D. Pearce

D. Pearce, S. Chattopadhyay, C. D. Cottone, 2001, European journal of paediatric neurology : EJPN : official journal of the European Paediatric Neurology Society.

Neural and extraneural expression of the neuronal ceroid lipofuscinoses genes CLN1, CLN2, and CLN3: functional implications for CLN3.

D. Pearce, S. Chattopadhyay, S. Chattopadhyay, 2000, Molecular genetics and metabolism.

Investigation of Batten disease with the yeast Saccharomyces cerevisiae.

F. Sherman, D. Pearce, 1999, Molecular genetics and metabolism.

Studies of pH regulation by Btn1p, the yeast homolog of human Cln3p.

F. Sherman, D. Pearce, S. A. Nosel, 1999, Molecular genetics and metabolism.

Sequential down-regulation of E-cadherin with squamous cell carcinoma progression: loss of E-cadherin via a prostaglandin E2-EP2 dependent posttranslational mechanism.

M. O’Banion, G. Scott, D. Pearce, 2007, Cancer research.

Acidified drinking water attenuates motor deficits and brain pathology in a mouse model of a childhood neurodegenerative disorder

D. Pearce, Logan M Langin, A. Kovács, 2022, Scientific Reports.

The role of nonsense-mediated decay in neuronal ceroid lipofuscinosis.

D. Pearce, Chun‐Hung Chan, Jake N. Miller, 2013, Human molecular genetics.

pH-dependent localization of Btn1p in the yeast model for Batten disease

D. Pearce, S. Padilla-Lopez, Devin M. Wolfe, 2010, Disease Models & Mechanisms.

Neurodevelopmental delay in the Cln3Δex7/8 mouse model for Batten disease

B. Sampaio-Marques, N. Osório, D. Pearce, 2009, Genes, brain, and behavior.

Transcript and in silico analysis of CLN3 in juvenile neuronal ceroid lipofuscinosis and associated mouse models.

H. Mitchison, D. Pearce, Chun‐Hung Chan, 2008, Human molecular genetics.

Immune system irregularities in lysosomal storage disorders

J. Cooper, D. Pearce, J. Castaneda, 2008, Acta Neuropathologica.

Genetic ataxia telangiectasia porcine model phenocopies the multisystemic features of the human disease.

D. Meyerholz, D. Pearce, J. Weimer, 2017, Biochimica et biophysica acta. Molecular basis of disease.

Protein product of CLN6 gene responsible for variant late‐onset infantile neuronal ceroid lipofuscinosis interacts with CRMP‐2

T. Gillingwater, T. Wishart, D. Pearce, 2009, Journal of neuroscience research.

Lysosome dysfunction in the pathogenesis of kidney diseases

D. Pearce, K. Surendran, Seasson P Vitiello, 2014, Pediatric Nephrology.

Genotype does not predict severity of behavioural phenotype in juvenile neuronal ceroid lipofuscinosis (Batten disease)

J. Mink, J. Kwon, F. Marshall, 2010, Developmental medicine and child neurology.

Nitric Oxide Signaling Is Disrupted in the Yeast Model for Batten Disease □ D

J. Laranjinha, C. Leão, A. Carvalho, 2007 .

Therapeutic landscape for Batten disease: current treatments and future prospects

Tyler B. Johnson, D. Pearce, J. Weimer, 2019, Nature Reviews Neurology.

Detailed Clinical Phenotype and Molecular Genetic Findings in CLN3-Associated Isolated Retinal Degeneration

G. Holder, F. Raymond, R. MacLaren, 2017, JAMA ophthalmology.

Strategies for data analyses in a high resolution 1H NMR based metabolomics study of a mouse model of Batten disease

R. Mortishire-Smith, J. Griffin, J. Cooper, 2007, Metabolomics.

IgG entry and deposition are components of the neuroimmune response in Batten disease

J. Cooper, C. Guérin, D. Pearce, 2007, Neurobiology of Disease.

The neuronal ceroid lipofuscinoses

D. Pearce, J. Weimer, Yasser M Elshatory, 2007, NeuroMolecular Medicine.

The neuronal ceroid lipofuscinoses: mutations in different proteins result in similar disease.

D. Pearce, J. Weimer, Yasser M Elshatory, 2002, Neuromolecular medicine.

Autoimmunity to glutamic acid decarboxylase in the neurodegenerative disorder Batten disease

P. Rothberg, C. Wasserfall, D. Schatz, 2005, Neurology.

Juvenile neuronal ceroid lipofuscinosis (JNCL) and the eye.

