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  1. Article: Hépatite C: une étude prédit un avenir coûteux si rien n'est fait maintenant.

    Perreault, Denyse

    Perspective infirmiere : revue officielle de l'Ordre des infirmieres et infirmiers du Quebec

    2014  Volume 11, Issue 4, Page(s) 14

    Title translation Hepatitis C: a study predicts a costly future if nothing is done now.
    MeSH term(s) Canada ; Cost of Illness ; Hepatitis C, Chronic/economics ; Hepatitis C, Chronic/epidemiology ; Humans ; Mass Screening ; United States
    Language French
    Publishing date 2014-09
    Publishing country Canada
    Document type Journal Article
    ZDB-ID 2132473-6
    ISSN 1708-1890
    ISSN 1708-1890
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Corrigendum to "C Fragment of Tetanus Toxin Hybrid Proteins Evaluated for Muscle-specific Transsynaptic Mapping of Spinal Motor Circuitry in the Newborn Mouse" [Neuroscience 141(2) (2006) 803-816].

    Perreault, M-C / Pastor-Bernier, A / Renaud, J-S / Roux, S / Glover, J C

    Neuroscience

    2019  Volume 424, Page(s) 211

    Language English
    Publishing date 2019-11-29
    Publishing country United States
    Document type Published Erratum
    ZDB-ID 196739-3
    ISSN 1873-7544 ; 0306-4522
    ISSN (online) 1873-7544
    ISSN 0306-4522
    DOI 10.1016/j.neuroscience.2019.11.019
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Incidence trends in pediatric central nervous system tumors in Canada: a 15 years report from Cancer and Young People in Canada (CYP-C) registry.

    Larouche, Valérie / Toupin, Annie-Kim / Lalonde, Benoît / Simonyan, David / Jabado, Nada / Perreault, Sébastien

    Neuro-oncology advances

    2020  Volume 2, Issue 1, Page(s) vdaa012

    Abstract: ... C) surveillance system that includes every patient less than 15 years of age with a tumor seen ...

    Abstract Background: The aim of this study is to present a national surveillance report on pediatric central nervous system (CNS) tumors in Canada during the period between 2001 and 2015.
    Methods: All pediatric patients with a diagnosis of primary CNS tumors were collected by the Cancer in Young People in Canada (CYP-C) surveillance system that includes every patient less than 15 years of age with a tumor seen in one of the 17 pediatric oncology centres in Canada. This registry included malignant and benign CNS tumors. We calculated the age-adjusted incidence rates (AAIRs) per 100 000 person-years for CNS tumors overall and by age group, major histology subgroups, and geographical distribution over the country.
    Results: Overall, 3306 patients less than 15 years old had been diagnosed with a CNS tumor in Canada in 2001-2015 with a 1.23:1 male to female ratio. The overall AAIR is 3.80. The three most frequent groups of tumors were low-grade gliomas (36.4%), high-grade gliomas (22.3%), and embryonal tumors (18.7%) with incidence rates of 1.41, 0.86, and 0.72 per 100 000 person-years, respectively. The incidence rate of pediatric CNS tumors is stable during the period 2001-2015 in Canada and no significant differences were seen between malignant and benign tumors over the country.
    Conclusions: These data represent all the pediatric patients 0-14 years old with a CNS tumor in the Canadian population. Incidence rates by age group, sex, and subgroups of tumors are similar to those seen in the literature.
    Language English
    Publishing date 2020-02-07
    Publishing country England
    Document type Journal Article
    ZDB-ID 3009682-0
    ISSN 2632-2498 ; 2632-2498
    ISSN (online) 2632-2498
    ISSN 2632-2498
    DOI 10.1093/noajnl/vdaa012
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Expanding the clinical phenotype of individuals with a 3-bp in-frame deletion of the NF1 gene (c.2970_2972del): an update of genotype-phenotype correlation.

