that are significantly different from that found in GNRA TR interactions. Read More

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December 2016

C9ORF72 interaction with cofilin modulates actin dynamics in motor neurons.

Nat Neurosci 2016 12 10;19(12):1610-1618. Epub 2016 Oct 10.

Institute of Clinical Neurobiology, University Hospital of Wuerzburg, Wuerzburg, Germany.

Intronic hexanucleotide expansions in C9ORF72 are common in amyotrophic lateral sclerosis (ALS) and frontotemporal dementia, but it is unknown whether loss of function, toxicity by the expanded RNA or dipeptides from non-ATG-initiated translation are responsible for the pathophysiology. We determined the interactome of C9ORF72 in motor neurons and found that C9ORF72 was present in a complex with cofilin and other actin binding proteins. Phosphorylation of cofilin was enhanced in C9ORF72-depleted motor neurons, in patient-derived lymphoblastoid cells, induced pluripotent stem cell-derived motor neurons and post-mortem brain samples from ALS patients. Read More

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December 2016

C9orf72's Interaction with Rab GTPases-Modulation of Membrane Traffic and Autophagy.

Bor L Tang

Front Cell Neurosci 2016 7;10:228. Epub 2016 Oct 7.

Department of Biochemistry, Yong Loo Lin School of Medicine, National University of SingaporeSingapore, Singapore; NUS Graduate School for Integrative Sciences and Engineering, National University of SingaporeSingapore, Singapore.

Hexanucleotide repeat expansion in an intron of Chromosome 9 open reading frame 72 () is the most common genetic cause of Amyotrophic Lateral Sclerosis (ALS) and Frontotemporal Dementia (FTD). While functional haploinsufficiency of C9orf72 resulting from the mutation may play a role in ALS/FTD, the actual cellular role of the protein has been unclear. Recent findings have now shown that C9orf72 physically and functionally interacts with multiple members of the Rab small GTPases family, consequently exerting important influences on cellular membrane traffic and the process of autophagy. Read More

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October 2016

The C9ORF72 GGGGCC expansion forms RNA G-quadruplex inclusions and sequesters hnRNP H to disrupt splicing in ALS brains.

Elife 2016 09 13;5. Epub 2016 Sep 13.

Department of Biological Sciences, Columbia University, New York, United States.

An expanded GGGGCC hexanucleotide in (C9) is the most frequent known cause of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). It has been proposed that expanded transcripts adopt G-quadruplex (G-Q) structures and associate with proteins, but whether this occurs and contributes to disease is unknown. Here we show first that the protein that predominantly associates with GGGGCC repeat RNA in vitro is the splicing factor hnRNP H, and that this interaction is linked to G-Q formation. Read More

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September 2016

Gain of Toxicity from ALS/FTD-Linked Repeat Expansions in C9ORF72 Is Alleviated by Antisense Oligonucleotides Targeting GGGGCC-Containing RNAs.

Neuron 2016 05 21;90(3):535-50. Epub 2016 Apr 21.

Ludwig Institute for Cancer Research, University of California, San Diego, La Jolla, CA 92093, USA; Department of Neurosciences, University of California, San Diego, La Jolla, CA 92093, USA. Electronic address:

Hexanucleotide expansions in C9ORF72 are the most frequent genetic cause of amyotrophic lateral sclerosis and frontotemporal dementia. Disease mechanisms were evaluated in mice expressing C9ORF72 RNAs with up to 450 GGGGCC repeats or with one or both C9orf72 alleles inactivated. Chronic 50% reduction of C9ORF72 did not provoke disease, while its absence produced splenomegaly, enlarged lymph nodes, and mild social interaction deficits, but not motor dysfunction. Read More

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Kissing-loop interaction between 5' and 3' ends of tick-borne Langat virus genome 'bridges the gap' between mosquito- and tick-borne flaviviruses in mechanisms of viral RNA cyclization: applications for virus attenuation and vaccine development.

Nucleic Acids Res 2016 Apr 4;44(7):3330-50. Epub 2016 Feb 4.

Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases (NIAID), National Institutes of Health (NIH), Bethesda, MD, 20892-3203 USA

Insertion of microRNA target sequences into the flavivirus genome results in selective tissue-specific attenuation and host-range restriction of live attenuated vaccine viruses. However, previous strategies for miRNA-targeting did not incorporate a mechanism to prevent target elimination under miRNA-mediated selective pressure, restricting their use in vaccine development. To overcome this limitation, we developed a new approach for miRNA-targeting of tick-borne flavivirus (Langat virus, LGTV) in the duplicated capsid gene region (DCGR). Read More

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Structural basis of nucleic-acid recognition and double-strand unwinding by the essential neuronal protein Pur-alpha.

Elife 2016 Jan 8;5. Epub 2016 Jan 8.

Institute of Structural Biology, Helmholtz Zentrum München - German Research Center for Environmental Health, Neuherberg, Germany.