M. Chung, D. Pearce, Mina M. Chung, 2009, Survey of ophthalmology.

Diagnosis of neuronal ceroid lipofuscinosis: mutation detection strategies.

P. Rothberg, D. Pearce, Amanda L. Getty, 2007, Expert opinion on medical diagnostics.

The Neuronal Ceroid Lipofuscinoses: Clinical Features and Molecular Basis of Disease

B. Davidson, D. Pearce, M. Cabrera-Salazar, 2007 .

BTN1, a Yeast Gene Corresponding to the Human Gene Responsible for Batten's Disease, is Not Essential for Viability, Mitochondrial Function, or Degradation of Mitochondrial ATP Synthase

F. Sherman, D. Pearce, 1997, Yeast.

Molecular correlates of axonal and synaptic pathology in mouse models of Batten disease

J. Cooper, T. Gillingwater, M. Sands, 2009, Human molecular genetics.

A Novel c.1135_1138delCTGT Mutation in CLN3 Leads to Juvenile Neuronal Ceroid Lipofuscinosis

A. Drack, D. Pearce, Jake N. Miller, 2013, Journal of child neurology.

A Novel c.776_777insA Mutation in CLN1 Leads to Infantile Neuronal Ceroid Lipofuscinosis

D. Pearce, Jake N. Miller, 2013, Journal of child neurology.

Altered glutamate receptor function in the cerebellum of the Ppt1−/− mouse, a murine model of infantile neuronal ceroid lipofuscinosis

R. Finn, D. Pearce, A. Kovács, 2012, Journal of neuroscience research.

A novel porcine model of CLN3 Batten disease recapitulates clinical phenotypes

Tyler B. Johnson, D. Pearce, C. Rogers, 2022, bioRxiv.

A Novel Porcine Model of CLN2 Batten Disease that Recapitulates Patient Phenotypes

Tyler B. Johnson, H. Johnson, D. Pearce, 2022, Neurotherapeutics.

A novel porcine model of ataxia telangiectasia reproduces neurological features and motor deficits of human disease.

D. Meyerholz, B. Darbro, Xiao-jun Wang, 2015, Human molecular genetics.

Altered sensitivity of cerebellar granule cells to glutamate receptor overactivation in the Cln3 Δex7/8 -knock-in mouse model of juvenile neuronal ceroid lipofuscinosis

R. Finn, D. Pearce, A. Kovács, 2011, Neurochemistry International.

Prenatal viral infection in mouse causes differential expression of genes in brains of mouse progeny: A potential animal model for schizophrenia and autism

A. Brooks, R. Sidwell, S. Fatemi, 2005, Synapse.

Maternal infection leads to abnormal gene regulation and brain atrophy in mouse offspring: Implications for genesis of neurodevelopmental disorders

Hao Huang, Georg Juckel, David A. Pearce, 2008, Schizophrenia Research.

Neuropsychological Symptoms of Juvenile-Onset Batten Disease: Experiences From 2 Studies

J. Mink, J. Kwon, F. Marshall, 2007, Journal of child neurology.

Comment on "Deletion of btn1, an orthologue of CLN3, increases glycolysis and perturbs amino acid metabolism in the fission yeast model of Batten disease".

D. Pearce, S. Padilla-Lopez, 2011, Molecular bioSystems.

Decreased sensitivity of palmitoyl protein thioesterase 1-deficient neurons to chemical anoxia

D. Pearce, A. Kovács, M. Meyer, 2017, Metabolic Brain Disease.

Chapter 148 – Paraplegin

D. Pearce, 2013 .

Comparative analysis of the gut microbiota composition in the Cln1R151X and Cln2R207X mouse models of Batten disease and in three wild-type mouse strains

Jing Zhao, D. Pearce, A. Kovács, 2020, Archives of Microbiology.

Age-dependent therapeutic effect of memantine in a mouse model of juvenile Batten disease

Angelika Saje, J. Cooper, D. Pearce, 2012, Neuropharmacology.

Temporary inhibition of AMPA receptors induces a prolonged improvement of motor performance in a mouse model of juvenile Batten disease

Angelika Saje, J. Cooper, É. Szabó, 2011, Neuropharmacology.