    Koczkowska, Magdalena / Callens, Tom / Gomes, Alicia / Sharp, Angela / Chen, Yunjia / Hicks, Alesha D / Aylsworth, Arthur S / Azizi, Amedeo A / Basel, Donald G / Bellus, Gary / Bird, Lynne M / Blazo, Maria A / Burke, Leah W / Cannon, Ashley / Collins, Felicity / DeFilippo, Colette / Denayer, Ellen / Digilio, Maria C / Dills, Shelley K /
    Dosa, Laura / Greenwood, Robert S / Griffis, Cristin / Gupta, Punita / Hachen, Rachel K / Hernández-Chico, Concepción / Janssens, Sandra / Jones, Kristi J / Jordan, Justin T / Kannu, Peter / Korf, Bruce R / Lewis, Andrea M / Listernick, Robert H / Lonardo, Fortunato / Mahoney, Maurice J / Ojeda, Mayra Martinez / McDonald, Marie T / McDougall, Carey / Mendelsohn, Nancy / Miller, David T / Mori, Mari / Oostenbrink, Rianne / Perreault, Sebastién / Pierpont, Mary Ella / Piscopo, Carmelo / Pond, Dinel A / Randolph, Linda M / Rauen, Katherine A / Rednam, Surya / Rutledge, S Lane / Saletti, Veronica / Schaefer, G Bradley / Schorry, Elizabeth K / Scott, Daryl A / Shugar, Andrea / Siqveland, Elizabeth / Starr, Lois J / Syed, Ashraf / Trapane, Pamela L / Ullrich, Nicole J / Wakefield, Emily G / Walsh, Laurence E / Wangler, Michael F / Zackai, Elaine / Claes, Kathleen B M / Wimmer, Katharina / van Minkelen, Rick / De Luca, Alessandro / Martin, Yolanda / Legius, Eric / Messiaen, Ludwine M

    Genetics in medicine : official journal of the American College of Medical Genetics

    2018  Volume 21, Issue 4, Page(s) 867–876

    Abstract: ... Exceptions are individuals heterozygous for the NF1 in-frame deletion, c.2970_2972del (p.Met992del ... disabilities. In an individual with the NF1 constitutional c.2970_2972del and three astrocytomas, we provided ... microsatellite markers and c.2970_2972del.: Conclusion: We demonstrate that individuals with the NF1 p.Met992del ...

    Abstract Purpose: Neurofibromatosis type 1 (NF1) is characterized by a highly variable clinical presentation, but almost all NF1-affected adults present with cutaneous and/or subcutaneous neurofibromas. Exceptions are individuals heterozygous for the NF1 in-frame deletion, c.2970_2972del (p.Met992del), associated with a mild phenotype without any externally visible tumors.
    Methods: A total of 135 individuals from 103 unrelated families, all carrying the constitutional NF1 p.Met992del pathogenic variant and clinically assessed using the same standardized phenotypic checklist form, were included in this study.
    Results: None of the individuals had externally visible plexiform or histopathologically confirmed cutaneous or subcutaneous neurofibromas. We did not identify any complications, such as symptomatic optic pathway gliomas (OPGs) or symptomatic spinal neurofibromas; however, 4.8% of individuals had nonoptic brain tumors, mostly low-grade and asymptomatic, and 38.8% had cognitive impairment/learning disabilities. In an individual with the NF1 constitutional c.2970_2972del and three astrocytomas, we provided proof that all were NF1-associated tumors given loss of heterozygosity at three intragenic NF1 microsatellite markers and c.2970_2972del.
    Conclusion: We demonstrate that individuals with the NF1 p.Met992del pathogenic variant have a mild NF1 phenotype lacking clinically suspected plexiform, cutaneous, or subcutaneous neurofibromas. However, learning difficulties are clearly part of the phenotypic presentation in these individuals and will require specialized care.
    MeSH term(s) Adolescent ; Adult ; Child ; Child, Preschool ; Female ; Genetic Association Studies ; Genetic Predisposition to Disease ; Heterozygote ; Humans ; Infant ; Learning Disabilities/genetics ; Learning Disabilities/physiopathology ; Male ; Mutation, Missense/genetics ; Neurofibroma, Plexiform/genetics ; Neurofibroma, Plexiform/physiopathology ; Neurofibromatosis 1/genetics ; Neurofibromatosis 1/pathology ; Neurofibromin 1/genetics ; Sequence Deletion ; Young Adult
    Chemical Substances Neurofibromin 1
    Language English
    Publishing date 2018-09-07
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1455352-1
    ISSN 1530-0366 ; 1098-3600
    ISSN (online) 1530-0366
    ISSN 1098-3600
    DOI 10.1038/s41436-018-0269-0
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  5. Article ; Online: Correction: Expanding the clinical phenotype of individuals with a 3-bp in-frame deletion of the NF1 gene (c.2970_2972del): an update of genotype-phenotype correlation.

