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[PMID]:29274490
[Au] Autor:Ghawanmeh AA; Chong KF; Sarkar SM; Bakar MA; Othaman R; Khalid RM
[Ad] Endereço:Faculty of Industrial Sciences & Technology, University Malaysia Pahang, Gambang, 26300 Kuantan, Pahang, Malaysia. Electronic address: gh.just4chem@hotmail.com.
[Ti] Título:Colchicine prodrugs and codrugs: Chemistry and bioactivities.
[So] Source:Eur J Med Chem;144:229-242, 2018 Jan 20.
[Is] ISSN:1768-3254
[Cp] País de publicação:France
[La] Idioma:eng
[Ab] Resumo:Antimitotic colchicine possesses low therapeutic index due to high toxicity effects in non-target cell. However, diverse colchicine analogs have been derivatized as intentions for toxicity reduction and structure-activity relationship (SAR) studying. Hybrid system of colchicine structure with nontoxic biofunctional compounds modified further affords a new entity in chemical structure with enhanced activity and selectivity. Moreover, nanocarrier formulation strategies have been used for colchicine delivery. This review paper focuses on colchicine nanoformulation, chemical synthesis of colchicine prodrugs and codrugs with different linkers, highlights linker chemical nature and biological activity of synthesized compounds. Additionally, classification of colchicine prodrugs based on type of conjugates is discussed, as biopolymers prodrugs, fluorescent prodrug, metal complexes prodrug, metal-labile prodrug and bioconjugate prodrug. Finally, we briefly summarized the biological importance of colchicine nanoformulation, colchicine prodrugs and codrugs.
[Mh] Termos MeSH primário: Colchicina/análogos & derivados
Colchicina/farmacologia
Pró-Fármacos/química
Pró-Fármacos/farmacologia
Moduladores de Tubulina/química
Moduladores de Tubulina/farmacologia
[Mh] Termos MeSH secundário: Animais
Desenho de Drogas
Seres Humanos
Mitose/efeitos dos fármacos
Relação Estrutura-Atividade
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Prodrugs); 0 (Tubulin Modulators); SML2Y3J35T (Colchicine)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171224
[St] Status:MEDLINE


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[PMID]:29268130
[Au] Autor:Lin HY; Han HW; Sun WX; Yang YS; Tang CY; Lu GH; Qi JL; Wang XM; Yang YH
[Ad] Endereço:State Key Laboratory of Pharmaceutical Biotechnology, NJU-NJFU Institute of Plant Molecular Biology, School of Life Sciences, Nanjing University, Nanjing, 210023, China; Co-Innovation Center for Sustainable Forestry in Southern China, Nanjing Forestry University, Nanjing, 210037, China.
[Ti] Título:Design and characterization of α-lipoic acyl shikonin ester twin drugs as tubulin and PDK1 dual inhibitors.
[So] Source:Eur J Med Chem;144:137-150, 2018 Jan 20.
[Is] ISSN:1768-3254
[Cp] País de publicação:France
[La] Idioma:eng
[Ab] Resumo:Shikonin exhibits powerful anticancer activities for various cancer cells, but its poor solubility and strong toxicity hinder its development as clinical anticancer agent. We previously confirmed that shikonin and its derivatives can disturb mitosis through targeting tubulin. In this study, α-lipoic acid, the naturally-occurring co-factor of pyruvate dehydrogenase (PDH), was introduced into shikonin to design the twin drugs against both mitosis (tubulin) and glycolysis (PDK). 18 kinds of α-lipoic acid shikonin ester derivatives were achieved through three rounds of screening process performed by computer assistant drug design method, being designated as the outstanding compounds. Among them, 1c displayed the most potent cytotoxicity towards cervical cancer cells (HeLa) with an IC value of 3.14 ± 0.58 µM and inhibited xenotransplanted tumor growth in a dose-dependent manner. Further pharmacologic study demonstrated that 1c can cause cell cycle arrest in G2/M phase as tubulin polymerization inhibitor. Moreover, it also showed good PDK1 inhibitory activity, promoting PDH activity and forced HeLa cells to process more aerobic metabolism to undergo cell apoptosis. We reported here the first dual inhibitors of tubulin and PDK1 based on shikonin. It may form a basis for shikonin optimization through twin drug design framework for the discovery of new and potent shikonin derivatives in the study of targeted cancer therapy.
