scholarly journals Contribution of Natural Inhibitors to the Understanding of the PI3K/PDK1/PKB Pathway in the Insulin-mediated Intracellular Signaling Cascade

2008 ◽  
Vol 9 (11) ◽  
pp. 2217-2230 ◽  
Author(s):  
Jae Cho ◽  
Jongsun Park
Keyword(s):  
Intracellular Signaling ◽  
Signaling Cascade ◽  
Intracellular Signaling Cascade ◽  
Natural Inhibitors

The Pleiotropic Intricacies of Hedgehog Signaling: From Craniofacial Patterning to Carcinogenesis

FACE ◽  
2021 ◽  
pp. 273250162110243
Author(s):  
Mikhail Pakvasa ◽  
Andrew B. Tucker ◽  
Timothy Shen ◽  
Tong-Chuan He ◽  
Russell R. Reid
Keyword(s):  
Intracellular Signaling ◽  
Limb Development ◽  
Hedgehog Signaling ◽  
Target Genes ◽  
Craniofacial Development ◽  
Signaling Cascade ◽  
Signaling Mechanisms ◽  
Intracellular Signaling Cascade ◽  
And Function

Hedgehog signaling was discovered more than 40 years ago in experiments demonstrating that it is a fundamental mediator of limb development. Since that time, it has been shown to be important in development, homeostasis, and disease. The hedgehog pathway proceeds through a pathway highly conserved throughout animals beginning with the extracellular diffusion of hedgehog ligands, proceeding through an intracellular signaling cascade, and ending with the activation of specific target genes. A vast amount of research has been done elucidating hedgehog signaling mechanisms and regulation. This research has found a complex system of genetics and signaling that helps determine how organisms develop and function. This review provides an overview of what is known about hedgehog genetics and signaling, followed by an in-depth discussion of the role of hedgehog signaling in craniofacial development and carcinogenesis.

scholarly journals Possible regulation of genes associated with intracellular signaling cascade in rat liver regeneration

2009 ◽  
Vol 44 (4) ◽  
pp. 462-470 ◽  
Author(s):  
Cun-Shuan Xu ◽  
Heng-Yi Shao ◽  
Shuai-Shuai Liu ◽  
Bo Qin ◽  
Xiu-Feng Sun ◽  
...  
Keyword(s):  
Liver Regeneration ◽  
Rat Liver ◽  
Intracellular Signaling ◽  
Signaling Cascade ◽  
Rat Liver Regeneration ◽  
Intracellular Signaling Cascade

scholarly journals IL-4 induces a wide-spectrum intracellular signaling cascade in CD8+T cells

2007 ◽  
Vol 81 (4) ◽  
pp. 1102-1110 ◽  
Author(s):  
Ana Acacia de Sa Pinheiro ◽  
Alexandre Morrot ◽  
Sumana Chakravarty ◽  
Michael Overstreet ◽  
Jay H. Bream ◽  
...  
Keyword(s):  
T Cells ◽  
Cd8 T Cells ◽  
Intracellular Signaling ◽  
Wide Spectrum ◽  
Signaling Cascade ◽  
Intracellular Signaling Cascade

scholarly journals The Complicated Body in Motion: Rediscovering the Mechanical Stimulations in Cell Models of Human Disease

2019 ◽  
Author(s):  
Tzyy-Yue Wong ◽  
Yu-Kai Tseng ◽  
Tung-Chen Yeh ◽  
Rong-Chang Jhong ◽  
Yue-Fang Wang ◽  
...  
Keyword(s):  
Mechanical Stimulation ◽  
Intracellular Signaling ◽  
The Body ◽  
Signaling Cascade ◽  
Physical Injury ◽  
Cell Models ◽  
Physical Stimulation ◽  
Intracellular Signaling Cascade ◽  
The Mind

Thought runs through the mind like blood runs through our body to keep us alive. Like the mind, the body does not stay inert and is in constant motion. Not a single cell in our body is left inert unless cell is under stress or dying. These scenarios are reflected upon when a person is sick, the person lies in bed with less movement; however, is active when the person is healthy. The topic of mechanical stimulation has emerged due to the increasing understanding of the physical stimulations we face each day. Further understanding of the mechanically-regulated mechanism can help us explore the pathological events in a disease. Here, we reviewed the role of sensory proteins in pathological events that are observed in cardiomyopathy, cancer, respiratory, renal, obesity, genetics, physical injury and bacterial infection. Taken together, sensory proteins are mechanically-activated which assist reception of external physical stimulation and convert into biochemical to trigger intracellular signaling cascade.