    Koczkowska, Magdalena / Callens, Tom / Gomes, Alicia / Sharp, Angela / Chen, Yunjia / Hicks, Alesha D / Aylsworth, Arthur S / Azizi, Amedeo A / Basel, Donald G / Bellus, Gary / Bird, Lynne M / Blazo, Maria A / Burke, Leah W / Cannon, Ashley / Collins, Felicity / DeFilippo, Colette / Denayer, Ellen / Digilio, Maria C / Dills, Shelley K /
    Dosa, Laura / Greenwood, Robert S / Griffis, Cristin / Gupta, Punita / Hachen, Rachel K / Hernández-Chico, Concepción / Janssens, Sandra / Jones, Kristi J / Jordan, Justin T / Kannu, Peter / Korf, Bruce R / Lewis, Andrea M / Listernick, Robert H / Lonardo, Fortunato / Mahoney, Maurice J / Ojeda, Mayra Martinez / McDonald, Marie T / McDougall, Carey / Mendelsohn, Nancy / Miller, David T / Mori, Mari / Oostenbrink, Rianne / Perreault, Sebastién / Pierpont, Mary Ella / Piscopo, Carmelo / Pond, Dinel A / Randolph, Linda M / Rauen, Katherine A / Rednam, Surya / Rutledge, S Lane / Saletti, Veronica / Schaefer, G Bradley / Schorry, Elizabeth K / Scott, Daryl A / Shugar, Andrea / Siqveland, Elizabeth / Starr, Lois J / Syed, Ashraf / Trapane, Pamela L / Ullrich, Nicole J / Wakefield, Emily G / Walsh, Laurence E / Wangler, Michael F / Zackai, Elaine / Claes, Kathleen B M / Wimmer, Katharina / van Minkelen, Rick / De Luca, Alessandro / Martin, Yolanda / Legius, Eric / Messiaen, Ludwine M

    Genetics in medicine : official journal of the American College of Medical Genetics

    2018  Volume 21, Issue 3, Page(s) 764–765

    Abstract: A correction has been published to this Article. The PDF and HTML have been updated accordingly. ...

    Abstract A correction has been published to this Article. The PDF and HTML have been updated accordingly.
    Keywords covid19
    Language English
    Publishing date 2018-08-11
    Publishing country United States
    Document type Journal Article ; Published Erratum
    ZDB-ID 1455352-1
    ISSN 1530-0366 ; 1098-3600
    ISSN (online) 1530-0366
    ISSN 1098-3600
    DOI 10.1038/s41436-018-0326-8
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  6. Article ; Online: Regulation of c-fos expression by the dopamine D1-D2 receptor heteromer.

    Perreault, M L / Shen, M Y F / Fan, T / George, S R

    Neuroscience

    2015  Volume 285, Page(s) 194–203

    Abstract: ... to rats induced significant c-fos expression in the nucleus accumbens that was significantly inhibited ... by TAT-D1 did not have any effects in any striatal subregions, but induced significant c-fos ... cortices and piriform cortex. The induction of c-fos by TAT-D1 was also evident in the anterior olfactory ...