The neuronal DNA-/RNA-binding protein Pur-alpha is a transcription regulator and core factor for mRNA localization. Pur-alpha-deficient mice die after birth with pleiotropic neuronal defects. Here, we report the crystal structure of the DNA-/RNA-binding domain of Pur-alpha in complex with ssDNA. Read More

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January 2016

Isoform-specific antibodies reveal distinct subcellular localizations of C9orf72 in amyotrophic lateral sclerosis.

Ann Neurol 2015 Oct 29;78(4):568-83. Epub 2015 Aug 29.

Tanz Center for Research in Neurodegenerative Diseases, University of Toronto, Toronto, Ontario, Canada.

Objective: A noncoding hexanucleotide repeat expansion in C9orf72 is the most common cause of amyotrophic lateral sclerosis (ALS) and frontotemporal lobar degeneration (FTLD). It has been reported that the repeat expansion causes a downregulation of C9orf72 transcripts, suggesting that haploinsufficiency may contribute to disease pathogenesis. Two protein isoforms are generated from three alternatively spliced transcripts of C9orf72; a long form (C9-L) and a short form (C9-S), and their function(s) are largely unknown owing to lack of specific antibodies. Read More

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October 2015

Bioinformatics Data Mining Approach Suggests Coexpression of AGTPBP1 with an ALS-linked Gene C9orf72.

J Cent Nerv Syst Dis 2015 8;7:15-26. Epub 2015 Jun 8.

Department of Bioinformatics and Molecular Neuropathology, Meiji Pharmaceutical University, Kiyose, Tokyo, Japan.

Background: Expanded GGGGCC hexanucleotide repeats located in the noncoding region of the chromosome 9 open reading frame 72 (C9orf72) gene represent the most common genetic abnormality for familial and sporadic amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). Formation of nuclear RNA foci, accumulation of repeat-associated non-ATG-translated dipeptide-repeat proteins, and haploinsufficiency of C9orf72 are proposed for pathological mechanisms of C9ALS/FTD. However, at present, the physiological function of C9orf72 remains largely unknown. Read More

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A Multiprotein DNA Translocation Complex Directs Intramycelial Plasmid Spreading during Streptomyces Conjugation.

mBio 2015 May 26;6(3):e02559-14. Epub 2015 May 26.

Interfakultaeres Institut für Mikrobiologie und Infektionsmedizin Tuebingen IMIT, Mikrobiologie, Biotechnologie, Eberhard Karls Universitaet Tuebingen, Tuebingen, Germany

Unlabelled: Conjugative DNA transfer in mycelial Streptomyces is a unique process involving the transfer of a double-stranded plasmid from the donor into the recipient and the subsequent spreading of the transferred plasmid within the recipient mycelium. This process is associated with growth retardation of the recipient and manifested by the formation of circular inhibition zones, named pocks. To characterize the unique Streptomyces DNA transfer machinery, we replaced each gene of the conjugative 12. Read More

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Thioester Bonds of Thiocoraline Can Be Replaced with NMe-Amide Bridges without Affecting Its DNA-Binding Properties.

ACS Med Chem Lett 2014 Jan 4;5(1):45-50. Epub 2013 Nov 4.

Centre for Biological Sciences, Life Sciences Building 85, University of Southampton , Southampton SO17 1BJ, U.K.

In the search for new drug candidates for DNA recognition, affinity and sequence selectivity are two of the most important features. NMe-azathiocoraline, a synthetic antitumor bisintercalator derived from the natural marine product thiocoraline, shows similar potency to the parent compound, as well as possessing enhanced stability. Analysis of the DNA-binding selectivity of NMe-azathiocoraline by DNase I footprinting using universal substrates with all 136 tetranucleotides and all possible symmetrical hexanucleotide sequences revealed that, although this ligand binds to all CpG steps with lower affinities than thiocoraline, it displays additional binding to AT-rich sites. Read More

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January 2014

No interaction between tau and TDP-43 pathologies in either frontotemporal lobar degeneration or motor neurone disease.

Neuropathol Appl Neurobiol 2014 Dec;40(7):844-54

Clinical and Cognitive Sciences Research Group, Institute of Brain, Behaviour and Mental Health, Faculty of Medical and Human Sciences, University of Manchester, Salford Royal Hospital, Salford.

Introduction: Frontotemporal lobar degeneration (FTLD) is classified mainly into FTLD-tau and FTLD-TDP according to the protein present within inclusion bodies. While such a classification implies only a single type of protein should be present, recent studies have demonstrated dual tau and TDP-43 proteinopathy can occur, particularly in inherited FTLD.

Methods: We therefore investigated 33 patients with FTLD-tau (including 9 with MAPT mutation) for TDP-43 pathological changes, and 45 patients with FTLD-TDP (including 12 with hexanucleotide expansion in C9ORF72 and 12 with GRN mutation), and 23 patients with motor neurone disease (3 with hexanucleotide expansion in C9ORF72), for tauopathy. Read More

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December 2014

Screening for protein-DNA interactions by automatable DNA-protein interaction ELISA.

PLoS One 2013 11;8(10):e75177. Epub 2013 Oct 11.