Immunosuppression alters disease severity in juvenile Batten disease mice

J. Cooper, D. Pearce, Chun‐Hung Chan, 2011, Journal of Neuroimmunology.

Attenuation of AMPA receptor activity improves motor skills in a mouse model of juvenile Batten disease

D. Pearce, A. Kovács, 2008, Experimental Neurology.

Cd2+, Mn2+, Ni2+ and Se2+ toxicity to Saccharomyces cerevisiae lacking YPK9p the orthologue of human ATP13A2.

D. Pearce, Barbara Stiller, Devin M. Wolfe, 2009, Biochemical and biophysical research communications.

Review: The Cct eukaryotic chaperonin subunits of Saccharomyces cerevisiae and other yeasts

F Sherman, F. Sherman, J. Ernst, 1996, Yeast.

Cerebellar defects in a mouse model of juvenile neuronal ceroid lipofuscinosis

J. Cooper, D. Pearce, Charlie C. Pontikis, 2009, Brain Research.

An autoantibody to GAD65 in sera of patients with juvenile neuronal ceroid lipofuscinoses

D. Pearce, D. Wenger, S. Chattopadhyay, 2002, Neurology.

Giardia duodenalis: exposure to metronidazole inhibits competitive interactions between isolates of the parasite in vitro.

B. Meloni, A. Lymbery, D. Pearce, 1996, The Journal of parasitology.

Enhanced stability in vivo of a thermodynamically stable mutant form of yeast iso-1-cytochrome c

F. Sherman, D. Pearce, 1995, Molecular and General Genetics MGG.

Altered arginine metabolism in the central nervous system (CNS) of the Cln3−/− mouse model of juvenile Batten disease

D. Pearce, Chun‐Hung Chan, D. Ramirez-Montealegre, 2009, Neuropathology and applied neurobiology.

Nitric oxide signaling is disrupted in the yeast model for Batten disease.

J. Laranjinha, C. Leão, A. Carvalho, 2007, Molecular biology of the cell.

CLN3, the protein associated with batten disease: Structure, function and localization

D. Pearce, J. Weimer, Jared W. Benedict, 2005, Journal of neuroscience research.

The Yeast Model for Batten Disease: Mutations inbtn1, btn2, and hsp30 Alter pH Homeostasis

F. Sherman, D. Pearce, Neda E. Muzaffar, 2000, Journal of bacteriology.

A novel interaction of CLN3 with nonmuscle myosin-IIB and defects in cell motility of Cln3(-/-) cells.

D. Pearce, Jared W. Benedict, Amanda L. Getty, 2011, Experimental cell research.

You say lipofuscin, we say ceroid: Defining autofluorescent storage material

D. Pearce, S. Seehafer, 2006, Neurobiology of Aging.

Nonsense-mediated decay in genetic disease: friend or foe?

D. Pearce, Jake N. Miller, 2014, Mutation research. Reviews in mutation research.

Interactions of the proteins of neuronal ceroid lipofuscinosis: clues to function

D. Pearce, Amanda L. Getty, 2011, Cellular and Molecular Life Sciences.

Interaction between Sdo1p and Btn1p in the Saccharomyces cerevisiae model for Batten disease.

D. Pearce, S. Padilla-Lopez, Jared W. Benedict, 2010, Human molecular genetics.

Phenotypic reversal of the btn1 defects in yeast by chloroquine: a yeast model for Batten disease.

F. Sherman, D. Pearce, B. Das, 1999, Proceedings of the National Academy of Sciences of the United States of America.

A yeast model for the study of Batten disease.

F. Sherman, D. Pearce, 1998, Proceedings of the National Academy of Sciences of the United States of America.

A metabolomic comparison of mouse models of the Neuronal Ceroid Lipofuscinoses

R. Salek, R. Mortishire-Smith, J. Griffin, 2011, Journal of biomolecular NMR.

Characterizing pathogenic processes in Batten disease: use of small eukaryotic model systems.

P. Taschner, Sandra Codlin, C. Korey, 2006, Biochimica et biophysica acta.

Novel CLN3 mutation predicted to cause complete loss of protein function does not modify the classical JNCL phenotype

J. Mink, P. Rothberg, A. Leman, 2005, Neuroscience Letters.

A role in vacuolar arginine transport for yeast Btn1p and for human CLN3, the protein defective in Batten disease

Yoojin M Kim, D. Pearce, D. Ramirez-Montealegre, 2003, Proceedings of the National Academy of Sciences of the United States of America.