    Abstract The dopamine D1 and D2 receptors form the D1-D2 receptor heteromer in a subset of neurons and couple to the Gq protein to regulate intracellular calcium signaling. In the present study the effect of D1-D2 heteromer activation and disruption on neuronal activation in the rat brain was mapped. This was accomplished using the dopamine agonist SKF 83959 to activate the D1-D2 heteromer in combination with a TAT-D1 disrupting peptide we developed, and which has been shown to disrupt the D1/D2 receptor interaction and antagonize D1-D2 heteromer-induced cell signaling and behavior. Acute SKF 83959 administration to rats induced significant c-fos expression in the nucleus accumbens that was significantly inhibited by TAT-D1 pretreatment. No effects of SKF 83959 were seen in caudate putamen. D1-D2 heteromer disruption by TAT-D1 did not have any effects in any striatal subregions, but induced significant c-fos immunoreactivity in a number of cortical regions including the orbitofrontal cortex, prelimbic and infralimbic cortices and piriform cortex. The induction of c-fos by TAT-D1 was also evident in the anterior olfactory nucleus, as well as the lateral habenula and thalamic nuclei. These findings show for the first time that the D1-D2 heteromer can differentially regulate c-fos expression in a region-dependent manner either through its activation or through tonic inhibition of neuronal activity.
    MeSH term(s) 2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine/analogs & derivatives ; 2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine/pharmacology ; Animals ; Brain/drug effects ; Brain/metabolism ; Cell Count ; Dimerization ; Dopamine Agonists/pharmacology ; Dopamine Antagonists/pharmacology ; Immunohistochemistry ; Male ; Neurons/drug effects ; Neurons/metabolism ; Proto-Oncogene Proteins c-fos/metabolism ; Rats, Sprague-Dawley ; Receptors, Dopamine D1/metabolism ; Receptors, Dopamine D2/metabolism
    Chemical Substances Dopamine Agonists ; Dopamine Antagonists ; Proto-Oncogene Proteins c-fos ; Receptors, Dopamine D1 ; Receptors, Dopamine D2 ; 2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine (67287-49-4) ; SK&F 83959 (80751-85-5)
    Language English
    Publishing date 2015-01-29
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 196739-3
    ISSN 1873-7544 ; 0306-4522
    ISSN (online) 1873-7544
    ISSN 0306-4522
    DOI 10.1016/j.neuroscience.2014.11.017
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  7. Article ; Online: [(11)C]-Acetoacetate PET imaging: a potential early marker for cardiac heart failure.

    Croteau, Etienne / Tremblay, Sébastien / Gascon, Suzanne / Dumulon-Perreault, Véronique / Labbé, Sébastien M / Rousseau, Jacques A / Cunnane, Stephen C / Carpentier, André C / Bénard, François / Lecomte, Roger

    Nuclear medicine and biology

    2014  Volume 41, Issue 10, Page(s) 863–870

    Abstract: ... the mitochondrial production of oxidative stress involved in cardiotoxicity. In this study, [(11)C]-acetoacetate was ... heart failure model was induced by doxorubicin, Dox(+). [(14)C]-Acetoacetate, a non-positron (β-) emitting ... Afterward, [(11)C]-acetoacetate (β+) myocardial PET images were obtained for kinetic analysis and heart ...