[Mh] Termos MeSH primário: Antineoplásicos/química
Antineoplásicos/farmacologia
Naftoquinonas/química
Naftoquinonas/farmacologia
Proteínas Serina-Treonina Quinases/antagonistas & inibidores
Moduladores de Tubulina/química
Moduladores de Tubulina/farmacologia
[Mh] Termos MeSH secundário: Apoptose/efeitos dos fármacos
Pontos de Checagem do Ciclo Celular/efeitos dos fármacos
Desenho de Drogas
Glicólise/efeitos dos fármacos
Células HeLa
Seres Humanos
Mitose/efeitos dos fármacos
Neoplasias/tratamento farmacológico
Neoplasias/metabolismo
Proteínas Serina-Treonina Quinases/metabolismo
Tubulina (Proteína)/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Naphthoquinones); 0 (Tubulin); 0 (Tubulin Modulators); 3IK6592UBW (shikonin); EC 2.7.11.1 (Protein-Serine-Threonine Kinases); EC 2.7.11.2 (pyruvate dehydrogenase (acetyl-transferring) kinase)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171222
[St] Status:MEDLINE


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[PMID]:28743762
[Au] Autor:Hum YF; Jinks-Robertson S
[Ad] Endereço:Department of Molecular Genetics and Microbiology, Duke University, Durham, North Carolina 27710.
[Ti] Título:Mitotic Gene Conversion Tracts Associated with Repair of a Defined Double-Strand Break in .
[So] Source:Genetics;207(1):115-128, 2017 09.
[Is] ISSN:1943-2631
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Mitotic recombination between homologous chromosomes leads to the uncovering of recessive alleles through loss of heterozygosity. In the current study, a defined double-strand break was used to initiate reciprocal loss of heterozygosity between diverged homologs of chromosome IV in These events resulted from the repair of two broken chromatids, one of which was repaired as a crossover and the other as a noncrossover. Associated gene conversion tracts resulting from the donor-directed repair of mismatches formed during strand exchange (heteroduplex DNA) were mapped using microarrays. Gene conversion tracts associated with individual crossover and noncrossover events were similar in size and position, with half of the tracts being unidirectional and mapping to only one side of the initiating break. Among crossover events, this likely reflected gene conversion on only one side of the break, with restoration-type repair occurring on the other side. For noncrossover events, an ectopic system was used to directly compare gene conversion tracts produced in a wild-type strain to heteroduplex DNA tracts generated in the absence of the Mlh1 mismatch-repair protein. There was a strong bias for unidirectional tracts in the absence, but not in the presence, of Mlh1 This suggests that mismatch repair acts on heteroduplex DNA that is only transiently present in noncrossover intermediates of the synthesis dependent strand annealing pathway. Although the molecular features of events associated with loss of heterozygosity generally agreed with those predicted by current recombination models, there were unexpected complexities in associated gene conversion tracts.
[Mh] Termos MeSH primário: Quebras de DNA de Cadeia Dupla
Conversão Gênica
Mitose/genética
Reparo de DNA por Recombinação
Saccharomyces cerevisiae/genética
[Mh] Termos MeSH secundário: Troca Genética
Saccharomyces cerevisiae/citologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170727
[St] Status:MEDLINE
[do] DOI:10.1534/genetics.117.300057


  4 / 43370 MEDLINE  
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[PMID]:28747316
[Au] Autor:Suresh S; Markossian S; Osmani AH; Osmani SA
[Ad] Endereço:Department of Molecular Genetics, The Ohio State University, Columbus, OH.
[Ti] Título:Mitotic nuclear pore complex segregation involves Nup2 in .
[So] Source:J Cell Biol;216(9):2813-2826, 2017 Sep 04.
[Is] ISSN:1540-8140
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Transport through nuclear pore complexes (NPCs) during interphase is facilitated by the nucleoporin Nup2 via its importin α- and Ran-binding domains. However, and vertebrate Nup2 also locate to chromatin during mitosis, suggestive of mitotic functions. In this study, we report that Nup2 is required for mitotic NPC inheritance in Interestingly, the role of Nup2 during mitotic NPC segregation is independent of its importin α- and Ran-binding domains but relies on a central targeting domain that is necessary for localization and viability. To test whether mitotic chromatin-associated Nup2 might function to bridge NPCs with chromatin during segregation, we provided an artificial link between NPCs and chromatin via Nup133 and histone H1. Using this approach, we bypassed the requirement of Nup2 for NPC segregation. This indicates that cells ensure accurate mitotic NPC segregation to daughter nuclei by linking mitotic DNA and NPC segregation via the mitotic specific chromatin association of Nup2.