Optic nerve degeneration in a murine model of juvenile ceroid lipofuscinosis.

Rebecca M. Sappington, D. Calkins, D. Pearce, 2003, Investigative ophthalmology & visual science.

Functional categorization of gene expression changes in the cerebellum of a Cln3-knockout mouse model for Batten disease.

R. Nussbaum, A. Brooks, H. Mitchison, 2003, Molecular genetics and metabolism.

11 Experimental models of NCL: The yeast model

D. Pearce, 2001 .

Batten disease: evaluation of CLN3 mutations on protein localization and function.

B. Davidson, M. Bennett, Ronald E. Haskell, 2000, Human molecular genetics.

Localization and processing of CLN3, the protein associated to batten disease: Where is it and what does it do?

D. Pearce, 2000, Journal of neuroscience research.

Action of BTN1, the yeast orthologue of the gene mutated in Batten disease

T. Ferea, F. Sherman, D. Pearce, 1999, Nature Genetics.

The novel Cln1(R151X) mouse model of infantile neuronal ceroid lipofuscinosis (INCL) for testing nonsense suppression therapy.

D. Pearce, A. Kovács, Jake N. Miller, 2015, Human molecular genetics.

Defective synaptic transmission causes disease signs in a mouse model of juvenile neuronal ceroid lipofuscinosis

H. Pape, H. Wiendl, C. Geis, 2017, eLife.

Role of the Lysosomal Membrane Protein, CLN3, in the Regulation of Cathepsin D Activity

D. Pearce, A. Kovács, J. Cárcel-Trullols, 2017, Journal of cellular biochemistry.

Lack of specificity of antibodies raised against CLN3, the lysosomal/endosomal transmembrane protein mutated in juvenile Batten disease

D. Pearce, A. Kovács, T. Nelson, 2017, Bioscience reports.

Abnormally increased surface expression of AMPA receptors in the cerebellum, cortex and striatum of Cln3−/− mice

D. Pearce, A. Kovács, Caitlin Hof, 2015, Neuroscience Letters.

Cell biology of the NCL proteins: What they do and don't do.

D. Pearce, A. Kovács, J. Cárcel-Trullols, 2015, Biochimica et biophysica acta.

Late onset neurodegeneration in the Cln3 −/− mouse model of juvenile neuronal ceroid lipofuscinosis is preceded by low level glial activation

W. Mobley, J. Cooper, P. Rezaie, 2004, Brain Research.

Altered Flurothyl Seizure Induction Latency, Phenotype, and Subsequent Mortality in a Mouse Model of Juvenile Neuronal Ceroid Lipofuscinosis/Batten Disease

D. Pearce, C. Applegate, T. Mhyre, 2002, Epilepsia.

An autoantibody inhibitory to glutamic acid decarboxylase in the neurodegenerative disorder Batten disease.

Masumi Ito, Jonathan D Cooper, J. Cooper, 2002, Human molecular genetics.

Homogeneous PCR nucleobase quenching assays to detect four mutations that cause neuronal ceroid lipofuscinosis: T75P and R151X in CLN1, and IVS5-1G>C and R208X in CLN2

P. Rothberg, A. Leman, S. Mole, 2006, Journal of Neuroscience Methods.

A clinical rating scale for Batten disease

J. Mink, P. Rothberg, J. Kwon, 2005, Neurology.

Homogeneous polymerase chain reaction nucleobase quenching assay to detect the 1-kbp deletion in CLN3 that causes Batten disease.

P. Rothberg, D. Pearce, D. Ramirez-Montealegre, 2004, The Journal of molecular diagnostics : JMD.

Tissue‐specific variation in nonsense mutant transcript level and drug‐induced read‐through efficiency in the Cln1 R151X mouse model of INCL

D. Pearce, A. Kovács, Jake N. Miller, 2015, Journal of cellular and molecular medicine.

Progressive oxidative damage in the central nervous system of a murine model for juvenile Batten disease

D. Pearce, Jared W. Benedict, Jared W. Benedict, 2007, Journal of neuroscience research.

Maize contains a Lon protease gene that can partially complement a yeast pim1-deletion mutant

F. Sherman, D. Pearce, W. D. Rapp, 1998, Plant Molecular Biology.

A tailored Cln3Q352X mouse model for testing therapeutic interventions in CLN3 Batten disease

Tyler B. Johnson, D. Pearce, Logan M Langin, 2020, Scientific Reports.

