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Referências encontradas : 254 [refinar]
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[PMID]:28911001
[Au] Autor:Franceschi S; Spugnesi L; Aretini P; Lessi F; Scarpitta R; Galli A; Congregati C; Caligo MA; Mazzanti CM
[Ad] Endereço:FPS - Fondazione Pisana per la Scienza, Pisa 56121, Italy.
[Ti] Título:Whole-exome analysis of a Li-Fraumeni family trio with a novel TP53 PRD mutation and anticipation profile.
[So] Source:Carcinogenesis;38(9):938-943, 2017 Sep 01.
[Is] ISSN:1460-2180
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Li-Fraumeni syndrome is a clinically heterogeneous familial cancer predisposition syndrome with autosomal-dominant inheritance caused by heterozygous germline mutations in the TP53 gene. We here analyze the genetic background of a family with a 4-year-proband presented with a Li-Fraumeni tumor. The mother developed breast cancer at age 37 and the proband died at age 8. We performed Sanger sequencing and whole-exome sequencing on peripheral blood DNA from proband and relatives. Data analysis selected only high-quality score and depth reads, rare variants and protein impact involving missense, non-sense, frameshift and splice disrupt mutations. Disease implicated variants and predicted deleterious alterations were also chosen. TP53 genetic testing revealed a never reported TP53 deletion arose as de novo mutation in the mother and inherited by the proband. We then performed whole-exome analysis of the trio to uncover inherited variants from the father that potentially worsen the already altered genetic background in the proband. No pathogenic variants were inherited in autosomal recessive, de novo dominant or X-linked recessive manner. Comparing proband and father exome we detected 25 predicted deleterious variants including a nonsense mutation in ERCC3. Those inherited mutations are possible candidate modifiers linked to TP53, explaining the proband accelerated tumor onset compared to the mother and providing a possible explanation of the genetic anticipation event in this Li-Fraumeni family.
[Mh] Termos MeSH primário: Antecipação Genética
Neoplasias da Mama/genética
Síndrome de Li-Fraumeni/genética
Proteína Supressora de Tumor p53/genética
[Mh] Termos MeSH secundário: Carcinoma Adrenocortical/terapia
Pré-Escolar
DNA Helicases/genética
Proteínas de Ligação a DNA/genética
Exoma/genética
Feminino
Genes p53
Predisposição Genética para Doença
Testes Genéticos
Mutação em Linhagem Germinativa
Heterozigoto
Humanos
Metástase Linfática
Masculino
Linhagem
Análise de Sequência de DNA
Deleção de Sequência
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (DNA-Binding Proteins); 0 (Tumor Suppressor Protein p53); 146045-44-5 (XPBC-ERCC-3 protein); EC 3.6.4.- (DNA Helicases)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171003
[Lr] Data última revisão:
171003
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170915
[St] Status:MEDLINE
[do] DOI:10.1093/carcin/bgx069


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[PMID]:28296734
[Au] Autor:Guo X; Fan C; Wang Y; Wang M; Cai C; Yang Y; Zhao S; Duan F; Li Y
[Ad] Endereço:aKey Laboratory of Clinical Trial Research in Cardiovascular Drugs, Ministry of Health, Fuwai Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China bAlfred I. DuPont Hospital for Children, Wilmington, DE cDepartment of Radiology dDepartment of Ultrasound, Fuwai Hospital, Beijing, China.
[Ti] Título:Genetic anticipation in a special form of hypertrophic cardiomyopathy with sudden cardiac death in a family with 74 members across 5 generations.
[So] Source:Medicine (Baltimore);96(11):e6249, 2017 Mar.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Hypertrophic cardiomyopathy (HCM) is the most common heritable heart disease. The genetic anticipation of HCM and its associated etiology, sudden cardiac death (SCD), remains unclear. The aim of this study was to investigate the mechanism underlying the genetic anticipation of HCM and associated SCD.An HCM family including 5 generations and 74 members was studied. Two-dimensional echocardiography was performed to diagnose HCM. The age of onset of HCM was defined as the age at first diagnosis according to hospital records. The information on SCD was confirmed by verification by ≥2 family members and a review of hospital records. Whole-genome sequencing was performed on 4 HCM subjects and 1 healthy control in the family. The identified mutations were screened in all available family members and 216 unrelated healthy controls by Sanger sequencing.The median ages of onset of HCM were 63.5, 38.5, and 18.0 years in members of the second, third, and fourth generations of the family, respectively, and the differences between the generations were significant (P < 0.001). The age at SCD also decreased with each subsequent generation (P < 0.05). In particular, among the third-generation family members, SCD occurred between 30 and 40 years of age at approximately 8 AM, whereas among the fourth-generation family members, all 5 males who experienced SCD were 16 years of age and died at approximately 8 AM. The sarcomere gene mutations MYH7-A719H and MYOZ2-L169G were detected in the HCM individuals in this pedigree. Increases in the number of mutations and the frequency of multiple gene mutations were observed in the younger generations. Moreover, a structural variant was present in the HCM phenotype-positive subjects but was absent in the HCM phenotype-negative subjects.HCM may exhibit genetic anticipation, with a decreased age of onset and increased severity in successive generations. Multiple gene mutations may contribute to genetic anticipation in HCM and thus may be of prognostic value.
[Mh] Termos MeSH primário: Antecipação Genética
Miosinas Cardíacas/genética
Cardiomiopatia Hipertrófica Familiar/genética
Proteínas de Transporte/genética
Morte Súbita Cardíaca/etiologia
Proteínas Musculares/genética
Cadeias Pesadas de Miosina/genética
[Mh] Termos MeSH secundário: Adolescente
Adulto
Idoso
Estudos de Casos e Controles
Criança
Feminino
Estudo de Associação Genômica Ampla
Humanos
Masculino
Meia-Idade
Análise de Sequência de DNA
Adulto Jovem
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Carrier Proteins); 0 (MYH7 protein, human); 0 (MYOZ2 protein, human); 0 (Muscle Proteins); EC 3.6.1.- (Cardiac Myosins); EC 3.6.4.1 (Myosin Heavy Chains)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170403
[Lr] Data última revisão:
170403
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170315
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000006249


