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4 edition of p53 protein expression in murine embryonic stem cells found in the catalog.

p53 protein expression in murine embryonic stem cells

Chen, Jianmin

p53 protein expression in murine embryonic stem cells

by Chen, Jianmin

  • 160 Want to read
  • 3 Currently reading

Published by National Library of Canada in Ottawa .
Written in English


Edition Notes

Thesis (M.Sc.)--University of Toronto, 1993.

SeriesCanadian theses = Thèses canadiennes
The Physical Object
FormatMicroform
Pagination1 microfiche : negative.
ID Numbers
Open LibraryOL15085685M
ISBN 100315835486
OCLC/WorldCa31515218

Product Data Sheet Total Protein – Murine Embryonic Stem Cell Line D3 CATALOG NUMBER: CBA STORAGE: 80ºC; avoid freeze/thaw QUANTITY AND CONCENTRATION: µg at mg/mL in NP Solubilization Buffer SHELF LIFE: 6 months from date of receipt under proper storage conditions Background Embryonic stem (ES) cells are continuous proliferating .   Indeed, only the large oligomers of this protein seems to possess a chaperone-like activity, can modulate ROS or glutathione levels, and are able to block tumor necrosis factor-induced cell death.2 3Hence, during the early differentiation of murine CGR8 embryonic stem cells, the transient accumulation of hsp27 may be accompanied with a.

Stem cell research requires cellular and molecular tools to confirm pluripotency or to help determine the utility of cells in downstream experiments. Whether analyzing proliferation, protein levels, gene expression, or epigenetic profiles, we have the right instruments, products, and services for your research. Request information.   In this chapter, we highlight in detail the current state of research on thyroid stem cells by focusing on (1) the description of the first experiments performed to obtain thyroid follicles from embryonic stem cells, (2) the identification of resident stem cells in the thyroid gland, and (3) the definition of the current translational in vivo Author: Giovanni Zito, Antonina Coppola, Giuseppe Pizzolanti, Carla Giordano.

Developmental biology, regenerative medicine and cancer biology are more and more interested in understanding the molecular mechanisms controlling pluripotency and self-renewal in stem cells. Pluripotency is maintained by a synergistic interplay between extrinsic stimuli and intrinsic circuitries, which allow sustainment of the undifferentiated and self-renewing by: Lin homolog A is a protein that in humans is encoded by the LIN28 gene.. LIN28 encodes an RNA-binding protein that binds to and enhances the translation of the IGF-2 (insulin-like growth factor 2) mRNA. Lin28 binds to the let-7 pre-microRNA and blocks production of the mature let-7 microRNA in mouse embryonic stem cells. In pluripotent embryonal carcinoma cells, LIN28 is Aliases: LIN28A, CSDD1, LIN, LIN28, ZCCHC1, .


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P53 protein expression in murine embryonic stem cells by Chen, Jianmin Download PDF EPUB FB2

Moreover, p53 RNA is more stable in embryonic stem cells and the p53 protein is more often transcribed. This is at least partly due to decreased expression of miRNAa and b in embryonic stem cells. Despite its cytoplasmic localisation, p53 is degraded in 26S proteasomes in embryonic stem by:   p53 and the proliferation of ESCs.

In differentiated cells, p53 is an important regulator of cell proliferation. By controlling expression of the p21 gene, which encodes a prominent inhibitor of cyclin-dependent kinases, p53 influences transition from G1 into S-phase of the cell cycle[].In addition, p53 is able to initiate apoptosis by both the extrinsic and intrinsic Cited by: The impeded anti-proliferative activity of p53 and the induction of certain proto-oncogenes by p53 in murine embryonic stem cells can explain why stem cells proliferate efficiently despite having.

The p53 protein appears to play a similar role in embryonic stem cells, where p53 represses expression of Nanog – which limits the pool of pluripotent cells [4,5]. In contrast, loss of p53 extends the repopulating activity of tissue-specific stem cells [6,7].

Disruption of BRCA1 also allows expansion of breast stem cells. The restriction of Cited by:   FIGURE 1. p53 is activated in DNA damage-induced apoptosis of hESCs.

A, flow cytometric analysis of apoptotic cells using Annexin-V surface staining and are dot plots of the fluorescein isothiocyanate-conjugated Annexin-V versus PI staining for hESCs (a) and hESCs 12 h post 20 J/m 2 UV irradiation (b).

B, immunofluorescent detection of p53 in hESCs. Browse the archive of articles on Nature. Explore how long a coronavirus vaccine will take, and how scientists will choose the best from the dozens in by:   The role of p53 as “a guardian of the genome” has been well established in somatic cells.

However, its role in pluripotent stem cells remains much more elusive. Here, we discuss research progress in understanding the role of p53 in pluripotent stem cells and in pluripotent stem cell-like cancer stem cells.