Searching for novel biomarkers using a mouse model of CLN3-Batten disease

T. Kielian, D. Pearce, J. Weimer, 2018, PloS one.

Finding the most appropriate mouse model of juvenile CLN3 (Batten) disease for therapeutic studies: the importance of genetic background and gender

D. Pearce, A. Kovács, 2015, Disease Models & Mechanisms.

Neuronal ceroid lipofuscinosis type CLN2: a new rationale for the construction of phenotypic subgroups based on a survey of 25 cases in South America.

K. Sims, D. Pearce, W. Xin, 2013, Gene.

Distinct patterns of serum immunoreactivity as evidence for multiple brain‐directed autoantibodies in juvenile neuronal ceroid lipofuscinosis

J. Cooper, D. Pearce, E. Bible, 2006, Neuropathology and applied neurobiology.

Selectively increased sensitivity of cerebellar granule cells to AMPA receptor-mediated excitotoxicity in a mouse model of Batten disease

D. Pearce, J. Weimer, A. Kovács, 2006, Neurobiology of Disease.

Altered amino acid levels in sera of a mouse model for juvenile neuronal ceroid lipofuscinoses.

R. Mooney, D. Pearce, S. Chattopadhyay, 2003, Clinica chimica acta; international journal of clinical chemistry.

Moving towards effective therapeutic strategies for Neuronal Ceroid Lipofuscinosis

T. Kielian, D. Pearce, J. Weimer, 2016, Orphanet Journal of Rare Diseases.

Absence of Btn1p in the yeast model for juvenile Batten disease may cause arginine to become toxic to yeast cells.

D. Pearce, Devin M. Wolfe, Seasson P Vitiello, 2007, Human molecular genetics.

Seizure Susceptibility, Phenotype, and Resultant Growth Delay in the nclf and mnd Mouse Models of Neuronal Ceroid Lipofuscinoses

D. Pearce, A. Kovács, Elizabeth Kriscenski-Perry, 2013, Journal of child neurology.

High Resolution 1H NMR-based Metabolomics Indicates a Neurotransmitter Cycling Deficit in Cerebral Tissue from a Mouse Model of Batten Disease*

Julian L Griffin, Jonathan D Cooper, R. Mortishire-Smith, 2005, Journal of Biological Chemistry.

Large Animal Models for Batten Disease

D. Pearce, Krystal L. Weber, 2013, Journal of child neurology.

Characterization of a novel porcine model of CLN3-Batten disease

Tyler B. Johnson, J. Cooper, A. Drack, 2019, Molecular Genetics and Metabolism.

Standardized assessment of behavior and adaptive living skills in juvenile neuronal ceroid lipofuscinosis

J. Mink, P. Rothberg, J. Kwon, 2006, Developmental medicine and child neurology.

A tailored mouse model of CLN2 disease: A nonsense mutant for testing personalized therapies

D. Pearce, Jill M Weimer, David A Pearce, 2017, PloS one.

Screening, diagnosis and epidemiology of Batten disease

D. Pearce, Elizabeth D. A. Wheeler, Natalie A Simpson, 2014 .

Comparative analysis of the gut microbiota composition in the Cln1R151X and Cln2R207X mouse models of Batten disease and in three wild-type mouse strains

D. Pearce, Jing Zhao, A. Kovács, 2020, Archives of Microbiology.

Treatment of the Ppt1–/– Mouse Model of Infantile Neuronal Ceroid Lipofuscinosis With the N-methyl-d-aspartate (NMDA) Receptor Antagonist Memantine

R. Finn, D. Pearce, A. Kovács, 2013, Journal of child neurology.

PIM1 encodes a mitochondrial ATP-dependent protease that is required for mitochondrial function in the yeast Saccharomyces cerevisiae.

F. Sherman, D. Pearce, L. van Dyck, 1994, The Journal of biological chemistry.

Alterations in striatal dopamine catabolism precede loss of substantia nigra neurons in a mouse model of juvenile neuronal ceroid lipofuscinosis

Deborah A. Ryan, J. Cooper, H. Federoff, 2007, Brain Research.

Chronic Olanzapine Treatment Causes Differential Expression of Genes in Frontal Cortex of Rats as Revealed by DNA Microarray Technique

Christopher J. Bell, Christopher Bell, D. Siderovski, 2006, Neuropsychopharmacology.

