Role of actin-binding proteins in cytoskeletal dynamics

1991 ◽  
Vol 19 (4) ◽  
pp. 1016-1020 ◽  
Author(s):  
A. G. Weeds ◽  
J. Gooch ◽  
M. Hawkins ◽  
B. Pope ◽  
M. Way
1985 ◽  
pp. 215-221 ◽  
Author(s):  
Victor E. Koteliansky ◽  
Vladimir P. Shirinsky ◽  
Gennady N. Gneushev ◽  
Michail A. Chernousov

2015 ◽  
Vol 113 (01) ◽  
pp. 20-36 ◽  
Author(s):  
Alexander García-Ponce ◽  
Alí Francisco Citalán-Madrid ◽  
Martha Velázquez-Avila ◽  
Hilda Vargas-Robles ◽  
Michael Schnoor

SummaryThe endothelial barrier of the vasculature is of utmost importance for separating the blood stream from underlying tissues. This barrier is formed by tight and adherens junctions (TJ and AJ) that form intercellular endothelial contacts. TJ and AJ are integral membrane structures that are connected to the actin cytoskeleton via various adaptor molecules. Consequently, the actin cytoskeleton plays a crucial role in regulating the stability of endothelial cell contacts and vascular permeability. While a circumferential cortical actin ring stabilises junctions, the formation of contractile stress fibres, e. g. under inflammatory conditions, can contribute to junction destabilisation. However, the role of actin-binding proteins (ABP) in the control of vascular permeability has long been underestimated. Naturally, ABP regulate permeability via regulation of actin remodelling but some actin-binding molecules can also act independently of actin and control vascular permeability via various signalling mechanisms such as activation of small GTPases. Several studies have recently been published highlighting the importance of actin-binding molecules such as cortactin, ezrin/ radixin/moesin, Arp2/3, VASP or WASP for the control of vascular permeability by various mechanisms. These proteins have been described to regulate vascular permeability under various pathophysiological conditions and are thus of clinical relevance as targets for the development of treatment strategies for disorders that are characterised by vascular hyperpermeability such as sepsis. This review highlights recent advances in determining the role of ABP in the control of endothelial cell contacts and vascular permeability.


2018 ◽  
Vol 2018 ◽  
pp. 1-13 ◽  
Author(s):  
Magdalena Izdebska ◽  
Wioletta Zielińska ◽  
Dariusz Grzanka ◽  
Maciej Gagat

Metastasis causes death of 90% of cancer patients, so it is the most significant issue associated with cancer disease. Thus, it is no surprise that many researchers are trying to develop drugs targeting or preventing them. The secondary tumour site formation is closely related to phenomena like epithelial-to-mesenchymal and its reverse, mesenchymal-to-epithelial transition. The change of the cells’ phenotype to mesenchymal involves the acquisition of migratory potential. Cancer cells movement is possible due to the development of invasive structures like invadopodia, lamellipodia, and filopodia. These changes are dependent on the reorganization of the actin cytoskeleton. In turn, the polymerization and depolymerization of actin are controlled by actin-binding proteins. In many tumour cells, the actin and actin-associated proteins are accumulated in the cell nucleus, suggesting that it may also affect the progression of cancer by regulating gene expression. Once the cancer cell reaches a new habitat it again acquires epithelial features and thus proliferative activity. Targeting of epithelial-to-mesenchymal or/and mesenchymal-to-epithelial transitions through regulation of their main components expression may be a potential solution to the problem of metastasis. This work focuses on the role of these processes in tumour progression and the assessment of therapeutic potential of agents targeting them.


Reproduction ◽  
2016 ◽  
Vol 151 (3) ◽  
pp. R29-R41 ◽  
Author(s):  
Nan Li ◽  
Elizabeth I Tang ◽  
C Yan Cheng

The blood–testis barrier (BTB) is an important ultrastructure in the testis, since the onset of meiosis and spermiogenesis coincides with the establishment of a functional barrier in rodents and humans. It is also noted that a delay in the assembly of a functional BTB following treatment of neonatal rats with drugs such as diethylstilbestrol or adjudin also delays the first wave of spermiation. While the BTB is one of the tightest blood–tissue barriers, it undergoes extensive remodeling, in particular, at stage VIII of the epithelial cycle to facilitate the transport of preleptotene spermatocytes connected in clones across the immunological barrier. Without this timely transport of preleptotene spermatocytes derived from type B spermatogonia, meiosis will be arrested, causing aspermatogenesis. Yet the biology and regulation of the BTB remains largely unexplored since the morphological studies in the 1970s. Recent studies, however, have shed new light on the biology of the BTB. Herein, we critically evaluate some of these findings, illustrating that the Sertoli cell BTB is regulated by actin-binding proteins (ABPs), likely supported by non-receptor protein kinases, to modulate the organization of actin microfilament bundles at the site. Furthermore, microtubule-based cytoskeleton is also working in concert with the actin-based cytoskeleton to confer BTB dynamics. This timely review provides an update on the unique biology and regulation of the BTB based on the latest findings in the field, focusing on the role of ABPs and non-receptor protein kinases.


2013 ◽  
Vol 88 (5) ◽  
pp. 279-287 ◽  
Author(s):  
Keisuke Sudo ◽  
Jong-In Park ◽  
Satomi Sakazono ◽  
Hiromi Masuko-Suzuki ◽  
Masaaki Osaka ◽  
...  

2017 ◽  
pp. 20-24
Author(s):  
Y Anu Shanu ◽  
Antonio Lauto ◽  
Simon J Myers

Coactosin is one of the numerous actin-binding proteins which regulate the actin cytoskeleton. Coactosin binds F-actin, and also interacts with 5-lipoxygenase, which is the first committed enzyme in leukotriene biosynthesis. Coactosin and human coactosin like protein 1 (COTL1) have the potential to play a role in the degradation or impairment of neuronal cells and their functioning. Its homology to other proteins that affect neuronal cells also contributes to this notion. The objective of this review is to explore its structural novelty, regulation and its significance in neurodegenerative diseases.


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