Embryonic stem cells (ESCs) have the potential to be used as unlimited resources for tissue replacement therapy, thereby compensating for organ donor shortage. To reach this goal, the molecular principles governing early differentiation events in the developing embryo need to be addressed, understood and properly implemented in vitro. Studies carried out in several vertebrate models have established that Nodal/Activin A, BMP, WNT and FGF signaling pathways regulate early embryo development and that these pathways are similarly used during germ layer formation by cultured ESCs. However, differences have also been identified in the way these pathways function or interact in mouse vs. human ESCs, making it sometimes difficult to extrapolate findings from one system to the other. In this review, we discuss and compare the role of the relevant signaling pathways and their crosstalk during undifferentiated growth and during the endoderm differentiation of mouse and human ESCs.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1387/ijdb.120115ls | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Intervention of a Communication Between PI3K/Akt and β-Catenin by (-)-Epigallocatechin-3-Gallate Suppresses TGF-β1-Promoted Epithelial-Mesenchymal Transition and Invasive Phenotype of NSCLC Cells.
Environ Toxicol
January 2025
Department of Medical Research, Chung Shan Medical University Hospital, Taichung, Taiwan.
The epithelial-mesenchymal transition (EMT) assists in the acquisition of invasiveness, relapse, and resistance in non-small cell lung cancer (NSCLC) and can be caused by the signaling of transforming growth factor-β1 (TGF-β1) through Smad-mediated or Smad-independent pathways. (-)-Epigallocatechin-3-gallate (EGCG), a multifunctional cancer-preventing bioconstituent found in tea polyphenols, has been shown to repress TGF-β1-triggered EMT in the human NSCLC A549 cell line by inhibiting the activation of Smad2 and Erk1/2 or reducing the acetylation of Smad2 and Smad3. However, its impact on the Smad-independent pathway remains unclear.
View Article and Find Full Text PDFCardiac Involvement and TBCK-Related Neurodevelopmental Disorder: Is It a New Feature of This Condition?
Am J Med Genet A
January 2025
Department of Experimental Medicine, Sapienza University of Rome, Rome, Italy.
TBCK (TBC1 Domain-Containing Kinase) encodes a protein playing a role in actin organization and cell growth/proliferation via the mTOR signaling pathway. Deleterious biallelic TBCK variants cause Hypotonia, infantile, with psychomotor retardation and characteristic facies 3. We report on three affected sibs, also displaying cardiac malformations.
View Article and Find Full Text PDFThe up-regulation of RIPK3 mediated by ac4C modification promotes oxidative stress-induced granulosa cell senescence by inhibiting the Nrf2/HO-1 pathway.
IUBMB Life
January 2025
Department of Reproductive Medical Center, First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan Province, China.
Abnormality of granulosa cells (GCs) is the critical cause of follicular atresia in premature ovarian failure (POF). RIPK3 is highly expressed in GCs derived from atretic follicles. We focus on uncovering how RIPK3 contributes to ovarian GC senescence.
View Article and Find Full Text PDFModeling the response to interleukin-21 to inform natural killer cell immunotherapy.
Immunol Cell Biol
January 2025
Steve and Cindy Rasmussen Institute for Genomic Medicine, Abigail Wexner Research Institute, Nationwide Children's Hospital, Columbus, OH, USA.
Natural killer (NK) cells are emerging agents for cancer therapy. Several different cytokines are used to generate NK cells for adoptive immunotherapy including interleukin (IL)-2, IL-12, IL-15 and IL-18 in solution, and membrane-bound IL-21. These cytokines drive NK cell activation through the integration of signal transducers and activators of transcription (STAT) and nuclear factor-kappa B (NF-κB) pathways, which overlap and synergize, making it challenging to predict optimal cytokine combinations for both proliferation and cytotoxicity.
View Article and Find Full Text PDFElevated LIF and JAK-STAT activation drive severe COVID-19 in myeloma patients receiving the BCMA-CD3 bispecific antibody Elranatamab.
J Transl Med
January 2025
Department of Hematology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences, No. 1 Shuaifuyuan, Beijing, 100730, China.
Background: Immunotherapy is a significant risk factor for severe COVID-19 in multiple myeloma (MM) patients. Understanding how immunotherapies lead to severe COVID-19 is crucial for improving patient outcomes.
Methods: Human protein microarrays were used to examine the expression of 440 protein molecules in MM patients treated with bispecific T-cell engagers (BiTe) (n = 9), anti-CD38 monoclonal antibodies (mAbs) (n = 10), and proteasome inhibitor (PI)-based regimens (n = 10).
Want AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!