    Abstract Unlabelled: The ketone body acetoacetate could be used as an alternate nutrient for the heart, and it also has the potential to improve cardiac function in an ischemic-reperfusion model or reduce the mitochondrial production of oxidative stress involved in cardiotoxicity. In this study, [(11)C]-acetoacetate was investigated as an early marker of intracellular damage in heart failure.
    Methods: A rat cardiotoxicity heart failure model was induced by doxorubicin, Dox(+). [(14)C]-Acetoacetate, a non-positron (β-) emitting radiotracer, was used to characterize the arterial blood input function and myocardial mitochondrial uptake. Afterward, [(11)C]-acetoacetate (β+) myocardial PET images were obtained for kinetic analysis and heart function assessment in control Dox(-) (n=15) and treated Dox(+) (n=6) rats. The uptake rate (K1) and myocardial clearance rate (k2or kmono) were extracted.
    Results: [(14)C]-Acetoacetate in the blood was increased in Dox(+), from 2 min post-injection until the last withdrawal point when the heart was harvested, as well as the uptake in the heart and myocardial mitochondria (unpaired t-test, p <0.05). PET kinetic analysis of [(11)C]-acetoacetate showed that rate constants K1, k2 and kmono were decreased in Dox(+) (p <0.05) combined with a reduction of 24% of the left ventricular ejection fraction (p <0.001).
    Conclusion: Radioactive acetoacetate ex vivo analysis [(14)C], and in vivo kinetic [(11)C] studies provided evidence that [(11)C]-acetoacetate can assess heart failure Dox(+). Contrary to myocardial flow reserve (rest-stress protocol), [(11)C]-acetoacetate can be used to assess reduced kinetic rate constants without requirement of hyperemic stress response. The proposed [(11)C]-acetoacetate cardiac radiotracer in the investigation of heart disease is novel and paves the way to a potential role for [(11)C]-acetoacetate in cardiac pathophysiology.
    MeSH term(s) Acetoacetates/blood ; Acetoacetates/pharmacokinetics ; Animals ; Antibiotics, Antineoplastic/toxicity ; Biomarkers/metabolism ; Carbon Radioisotopes/pharmacokinetics ; Doxorubicin/toxicity ; Heart Failure/chemically induced ; Heart Failure/diagnostic imaging ; Heart Failure/metabolism ; Male ; Positron-Emission Tomography/methods ; Rats ; Rats, Inbred F344 ; Tissue Distribution ; Ventricular Function, Left
    Chemical Substances Acetoacetates ; Antibiotics, Antineoplastic ; Biomarkers ; Carbon Radioisotopes ; acetoacetic acid (4ZI204Y1MC) ; Doxorubicin (80168379AG)
    Language English
    Publishing date 2014-11
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1138098-6
    ISSN 1872-9614 ; 0883-2897 ; 0969-8051
    ISSN (online) 1872-9614
    ISSN 0883-2897 ; 0969-8051
    DOI 10.1016/j.nucmedbio.2014.08.006
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  8. Article ; Online: Adiponectin, C-reactive protein, fibrinogen and tissue plasminogen activator antigen levels among glucose-intolerant women with and without histories of gestational diabetes.

    Kim, C / Christophi, C A / Goldberg, R B / Perreault, L / Dabelea, D / Marcovina, S M / Pi-Sunyer, X / Barrett-Connor, E

    Diabetic medicine : a journal of the British Diabetic Association

    2015  Volume 33, Issue 1, Page(s) 32–38

    Abstract: Aim: To examine concentrations of biomarkers (adiponectin, C-reactive protein, fibrinogen and ... 0001) and greater log C-reactive protein (-0.90 mg/l vs. -0.78 mg/l, p = 0.04) levels than women ...

