Sentences with phrase «pluripotency markers»

(A) Expression of pluripotency markers from iPSCs (HiPSC - 1 control) generated following retroviral transduction of unsorted HUF1 cells.

They display typical undifferentiated morphology and express pluripotency markers Oct4 and Sox2.

These data show that pluripotency markers in the expanded clones are maintained at levels comparable to those in the parental line, ChiPSC18.

RT - PCR analysis of RNA samples from EBs on days 3, 6 and 9 revealed a gradual decrease in expression of endogenous pluripotency markers such as Nanog, Rex1, Oct4 and Sox2 as compared to their expression in undifferentiated iPS cells (Figure 4B, upper panel).

Panel B. CD81 - negative cells were examined for pluripotency markers Oct ‑ 4, TRA ‑ 1 ‑ 60, and SSEA - 4.

Furthermore, data from RT - PCR analysis showed that transgenic 4 factors were completely silenced and endogenous pluripotency markers Oct4, Sox2, Rex1 as well as Nanog were successfully activated (Figure 3C).

Whitehead Institute researchers have determined that the transcription factor Nanog, which plays a critical role in the self - renewal of embryonic stem cells, is expressed in a manner similar to other pluripotency markers.

Individual, edited (CD81 knockout) hiPS cells were expanded into clonal lines and analyzed for expression of CD81 and three pluripotency markers via flow cytometry using antibodies against CD81, Oct ‑ 4, TRA ‑ 1 ‑ 60, and SSEA - 4.

(B) During EB formation processes, various pluripotency markers and differentiation markers were determined using RT - PCR.

All iPS lines (iPS1 - iPS3) showed the full complement of pluripotency markers utilized.

But Dppa5a is a well known mESC pluripotency marker, and Ckb is known to be highly abundant in brain (NSC's are neural stem cells).

Control and gesicle - treated hiPS cells were assessed for AcGFP1 expression (green), labeled with an antibody specific to pluripotency marker Oct ‑ 4, visualized with a fluorescent - labeled secondary antibody (red), and nuclear - labeled with DAPI (blue).

(C) RT - PCR results using specific primers against transgenic 4 factors and endogenous pluripotency markers.

We also interrogated the population of sorted, CD81 - negative cells for the expression of pluripotency markers (Figure 4, Panel B) and identified that successfully edited hiPS cells were 92.6 % Oct ‑ 4 positive, 99.7 % TRA ‑ 1 ‑ 60 positive, and 99.99 % SSEA - 4 positive.

To determine pluripotency and AcGFP1 knockout efficiency in gesicle - treated cells, cells were labeled with a fluorescently labeled antibody specific to the pluripotency marker SSEA - 4.

Pluripotency was maintained in all edited clonal lines, as evidenced by the persistent expression of the three pluripotency markers.

After, cells were analyzed by flow cytometry or immunocytochemistry for AcGFP1 and pluripotency markers.

Mouse NPCs were efficiently reprogrammed into typical iPS cells, where endogenous expression of pluripotency markers was fully activated and transgenes were completely silenced.

Towards the center of the colony, ∼ 40 % of the cells had lost expression of all pluripotency markers, and we found a number of cells that were null - expressing no markers of pluripotency or lineage commitment, only the housekeeping gene cyclophilin a. However, many cells in this region still expressed Oct - 4.

The lack of co-expression of pluripotency markers and lineage specific markers at the protein level despite robust co-expression of transcripts of both classes of gene suggests a role for post-translational regulation of expression, perhaps by small RNAs.

Expression of pluripotency markers was highest and most consistent at the edge of the colony, where most cells expressed between 3 — 5 of the pluripotency markers shown (Figure 2b — c).

SSEA - 3 positive cells accounted for most of the colony forming ability, and they expressed higher levels of pluripotency markers than did the SSEA - 3 negative compartment.

In the edge and the middle zones, we observed a proportion of cells expressing a combination of pluripotency markers and lineage specific genes.