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1 on of male and female haploid gametes into a diploid cell.
2 isolated cytogenetic finding in an otherwise diploid cell.
3 from only one of two homologous alleles in a diploid cell.
4 regation yield four haploid gametes from one diploid cell.
5 ts influence expression of both alleles in a diploid cell.
6 ifferences in expression of two alleles in a diploid cell.
7 disadvantage of haploid cells compared with diploid cells.
8 DNA ploidy but results in immortalization of diploid cells.
9 /Bud10 in haploid cells and Bud8 and Bud9 in diploid cells.
10 nhances the invasive behavior of haploid and diploid cells.
11 sting it is imported via the same pathway in diploid cells.
12 of different mating type combine to produce diploid cells.
13 ortalized human cell lines as well as normal diploid cells.
14 mine chromatin organization in polyploid and diploid cells.
15 operate during initiation of instability in diploid cells.
16 phase transition of NIH 3T3 and normal human diploid cells.
17 complexes repress haploid-specific genes in diploid cells.
18 tioned adjacent to the a1-alpha2 operator in diploid cells.
19 odifications increased cytotoxicity in human diploid cells.
20 he vast majority of oocytes enter meiosis as diploid cells.
21 id cells and is necessary for sporulation in diploid cells.
22 r inactive X alleles present in normal human diploid cells.
23 in complete remission, all but 2 showed all diploid cells.
24 populations had the allelic loss present in diploid cells.
25 as affected, as demonstrated in heterozygous diploid cells.
26 e to environmental stresses not tolerated by diploid cells.
27 but does not obviously affect proliferating diploid cells.
28 is a clear determinant of gene expression in diploid cells.
29 referentially sensitive to AICAR compared to diploid cells.
30 etween human embryonic stem (hES) and normal diploid cells.
31 e, we examine genetic stability in tel1 mec1 diploid cells.
32 not seen in vegetatively dividing haploid or diploid cells.
33 Mmi1 cause high levels of UPD in vegetative diploid cells.
34 uirement for Plk1 than normal nontransformed diploid cells.
35 oses generates CIN in otherwise stable, near-diploid cells.
36 ic imprinted expression in the reconstructed diploid cells.
37 ement, producing haploid gametes/spores from diploid cells.
38 of template DNA, which is equivalent to 1-2 diploid cells.
39 MIP1, to be evaluated in vivo in haploid and diploid cells.
40 in organisms that are primarily comprised of diploid cells.
41 ence of a competing homologous chromosome in diploid cells.
42 er, were reduced in tetraploid compared with diploid cells.
45 -prostate cancer cells, including WI-38 lung diploid cells, A-431 epidermoid carcinoma cells, and HeL
47 n mating-type gene expression in haploid and diploid cells affect NHEJ function, resulting in distinc
49 bition of Hsp90 with macbecin in sporulating diploid cells also blocked spore formation, underscoring
51 clear homodimers in contact inhibited normal diploid cells and dimerization of p12 is a necessary pro
53 d poliovirus vaccine (IPV) produced in human diploid cells and live attenuated oral poliovirus vaccin
55 deletions of one copy of essential genes in diploid cells and purified spores containing the deletio
56 gnificant correlations between levels of not-diploid cells and senescence-associated features (SAFs).
57 ersions of the G subunit were expressed in a diploid cell, and affinity purification of cytosolic V1
59 ng force in the evolution of mitotic/somatic diploid cells, and cellular changes that increase the ra
61 cterized using a large dataset of 129 normal diploid cells, and is shown to exceed previously reporte
62 that the replication profiles of haploid and diploid cells are indistinguishable, indicating that bot
63 ly stall at such barriers in late S phase of diploid cells are left unresolved in the shortened S pha
65 null-targeting method can be applied to any diploid cell, at any locus for which a negative selectio
66 CDKN2 mutations develop as early lesions in diploid cells before aneuploidy and cancer during neopla
72 of both RST1 and RST2 (rst-) causes a/alpha diploid cells constitutively to express a-specific genes
74 we propose that Ume6 serves a unique role in diploid cells, coupling metabolic responses to nutrition
75 demonstrates that the loss of FoxM1 elicits diploid cell deficiency with enhanced arrests prior to m
76 ortex; in particular, the bipolar budding of diploid cells depends on persistent landmarks at the bir
83 A replication and promoting proliferation in diploid cells, even when developmental signals normally
87 neage undergo mitotic proliferation to yield diploid cells, followed by endomitosis and acquisition o
88 of filamentous growth was also observed for diploid cells following MEK/ERK expression in liquid cul
89 ynamics observed in vivo in both haploid and diploid cells follows a process of dissociation-aggregat
90 velopmental switch: when FLO11 is expressed, diploid cells form pseudohyphal filaments; when FLO11 is
