Tgf-beta-r2 Knockout
Tgf-beta-r2 Knockout - Related Videos
09:18
Spheroid Assay to Measure TGF-β-induced Invasion
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Cited by 41 •
2011
An assay to quantitatively measure Transforming Growth Factor (TGF)-β-induced invasion in 3-dimensional collagen gels is described. This assay takes advantage of the MCF10A series of cell lines, which represent different stages of breast cancer development. This method can be adopted to be used with other cell lines and might be used to investigate other potential activators or inhibitors of invasion.
01:25
Beta
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2024
Beta is a crucial metric in finance used to assess an investment's risk and expected return relative to the overall market. It is calculated as the slope of the line in a scatterplot that compares the returns of an individual stock to the returns of the market benchmark, typically represented by a broad market index. Beta quantifies how much a stock's price moves in response to market movements, providing insight into its volatility and systematic risk. A beta of one indicates that the stock's...
01:16
TGF - β Signaling Pathway
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2023
The TGF-β signaling pathway regulates cell growth, differentiation, adhesion, motility, and development. TGF-β ligands that induce TGF-β signaling are synthesized in their latent form. Several proteases or cell surface receptors such as integrins act upon the latent form, releasing the active ligand. There are three types of mammalian TGF-βs: (TGF-β1, TGF-β2, and TGF-β3) that bind as homodimers or heterodimers to TGF-β receptors. The TGF-β receptors are of three kinds RI, RII, and RIII. The RI...
09:50
In situ Quantification of Pancreatic Beta-cell Mass in Mice
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Cited by 6 •
2010
The following protocol outlines the process of pancreatic dissection for virtual slice imaging, and the subsequent quantification of all GFP-tagged beta-cells in the entire pancreas.
06:34
A Tailored HPLC Purification Protocol That Yields High-purity Amyloid Beta 42 and Amyloid Beta 40 Peptides, Capable of Oligomer Formation
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Cited by 6 •
2017
Herein we report a tailored HPLC purification protocol that yields high-purity amyloid beta 42 (Aβ42) and amyloid beta 40 (Aβ40) peptides, capable of oligomer formation. Amyloid beta is a highly aggregation prone, hydrophobic peptide implicated in Alzheimer's disease. The amyloidogenic nature of the peptide makes its purification a challenge.
FAQs
At the signaling level, receptor loss interrupts the handoff between the two receptor classes. Without functional TGF-βR2, the type I receptor is not recruited and phosphorylated after ligand binding, so downstream SMAD2/3 signaling and associated gene-expression changes are reduced or absent in the targeted cells. This links the genetic alteration to measurable changes in cellular behavior.
Because the pathway influences proliferation, differentiation, migration, and immune responses, removing TGF-βR2 can expose which of these processes depend on signaling in a particular cellular or tissue setting. The resulting phenotype is not limited to one endpoint: it may reveal altered inflammatory activity, tissue development, or disease-associated behavior, helping connect receptor function with broader biological outcomes.
Restricting receptor disruption to specified cells or tissues allows the model to associate signaling loss with local functions rather than treating every biological effect as identical. This is especially relevant because TGF-β signaling can influence multiple processes, including immune responses, migration, differentiation, and tissue development. Targeting therefore helps clarify where a mechanism operates.
A study establishes receptor disruption in selected cells or tissues and then examines the resulting changes in signaling-related biology. Researchers can assess effects on gene expression, cellular behavior, inflammation, fibrosis, cancer-related processes, or tissue development. Relating these observations to the targeted location helps identify the receptor’s contribution to health and disease.
These models allow researchers to examine whether loss of TGF-βR2 changes signaling associated with fibrotic disease. By observing altered cellular or tissue responses after pathway disruption, investigators can connect receptor activity with fibrosis-related mechanisms and evaluate whether modifying this signaling axis might represent a useful therapeutic strategy.
Disrupting the receptor can reveal how TGF-β signaling contributes to inflammatory responses and cancer-associated cellular behavior. Researchers may use the resulting changes to clarify disease mechanisms, identify processes influenced by receptor activity, and assess potential therapeutic strategies. The model is therefore useful for linking a defined genetic alteration to medically relevant outcomes.