What are the disadvantages of pluripotent stem cells?
Disadvantages. The main issue is the use of retroviruses to generate iPSCs as they are associated with cancer. More specifically, retroviruses can insert their DNA anywhere in the genome and subsequently trigger cancer-causing gene expression.
What are the advantages of pluripotent stem cells?
The primary advantages of iPSCs compared to other stem cells are: a) iPSCs can be created from the tissue of the same patient that will receive the transplantation, thus avoiding immune rejection, and b) the lack of ethical implications because cells are harvested from a willing adult without harming them.
Where does fibroblast growth factor come from?
FGF, which was first discovered in pituitary extracts in 1973, is widely expressed in cells and tissues. Acidic FGF (FGF1) and basic FGF (FGF2) were originally isolated from the brain and pituitary gland as growth factors for fibroblasts.
What does pluripotent represent?
: not fixed as to developmental potentialities especially : capable of differentiating into one of many cell types pluripotent stem cells.
How is FGF a key regulator of pluripotent stem cells?
In the current review, we summarize the role of FGF signaling in the maintenance of pluripotency state of stem cells through regulation of key transcriptional factors. | Extrinsic signaling pathways governing stemness of pluripotent stem cells.
What are the functions of FGF and FGFR?
FGF/FGFR signaling governs fundamental cellular processes such as cell survival, proliferation, migration, differentiation, embryonic development, organogenesis, tissue repair/regeneration, and metabolism.
Which is a downstream regulator of Fgf4 signaling?
FGF4/ERK signaling promotes differentiation of mESCs through JNK/c-JUN and MEK/ERK pathways as downstream regulators. (B) Primed state of pluripotency in mEpiSCs, hESC, and hiPSCs is mainly controlled by FGF2/ERK and TGFβ/Activin/Nodal pathways. FGF2 acts through PI3K/AKT, PLCγ and MEK/ERK.
Which is part of the FGF signaling pathway?
(A) Mouse naïve pluripotency mainly controlled by LIF/STAT3, BMP4, Wnt/β-Catenin, and FGF4/ERK signaling pathways. LIF maintains pluripotency through binding to its receptor, gp130/LIFR, followed by activation of JAK/STAT3. Phosphorylated STAT3 interacts with KLF4 and maintains the pluripotency through OCT3/4.
