scholarly journals The N-terminal RASSF family: a new group of Ras-association-domaincontaining proteins, with emerging links to cancer formation

2009 ◽  
Vol 425 (2) ◽  
pp. 303-311 ◽  
Author(s):  
Victoria Sherwood ◽  
Asha Recino ◽  
Alex Jeffries ◽  
Andrew Ward ◽  
Andrew D. Chalmers

The RASSF (Ras-association domain family) has recently gained several new members and now contains ten proteins (RASSF1–10), several of which are potential tumour suppressors. The family can be split into two groups, the classical RASSF proteins (RASSF1–6) and the four recently added N-terminal RASSF proteins (RASSF7–10). The N-terminal RASSF proteins have a number of differences from the classical RASSF members and represent a newly defined set of potential Ras effectors. They have been linked to key biological processes, including cell death, proliferation, microtubule stability, promoter methylation, vesicle trafficking and response to hypoxia. Two members of the N-terminal RASSF family have also been highlighted as potential tumour suppressors. The present review will summarize what is known about the N-terminal RASSF proteins, addressing their function and possible links to cancer formation. It will also compare the N-terminal RASSF proteins with the classical RASSF proteins and ask whether the N-terminal RASSF proteins should be considered as genuine members or imposters in the RASSF family.

Author(s):  
Yini Liu ◽  
Chunyan Duan ◽  
Rongyang Dai ◽  
Yi Zeng

Ferroptosis is a recently recognized form of non-apoptotic regulated cell death and usually driven by iron-dependent lipid peroxidation and has arisen to play a significant role in cancer biology. Distinct from other types of cell death in morphology, genetics, and biochemistry, ferroptosis is characterized by the accumulation of lipid peroxides and lethal reactive oxygen species controlled by integrated oxidant and antioxidant systems. Increasing evidence indicates that a variety of biological processes, including amino acid, iron, lactate, and lipid metabolism, as well as glutathione, phospholipids, NADPH, and coenzyme Q10 biosynthesis, are closely related to ferroptosis sensitivity. Abnormal ferroptotic response may modulate cancer progression by reprogramming the tumor microenvironment (TME). The TME is widely associated with tumor occurrence because it is the carrier of tumor cells, which interacts with surrounding cells through the circulatory and the lymphatic system, thus influencing the development and progression of cancer. Furthermore, the metabolism processes play roles in maintaining the homeostasis and evolution of the TME. Here, this review focuses on the ferroptosis-mediated crosstalk in the TME, as well as discussing the novel therapeutic strategies for cancer treatment.


2009 ◽  
Vol 7 (44) ◽  
pp. 549-560 ◽  
Author(s):  
Michi Izumi ◽  
Alison M. Sweeney ◽  
Daniel DeMartini ◽  
James C. Weaver ◽  
Meghan L. Powers ◽  
...  

Many cephalopods exhibit remarkable dermal iridescence, a component of their complex, dynamic camouflage and communication. In the species Euprymna scolopes , the light-organ iridescence is static and is due to reflectin protein-based platelets assembled into lamellar thin-film reflectors called iridosomes, contained within iridescent cells called iridocytes. Squid in the family Loliginidae appear to be unique in which the dermis possesses a dynamic iridescent component with reflective, coloured structures that are assembled and disassembled under the control of the muscarinic cholinergic system and the associated neurotransmitter acetylcholine (ACh). Here we present the sequences and characterization of three new members of the reflectin family associated with the dynamically changeable iridescence in Loligo and not found in static Euprymna iridophores. In addition, we show that application of genistein, a protein tyrosine kinase inhibitor, suppresses ACh- and calcium-induced iridescence in Loligo . We further demonstrate that two of these novel reflectins are extensively phosphorylated in concert with the activation of iridescence by exogenous ACh. This phosphorylation and the correlated iridescence can be blocked with genistein. Our results suggest that tyrosine phosphorylation of reflectin proteins is involved in the regulation of dynamic iridescence in Loligo .


2020 ◽  
Vol 78 (Supplement_2) ◽  
pp. 80-90 ◽  
Author(s):  
Guadalupe Estrada-Gutiérrez ◽  
Elena Zambrano ◽  
Ernestina Polo-Oteyza ◽  
Arturo Cardona-Pérez ◽  
Felipe Vadillo-Ortega

Abstract Health systems and society are facing the growing problem of obesity and its accompanying comorbidities. New approaches to reduce these problems must be oriented to population groups in which long-lasting effects of interventions may occur. Biological processes occurring during the first 1000 days of life, which may be modulated by environmental modifications and result in phenotypes with differential risk for noncommunicable chronic disease, constitute an opportunity for interventions. The nutritional and general health conditions of pregnant women and the fetus, as well as toddlers, can be improved with interventions during the first 1000 days, offering pregnancy care, promoting breastfeeding, instructing on the use of complementary foods, and educating on the adequacy of the family dietary patterns for children. Evidence that interventions during this period result in promotion of children’s growth and development, influencing the risk for development of obesity in infancy, is available. In this article, an ongoing program in Mexico City directed to offer continuum of care during the first 1000 days is described.


Science ◽  
2015 ◽  
Vol 351 (6268) ◽  
pp. 7-7
Author(s):  
M. McNutt
Keyword(s):  

2017 ◽  
Vol 114 (28) ◽  
pp. 7361-7366 ◽  
Author(s):  
Jae Young Choi ◽  
Qi Qiao ◽  
Se-Hoon Hong ◽  
Chang Min Kim ◽  
Jae-Hee Jeong ◽  
...  

Cell death-inducing DFF45-like effector (CIDE) domains, initially identified in apoptotic nucleases, form a family with diverse functions ranging from cell death to lipid homeostasis. Here we show that the CIDE domains of Drosophila and human apoptotic nucleases Drep2, Drep4, and DFF40 all form head-to-tail helical filaments. Opposing positively and negatively charged interfaces mediate the helical structures, and mutations on these surfaces abolish nuclease activation for apoptotic DNA fragmentation. Conserved filamentous structures are observed in CIDE family members involved in lipid homeostasis, and mutations on the charged interfaces compromise lipid droplet fusion, suggesting that CIDE domains represent a scaffold for higher-order assembly in DNA fragmentation and other biological processes such as lipid homeostasis.


2015 ◽  
Vol 468 (1) ◽  
pp. 17-24 ◽  
Author(s):  
Simone L. Reynolds ◽  
Katja Fischer

Catalytically inactive enzymes (also known as pseudoproteases, protease homologues or paralogues, non-peptidase homologues, non-enzymes and pseudoenzymes) have traditionally been hypothesized to act as regulators of their active homologues. However, those that have been characterized demonstrate that inactive enzymes have an extensive and expanding role in biological processes, including regulation, inhibition and immune modulation. With the emergence of each new genome, more inactive enzymes are being identified, and their abundance and potential as therapeutic targets has been realized. In the light of the growing interest in this emerging field the present review focuses on the classification, structure, function and mechanism of inactive enzymes. Examples of how inactivity is defined, how this is reflected in the structure, functions of inactive enzymes in biological processes and their mode of action are discussed.


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