5-biphosphate 3-kinase
5-biphosphate 3-kinase - Related Videos
01:27
Chemotherapy-Induced Nausea and Vomiting: 5-HT3 Receptor Antagonists
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2024
5-HT3 receptor antagonists, such as dolasetron, granisetron (Kytril), ondansetron (Zofran), and palonosetron (Axoli), are crucial in managing chemotherapy-induced nausea and vomiting (CINV) and postoperative nausea. These drugs selectively block 5-HT3 receptors in the visceral vagal and spinal afferent nerves, chemoreceptor trigger zone, and the vomiting center. They have a rapid onset of action and can be given as a single dose before chemotherapy. Ondansetron and granisetron, in particular,...
02:54
Protein Kinases and Phosphatases
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2020
Proteins undergo chemical modifications that trigger changes in the charge, structure, and conformation of the proteins. Phosphorylation, acetylation, glycosylation, nitrosylation, ubiquitination, lipidation, methylation, and proteolysis are various protein modifications that regulate protein activity. Such modifications are usually enzyme-driven. Protein kinases Many proteins in the cell are regulated by phosphorylation, the addition of a phosphate group. A family of enzymes called kinases...
07:26
Single-molecule Super-resolution Imaging of Phosphatidylinositol 4,5-bisphosphate in the Plasma Membrane with Novel Fluorescent Probes
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Cited by 9 •
2016
PI(4,5)P2 regulates various cellular functions, but its nanoscale organization in the cell plasma membrane is poorly understood. By labeling PI(4,5)P2 with a dual-color fluorescent probe fused to the Pleckstrin Homology domain, we describe a novel approach to study the PI(4,5)P2 spatial distribution in the plasma membrane at the nanometer scale.
06:42
Identifying Kinase Inhibitors that Modulate the Thymocyte Response to Strong TCR Signals
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2025
In this video, we describe a method to identify the small-molecule kinase inhibitors that modulate the apoptosis of self-reactive CD4+CD8+ double-positive immature thymocytes. Apoptosis is induced in the double-positive thymocytes by activating them with anti-CD3- and anti-CD28-coated magnetic beads; this is followed by a small-molecule inhibitor treatment and flow cytometry analysis to detect if the inhibitors modulate the apoptotic marker expression.
06:09
Assaying the Kinase Activity of LRRK2 in vitro
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Cited by 3 •
2012
Leucine Rich Repeat Kinase 2 is a large multidomain kinase, mutations in which are the most common genetic cause of Parkinson's disease. Analysis of the kinase activity of this protein has proven to be a crucial tool in understanding the biology and dysfunction of this protein. In this paper, in vitro assaying of the kinase activity of LRRK2 and a selection of its mutants is described, providing an experimental system to examine phosphorylation of putative substrates and potential dysfunction...
FAQs
Activation of PI3K converts phosphatidylinositol-4,5-bisphosphate, or PIP2, into phosphatidylinositol-3,4,5-trisphosphate, or PIP3. This change creates a lipid signaling state that recruits proteins involved in downstream pathway activation. In tumors, excessive upstream stimulation or genetic alterations can maintain this state, helping explain how abnormal signaling supports continued growth and survival.
PIP3 recruits signaling proteins such as AKT to the signaling environment at the cell membrane, enabling downstream pathway activity. This connection links PI3K activation with cellular processes including growth, survival, and metabolism. Because these functions can favor tumor development when signaling remains active, AKT provides an important mechanistic bridge between altered lipid signaling and cancer-related behavior.
Persistent activity across the PI3K-AKT-mTOR pathway can reinforce several biological programs that tumors depend on, including proliferation, survival, and metabolism. The pathway may become continuously stimulated through genetic alterations or excessive signals from upstream receptors. Its sustained activity therefore helps connect initiating molecular abnormalities with tumor development and resistance to treatment.
Receptor tyrosine kinases can provide cell-surface signals that activate PI3K and initiate downstream production of PIP3. This places PI3K between extracellular signaling and intracellular growth-control programs. Studying that relationship helps researchers determine whether abnormal pathway activity originates from excessive upstream stimulation, a genetic alteration, or both, which can clarify cancer mechanisms.
Researchers examine pathway activity and relevant genetic alterations to identify biomarkers associated with abnormal PI3K-AKT-mTOR signaling. Such biomarkers can help clarify which tumors show persistent pathway activation and may support investigation of treatment responses. In this context, biomarker studies connect molecular features with tumor development, signaling behavior, and the rationale for pathway-targeted therapy.
Cancer studies use the pathway to investigate therapies directed against PI3K or related signaling components. Researchers first consider how receptor signals, genetic alterations, and downstream AKT-mTOR activity may sustain tumor behavior, then evaluate whether pathway targeting addresses those mechanisms. This approach can guide therapy development while also helping explain treatment resistance linked to persistent signaling.