91 losses were also found in the corresponding diploid cells from premalignant epithelium in all three
94 Meiosis is the cellular program by which a diploid cell gives rise to haploid gametes for sexual re
95 tion of interphase is similar in haploid and diploid cells, haploid cells spend longer in mitosis, in
96 tract-length changes are half as frequent in diploid cells harboring heterozygous HRAS1 minisatellite
102 cells: (i) normal telomerase-negative human diploid cells; (ii) normal cells transfected with the hu
103 acking of the two copies of the GAL locus in diploid cells in both activating and repressive conditio
104 egulated in meiosis-competent MATa/MAT alpha diploid cells in comparison with diploids or haploids ex
106 yeast Saccharomyces cerevisiae is induced in diploid cells in response to nitrogen starvation and abu
107 romatin we have established 'isogenic' human diploid cells in which PARP1 and/or PARP2, or PARP3 are
108 o developed a protocol for null targeting of diploid cells, in which transfection of a DHFR-TS deleti
109 segregation compromises the proliferation of diploid cells, indicating that phenotypic changes that p
110 ed in G(1), S, and M phases and from meiotic diploid cells, indicating that they are constitutive com
111 a significant increase in the proportion of diploid cells, indicative of cell cycle arrest in G0-G1,
113 nclear because the proliferation of cultured diploid cells is compromised by chromosome missegregatio
121 traploid isogenic cells that had arisen from diploid cell lines displayed lower drug sensitivity than
122 nd apoptosis in cancer cells, whereas normal diploid cell lines, hTERT-RPE1 and MCF10A, survived a si
123 bsence of RAD52, repair is nearly absent and diploid cells lose the broken chromosome; however, in ce
124 tumors, but the mechanisms by which a stable diploid cell loses the ability to maintain genomic integ
126 p53 inactivation and c-myc overexpression in diploid cells markedly accelerates the spontaneous devel
132 resses this subject for vegetatively growing diploid cells of fission yeast Schizosaccharomyces pombe
134 e ratio of normal to aneuploid nuclei in the diploid cells of patients with impaired spermatogenesis
140 consequences of removing one copy of MAD2 in diploid cells of the budding yeast, Saccharomyces cerevi
141 salivary gland but not in the predominantly diploid cells of the embryo or larval imaginal discs and
146 ion in the presence of a poor carbon source, diploid cells of the yeast Saccharomyces cerevisiae unde
148 se regulatory pathways that also function in diploid cells, particularly those involved in S phase en
150 e regulation of genes specific to haploid or diploid cells plays a key role in determining which path
153 tify a population of proliferating Blimp1(+) diploid cells present within the spongiotrophoblast laye
163 of G1 to S phase transition in normal human diploid cells such as WI38, suggesting that the genetic
164 ice was able to yield HCCs composed of small diploid cells, suggesting that initiated cells are gener
165 d version of the E subunit from heterozygous diploid cells, suggesting that more than one E subunit i
166 i5 activator protein is not bound to URS1 in diploid cells, suggesting that recruitment of the Tup1-C
167 e give rise to teliospores, which are round, diploid cells surrounded by a specialized cell wall.
169 lves the fusion of haploid gametes to form a diploid cell that subsequently undergoes meiosis to gene
170 otype will surpass the viability of a normal diploid cell, the evolution of a neoplastic cell species
173 defects in late anaphase and cytokinesis in diploid cells; thus one hypothesis is that the expressio
175 RC) protein Cdc6 causes human nontransformed diploid cells to arrest nonlethally in G1-G1/S and S pha
177 essential because they are better able than diploid cells to mechanically stabilize wounds, especial
180 there are similarities between haploids and diploids, cell type-specific differences clearly alter t
182 iable haploid state that can be derived from diploid cells under in vitro and in vivo conditions, and
183 oublings (PDs), cultures of normal mammalian diploid cells undergo an irreversible growth arrest know
185 -labeled cells showed that the percentage of diploid cells undergoing DNA synthesis, the progression
188 paired in vegetatively growing budding yeast diploid cells, via multiple interstitial interactions, a
189 directs bud emergence to the distal pole of diploid cells, was localized to the distal pole of haplo
190 hat proteins required for bipolar budding in diploid cells were required for haploid invasive growth.
191 ociation with pericentric heterochromatin in diploid cells, where it appears to have roles in chromos
194 sizes in different model systems, including diploid cells with a chromosomal breakpoint that has bee
196 n with the homologous chromosome, whereas in diploid cells with an alpha mating type (matDelta/MATalp
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