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	<id>https://wikimd.org/index.php?action=history&amp;feed=atom&amp;title=RTK</id>
	<title>RTK - Revision history</title>
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	<updated>2026-04-25T17:27:52Z</updated>
	<subtitle>Revision history for this page on the wiki</subtitle>
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	<entry>
		<id>https://wikimd.org/index.php?title=RTK&amp;diff=5344520&amp;oldid=prev</id>
		<title>Prab: CSV import</title>
		<link rel="alternate" type="text/html" href="https://wikimd.org/index.php?title=RTK&amp;diff=5344520&amp;oldid=prev"/>
		<updated>2024-03-02T16:13:28Z</updated>

		<summary type="html">&lt;p&gt;CSV import&lt;/p&gt;
&lt;p&gt;&lt;b&gt;New page&lt;/b&gt;&lt;/p&gt;&lt;div&gt;&amp;#039;&amp;#039;&amp;#039;RTK&amp;#039;&amp;#039;&amp;#039; or &amp;#039;&amp;#039;&amp;#039;Receptor Tyrosine Kinase&amp;#039;&amp;#039;&amp;#039; is a high-affinity cell surface receptor for many polypeptide growth factors, cytokines, and hormones. Of the 90 unique tyrosine kinase genes identified in the human genome, 58 encode receptor tyrosine kinase proteins.&lt;br /&gt;
&lt;br /&gt;
== Structure ==&lt;br /&gt;
RTKs are composed of an extracellular domain, which is able to bind a specific growth factor, a single transmembrane helix, and an intracellular domain, which possesses tyrosine kinase activity. The extracellular domain is often rich in [[Cysteine|cysteine]] residues, which form disulfide bonds to stabilize the receptor structure.&lt;br /&gt;
&lt;br /&gt;
== Function ==&lt;br /&gt;
Upon binding of a ligand to the extracellular domain, RTKs form dimers. Dimerization leads to a close proximity of the intracellular domains stimulating autophosphorylation of tyrosines within the tyrosine kinase domains of the RTK monomers. This autophosphorylation leads to the activation of the RTKs, initiating a variety of intracellular signaling cascades.&lt;br /&gt;
&lt;br /&gt;
== Signaling Pathways ==&lt;br /&gt;
RTKs are key regulators of normal cellular processes, but may also lead to cancer and other diseases when they are overexpressed or mutated. RTKs activate several signaling pathways, including the [[Ras (protein)|RAS]]/[[Mitogen-activated protein kinase|MAPK]], [[Phosphoinositide 3-kinase|PI3K]]/[[AKT]] and [[Janus kinase|JAK]]/[[Signal transducer and activator of transcription|STAT]] pathways.&lt;br /&gt;
&lt;br /&gt;
== Clinical Significance ==&lt;br /&gt;
Several RTKs have been classified as oncogenes, and mutations in these genes often lead to uncontrolled cell growth and cancer. Therefore, RTKs have become popular targets for the development of anti-cancer drugs.&lt;br /&gt;
&lt;br /&gt;
[[Category:Cell biology]]&lt;br /&gt;
[[Category:Signal transduction]]&lt;br /&gt;
[[Category:Tyrosine kinases]]&lt;br /&gt;
{{Cell-biology-stub}}&lt;br /&gt;
{{Medicine-stub}}&lt;/div&gt;</summary>
		<author><name>Prab</name></author>
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