Integrated microfluidic devices with enhanced separation performance: Application to phosphoproteome analyses of differentiated cell model systems

2006 ◽  
Vol 29 (11) ◽  
pp. 1539-1549 ◽  
Author(s):  
Mihaela Ghitun ◽  
Eric Bonneil ◽  
Marie-Helene Fortier ◽  
Hongfeng Yin ◽  
Kevin Killeen ◽  
...  
Keyword(s):  
Cell Model ◽  
Microfluidic Devices ◽  
Model Systems ◽  
Separation Performance

scholarly journals The TGFβ Family in Human Placental Development at the Fetal-Maternal Interface

Biomolecules ◽  
2020 ◽  
Vol 10 (3) ◽  
pp. 453
Author(s):  
Susana M. Chuva de Sousa Lopes ◽  
Marta S. Alexdottir ◽  
Gudrun Valdimarsdottir
Keyword(s):  
Stem Cell ◽  
Transforming Growth Factor Beta ◽  
Molecular Mechanisms ◽  
Transforming Growth Factor ◽  
Cell Model ◽  
Embryonic Stem ◽  
Model Systems ◽  
Special Focus ◽  
Placental Development

Emerging data suggest that a trophoblast stem cell (TSC) population exists in the early human placenta. However, in vitro stem cell culture models are still in development and it remains under debate how well they reflect primary trophoblast (TB) cells. The absence of robust protocols to generate TSCs from humans has resulted in limited knowledge of the molecular mechanisms that regulate human placental development and TB lineage specification when compared to other human embryonic stem cells (hESCs). As placentation in mouse and human differ considerably, it is only with the development of human-based disease models using TSCs that we will be able to understand the various diseases caused by abnormal placentation in humans, such as preeclampsia. In this review, we summarize the knowledge on normal human placental development, the placental disease preeclampsia, and current stem cell model systems used to mimic TB differentiation. A special focus is given to the transforming growth factor-beta (TGFβ) family as it has been shown that the TGFβ family has an important role in human placental development and disease.

Microbicides for HIV/AIDS. 2. Electrophoretic Fingerprinting of CD4+ T-Cell Model Systems

Langmuir ◽  
2007 ◽  
Vol 23 (5) ◽  
pp. 2680-2687 ◽  
Author(s):  
D. Fairhurst ◽  
R. L. Rowell ◽  
I. M. Monahan ◽  
S. Key ◽  
D. Stieh ◽  
...  
Keyword(s):  
T Cell ◽  
Cell Model ◽  
Model Systems ◽  
Cd4 T Cell ◽  
Hiv Aids

Establishment and Genetic Landscape of Precancer Cell Model Systems from the Head and Neck Mucosal Lining

2018 ◽  
Vol 17 (1) ◽  
pp. 120-130 ◽  
Author(s):  
D. Vicky de Boer ◽  
Arjen Brink ◽  
Marijke Buijze ◽  
Marijke Stigter-van Walsum ◽  
Keith D. Hunter ◽  
...  
Keyword(s):  
Head And Neck ◽  
Cell Model ◽  
Model Systems ◽  
Genetic Landscape ◽  
Mucosal Lining

Molecular mechanism of secretory vesicle docking

2010 ◽  
Vol 38 (1) ◽  
pp. 192-198 ◽  
Author(s):  
Heidi de Wit
Keyword(s):  
Plasma Membrane ◽  
Cell Model ◽  
Secretory Vesicle ◽  
Model Systems ◽  
Secretory Vesicles ◽  
Filamentous Actin ◽  
Embryonic Mouse ◽  
Vesicle Docking ◽  
Bovine Chromaffin Cell ◽  
Stable Association

Docking, the stable association of secretory vesicles with the plasma membrane, is considered to be the necessary first step before vesicles gain fusion-competence, but it is unclear how vesicles dock. In adrenal medullary chromaffin cells, access of secretory vesicles to docking sites is controlled by dense F-actin (filamentous actin) beneath the plasma membrane. Recently, we found that, in the absence of Munc18-1, the number of docked vesicles and the thickness of cortical F-actin are affected. In the present paper, I discuss the possible mechanism by which Munc18-1 modulates cortical F-actin and how it orchestrates the docking machinery via an interaction with syntaxin-1. Finally, a comparison of Munc18's role in embryonic mouse and adult bovine chromaffin cell model systems will be made to clarify observed differences in cortical F-actin as well as docking phenotypes.

scholarly journals Caveolins in glial cell model systems: from detection to significance

2007 ◽  
Vol 103 (s1) ◽  
pp. 101-112 ◽  
Author(s):  
W. I. Silva ◽  
H. M. Maldonado ◽  
G. Velázquez ◽  
J. O. García ◽  
F. A. González
Keyword(s):  
Glial Cell ◽  
Cell Model ◽  
Model Systems

scholarly journals An In-Depth Comparison of Latent HIV-1 Reactivation in Multiple Cell Model Systems and Resting CD4+ T Cells from Aviremic Patients

2013 ◽  
Vol 9 (12) ◽  
pp. e1003834 ◽  
Author(s):  
Celsa A. Spina ◽  
Jenny Anderson ◽  
Nancie M. Archin ◽  
Alberto Bosque ◽  
Jonathan Chan ◽  
...  
Keyword(s):  
T Cells ◽  
Cd4 T Cells ◽  
Cell Model ◽  
Model Systems ◽  
Multiple Cell ◽  
Latent Hiv ◽  
Hiv 1

c-Maf Induces Monocytic Differentiation and Apoptosis in Bipotent Myeloid Progenitors

Blood ◽  
1999 ◽  
Vol 94 (5) ◽  
pp. 1578-1589 ◽  
Author(s):  
Shrikanth P. Hegde ◽  
JingFeng Zhao ◽  
Richard A. Ashmun ◽  
Linda H. Shapiro
Keyword(s):  
Target Genes ◽  
Cell Model ◽  
Myeloid Cell ◽  
Model Systems ◽  
Monocytic Differentiation ◽  
Developmentally Regulated ◽  
Myeloid Progenitor ◽  
Myeloid Progenitor Cells ◽  
Direct Binding ◽  
Myeloid Progenitors

Abstract The transcriptional mechanisms that drive colony-forming unit granulocyte-macrophage (CFU-GM) myeloid progenitors to differentiate into cells of either the granulocytic or monocytic lineage are not fully understood. We have shown that the c-Maf and c-Myb transcription factors physically interact in myeloid cells to form inhibitory complexes that hinder transactivation of c-Myb target genes through direct binding to Myb consensus sites. These complexes arise in a developmentally regulated pattern, peaking at the promyelocyte stage, or in cell model systems, appearing soon after the induction of monocytic differentiation. We wished to determine if this developmentally related interaction is a consequence of myeloid differentiation or an intrinsic differentiating stimulus. Because the elevated Myb:Maf status seen in differentiating cells can be recapitulated by overexpression of c-Maf in myeloid cell lines, we inducibly expressed the c-Maf cDNA in 2 bipotent human myeloid progenitor cells. Elevated levels of c-Maf protein led to marked increases in Myb:Maf complexes and the accumulation of monocyte/macrophage cells, followed by eventual programmed cell death. Analysis of targets that could mediate these phenotypic changes indicated that c-Maf likely plays a key role in myeloid cell development through dual mechanisms; inhibition of a select set of c-Myb regulated targets, such as Bcl-2 and CD13/APN, coupled with the activation of as yet undefined differentiation-promoting genes.

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