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The effects of transforming growth factor-β (TGF-β) are determined by cellular context. There are three kinds of contextual factors that determine the shape the TGF-β response: the signal transduction components, the transcriptional cofactors and the epigenetic state of the cell. The different ligands and receptors of TGF-β are significant ...
The PI3K-Akt pathway has many downstream effects and must be carefully regulated. One of the ways the pathway is negatively regulated is by reducing PIP 3 levels. Phosphatase and tensin homolog (PTEN) antagonises PI3K by converting PI(3,4,5)P 3 into PI(4,5)P 2.
The downstream effects of these signaling pathways may include additional enzymatic activities such as proteolytic cleavage, phosphorylation, methylation, and ubiquitinylation. Signaling molecules can be synthesized from various biosynthetic pathways and released through passive or active transports, or even from cell damage.
AKT can have a number of downstream effects such as activating CREB, [2] inhibiting p27, [3] localizing FOXO in the cytoplasm, [3] activating PtdIns-3ps, [4] and activating mTOR [3] which can affect transcription of p70 or 4EBP1. [3] There are many known factors that enhance the PI3K/AKT pathway including EGF, [5] shh, [2] IGF-1, [2] insulin ...
A downstream effect of the ER stress is a significant decrease in insulin-stimulated phosphorylation of tyrosine residues of insulin receptor substrate (IRS-1), which is the substrate for insulin tyrosine kinase (the insulin receptor).
Due to the anti-parallel nature of DNA, this means the 3' end of the template strand is upstream of the gene and the 5' end is downstream. Some genes on the same DNA molecule may be transcribed in opposite directions. This means the upstream and downstream areas of the molecule may change depending on which gene is used as the reference.
One of the downstream effects of active TAAR1 is to increase cAMP in the presynaptic cell via Gα s G-protein activation of adenylyl cyclase. [10] [11] [13] This alone can have a multitude of cellular consequences. A main function of the cAMP may be to up-regulate the expression of trace amines in the cell cytoplasm. [30]
The normal function of agonist binding is the generation of cellular changes leading to various downstream effects; these effects range from altering membrane potential to initiation of signaling cascades. [11] Conversely, when open channel blockers bind to the cell they prevent the normal function of agonist binding.