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Research Areas Translation regulatory factor RBM3 ... a proto - oncogenepreventsmitotic catastrophe
cumulative DNA damage(passive) caused bymitotic catastrophe
Sureban SM , Ramalingam S , Natarajan G , May R , Subramaniam D , Bishnupuri KS , Morrison AR , Dieckgraefe BK , Brackett DJ , Postier RG , Houchen CW , Anant S. Translation regulatory factor RBM3 ... a proto - oncogenepreventsmitotic catastrophe
1125016413.Replication checkpointpreventingmitotic catastrophe
Topoisomerase II deficiency Article Snippet(passive) provoked bya mitotic catastrophe
Topoisomerase II deficiency - Full Text Cytological And Genetic Consequences Fo(passive) provoked bya mitotic catastrophe
the DNA damage - induced , Chk1-dependent checkpoint ( 30(passive) can also be triggered byMitotic catastrophe
that the CUL4A / B deficiency allows for entering mitosis despite irreparable DNA damagethereby causingmitotic catastrophe
Cdk1 is sequestered in the cytoplasm upon DNA damage in a 14 - 3 - 3-dependent mannerto preventmitotic catastrophe
a decreased DNA repair capability and results in more residual DNA damage in the cells , including the mitotic cellspromptsthe mitotic catastrophe
Oct 2.PMID : 11593014 Free PMC ArticleSimilar articles Select item 112501642.Replication checkpointpreventingmitotic catastrophe
in G1 and subsequent G1 arrest associated with senescence or ( ii ) premature mitotic entry in the absence of p53 / p21WAF1causingmitotic catastrophe
Combining PARP inhibitor Olaparib with the BET inhibitor , we observed a synergistic increase in DNA damage and checkpoint defects , which allowed cells to enter mitosis despite the accumulation of DNA damageultimately causingmitotic catastrophe
BCR - ABL - mediated inhibition of DNA damage - induced apoptosis is associated with a prolongation of cell cycle arrest at the G2 / M restriction point ; the delay of G2 / M transition may allow time to repair and complete DNA replication and chromosomal segregationthereby preventinga mitotic catastrophe
rapid progression(passive) can be caused byMitotic catastrophe
premature exit from mitosis(passive) is ... caused bymitotic catastrophe
to “ facilitate ” the reentry of cells into mitosisthus causingmitotic catastrophe
aberrant mitosis and executed either during mitosis or in the subsequent interphase.5 , 8(passive) are triggered bymitotic catastrophe
Cells experiencing impairment of the mitotic machinery can undergo apoptosis within mitosis (resultingfrom mitotic “ catastrophe
drugs that target microtubules or affect the progression of mitosis(passive) could be caused byMitotic catastrophe
key cell - cycle and mitosis genescausingmitotic catastrophe
mitotic errors leading to widespread chromosomal rearrangements [ 14(passive) caused byMitotic catastrophe
microtubule instability leading to an abnormal mitotic checkpoint ( 19(passive) can also be triggered byMitotic catastrophe
cell deathresultingfrom mitotic catastrophe
in addition to inducing apoptosismay causemitotic catastrophe
Replisome degradationpreventsmitotic catastrophes
repeated aberrant mitosis(passive) caused bymitotic catastrophe
MnTE-2-PyP(passive) caused bymitotic catastrophes
premature mitotic entrance with either unrepaired DNA harm or(passive) caused bymitotic catastrophe
these dying cellsresultedfrom mitotic catastrophe
when overexpressed in the presence of the DNA‐damaging agent methyl methanesulphonate ( MMScausedmitotic catastrophe
agents that affect the stability of microtubules as well as by mitotic failure that results from impaired cell cycle checkpoints(passive) is also triggered byMitotic catastrophe
Constitutive SOCEcausesmitotic catastrophe
agents that damage microtubules and disrupt the mitotic spindle(passive) is also caused byMitotic catastrophe
The dashed arrows point to cells that underwent endoreduplicationeventually causingmitotic catastrophe
colorectal carcinoma cellstriggersa mitotic catastrophe
Radiationcausesmitotic catastrophe
To determinecan causemitotic catastrophe
in particular(passive) can ... be triggeredMitotic catastrophe
difficulties with tubulin arrangement in the mitotic spindle(passive) caused bythe mitotic catastrophe
to different types of cell deathcan leadto different types of cell death
to cell death in intestinal stem cellscontributesto cell death in intestinal stem cells
to abnormal nucleus division and cell death without DNA fragmentation through activation of caspaseleadsto abnormal nucleus division and cell death without DNA fragmentation through activation of caspase
a P73-dependent apoptotic cell death in chronic myelogenous leukemia cells ( K562(passive) was triggered bya P73-dependent apoptotic cell death in chronic myelogenous leukemia cells ( K562
to neuronal dysfunction and neurodegeneration in AD.PMIDleadsto neuronal dysfunction and neurodegeneration in AD.PMID
