scholarly journals Morpholino studies shed light on the signaling pathways regulating axon regeneration in lampreys

2022 ◽  
Vol 17 (7) ◽  
pp. 1475
Author(s):  
Antón Barreiro-Iglesias ◽  
Daniel Sobrido-Camean
2013 ◽  
Vol 304 (3) ◽  
pp. R177-R188 ◽  
Author(s):  
Wendi S. Neckameyer ◽  
Kathryn J. Argue

Numerous studies have detailed the extensive conservation of developmental signaling pathways between the model system, Drosophila melanogaster, and mammalian models, but researchers have also profited from the unique and highly tractable genetic tools available in this system to address critical questions in physiology. In this review, we have described contributions that Drosophila researchers have made to mathematical dynamics of pattern formation, cardiac pathologies, the way in which pain circuits are integrated to elicit responses from sensation, as well as the ways in which gene expression can modulate diverse behaviors and shed light on human cognitive disorders. The broad and diverse array of contributions from Drosophila underscore its translational relevance to modeling human disease.


2017 ◽  
Vol 4 (1) ◽  
pp. 100051 ◽  
Author(s):  
Barbara Knapp ◽  
Deva Krupakar Kusuluri ◽  
Nicola Horn ◽  
Karsten Boldt ◽  
Marius Ueffing ◽  
...  

Authors aimed to identify novel VLGR1-associated protein networks to shed light on its integration into signaling pathways and the cellular compartments in which VLGR1 functions using high-resolution affinity proteomics based on tandem affinity purifications (TAPs).


Author(s):  
Afshin Derakhshani ◽  
Zeinab Rostami ◽  
Hossein Safarpour ◽  
Sina Taefehshokr ◽  
Neda Jalili Tabrizi ◽  
...  

Cancer is the second leading cause of death worldwide. It is theorized that underlying genetic and epigenetic changes enable cells to proliferate out of control by escaping regulatory mechanisms. Although traditional molecular profiling techniques, i.e., bulk sequencing, can identify common mutations and gene expression patterns in cancer cells, they cannot detect tumour heterogeneity. However, single-cell technology has provided an ample opportunity to overcome this difficulty. Since this technology allows us to detect the heterogeneous properties of all cancer cells, this can further our knowledge of the signaling pathways in cancer cells. Indeed, single-cell transcriptomics technology has paved the road for identifying novel biomarkers and signaling pathways, which can serve as targets. This study aims to review the current knowledge about pathways involved in developing cancer cells and shed light on single-cell studies as promising therapeutic approaches.


2013 ◽  
Vol 29 (4) ◽  
pp. 411-420 ◽  
Author(s):  
Saijilafu ◽  
Bo-Yin Zhang ◽  
Feng-Quan Zhou

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Negar Noorbakhsh ◽  
Bentolhoda Hayatmoghadam ◽  
Marzieh Jamali ◽  
Maryam Golmohammadi ◽  
Maria Kavianpour

AbstractCancer can be considered as a communication disease between and within cells; nevertheless, there is no effective therapy for the condition, and this disease is typically identified at its late stage. Chemotherapy, radiation, and molecular-targeted treatment are typically ineffective against cancer cells. A better grasp of the processes of carcinogenesis, aggressiveness, metastasis, treatment resistance, detection of the illness at an earlier stage, and obtaining a better therapeutic response will be made possible. Researchers have discovered that cancerous mutations mainly affect signaling pathways. The Hippo pathway, as one of the main signaling pathways of a cell, has a unique ability to cause cancer. In order to treat cancer, a complete understanding of the Hippo signaling system will be required. On the other hand, interaction with other pathways like Wnt, TGF-β, AMPK, Notch, JNK, mTOR, and Ras/MAP kinase pathways can contribute to carcinogenesis. Phosphorylation of oncogene YAP and TAZ could lead to leukemogenesis, which this process could be regulated via other signaling pathways. This review article aimed to shed light on how the Hippo pathway interacts with other cellular signaling networks and its functions in leukemia.


2019 ◽  
Vol 39 (29) ◽  
pp. 5662-5672 ◽  
Author(s):  
Naoki Hisamoto ◽  
Tatsuhiro Shimizu ◽  
Kazuma Asai ◽  
Yoshiki Sakai ◽  
Strahil I. Pastuhov ◽  
...  

Author(s):  
Weida Ren ◽  
Wanyu Zhao ◽  
Lingbo Cao ◽  
Junqi Huang

Programmed cell death (PCD) depicts a genetically encoded and an orderly mode of cellular mortality. When triggered by internal or external stimuli, cells initiate PCDs through evolutionary conserved regulatory mechanisms. Actin, as a multifunctional cytoskeleton protein that forms microfilament, its integrity and dynamics are essential for a variety of cellular processes (e.g., morphogenesis, membrane blebbing and intracellular transport). Decades of work have broadened our knowledge about different types of PCDs and their distinguished signaling pathways. However, an ever-increasing pool of evidences indicate that the delicate relationship between PCDs and the actin cytoskeleton is beginning to be elucidated. The purpose of this article is to review the current understanding of the relationships between different PCDs and the actin machinery (actin, actin-binding proteins and proteins involved in different actin signaling pathways), in the hope that this attempt can shed light on ensuing studies and the development of new therapeutic strategies.


2020 ◽  
Author(s):  
Kelsie J. Anson ◽  
Giulia A. Corbet ◽  
Amy E. Palmer

AbstractZinc (Zn2+) is an essential metal in biology and its bioavailability is highly regulated. Many cell types exhibit fluctuations in Zn2+ that appear to play an important role in cellular function. However, the detailed molecular mechanisms by which Zn2+ dynamics influence cell physiology remain enigmatic. Here, we use a combination of fluorescent biosensors and cell perturbations to define how changes in intracellular Zn2+ impact kinase signaling pathways. By simultaneously monitoring Zn2+ dynamics and kinase activity in individual cells, we quantify changes in labile Zn2+ and directly correlate changes in Zn2+ with ERK and Akt activity. Under our experimental conditions, Zn2+ fluctuations are not toxic and do not activate stress-dependent kinase signaling. We demonstrate that while Zn2+ can non-specifically inhibit phosphatases leading to sustained kinase activation, ERK and Akt are predominantly activated via upstream signaling, and through a common node via Ras. We provide a framework for quantification of Zn2+ fluctuations and correlate these fluctuations with signaling events in single cells to shed light on the role that Zn2+ dynamics play in healthy cell signaling.Significance StatementWhile zinc (Zn2+) is a vital ion for cell function and human health, little is known about the role it plays in regulating cell signaling. Here, we use fluorescent tools to study the interaction between Zn2+ and cell signaling pathways that play a role in cell growth and proliferation. Importantly, we use small, non-toxic Zn2+concentrations to ensure that our Zn2+ changes are closer to what cells would experience in the body and not stress-inducing. We also demonstrate that these signaling changes are driven by Ras activation, which contradicts one of the major hypotheses in the field. Our sensors shed light on how cells respond to a very important micronutrient in real time.


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