The p53 protein, which plays a key role in Cited by: Differentiated cells can be reprogrammed to an embryonic-like state by transfer of nuclear contents into oocytes or by fusion with embryonic stem (ES) cells. Little is known about factors that induce this reprogramming.

Here, we demonstrate induction of pluripotent stem cells from mouse embryonic or adult fibroblasts by introducing four factors, Oct3/4, Sox2, c-Myc, and Cited by: These findings, and the link between the p53 family, stem cells, and aging, suggest that TAp73 might play a previously unanticipated role in maintenance of neural stem cells.

Relationships bewteen promoter DNA hypermethylation, genes which regulate stem/progenitor cells, and initiation of human cancer. The leading risk factors for the most prevalent forms of human cancer involve settings such as aging and chronic inflammation and which induce chronic increases in attempted cell renewal (Balkwill and Coussens, ; Nelson et al., ; Lu et.

The authors surveyed whole-exome and RNA-sequencing data from unique pluripotent stem cell lines, some of which are in the pipeline for clinical use, and found that approximately 5% of cell Cited by: Its expression both removes the unhealthy cells from the stem-cell pool by promoting programmed cell death or differentiation.

At the same time, p53 activates the Wnt pathway to inhibit the differentiation of surrounding, healthy embryonic stem cells to maintain a population for the development of the organism. @article{osti_, title = {Knockdown of p53 suppresses Nanog expression in embryonic stem cells}, author = {Abdelalim, Essam Mohamed, E-mail: [email protected] and Molecular Neuroscience Research Center, Shiga University of Medical Science, Setatsukinowa-cho, Otsu, Shiga and Department of Cytology and Histology, Faculty of Veterinary Medicine.

In this context, p53 suppresses the self-renewal of embryonic stem cells after DNA damage and blocks the reprogramming of somatic cells into induced pluripotent stem cells (iPSCs). If the inactivation of p53 pathway is a prerequisite for successful reprogramming, these findings raise concerns for the genomic stability and tumorigenecity of.

Abstract. The p53 protein plays a passive and an active role in stem cells. The transcriptional activities of p53 for cell-cycle arrest and DNA repair are largely turned off in stem cells, but there is some indication that long-term stem-cell viability may require other pregulated by: p53 and p73 Regulate Apoptosis but Not Cell-Cycle Progression in Mouse Embryonic Stem Cells upon DNA Damage and Differentiation Doxorubicin Induces RB Protein Expression in R1 Cells in a pDependent Manner Y.

XuPhosphorylation of murine p53 at ser regulates the p53 responses to DNA damage. Proc. Natl. Acad. Sci. USA, 97 (), pp Cited by: 9.

Since it was found that p53 is highly expressed in murine embryonic stem cells, it remained a mystery whether p53 is active in this cell type. We show that a significant part of p53 is localised in the nucleus of murine embryonic stem cells and that the majority of this nuclear p53 is bound to DNA.

According to its nuclear localisation, we show that p53 alters the transcriptional program. Surprisingly, Bak and not Bax is essential for actinomycin-D-induced apoptosis in human embryonic stem cells.

Finally, P53 is degraded rapidly in an ubiquitin-proteasome-dependent pathway in hPSCs at steady state but quickly accumulates and induces apoptosis when Mdm2 function is impaired.

Perinatal stem cells can be derived from postembryonic tissues, which include the tissues sourced at the time of birth, but also comprise the time period from the 16th week of gestation through the neonatal period [4,5].These tissues include the amniotic fluid, the placenta, placental membranes (amnion, chorion and Wharton jelly) and umbilical cord [6,7,8,9,10].Author: Melissa Rodrigues, Christine Blattner, Liborio Stuppia.

As mentioned above, p53 protein has a very short half-life ( min), and its level is actively regulated by protein degradation by both the calpain and the proteasome pathways. Thus we examined the expression level of p53 protein with altered CRT expression. There was a significant decrease in the level of p53 protein in the crt-/- cells (.

-- Abstract: Recent studies have reported the role of p53 in suppressing the pluripotency of embryonic stem (ES) cells after DNA damage and blocking the reprogramming of somatic cells into induced pluripotent stem (iPS) cells.

However, to date no evidence has been presented to support the function of p53 in unstressed ES cells.Alternatively, embryonic stem cells, which are pluripotent cells derived from the inner cell mass of the embryonic blastocyst, can be differentiated into the desired tissue-specific stem cell.

The use of human embryonic stem cells has been controversial for ethical reasons because of the need to isolate them from human embryos.

The history of the p53 field has made several turns. When it was first discovered as a SV40 binding protein, it was believed to be an oncoprotein because it is highly expressed in many types of tumors and the p53 cDNA from these tumors can transform normal cells together with H-Ras [1–6].Later on, studies by several laboratories convincingly showed that wild type Cited by: 5.