[Mh] Termos MeSH primário: Aspergillus nidulans/metabolismo
Proteínas Fúngicas/metabolismo
Mitose
Complexo de Proteínas Formadoras de Poros Nucleares/metabolismo
Poro Nuclear/metabolismo
[Mh] Termos MeSH secundário: Aspergillus nidulans/genética
Aspergillus nidulans/crescimento & desenvolvimento
Cromatina/genética
Cromatina/metabolismo
DNA Fúngico/genética
DNA Fúngico/metabolismo
Proteínas Fúngicas/genética
Histonas/metabolismo
Microscopia de Fluorescência
Mutação
Poro Nuclear/genética
Complexo de Proteínas Formadoras de Poros Nucleares/genética
Transdução de Sinais
Fatores de Tempo
Imagem com Lapso de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Chromatin); 0 (DNA, Fungal); 0 (Fungal Proteins); 0 (Histones); 0 (Nuclear Pore Complex Proteins)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170728
[St] Status:MEDLINE
[do] DOI:10.1083/jcb.201610019


  5 / 43370 MEDLINE  
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[PMID]:28457629
[Au] Autor:McCoy RC
[Ad] Endereço:Department of Genome Sciences, University of Washington, Seattle, WA, USA. Electronic address: rcmccoy@uw.edu.
[Ti] Título:Mosaicism in Preimplantation Human Embryos: When Chromosomal Abnormalities Are the Norm.
[So] Source:Trends Genet;33(7):448-463, 2017 07.
[Is] ISSN:0168-9525
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Along with errors in meiosis, mitotic errors during post-zygotic cell division contribute to pervasive aneuploidy in human embryos. Relatively little is known, however, about the genesis of these errors or their fitness consequences. Rapid technological advances are helping to close this gap, revealing diverse molecular mechanisms contributing to mitotic error. These include altered cell cycle checkpoints, aberrations of the centrosome, and failed chromatid cohesion, mirroring findings from cancer biology. Recent studies are challenging the idea that mitotic error is abnormal, emphasizing that the fitness impacts of mosaicism depend on its scope and severity. In light of these findings, technical and philosophical limitations of various screening approaches are discussed, along with avenues for future research.
[Mh] Termos MeSH primário: Blastocisto
Aberrações Cromossômicas
Mosaicismo
[Mh] Termos MeSH secundário: Aneuploidia
Seres Humanos
Meiose
Mitose
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180228
[Lr] Data última revisão:
180228
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170502
[St] Status:MEDLINE


  6 / 43370 MEDLINE  
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Registro de Ensaios Clínicos
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[PMID]:29260225
[Au] Autor:Stupp R; Taillibert S; Kanner A; Read W; Steinberg DM; Lhermitte B; Toms S; Idbaih A; Ahluwalia MS; Fink K; Di Meco F; Lieberman F; Zhu JJ; Stragliotto G; Tran DD; Brem S; Hottinger AF; Kirson ED; Lavy-Shahaf G; Weinberg U; Kim CY; Paek SH; Nicholas G; Burna J; Hirte H; Weller M; Palti Y; Hegi ME; Ram Z
[Ad] Endereço:Lou and Jean MalnatiBrain Tumor Institute of the Robert H. Lurie Comprehensive Cancer Center of Northwestern University Feinberg School of Medicine, Chicago, Illinois.
[Ti] Título:Effect of Tumor-Treating Fields Plus Maintenance Temozolomide vs Maintenance Temozolomide Alone on Survival in Patients With Glioblastoma: A Randomized Clinical Trial.
[So] Source:JAMA;318(23):2306-2316, 2017 12 19.
