Src-family kinase signaling, actin-mediated membrane trafficking and organellar dynamics in the control of cell fate: Lessons to be learned from the adenovirus E4orf4 death factor

2010 ◽  
Vol 22 (11) ◽  
pp. 1604-1614 ◽  
Author(s):  
Josée N. Lavoie ◽  
Marie-Claude Landry ◽  
Robert L. Faure ◽  
Claudia Champagne
Keyword(s):  
Cell Fate ◽  
Membrane Trafficking ◽  
Kinase Signaling ◽  
Src Family Kinase

scholarly journals Redox and Src family kinase signaling control leukocyte wound attraction and neutrophil reverse migration

2014 ◽  
Vol 207 (5) ◽  
pp. 589-598 ◽  
Author(s):  
Sebastien Tauzin ◽  
Taylor W. Starnes ◽  
Francisco Barros Becker ◽  
Pui-ying Lam ◽  
Anna Huttenlocher
Keyword(s):  
Tissue Regeneration ◽  
Tissue Damage ◽  
Redox Signaling ◽  
Kinase Signaling ◽  
Src Family Kinase ◽  
Reverse Migration ◽  
Early Recruitment

Tissue damage induces early recruitment of neutrophils through redox-regulated Src family kinase (SFK) signaling in neutrophils. Redox-SFK signaling in epithelium is also necessary for wound resolution and tissue regeneration. How neutrophil-mediated inflammation resolves remains unclear. In this paper, we studied the interactions between macrophages and neutrophils in response to tissue damage in zebrafish and found that macrophages contact neutrophils and induce resolution via neutrophil reverse migration. We found that redox-SFK signaling through p22phox and Yes-related kinase is necessary for macrophage wound attraction and the subsequent reverse migration of neutrophils. Importantly, macrophage-specific reconstitution of p22phox revealed that macrophage redox signaling is necessary for neutrophil reverse migration. Thus, redox-SFK signaling in adjacent tissues is essential for coordinated leukocyte wound attraction and repulsion through pathways that involve contact-mediated guidance.

scholarly journals Crucial Roles of the Arp2/3 Complex during Mammalian Corticogenesis

2015 ◽  
Author(s):  
Pei-Shan Wang ◽  
Fu-Sheng Chou ◽  
Fengli Guo ◽  
Praveen Suraneni ◽  
Sheng Xia ◽  
...  
Keyword(s):  
Cell Fate ◽  
Membrane Trafficking ◽  
Neuronal Migration ◽  
Neuronal Cell ◽  
Leading Edge ◽  
Radial Glial Cells ◽  
A Cell ◽  
Radial Glial ◽  
Altered Cell ◽  
Actin Nucleator

The polarity and organization of radial glial cells (RGCs), which serve as both stem cells and scaffolds for neuronal migration, are crucial for cortical development. However, the cytoskeletal mechanisms that drive radial glial outgrowth and maintain RGC polarity remain poorly understood. Here, we show that the Arp2/3 complex, the unique actin nucleator that produces branched actin networks, plays essential roles in RGC polarity and morphogenesis. Disruption of the Arp2/3 complex in RGCs retards process outgrowth toward the basal surface and impairs apical polarity and adherens junctions. Whereas the former is correlated with abnormal actin-based leading edge, the latter is consistent with blockage in membrane trafficking. These defects result in altered cell fate, disrupted cortical lamination and abnormal angiogenesis. In addition, we present evidence that the Arp2/3 complex is a cell-autonomous regulator of neuronal migration. Our data suggest that Arp2/3-mediated actin assembly may be particularly important for neuronal cell motility in soft or poorly adhesive matrix environment.

scholarly journals Protein Kinases and Their Inhibitors in Pluripotent Stem Cell Fate Regulation

2019 ◽  
Vol 2019 ◽  
pp. 1-10 ◽  
Author(s):  
Jungwoon Lee ◽  
Young-Jun Park ◽  
Haiyoung Jung
Keyword(s):  
Stem Cells ◽  
Signaling Pathways ◽  
Protein Kinases ◽  
Cell Fate ◽  
Pluripotent Stem Cells ◽  
Intracellular Signaling ◽  
Regulatory Networks ◽  
Kinase Signaling ◽  
Self Renewal ◽  
Lineage Differentiation