Plant Physiology, Center for Plant Molecular Biology, University of Tuebingen, Tuebingen, Germany.

DNA-binding proteins (DBPs), such as transcription factors, constitute about 10% of the protein-coding genes in eukaryotic genomes and play pivotal roles in the regulation of chromatin structure and gene expression by binding to short stretches of DNA. Despite their number and importance, only for a minor portion of DBPs the binding sequence had been disclosed. Methods that allow the de novo identification of DNA-binding motifs of known DBPs, such as protein binding microarray technology or SELEX, are not yet suited for high-throughput and automation. Read More

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NMR-based structure of anticancer drug mitoxantrone stacked with terminal base pair of DNA hexamer sequence d-(ATCGAT)2.

J Biomol Struct Dyn 2014 1;32(7):1164-83. Epub 2013 Jul 1.

a Department of Chemistry , National Institute of Technology Hamirpur , Hamirpur , 177 001 , India .

Mitoxantrone is a promising antitumor drug having considerably reduced cardiotoxicity as compared to anthracyclines. Its binding to deoxyhexanucleotides sequence d-(ATCGAT)2 has been studied by proton and phosphorous-31 nuclear magnetic resonance spectroscopy. The stoichiometry reveals that 1:1 and 2:1 mitoxantrone-d(ATCGAT)2 complexes are formed in solution. Read More

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Novel TARDBP sequence variant and C9ORF72 repeat expansion in a family with frontotemporal dementia.

Alzheimer Dis Assoc Disord 2014 Apr-Jun;28(2):190-3

Departments of *Neurology ‡Ophthalmology, Institute of Clinical Medicine, University of Oulu †Clinical Research Center, Oulu University Hospital, Oulu, Finland §Neuromuscular Diseases Research Unit, Laboratory of Neurogenetics, National Institute on Aging, National Institutes of Health, Bethesda, MD ∥Department of Neurology, Institute of Clinical Medicine, University of Eastern Finland ¶Department of Neurology, Kuopio University Hospital, Kuopio, Finland.

Frontotemporal lobar degeneration (FTLD) is a genetically heterogenous syndrome and has been associated most recently with a hexanucleotide repeat expansion within the C9ORF72 gene. Pathogenic TDP-43 gene (TARDBP) mutations have been identified in amyotrophic lateral sclerosis, but the role of TARDBP mutations in FTLD is more contradictory. To investigate the role of TARDBP mutations in a clinical series of Finnish FTLD patients, we sequenced TARDBP exons 1 to 6 in 77 FTLD patients. Read More

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January 2015

Hexanucleotide motifs mediate recruitment of the RNA elimination machinery to silent meiotic genes.

Open Biol 2012 Mar;2(3):120014

Department of Biophysics and Biochemistry, Graduate School of Science, University of Tokyo, Hongo, Tokyo 113-0033, Japan.

The selective elimination system blocks the accumulation of meiosis-specific mRNAs during the mitotic cell cycle in fission yeast. These mRNAs harbour a region, the determinant of selective removal (DSR), which is recognized by a YTH-family RNA-binding protein, Mmi1. Mmi1 directs target transcripts to destruction in association with nuclear exosomes. Read More

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Functional analysis of sequence motifs involved in the polyadenylation of Trichomonas vaginalis mRNAs.

Eukaryot Cell 2012 Jun 30;11(6):725-34. Epub 2012 Mar 30.

Departamento de Biología Molecular y Biotecnología, Instituto de Investigaciones Biomédicas, Universidad Nacional Autónoma de México, México DF, México.

Synthesis of functional mRNA in eukaryotes involves processing of precursor transcripts, including the addition of a poly(A) tail at the 3' end. A multiprotein complex recognizes a polyadenylation signal, generally the hexanucleotide AAUAAA in metazoans, to direct processing of the pre-mRNA. Based on sequence analysis of several cDNAs, we have previously suggested that the UAAA tetranucleotide (which may include the UAA translation stop codon) could be the polyadenylation signal in Trichomonas vaginalis, a parasitic protozoon that causes human trichomoniasis. Read More

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Platinated DNA affects zinc finger conformation. Interaction of a platinated single-stranded oligonucleotide and the C-terminal zinc finger of nucleocapsid protein HIVNCp7.

Biochemistry 2012 Feb 14;51(8):1752-61. Epub 2012 Feb 14.

Department of Chemistry, Virginia Commonwealth University, Richmond, Virginia 23284, United States.

This paper describes for the first time the intimate molecular details of the association between a platinated oligonucleotide and a zinc finger peptide. Site-specific platination of the guanine in a single-stranded hexanucleotide gave {[Pt(dien)d(5'-TACGCC-3')], Pt(dien)(6-mer)} (II) characterized by mass spectrometry and (1)H nuclear magnetic resonance (NMR) spectroscopy. The work extends the study of platinum-nucleobase complex-zinc finger interactions using small molecules such as [Pt(dien)(9-EtGua)](2+) (I). Read More

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February 2012