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[PMID]:27270116
[Au] Autor:Nguyen CE; Campbell C
[Ad] Endereço:Department of Paediatrics (Nguyen), London Health Sciences Centre; Paediatric Neurology Clinic (Campbell), Children's Hospital, London Health Sciences Centre; Department of Epidemiology and Clinical Neurological Sciences, Western University, London, Ont.
[Ti] Título:Myotonic dystrophy type 1.
[So] Source:CMAJ;188(14):1033, 2016 Oct 04.
[Is] ISSN:1488-2329
[Cp] País de publicação:Canada
[La] Idioma:eng
[Mh] Termos MeSH primário: Arritmias Cardíacas/fisiopatologia
Distrofia Miotônica/fisiopatologia
[Mh] Termos MeSH secundário: Idade de Início
Antecipação Genética/genética
Arritmias Cardíacas/mortalidade
Causas de Morte
Humanos
Mexiletina/uso terapêutico
Distrofia Miotônica/quimioterapia
Distrofia Miotônica/epidemiologia
Distrofia Miotônica/genética
Bloqueadores do Canal de Sódio Disparado por Voltagem/uso terapêutico
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Voltage-Gated Sodium Channel Blockers); 1U511HHV4Z (Mexiletine)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170403
[Lr] Data última revisão:
170403
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:160608
[St] Status:MEDLINE


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[PMID]:26574783
[Au] Autor:Prigigallo MI; Abdelfattah A; Cacciola SO; Faedda R; Sanzani SM; Cooke DE; Schena L
[Ad] Endereço:First, second, and seventh authors: Dipartimento di Agraria, Università Mediterranea di Reggio Calabria, Località Feo di Vito, 89122 Reggio Calabria, Italy; third and fourth authors: Dipartimento di Agricoltura, Alimentazione e Ambiente, Università degli Studi, Via S. Sofia 100, 95123 Catania, Italy
[Ti] Título:Metabarcoding Analysis of Phytophthora Diversity Using Genus-Specific Primers and 454 Pyrosequencing.
[So] Source:Phytopathology;106(3):305-13, 2016 Mar.
[Is] ISSN:0031-949X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:A metabarcoding method based on genus-specific primers and 454 pyrosequencing was utilized to investigate the genetic diversity of Phytophthora spp. in soil and root samples of potted plants, from eight nurseries. Pyrosequencing enabled the detection of 25 Phytophthora phylotypes distributed in seven different clades and provided a much higher resolution than a corresponding cloning/Sanger sequencing approach. Eleven of these phylotypes, including P. cactorum, P. citricola s.str., P. palmivora, P. palmivora-like, P. megasperma or P. gonapodyides, P. ramorum, and five putative new Phytophthora species phylogenetically related to clades 1, 2, 4, 6, and 7 were detected only with the 454 pyrosequencing approach. We also found an additional 18 novel records of a phylotype in a particular nursery that were not detected with cloning/Sanger sequencing. Several aspects confirmed the reliability of the method: (i) many identical sequence types were identified independently in different nurseries, (ii) most sequence types identified with 454 pyrosequencing were identical to those from the cloning/Sanger sequencing approach and/or perfectly matched GenBank deposited sequences, and (iii) the divergence noted between sequence types of putative new Phytophthora species and all other detected sequences was sufficient to rule out sequencing errors. The proposed method represents a powerful tool to study Phytophthora diversity providing that particular attention is paid to the analysis of 454 pyrosequencing raw read sequences and to the identification of sequence types.
[Mh] Termos MeSH primário: Código de Barras de DNA Taxonômico
DNA Fúngico/genética
Regulação Fúngica da Expressão Gênica/fisiologia
[Mh] Termos MeSH secundário: Antecipação Genética
Técnicas de Amplificação de Ácido Nucleico
Phytophthora/classificação
Phytophthora/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (DNA, Fungal)
[Em] Mês de entrada:1605
[Cu] Atualização por classe:160319
[Lr] Data última revisão:
160319
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160319
[St] Status:MEDLINE
[do] DOI:10.1094/PHYTO-07-15-0167-R


