INT282590
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
Increased mRNA levels and increased OCT-4 protein expression were significantly correlated (Pearson's correlation coefficient 0.8). | |||||||||||||||
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This rejects our study hypothesis that OCT-4 is overexpressed during endometrial proliferation in the follicular phase and downregulated during the secretory transformation of the endometrium in the luteal phase. | |||||||||||||||
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Increased mRNA levels and increased OCT-4 protein expression were significantly correlated (Pearson's correlation coefficient 0.8). | |||||||||||||||
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Figure 3 shows follicular and luteal phase endometrial samples with and without OCT-4 overexpression. | |||||||||||||||
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OCT-4 protein overexpression in the follicular and luteal phase was found in 33/49 (67%) and 23/40 (58%) of women, respectively (p = 0.5). | |||||||||||||||
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OCT-4 protein overexpression was identified in 56/89 (63%) samples. | |||||||||||||||
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Oct4 overexpression in ATSC as evidenced by various cell reprogramming behaviors via the expression of stemness genes | |||||||||||||||
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We studied the effect of Oct4 overexpression on mesodermal lineage differentiation into fat, bone, and chondrocyte of ATSCs. | |||||||||||||||
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In our study, Oct4/ATSCs overexpress not only Oct4, Sox-2, Nanog, and Rex1, but also c-Myc to obtain active self-renewal activity with pluripotency after exogenic Oct4 transfection. | |||||||||||||||
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When Oct4 expression was recovered by exogenic Oct4 gene overexpression in damaged cells, ATSCs recovered to normal and viable cell with cell survival related signal pathway molecule such as Akt/PI3K, Bcl2, and ERK1/2. | |||||||||||||||
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Our results showed that Oct4/ATSC can increase developmental potential following reprogramming via the overexpression of the embryonic transcription factors, Rex1, Oct4, and Oct4-dependent Nanog and Sox2. | |||||||||||||||
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The Oct4-overexpressed ATSC cells showed prominent effects on upregulation of a variety of proliferation-associated genes, including RUNX3, CDK2 and CDK4, and telomere reverse transcriptase (TERT; Fig. 1D). | |||||||||||||||
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In a univariate regression model, the day of the menstrual cycle, using 3-day intervals, did not influence OCT-4 protein expression, when comparing an IRS <6 vs. ? | |||||||||||||||
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Specifically, we aimed to answer the question whether or not OCT-4 is overexpressed during endometrial proliferation in the follicular phase and downregulated during the secretory transformation of the endometrium in the luteal phase.
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Increased expression of OCT-4 protein in the follicular and luteal phases was found in 33/49 (67%) and 23/40 (58%) of women, respectively (p = 0.5).
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Increased expression of OCT-4 protein was identified in 56/89 (63%) samples. | |||||||||||||||
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And Oct4/ATSCs overexpressed the oncogenic gene, c-myc with prominently extended the S phase in cell cycles (Fig. 1C). | |||||||||||||||
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Evaluation of trans-differentiation properties of Oct4 overexpressed cells in vitro and in vivo BT mouse model | |||||||||||||||
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Differential expression of selected genes was verified independently using real time PCR and prepared from Oct4 overexpressed ATSCs or control ATSCs (Fig. 4). | |||||||||||||||
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The inhibition of ATSC growth was detected by transfection of Oct4 siRNA into ATSCs cells and counted dye-exclusive viable cells for 6 days.
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