scholarly journals Semaphorin4D induces inhibitory synapse formation by rapid stabilization of presynaptic boutons via MET co-activation

2017 ◽  
Author(s):  
Cátia P. Frias ◽  
Tom Bresser ◽  
Lisa Scheefhals ◽  
Hai Yin Hu ◽  
Paul M. P. van Bergen en Henegouwen ◽  
...  
Keyword(s):  
Intracellular Signaling ◽  
Synapse Formation ◽  
Inhibitory Synapse ◽  
Network Activity ◽  
Inhibitory Synapses ◽  
Signaling Cascade ◽  
Molecular Processes ◽  
Intracellular Signaling Cascade ◽  
Gabaergic Synapses ◽  
Presynaptic Boutons

ABSTRACTChanges in inhibitory connections are essential for experience-dependent circuit adaptations. Defects in inhibitory synapses are linked to neurodevelopmental disorders, but the molecular processes underlying inhibitory synapse formation are not well understood. Here we use high resolution two-photon microscopy in organotypic hippocampal slices to examine the signaling pathways induced by the postsynaptic signaling molecule Semaphorin4D (Sema4D) during inhibitory synapse formation. By monitoring changes in individual GFP-labeled presynaptic boutons we found that the primary action of Sema4D is to induce stabilization of presynaptic boutons within tens of minutes. Stabilizing boutons rapidly recruited synaptic vesicles, which was followed by accumulation of postsynaptic gephyrin. Newly formed inhibitory synapses were complete and functional after 24 hours, as determined by electrophysiology and immunohistochemistry. We further showed that Sema4D signaling is regulated by network activity and can induce a local increase in bouton density, suggesting a possible role in circuit adaptation. We further examined the intracellular signaling cascade triggered by Sema4D and found that bouton stabilization occurred through rapid remodeling of actin, and this could be mimicked by the actin-depolymerizing drug Latrunculin B or by reducing ROCK activity. The intracellular signaling cascade required activation of the receptor tyrosine kinase MET, which is a well-known autism risk factor. Our immunohistochemistry data suggests that MET may be localized to presynaptic inhibitory axons. Together, our data yield important insights in the molecular pathway underlying activity-dependent Sema4D-induced synapse formation and reveal a novel role for MET in inhibitory synapses.Significance StatementGABAergic synapses provide the main inhibitory control of neuronal activity in the brain. We make important steps in unraveling the molecular processes that take place when formation of inhibitory synapses is triggered by a specific signaling molecule, Sema4D. We find that this process depends on network activity and involves specific remodeling of the intracellular actin cytoskeleton. We also reveal a previously unknown role for MET in inhibitory synapses. As defects in GABAergic synapses have been implied in many brain disorders, and mutations in MET are strong risk factors for autism, our findings urge for a further investigation of the role of MET at inhibitory synapses.

scholarly journals β2 Integrin Signaling Cascade in Neutrophils: More Than a Single Function

2021 ◽  
Vol 11 ◽  
Author(s):  
Panagiota Bouti ◽  
Steven D. S. Webbers ◽  
Susanna C. Fagerholm ◽  
Ronen Alon ◽  
Markus Moser ◽  
...  
Keyword(s):  
Cancer Progression ◽  
Intracellular Signaling ◽  
Fungal Pathogens ◽  
Therapeutic Potential ◽  
Integrin Signaling ◽  
Signaling Cascade ◽  
Inflammatory Conditions ◽  
Single Function ◽  
Intracellular Signaling Cascade ◽  
Integrin Ligand

Neutrophils are the most prevalent leukocytes in the human body. They have a pivotal role in the innate immune response against invading bacterial and fungal pathogens, while recent emerging evidence also demonstrates their role in cancer progression and anti-tumor responses. The efficient execution of many neutrophil effector responses requires the presence of β2 integrins, in particular CD11a/CD18 or CD11b/CD18 heterodimers. Although extensively studied at the molecular level, the exact signaling cascades downstream of β2 integrins still remain to be fully elucidated. In this review, we focus mainly on inside-out and outside-in signaling of these two β2 integrin members expressed on neutrophils and describe differences between various neutrophil stimuli with respect to integrin activation, integrin ligand binding, and the pertinent differences between mouse and human studies. Last, we discuss how integrin signaling studies could be used to explore the therapeutic potential of targeting β2 integrins and the intracellular signaling cascade in neutrophils in several, among other, inflammatory conditions in which neutrophil activity should be dampened to mitigate disease.

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