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[PMID]:26817350
[Au] Autor:Blaszczyk M; Boczarska-Jedynak M; Rudzinska M
[Ti] Título:[Clinical variability of Juvenile Huntington's Disease phenotype].
[Ti] Título:Odmiennosc kliniczna mlodzienczej postaci choroby Huntingtona..
[So] Source:Przegl Lek;72(7):366-70, 2015.
[Is] ISSN:0033-2240
[Cp] País de publicação:Poland
[La] Idioma:pol
[Ab] Resumo:Huntington's disease is rare, genetically determinated, neurodegenerative disorder. It is determined by dynamic mutation of IT15 gene on short arm of 4 chromosome. Characteristic symptomatology include involuntary movements, cognitive decline and wide spectrum of mood and behaviour disorders. It typically becomes noticeable in mid-adult life, but there are reported cases of appaers of symptoms between 2 and 80 year of life. Especially interesting is juvenile Huntington's disease- the Westphal variant with the beginning in childchood (before 20 year of age) because of clinical differences causing diagnostic difficulties. It affects 5-10% of carries of the mutant gene. Symptoms became noticeable before 10 year of age only in 1% of them.
[Mh] Termos MeSH primário: Doença de Huntington/diagnóstico
[Mh] Termos MeSH secundário: Adolescente
Adulto
Idade de Início
Idoso
Idoso de 80 Anos ou mais
Antecipação Genética
Criança
Pré-Escolar
Humanos
Proteína Huntingtina
Doença de Huntington/epidemiologia
Doença de Huntington/genética
Meia-Idade
Proteínas do Tecido Nervoso/genética
Fenótipo
Avaliação de Sintomas
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (HTT protein, human); 0 (Huntingtin Protein); 0 (Nerve Tissue Proteins)
[Em] Mês de entrada:1603
[Cu] Atualização por classe:161126
[Lr] Data última revisão:
161126
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160127
[St] Status:MEDLINE


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[PMID]:26259297
[Au] Autor:Kavoussi SC; Lesser RL
[Ti] Título:Genetic Anticipation in Familial Neuromyelitis Optica: Case and Literature Review.
[So] Source:Conn Med;79(4):207-9, 2015 Apr.
[Is] ISSN:0010-6178
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVES: To describe genetic anticipation in a mother and daughter with antiaquaporin 4 (AQP4) antibody-positive neuromyelitisoptica (NMO). METHODS: Retrospective case review. RESULTS: A woman with onset of transverse myelitis at age 38 was found to have a positive AQP4 antibody during work-up of recurrent symptoms. Subsequently, she developed intermittent episodes of monocular vision loss with optic nerve involvement that were treated with intravenous methylprednisolone and chronic rituximab. Eighteen years after initial presentation, her 78-year-old mother, with a history of recurrent urinary tract infections, also developed monocular vision loss and her anti-AQP4 antibody was positive. Previous reports of genetic anticipation in familial NMO are identified and discussed. CONCLUSIONS: These cases highlight genetic anticipation in familial NMO. Disease onset can occur with a chronological age difference of as much as 40 years between parent and child. Patients with NMO should be counseled regarding the possibility of subsequent disease onset in family members, particularly parents, with significant differences in calendar or chronological year of onset.
[Mh] Termos MeSH primário: Antecipação Genética
Aquaporina 4/imunologia
Mielite Transversa/genética
Neuromielite Óptica/genética
[Mh] Termos MeSH secundário: Adulto
Idade de Início
Idoso
Anticorpos Monoclonais Murinos/uso terapêutico
Feminino
Humanos
Metilprednisolona/uso terapêutico
Mielite Transversa/epidemiologia
Mielite Transversa/imunologia
Neuromielite Óptica/epidemiologia
Neuromielite Óptica/imunologia
Estudos Retrospectivos
Rituximab
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Antibodies, Monoclonal, Murine-Derived); 0 (Aquaporin 4); 4F4X42SYQ6 (Rituximab); X4W7ZR7023 (Methylprednisolone)
[Em] Mês de entrada:1508
[Cu] Atualização por classe:151119
[Lr] Data última revisão:
151119
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150811
[St] Status:MEDLINE


