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Upregulation of receptors, on the other hand, can result in super-sensitized cells, especially after repeated exposure to an antagonistic drug or prolonged absence of the ligand. Some receptor agonists may cause downregulation of their respective receptors, while most receptor antagonists temporarily upregulate their respective receptors.
Up-regulation is a process which occurs within a cell triggered by a signal (originating internal or external to the cell), which results in increased expression of one or more genes and as a result the proteins encoded by those genes. Conversely, down-regulation is a process resulting in decreased gene and corresponding protein expression.
IRS-1 protein is known to be involved in various types of cancer, including colorectal, [37] lung, [38] prostate and breast cancer. [39] IRS-1 integrates signalling from insulin receptor (InsR), insulin-like growth factor-1 receptor (IGF1R) and many other cytokine receptors and is elevated in β-catenin induced cells.
Receptor mediated endocytosis is common way of turning receptors "off". Endocytic down regulation is regarded as a means for reducing receptor signaling. [40] The process involves the binding of a ligand to the receptor, which then triggers the formation of coated pits, the coated pits transform to coated vesicles and are transported to the ...
Another receptor that often plays a role in breast cancer, although it is not a hormone receptor, is the human epidermal growth factor receptor 2 (HER2). The overexpression of HER2 is determined by immunohistochemistry (IHC), or with fluorescent in situ hybridization in those equivocal cases where IHC does not provide a clear result.
Androgen receptors interact with other proteins in the nucleus, resulting in up- or down-regulation of specific gene transcription. [25] Up-regulation or activation of transcription results in increased synthesis of messenger RNA, which, in turn, is translated by ribosomes to produce specific proteins.
In cancer, Wnt signaling can become independent of regular stimuli, through mutations in downstream oncogenes and tumor suppressor genes that become permanently activated even though the normal receptor has not received a signal. β-catenin binds to transcription factors such as the protein TCF4 and in combination the molecules activate the ...
These receptors may have intrinsic catalytic activity or may be coupled to effector enzymes, or may also be associated to ionic channels. Therefore, there are four main transmembrane receptor types: G protein coupled receptors (GPCRs), tyrosine kinase receptors (RTKs), serine/threonine kinase receptors (RSTKs), and ligand-gated ion channels ...