Gene symbol: CLN3. Disease: Juvenile neuronal ceroid lipofuscinosis (Batten disease).

P. Rothberg, A. Leman, D. Pearce, 2005, Human Genetics.

Antigen presenting cell abnormalities in the Cln3(-/-) mouse model of juvenile neuronal ceroid lipofuscinosis.

D. Pearce, A. Kovács, Samantha L. Hersrud, 2016, Biochimica et biophysica acta.

Characterization of lipid-linked oligosaccharide accumulation in mouse models of Batten disease.

M. Lehrman, D. Pearce, S. Hofmann, 2005, Glycobiology.

Maternal antibrain antibodies in autism

L. Lee, H. Singer, A. Zimmerman, 2007, Brain, Behavior, and Immunity.

Enhanced mitochondrial degradation of yeast cytochrome c with amphipathic structures

F. Sherman, D. Pearce, R. Moerschell, 2005, Current Genetics.

Hereditary spastic paraplegia: mitochondrial metalloproteases of yeast

D. Pearce, 1999, Human Genetics.

Location- and sex-specific differences in weight and motor coordination in two commonly used mouse strains

D. Pearce, A. Kovács, 2013, Scientific Reports.

Degradation of yeast cytochromes c dependent and independent on its physiological partners.

F. Sherman, D. Pearce, 1998, Archives of biochemistry and biophysics.

Identification of alpha-fetoprotein as an autoantigen in juvenile Batten disease.

D. Pearce, J. Castaneda, 2008, Neurobiology of disease.

Diminished degradation of yeast cytochrome c by interactions with its physiological partners.

F. Sherman, D. Pearce, 1995, Proceedings of the National Academy of Sciences of the United States of America.

Differential Ubiquitin-dependent Degradation of the Yeast Apo-cytochrome c Isozymes*

F Sherman, F. Sherman, D. Pearce, 1997, The Journal of Biological Chemistry.

Disruption of a cystine transporter downregulates expression of genes involved in sulfur regulation and cellular respiration

D. Pearce, Emily A. Weber, B. Ahlers, 2016, Biology Open.

Pharmacological Effects on Ceroid Lipofuscin and Neuronal Structure in Cln3∆ex7/8 Mouse Brain Cultures

D. Brenneman, D. Pearce, A. Kovács, 2017, Journal of Molecular Neuroscience.

Prospects for stem cell therapy in neuronal ceroid lipofuscinosis.

R. Steiner, P. Orchard, D. Pearce, 2013, Regenerative medicine.

"Additional trials are clearly needed to establish when and whether stem cell therapies should be applied to neuronal ceroid lipofuscinosis, and, if so, which forms of the disease are most likely to benefit from such therapies. "

R. Steiner, P. Orchard, D. Pearce, 2013 .

Batten Disease

J. Mink, B. Maria, D. Pearce, 2013, Journal of Child Neurology.

Imaging of late infantile neuronal ceroid lipofuscinosis

D. Pearce, D. Ramirez-Montealegre, 2007, Neurology.

Requirements of Cyc2p and the porin, Por1p, for ionic stability and mitochondrial integrity in Saccharomyces cerevisiae.

F. Sherman, T. S. Cardillo, D. Pearce, 2001, Archives of biochemistry and biophysics.

Identification of α-fetoprotein as an autoantigen in juvenile Batten disease

D. Pearce, J. Castaneda, 2008, Neurobiology of Disease.

Altered sensitivity to excitotoxic cell death and glutamate receptor expression between two commonly studied mouse strains

R. Finn, D. Pearce, A. Kovács, 2010, Journal of neuroscience research.

Review: The Cct eukaryotic chaperonin subunits of Saccharomyces cerevisiae and other yeasts

F. Sherman, J. Ernst, D. Pearce, 1996, Yeast.

Air proteins control differential TRAMP substrate specificity for nuclear RNA surveillance.

D. Mathews, J. Butler, Z. Xu, 2012, RNA.

The Paracoccus denitrificans ccmA, B and C genes: cloning and sequencing, and analysis of the potential of their products to form a haem or apo- c-type cytochrome transporter.

M. D. Page, S. Ferguson, D. Pearce, 1997, Microbiology.

Toxicity of Copper, Cobalt, and Nickel Salts Is Dependent on Histidine Metabolism in the YeastSaccharomyces cerevisiae

F. Sherman, D. Pearce, 1999, Journal of bacteriology.