[Is] ISSN:1538-3598
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Importance: Tumor-treating fields (TTFields) is an antimitotic treatment modality that interferes with glioblastoma cell division and organelle assembly by delivering low-intensity alternating electric fields to the tumor. Objective: To investigate whether TTFields improves progression-free and overall survival of patients with glioblastoma, a fatal disease that commonly recurs at the initial tumor site or in the central nervous system. Design, Setting, and Participants: In this randomized, open-label trial, 695 patients with glioblastoma whose tumor was resected or biopsied and had completed concomitant radiochemotherapy (median time from diagnosis to randomization, 3.8 months) were enrolled at 83 centers (July 2009-2014) and followed up through December 2016. A preliminary report from this trial was published in 2015; this report describes the final analysis. Interventions: Patients were randomized 2:1 to TTFields plus maintenance temozolomide chemotherapy (n = 466) or temozolomide alone (n = 229). The TTFields, consisting of low-intensity, 200 kHz frequency, alternating electric fields, was delivered (≥ 18 hours/d) via 4 transducer arrays on the shaved scalp and connected to a portable device. Temozolomide was administered to both groups (150-200 mg/m2) for 5 days per 28-day cycle (6-12 cycles). Main Outcomes and Measures: Progression-free survival (tested at α = .046). The secondary end point was overall survival (tested hierarchically at α = .048). Analyses were performed for the intent-to-treat population. Adverse events were compared by group. Results: Of the 695 randomized patients (median age, 56 years; IQR, 48-63; 473 men [68%]), 637 (92%) completed the trial. Median progression-free survival from randomization was 6.7 months in the TTFields-temozolomide group and 4.0 months in the temozolomide-alone group (HR, 0.63; 95% CI, 0.52-0.76; P < .001). Median overall survival was 20.9 months in the TTFields-temozolomide group vs 16.0 months in the temozolomide-alone group (HR, 0.63; 95% CI, 0.53-0.76; P < .001). Systemic adverse event frequency was 48% in the TTFields-temozolomide group and 44% in the temozolomide-alone group. Mild to moderate skin toxicity underneath the transducer arrays occurred in 52% of patients who received TTFields-temozolomide vs no patients who received temozolomide alone. Conclusions and Relevance: In the final analysis of this randomized clinical trial of patients with glioblastoma who had received standard radiochemotherapy, the addition of TTFields to maintenance temozolomide chemotherapy vs maintenance temozolomide alone, resulted in statistically significant improvement in progression-free survival and overall survival. These results are consistent with the previous interim analysis. Trial Registration: clinicaltrials.gov Identifier: NCT00916409.
[Mh] Termos MeSH primário: Antineoplásicos Alquilantes/uso terapêutico
Dacarbazina/análogos & derivados
Terapia por Estimulação Elétrica
Glioblastoma/tratamento farmacológico
[Mh] Termos MeSH secundário: Adulto
Idoso
Antineoplásicos Alquilantes/efeitos adversos
Quimiorradioterapia
Dacarbazina/efeitos adversos
Dacarbazina/uso terapêutico
Intervalo Livre de Doença
Feminino
Seguimentos
Glioblastoma/radioterapia
Glioblastoma/cirurgia
Seres Humanos
Quimioterapia de Manutenção
Masculino
Meia-Idade
Mitose
Análise de Sobrevida
[Pt] Tipo de publicação:CLINICAL TRIAL, PHASE III; COMPARATIVE STUDY; JOURNAL ARTICLE; MULTICENTER STUDY; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
0 (Antineoplastic Agents, Alkylating); 7GR28W0FJI (Dacarbazine); YF1K15M17Y (temozolomide)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180228
[Lr] Data última revisão:
180228
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171221
[Cl] Clinical Trial:ClinicalTrial
[St] Status:MEDLINE
[do] DOI:10.1001/jama.2017.18718


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[PMID]:29342186
[Au] Autor:Hultman I; Haeggblom L; Rognmo I; Jansson Edqvist J; Blomberg E; Ali R; Phillips L; Sandstedt B; Kogner P; Shirazi Fard S; Ährlund-Richter L
[Ad] Endereço:Department of Women's and Children's Health, Karolinska Institutet, Stockholm. Sweden.
[Ti] Título:Doxorubicin-provoked increase of mitotic activity and concomitant drain of G0-pool in therapy-resistant BE(2)-C neuroblastoma.
[So] Source:PLoS One;13(1):e0190970, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:In this study chemotherapy response in neuroblastoma (NB) was assessed for the first time in a transplantation model comprising non-malignant human embryonic microenvironment of pluripotent stem cell teratoma (PSCT) derived from diploid bona fide hESC. Two NB cell lines with known high-risk phenotypes; the multi-resistant BE(2)-C and the drug sensitive IMR-32, were transplanted to the PSCT model and the tumour growth was exposed to single or repeated treatments with doxorubicin, and thereafter evaluated for cell death, apoptosis, and proliferation. Dose dependent cytotoxic effects were observed, this way corroborating the experimental platform for this type of analysis. Notably, analysis of doxorubicin-resilient BE(2)-C growth in the PSCT model revealed an unexpected 1,5-fold increase in Ki67-index (p<0.05), indicating that non-cycling (G0) cells entered the cell cycle following the doxorubicin exposure. Support for this notion was obtained also in vitro. A pharmacologically relevant dose (1µM) resulted in a marked accumulation of Ki67 positive BE(2)-C cells (p<0.0001), as well as a >3-fold increase in active cell cycle (i.e. cells positive staining for PH3 together with incorporation of EdU) (p<0.01). Considering the clinical challenge for treating high-risk NB, the discovery of a therapy-provoked growth-stimulating effect in the multi-resistant and p53-mutated BE(2)-C cell line, but not in the drug-sensitive p53wt IMR-32 cell line, warrants further studies concerning generality and clinical significance of this new observation.