    Abstract Aim: To examine concentrations of biomarkers (adiponectin, C-reactive protein, fibrinogen and tissue plasminogen-activator antigen) associated with glucose homeostasis and diabetes risk by history of gestational diabetes (GDM).
    Methods: We conducted a secondary analysis of the Diabetes Prevention Program, a randomized trial of lifestyle intervention or metformin for diabetes prevention. At baseline, participants were overweight and had impaired glucose tolerance. Biomarkers at baseline and 1 year after enrolment were compared between parous women with (n = 350) and without histories of GDM (n = 1466). Cox proportional hazard models evaluated whether history of GDM was associated with diabetes risk, after adjustment for baseline biomarker levels as well as for change in biomarker levels, demographic factors and anthropometrics.
    Results: At baseline, women with histories of GDM had lower adiponectin (7.5 μg/ml vs. 8.7 μg/ml; p < 0.0001) and greater log C-reactive protein (-0.90 mg/l vs. -0.78 mg/l, p = 0.04) levels than women without histories of GDM, but these associations did not persist after adjustment for demographic factors. Fibrinogen and tissue plasminogen-activator antigen were similar between women with and without histories of GDM. Women with and without histories of GDM had a similar pattern of changes in biomarkers within randomization arm. Adjustment for age, race/ethnicity, baseline weight, change in weight, baseline biomarker level and change in biomarker level did not significantly alter the association between history of GDM, and diabetes risk.
    Conclusions: Among women with impaired glucose tolerance, biomarkers in women with and without histories of GDM are similar and respond similarly to lifestyle changes and metformin. Adjustment for biomarker levels did not explain the higher risk of diabetes observed in women with histories of GDM.
    MeSH term(s) Adiponectin/blood ; Adult ; Biomarkers/blood ; Body Mass Index ; C-Reactive Protein/analysis ; Cohort Studies ; Combined Modality Therapy ; Diabetes Mellitus, Type 2/complications ; Diabetes Mellitus, Type 2/epidemiology ; Diabetes Mellitus, Type 2/etiology ; Diabetes Mellitus, Type 2/prevention & control ; Diabetes, Gestational/physiopathology ; Diet, Reducing ; Female ; Fibrinogen/analysis ; Glucose Intolerance/blood ; Glucose Intolerance/complications ; Glucose Intolerance/etiology ; Glucose Intolerance/therapy ; Humans ; Hypoglycemic Agents/therapeutic use ; Life Style ; Middle Aged ; Motor Activity ; Overweight/complications ; Overweight/therapy ; Pregnancy ; Risk ; Tissue Plasminogen Activator/blood ; United States/epidemiology ; Weight Loss
    Chemical Substances ADIPOQ protein, human ; Adiponectin ; Biomarkers ; Hypoglycemic Agents ; Fibrinogen (9001-32-5) ; C-Reactive Protein (9007-41-4) ; Tissue Plasminogen Activator (EC 3.4.21.68)
    Language English
    Publishing date 2015-05-29
    Publishing country England
    Document type Comparative Study ; Journal Article ; Multicenter Study ; Randomized Controlled Trial ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 605769-x
    ISSN 1464-5491 ; 0742-3071 ; 1466-5468
    ISSN (online) 1464-5491
    ISSN 0742-3071 ; 1466-5468
    DOI 10.1111/dme.12799
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  9. Article ; Online: Depletion of WRN protein causes RACK1 to activate several protein kinase C isoforms.

    Massip, L / Garand, C / Labbé, A / Perreault, E / Turaga, R V N / Bohr, V A / Lebel, M

    Oncogene

    2009  Volume 29, Issue 10, Page(s) 1486–1497

    Abstract: ... of several protein kinase C (PKC) enzymes. Using a tandem affinity purification strategy, we found that WRN physically and ... functionally interacts with receptor for activated C-kinase 1 (RACK1), a highly conserved anchoring protein ...