Protein kinases modulate the reversible postmodifications of substrate proteins to their phosphorylated forms as an essential process in regulating intracellular signaling transduction cascades. Moreover, phosphorylation has recently been shown to tightly control the regulatory network of kinases responsible for the induction and maintenance of pluripotency, defined as the particular ability to differentiate pluripotent stem cells (PSCs) into every cell type in the adult body. In particular, emerging evidence indicates that the balance between the self-renewal and differentiation of PSCs is regulated by the small molecules that modulate kinase signaling pathways. Furthermore, new reprogramming technologies have been developed using kinase modulators, which have provided novel insight of the mechanisms underlying the kinase regulatory networks involved in the generation of induced pluripotent stem cells (iPSCs). In this review, we highlight the recent progress made in defining the roles of protein kinase signaling pathways and their small molecule modulators in regulating the pluripotent states, self-renewal, reprogramming process, and lineage differentiation of PSCs.

scholarly journals Inhibiting EGF Receptor or SRC Family Kinase Signaling Overcomes BRAF Inhibitor Resistance in Melanoma

2012 ◽  
Vol 3 (2) ◽  
pp. 158-167 ◽  
Author(s):  
Maria R. Girotti ◽  
Malin Pedersen ◽  
Berta Sanchez-Laorden ◽  
Amaya Viros ◽  
Samra Turajlic ◽  
...  
Keyword(s):  
Egf Receptor ◽  
Braf Inhibitor ◽  
Kinase Signaling ◽  
Src Family Kinase ◽  
Inhibitor Resistance

Multiplex Analysis of Src Family Kinase Signaling by Microbead Suspension Arrays

2010 ◽  
Vol 8 (4) ◽  
pp. 488-496 ◽  
Author(s):  
Mel Campbell ◽  
Wen-Rong Lie ◽  
Jing Zhao ◽  
David Hayes ◽  
Jehangir Mistry ◽  
...  
Keyword(s):  
Kinase Signaling ◽  
Src Family Kinase ◽  
Multiplex Analysis

scholarly journals Molecular interdiction of Src-family kinase signaling in hematopoietic cells

Oncogene ◽  
2004 ◽  
Vol 23 (48) ◽  
pp. 8024-8032 ◽  
Author(s):  
Robert L Geahlen ◽  
Misty D Handley ◽  
Marietta L Harrison
Keyword(s):  
Hematopoietic Cells ◽  
Kinase Signaling ◽  
Src Family Kinase

Abstract 3404: Inhibiting EGF receptor or SRC family kinase signaling overcomes BRAF inhibitor resistance in melanoma.

2013 ◽  
Author(s):  
Maria R. Girotti ◽  
Malin Pedersen ◽  
Berta Sanchez-Laorden ◽  
Amaya Viros ◽  
Samra Turajlic ◽  
...  
Keyword(s):  
Egf Receptor ◽  
Braf Inhibitor ◽  
Kinase Signaling ◽  
Src Family Kinase ◽  
Inhibitor Resistance

scholarly journals MAP Kinase Signaling Antagonizes PAR-1 Function During Polarization of the Early Caenorhabditis elegans Embryo

Genetics ◽  
2009 ◽  
Vol 183 (3) ◽  
pp. 965-977 ◽  
Author(s):  
Annina C. Spilker ◽  
Alexia Rabilotta ◽  
Caroline Zbinden ◽  
Jean-Claude Labbé ◽  
Monica Gotta
Keyword(s):  
Cell Division ◽  
Caenorhabditis Elegans ◽  
Map Kinase ◽  
Cell Fate ◽  
Asymmetric Cell Division ◽  
Asymmetric Distribution ◽  
Kinase Signaling ◽  
C Elegans ◽  
Link Type ◽  
Map Kinase Signaling

PAR proteins (partitioning defective) are major regulators of cell polarity and asymmetric cell division. One of the par genes, par-1, encodes a Ser/Thr kinase that is conserved from yeast to mammals. In Caenorhabditis elegans, par-1 governs asymmetric cell division by ensuring the polar distribution of cell fate determinants. However the precise mechanisms by which PAR-1 regulates asymmetric cell division in C. elegans remain to be elucidated. We performed a genomewide RNAi screen and identified six genes that specifically suppress the embryonic lethal phenotype associated with mutations in par-1. One of these suppressors is mpk-1, the C. elegans homolog of the conserved mitogen activated protein (MAP) kinase ERK. Loss of function of mpk-1 restored embryonic viability, asynchronous cell divisions, the asymmetric distribution of cell fate specification markers, and the distribution of PAR-1 protein in par-1 mutant embryos, indicating that this genetic interaction is functionally relevant for embryonic development. Furthermore, disrupting the function of other components of the MAPK signaling pathway resulted in suppression of par-1 embryonic lethality. Our data therefore indicates that MAP kinase signaling antagonizes PAR-1 signaling during early C. elegans embryonic polarization.

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