[Mh] Termos MeSH primário: Doxorrubicina/farmacologia
Mitose/efeitos dos fármacos
Neuroblastoma/patologia
Fase de Repouso do Ciclo Celular
[Mh] Termos MeSH secundário: Animais
Morte Celular/efeitos dos fármacos
Linhagem Celular Tumoral
Proliferação Celular
Seres Humanos
Camundongos
Camundongos Endogâmicos NOD
Camundongos SCID
Modelos Biológicos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
80168379AG (Doxorubicin)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180226
[Lr] Data última revisão:
180226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180118
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0190970


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[PMID]:28468989
[Au] Autor:D'Avino PP
[Ad] Endereço:Department of Pathology, University of Cambridge, Tennis Court Road, Cambridge, CB2 1QP, UK ppd21@cam.ac.uk.
[Ti] Título:Citron kinase - renaissance of a neglected mitotic kinase.
[So] Source:J Cell Sci;130(10):1701-1708, 2017 May 15.
[Is] ISSN:1477-9137
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Cell division controls the faithful segregation of genomic and cytoplasmic materials between the two nascent daughter cells. Members of the Aurora, Polo and cyclin-dependent (Cdk) kinase families are known to regulate multiple events throughout cell division, whereas another kinase, citron kinase (CIT-K), for a long time has been considered to function solely during cytokinesis, the last phase of cell division. CIT-K was originally proposed to regulate the ingression of the cleavage furrow that forms at the equatorial cortex of the dividing cell after chromosome segregation. However, studies in the last decade have clarified that this kinase is, instead, required for the organization of the midbody in late cytokinesis, and also revealed novel functions of CIT-K earlier in mitosis and in DNA damage control. Moreover, CIT-K mutations have recently been linked to the development of human microcephaly, and CIT-K has been identified as a potential target in cancer therapy. In this Commentary, I describe and re-evaluate the functions and regulation of CIT-K during cell division and its involvement in human disease. Finally, I offer my perspectives on the open questions and future challenges that are necessary to address, in order to fully understand this important and yet unjustly neglected mitotic kinase.
[Mh] Termos MeSH primário: Peptídeos e Proteínas de Sinalização Intracelular/metabolismo
Mitose
Proteínas Serina-Treonina Quinases/metabolismo
[Mh] Termos MeSH secundário: Animais
Citocinese
Seres Humanos
Modelos Biológicos
Transdução de Sinais
Proteínas rho de Ligação ao GTP/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Intracellular Signaling Peptides and Proteins); EC 2.7.1.- (citron-kinase); EC 2.7.11.1 (Protein-Serine-Threonine Kinases); EC 3.6.5.2 (rho GTP-Binding Proteins)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180223
[Lr] Data última revisão:
180223
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE
[do] DOI:10.1242/jcs.200253


  9 / 43370 MEDLINE  
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[PMID]:29262707
[Au] Autor:Atalay PB; Asci O; Kaya FO; Tuna BG
[Ad] Endereço:1 Department of Medical Biology and Genetics, Faculty of Medicine, Maltepe University , Istanbul , Turkey.
[Ti] Título:Hydrogen peroxide prolongs mitotic arrest in a dose dependent manner and independently of the spindle assembly checkpoint activity in Saccharomyces cerevisiae.
[So] Source:Acta Biol Hung;68(4):477-489, 2017 Dec.