    Abstract Werner's syndrome (WS) is a rare autosomal disease characterized by the premature onset of several age-associated pathologies. The protein defective in patients with WS (WRN) is a helicase/exonuclease involved in DNA repair, replication, transcription and telomere maintenance. In this study, we show that a knock down of the WRN protein in normal human fibroblasts induces phosphorylation and activation of several protein kinase C (PKC) enzymes. Using a tandem affinity purification strategy, we found that WRN physically and functionally interacts with receptor for activated C-kinase 1 (RACK1), a highly conserved anchoring protein involved in various biological processes, such as cell growth and proliferation. RACK1 binds strongly to the RQC domain of WRN and weakly to its acidic repeat region. Purified RACK1 has no impact on the helicase activity of WRN, but selectively inhibits WRN exonuclease activity in vitro. Interestingly, knocking down RACK1 increased the cellular frequency of DNA breaks. Depletion of the WRN protein in return caused a fraction of nuclear RACK1 to translocate out of the nucleus to bind and activate PKCdelta and PKCbetaII in the membrane fraction of cells. In contrast, different DNA-damaging treatments known to activate PKCs did not induce RACK1/PKCs association in cells. Overall, our results indicate that a depletion of the WRN protein in normal fibroblasts causes the activation of several PKCs through translocation and association of RACK1 with such kinases.
    MeSH term(s) Blotting, Western ; Cell Line, Tumor ; Cells, Cultured ; DNA Damage ; Enzyme Activation ; Exodeoxyribonucleases/genetics ; Exodeoxyribonucleases/metabolism ; Fibroblasts/cytology ; Fibroblasts/metabolism ; GTP-Binding Proteins/genetics ; GTP-Binding Proteins/metabolism ; Humans ; Neoplasm Proteins/genetics ; Neoplasm Proteins/metabolism ; Phosphoproteins/metabolism ; Phosphorylation ; Protein Binding ; Protein Kinase C/metabolism ; Protein Kinase C beta ; Protein Kinase C-delta/metabolism ; RNA Interference ; RecQ Helicases/genetics ; RecQ Helicases/metabolism ; Receptors for Activated C Kinase ; Receptors, Cell Surface/genetics ; Receptors, Cell Surface/metabolism ; Werner Syndrome Helicase ; p38 Mitogen-Activated Protein Kinases/metabolism
    Chemical Substances Neoplasm Proteins ; Phosphoproteins ; RACK1 protein, human ; Receptors for Activated C Kinase ; Receptors, Cell Surface ; Protein Kinase C (EC 2.7.11.13) ; Protein Kinase C beta (EC 2.7.11.13) ; Protein Kinase C-delta (EC 2.7.11.13) ; p38 Mitogen-Activated Protein Kinases (EC 2.7.11.24) ; Exodeoxyribonucleases (EC 3.1.-) ; GTP-Binding Proteins (EC 3.6.1.-) ; RecQ Helicases (EC 3.6.4.12) ; WRN protein, human (EC 3.6.4.12) ; Werner Syndrome Helicase (EC 3.6.4.12)
    Language English
    Publishing date 2009-12-07
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Intramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 639046-8
    ISSN 1476-5594 ; 0950-9232
    ISSN (online) 1476-5594
    ISSN 0950-9232
    DOI 10.1038/onc.2009.443
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  10. Article ; Online: Killer granzyme B linked to N-myc- and c-myc-dependent HSC survival: isn't that comyc?

    Sauvageau, Guy / Perreault, Claude

    Cell stem cell

    2008  Volume 3, Issue 6, Page(s) 579–580

    Abstract: c-myc is a key regulator of hemopoietic stem cell (HSC) activity. In this issue of Cell Stem Cell ... Laurenti et al. (2008) show that c-myc and N-myc control HSC survival and link this finding ...

    Abstract c-myc is a key regulator of hemopoietic stem cell (HSC) activity. In this issue of Cell Stem Cell, Laurenti et al. (2008) show that c-myc and N-myc control HSC survival and link this finding to the regulation of granzyme B expression.
    MeSH term(s) Animals ; Cell Differentiation/genetics ; Cell Survival/genetics ; Gene Expression Regulation, Enzymologic/genetics ; Granzymes/genetics ; Granzymes/metabolism ; Hematopoiesis/genetics ; Hematopoietic Stem Cells/enzymology ; Mice ; Proto-Oncogene Proteins c-myc/genetics ; Proto-Oncogene Proteins c-myc/metabolism ; Secretory Vesicles/enzymology ; Secretory Vesicles/secretion
    Chemical Substances Proto-Oncogene Proteins c-myc ; Granzymes (EC 3.4.21.-)
    Language English
    Publishing date 2008-12-04
    Publishing country United States
    Document type Comment ; Journal Article ; Review
    ZDB-ID 2375354-7
    ISSN 1875-9777 ; 1934-5909
    ISSN (online) 1875-9777
    ISSN 1934-5909
    DOI 10.1016/j.stem.2008.11.003
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