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[PMID]:25850851
[Au] Autor:Church J; Kravochuck S
[Ad] Endereço:Cleveland, Ohio.
[Ti] Título:Variation in lynch syndrome.
[So] Source:Dis Colon Rectum;58(5):e77; quiz e79, 2015 May.
[Is] ISSN:1530-0358
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Antecipação Genética
Neoplasias Colorretais Hereditárias sem Polipose/genética
Reparo de Erro de Pareamento de DNA
[Mh] Termos MeSH secundário: Humanos
[Pt] Tipo de publicação:COMMENT; LETTER
[Em] Mês de entrada:1505
[Cu] Atualização por classe:150408
[Lr] Data última revisão:
150408
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150408
[St] Status:MEDLINE
[do] DOI:10.1097/DCR.0000000000000355


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[PMID]:25785264
[Au] Autor:Martirosyan A; Petrek M; Navratilova Z; Blbulyan A; Boyajyan A; Manukyan G
[Ad] Endereço:Department of Pathological Physiology, Faculty of Medicine and Dentistry, Palacky University, 775 20 Olomouc, Czech Republic ; Group of Molecular and Cellular Immunology, Institute of Molecular Biology, National Academy of Sciences, 0014 Yerevan, Armenia.
[Ti] Título:Differential regulation of proinflammatory mediators following LPS- and ATP-induced activation of monocytes from patients with antiphospholipid syndrome.
[So] Source:Biomed Res Int;2015:292851, 2015.
[Is] ISSN:2314-6141
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Antiphospholipid syndrome (APS) is an acquired autoimmune disorder characterized by recurrent thrombosis and pregnancy morbidity in association with the presence of antiphospholipid antibodies. Growing evidence supports the involvement of monocytes in APS pathogenesis. Inflammatory activation of monocytes promotes thrombus formation and other APS complications. However, mechanisms underlying their activation are poorly investigated. We aimed to determine transcriptional activity of monocytes after exposing them to low concentrations of lipopolysaccharide (LPS) and LPS + adenosine triphosphate (ATP) using comparative qRT-PCR. The results showed that LPS significantly increased transcriptional levels of TLR2, IL-23, CCL2, CXCL10, IL-1ß, and IL-6 in APS cells, while, in cells from healthy donors, LPS resulted in IL-6 and STAT3 elevated mRNAs. Double stimulation of the cells resulted in decreased mRNA levels of NLRP3 in monocytes isolated from healthy donors and CCL2, IL-1ß in APS cells. By contrast, TLR2 mRNAs were elevated in both investigated groups after culture of the cells with LPS + ATP. Thus, the findings indicate increased sensitivity of APS cells to LPS that may contribute to thrombus formation and enhance development or progression of autoimmune processes. Low concentrations of ATP diminish LPS-induced inflammatory state of APS monocytes which might be a potential mechanism which regulates inflammatory state of the cells.
[Mh] Termos MeSH primário: Trifosfato de Adenosina/farmacologia
Síndrome Antifosfolipídica/metabolismo
Inflamação/metabolismo
Lipopolissacarídeos/farmacologia
Monócitos/efeitos de drogas
Monócitos/metabolismo
[Mh] Termos MeSH secundário: Adulto
Antecipação Genética/efeitos de drogas
Estudos de Casos e Controles
Quimiocina CCL2/metabolismo
Quimiocina CXCL10
Feminino
Humanos
Interleucinas/metabolismo
RNA Mensageiro/metabolismo
Fator de Transcrição STAT3/metabolismo
Receptor 2 Toll-Like/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (CCL2 protein, human); 0 (CXCL10 protein, human); 0 (Chemokine CCL2); 0 (Chemokine CXCL10); 0 (Interleukins); 0 (Lipopolysaccharides); 0 (RNA, Messenger); 0 (STAT3 Transcription Factor); 0 (STAT3 protein, human); 0 (TLR2 protein, human); 0 (Toll-Like Receptor 2); 8L70Q75FXE (Adenosine Triphosphate)
[Em] Mês de entrada:1511
[Cu] Atualização por classe:150321
[Lr] Data última revisão:
150321
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150318
[St] Status:MEDLINE
[do] DOI:10.1155/2015/292851