[Is] ISSN:0236-5383
[Cp] País de publicação:Hungary
[La] Idioma:eng
[Ab] Resumo:Oxidative stress and chromosome missegregation are important factors that are linked to aneuploidy. A major reason for chromosome missegragation is the inappropriate activity of the spindle assembly checkpoint (SAC), a conserved surveillance mechanism that monitors the state of kinetochore-microtubule attachments to ensure equal chromosome segregation in mitosis. SAC-activation induces a prolonged mitotic arrest. Mitosis is considered the most vulnerable cell cycle phase to several external signals, therefore increasing the time cells spent in this phase via mitotic arrest induction by SAC-activating agents is favorable for cancer therapy. Cancer cells also display elevated oxidative stress due to abnormally high production of reactive oxygen species (ROS). However, the effect of increased oxidative stress on the duration of mitotic arrest remains largely unknown. In this study, we investigated the effect of H O -induced oxidative stress on the mitotic arrest induced by a SAC-activating agent (nocodazole) in Saccharomyces cerevisiae. Our data suggest that oxidative stress prolongs SAC-activation induced mitotic arrest in a dose dependent manner. We, in addition, investigated the effect of H O treatment on the mitotic arrest induced independently of SAC-activation by using a conditional mutant (cdc23) and showed that the effect of H O -induced oxidative stress on mitotic arrest is independent of the SAC activity.
[Mh] Termos MeSH primário: Pontos de Checagem do Ciclo Celular/efeitos dos fármacos
Peróxido de Hidrogênio/farmacologia
Mitose/efeitos dos fármacos
Saccharomyces cerevisiae/metabolismo
Fuso Acromático/metabolismo
[Mh] Termos MeSH secundário: Subunidade Apc8 do Ciclossomo-Complexo Promotor de Anáfase/genética
Subunidade Apc8 do Ciclossomo-Complexo Promotor de Anáfase/metabolismo
Pontos de Checagem do Ciclo Celular/genética
Relação Dose-Resposta a Droga
Mitose/genética
Mutação
Saccharomyces cerevisiae/genética
Proteínas de Saccharomyces cerevisiae/genética
Proteínas de Saccharomyces cerevisiae/metabolismo
Fuso Acromático/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Apc8 Subunit, Anaphase-Promoting Complex-Cyclosome); 0 (CDC23 protein, S cerevisiae); 0 (Saccharomyces cerevisiae Proteins); BBX060AN9V (Hydrogen Peroxide)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180216
[Lr] Data última revisão:
180216
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171222
[St] Status:MEDLINE
[do] DOI:10.1556/018.68.2017.4.12


  10 / 43370 MEDLINE  
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[PMID]:29371677
[Au] Autor:An Z; Sabalic M; Bloomquist RF; Fowler TE; Streelman T; Sharpe PT
[Ad] Endereço:Centre for Craniofacial and Regenerative Biology, Dental Institute, Kings College London, London, SE1 9RT, UK.
[Ti] Título:A quiescent cell population replenishes mesenchymal stem cells to drive accelerated growth in mouse incisors.
[So] Source:Nat Commun;9(1):378, 2018 01 25.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The extent to which heterogeneity within mesenchymal stem cell (MSC) populations is related to function is not understood. Using the archetypal MSC in vitro surface marker, CD90/Thy1, here we show that 30% of the MSCs in the continuously growing mouse incisor express CD90/Thy1 and these cells give rise to 30% of the differentiated cell progeny during postnatal development. In adulthood, when growth rate homeostasis is established, the CD90/Thy1 MSCs decrease dramatically in number. When adult incisors are cut, the growth rate increases to rapidly re-establish tooth length and homeostasis. This accelerated growth rate correlates with the re-appearance of CD90/Thy MSCs and re-establishment of their contribution to cell differentiation. A population of Celsr1 quiescent cells becomes mitotic following clipping and replenishes the CD90/Thy1 population. A sub-population of MSCs thus exists in the mouse incisor, distinguished by expression of CD90/Thy1 that plays a specific role only during periods of increased growth rate.
[Mh] Termos MeSH primário: Linhagem da Célula/genética
Incisivo/citologia
Células Mesenquimais Estromais/citologia
Osteogênese/genética
Antígenos Thy-1/genética
[Mh] Termos MeSH secundário: Animais
Biomarcadores/metabolismo
Contagem de Células
Diferenciação Celular
Proliferação Celular
Citometria de Fluxo
Expressão Gênica
Incisivo/crescimento & desenvolvimento
Incisivo/metabolismo
Células Mesenquimais Estromais/metabolismo
Camundongos
Camundongos Transgênicos
Mitose
Receptores Acoplados a Proteínas-G/genética
Receptores Acoplados a Proteínas-G/metabolismo
Antígenos Thy-1/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Biomarkers); 0 (Celsr1 protein, mouse); 0 (Receptors, G-Protein-Coupled); 0 (Thy-1 Antigens)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180215
[Lr] Data última revisão:
180215
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180127
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-017-02785-6



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