in fatal dilated cardiomyopathy , " Circulation Researchresultingin fatal dilated cardiomyopathy , " Circulation Research
in delayed apoptosisresultingin delayed apoptosis
in apoptosis[29resultsin apoptosis[29
to necrosis and apoptosisledto necrosis and apoptosis
in fatal dilated cardiomyopathy — Penn State Rationaleresultingin fatal dilated cardiomyopathy — Penn State Rationale
in caspase dependent apoptosisresultin caspase dependent apoptosis
to apoptosis and senescence in TNBCleadsto apoptosis and senescence in TNBC
generic secondary apoptosis(passive) triggered bygeneric secondary apoptosis
to apoptosis followed by PARP and Laminleadsto apoptosis followed by PARP and Lamin
in apoptosis by downregulating CDC20 in glioma cellsresultsin apoptosis by downregulating CDC20 in glioma cells
to apoptosis or necrosis in p53-deficient cellsleadingto apoptosis or necrosis in p53-deficient cells
in fatal dilated cardiomyopathy AU - Ahmad , Firdos AU - Parikh , Shan AU - Hoffman , Nichole E. AU - Verma , Vipin K. AU - Yuan , Ancai AU - Guo , Yuanjun AU - Lal , Hind N2 - Rationaleresultingin fatal dilated cardiomyopathy AU - Ahmad , Firdos AU - Parikh , Shan AU - Hoffman , Nichole E. AU - Verma , Vipin K. AU - Yuan , Ancai AU - Guo , Yuanjun AU - Lal , Hind N2 - Rationale
in the activation of three distinct oncosuppressive mechanisms , i.e. , apoptosis , necrosis and senescence , and cancer cellscan resultin the activation of three distinct oncosuppressive mechanisms , i.e. , apoptosis , necrosis and senescence , and cancer cells
to p53-independent apoptosis or necrotic death.37 Lethal hematopoietic syndrome resulting from an acute p53 responseleadingto p53-independent apoptosis or necrotic death.37 Lethal hematopoietic syndrome resulting from an acute p53 response
in fatal dilated cardiomyopathy Zhou , J. , Ahmad , F. , Parikh , S. , Hoffman , N. E. , Rajan , S. , Verma , V. K. , Song , J. , Yuan , A. , Shanmughapriya , S. , Guo , Y. , Gao , E. , Koch , W. , Woodgett , J. R. , Madesh , M. , Kishore , R. , Lal , H. & Force , T. , Apr 15 2016resultingin fatal dilated cardiomyopathy Zhou , J. , Ahmad , F. , Parikh , S. , Hoffman , N. E. , Rajan , S. , Verma , V. K. , Song , J. , Yuan , A. , Shanmughapriya , S. , Guo , Y. , Gao , E. , Koch , W. , Woodgett , J. R. , Madesh , M. , Kishore , R. , Lal , H. & Force , T. , Apr 15 2016
massive die - off of the affected cellscausesmassive die - off of the affected cells
either to apoptotic morphology or to necrosiscan leadeither to apoptotic morphology or to necrosis
in a loss of functional cardiac myocytesresultingin a loss of functional cardiac myocytes
from chromosomal instability after DNA damageresultingfrom chromosomal instability after DNA damage
abnormal mitosis(passive) caused byabnormal mitosis
in senescence , or irreversible cell cycle arrest precluding generation of genomic unstable cellsresultingin senescence , or irreversible cell cycle arrest precluding generation of genomic unstable cells
in human cancer cellstriggeredin human cancer cells
to arrest in mitosis or , alternatively , to the formation of cells with multiple nuclei or a single giant nucleus ( 12 , 13leadsto arrest in mitosis or , alternatively , to the formation of cells with multiple nuclei or a single giant nucleus ( 12 , 13
in remote desktop , polyploidy , or failure to identify cytokinesisresultingin remote desktop , polyploidy , or failure to identify cytokinesis
Many different cell fates(passive) could be caused byMany different cell fates
to arrest in mitosis , or alternatively to the formation of cells with multiple nuclei or a single giant nucleus ( Gisselsson et al .leadsto arrest in mitosis , or alternatively to the formation of cells with multiple nuclei or a single giant nucleus ( Gisselsson et al .
survival of cells with extensively damaged chromosomes ( Figure 1preventingsurvival of cells with extensively damaged chromosomes ( Figure 1
endopolyploidy , giant cell formationprovokesendopolyploidy , giant cell formation
normallycausednormally
from a combination of deficient cell - cycle checkpoints , in particular DNA structure checkpoints and the spindle assembly checkpoint , and cellular damage [ 1 ] Defective cell cycle checkpointmay resultfrom a combination of deficient cell - cycle checkpoints , in particular DNA structure checkpoints and the spindle assembly checkpoint , and cellular damage [ 1 ] Defective cell cycle checkpoint
to missegregation of chromosomal DNA that is trapped between two cells ( cut phenotypeleadingto missegregation of chromosomal DNA that is trapped between two cells ( cut phenotype
in a sub - G0 peakcould resultin a sub - G0 peak
to cellular necrosisleadingto cellular necrosis
in the ultimate development of fatal heart failureresultingin the ultimate development of fatal heart failure
in cell fusion , polyploidy , forex in india 2017resultingin cell fusion , polyploidy , forex in india 2017