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[PMID]:25712547
[Au] Autor:Pratte A; Prévost C; Puymirat J; Mathieu J
[Ad] Endereço:Division of Genetic Counseling, CSSS Chicoutimi, Chicoutimi, Quebec, Canada.
[Ti] Título:Anticipation in myotonic dystrophy type 1 parents with small CTG expansions.
[So] Source:Am J Med Genet A;167A(4):708-14, 2015 Apr.
[Is] ISSN:1552-4833
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Myotonic dystrophy type 1 is the most common form of adult muscular dystrophy and has the world's highest prevalence in the Saguenay-Lac-St-Jean region, due to a founder effect. This autosomal dominant disorder results from an unstable CTG repeat expansion in DMPK. This region of Canada has had a family screening and predictive testing program for this disorder since 1988. Heterozygotes for small expansions (50-100 CTG repeats) can be asymptomatic or minimally affected. The aim of this study was to assess anticipation for these individuals. At the time of this study, the molecular data of 40 individuals and their 76 affected children were available. We compared 76 parent-child pairs. Most offspring (92.1%) had a larger number of repeats than their parent and the median number of repeats in the offspring was 325 (range, 57-2000). The number of CTG repeats was significantly greater when the mutation was transmitted by a father (median, 425 repeats; range, 70-2000), than when it was transmitted by a mother (median, 200 repeats; range, 57-1400). The majority (65.8%) of children also had a more severe phenotype than their parent but the sex of the parent had no significant influence on the severity of the child's phenotype. No congenital phenotype was observed. These results confirm that anticipation is present even when the parent is heterozygous for a small CTG expansion. The parental sex has an impact on the size of the repeat in the next generation, larger increases being transmitted by males with a small expansion.
[Mh] Termos MeSH primário: Distrofia Miotônica/genética
[Mh] Termos MeSH secundário: Adulto
Idade de Início
Antecipação Genética
Criança
Feminino
Humanos
Masculino
Distrofia Miotônica/patologia
Pais
Linhagem
Expansão das Repetições de Trinucleotídeos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Em] Mês de entrada:1512
[Cu] Atualização por classe:150330
[Lr] Data última revisão:
150330
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150330
[St] Status:MEDLINE
[do] DOI:10.1002/ajmg.a.36950


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[PMID]:25489706
[Au] Autor:You YN
[Ad] Endereço:Houston, Texas.
[Ti] Título:Anticipating phenotypic differences from genetic mutations.
[So] Source:Dis Colon Rectum;58(1):143-4, 2015 Jan.
[Is] ISSN:1530-0358
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Antecipação Genética
Neoplasias Colorretais Hereditárias sem Polipose/genética
Reparo de Erro de Pareamento de DNA
[Mh] Termos MeSH secundário: Proteínas Adaptadoras de Transdução de Sinal/genética
Adenosina Trifosfatases/genética
Enzimas Reparadoras do DNA/genética
Proteínas de Ligação a DNA/genética
Genótipo
Mutação em Linhagem Germinativa
Humanos
Endonuclease PMS2 de Reparo de Erro de Pareamento
Proteína 1 Homóloga a MutL
Proteína 2 Homóloga a MutS/genética
Proteínas Nucleares/genética
Fenótipo
Medição de Risco
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Adaptor Proteins, Signal Transducing); 0 (DNA-Binding Proteins); 0 (G-T mismatch-binding protein); 0 (MLH1 protein, human); 0 (Nuclear Proteins); EC 3.6.1.- (Adenosine Triphosphatases); EC 3.6.1.- (PMS2 protein, human); EC 3.6.1.3 (MSH2 protein, human); EC 3.6.1.3 (Mismatch Repair Endonuclease PMS2); EC 3.6.1.3 (MutL Protein Homolog 1); EC 3.6.1.3 (MutS Homolog 2 Protein); EC 6.5.1.- (DNA Repair Enzymes)
[Em] Mês de entrada:1502
[Cu] Atualização por classe:161125
[Lr] Data última revisão:
161125
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:141210
[St] Status:MEDLINE
[do] DOI:10.1097/DCR.0000000000000271



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