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	<id>https://wikimd.org/index.php?action=history&amp;feed=atom&amp;title=Granulocyte_colony-stimulating_factor_receptor</id>
	<title>Granulocyte colony-stimulating factor receptor - Revision history</title>
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	<updated>2026-04-28T04:52:45Z</updated>
	<subtitle>Revision history for this page on the wiki</subtitle>
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	<entry>
		<id>https://wikimd.org/index.php?title=Granulocyte_colony-stimulating_factor_receptor&amp;diff=6508486&amp;oldid=prev</id>
		<title>Prab: CSV import</title>
		<link rel="alternate" type="text/html" href="https://wikimd.org/index.php?title=Granulocyte_colony-stimulating_factor_receptor&amp;diff=6508486&amp;oldid=prev"/>
		<updated>2025-03-17T13:41:43Z</updated>

		<summary type="html">&lt;p&gt;CSV import&lt;/p&gt;
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				&lt;td colspan=&quot;2&quot; style=&quot;background-color: #fff; color: #202122; text-align: center;&quot;&gt;Revision as of 13:41, 17 March 2025&lt;/td&gt;
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		<author><name>Prab</name></author>
	</entry>
	<entry>
		<id>https://wikimd.org/index.php?title=Granulocyte_colony-stimulating_factor_receptor&amp;diff=6230181&amp;oldid=prev</id>
		<title>Prab: CSV import</title>
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		<updated>2025-02-10T16:15:51Z</updated>

		<summary type="html">&lt;p&gt;CSV import&lt;/p&gt;
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				&lt;td colspan=&quot;2&quot; style=&quot;background-color: #fff; color: #202122; text-align: center;&quot;&gt;← Older revision&lt;/td&gt;
				&lt;td colspan=&quot;2&quot; style=&quot;background-color: #fff; color: #202122; text-align: center;&quot;&gt;Revision as of 16:15, 10 February 2025&lt;/td&gt;
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&lt;/table&gt;</summary>
		<author><name>Prab</name></author>
	</entry>
	<entry>
		<id>https://wikimd.org/index.php?title=Granulocyte_colony-stimulating_factor_receptor&amp;diff=5585803&amp;oldid=prev</id>
		<title>Prab: CSV import</title>
		<link rel="alternate" type="text/html" href="https://wikimd.org/index.php?title=Granulocyte_colony-stimulating_factor_receptor&amp;diff=5585803&amp;oldid=prev"/>
		<updated>2024-04-13T21:04:10Z</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;Granulocyte colony-stimulating factor receptor&amp;#039;&amp;#039;&amp;#039; (G-CSFR) is a [[cell surface receptor]] that specifically binds and responds to the [[granulocyte colony-stimulating factor]] (G-CSF), a [[cytokine]] that plays a crucial role in the production, differentiation, and function of [[granulocyte]]s, a category of [[white blood cells]] (WBCs) involved in the immune response. The G-CSFR is encoded by the &amp;#039;&amp;#039;CSF3R&amp;#039;&amp;#039; gene in humans.&lt;br /&gt;
&lt;br /&gt;
==Structure==&lt;br /&gt;
The G-CSFR is a member of the cytokine receptor family and is characterized by a modular structure that includes an extracellular domain, which binds G-CSF, a single [[transmembrane domain]], and an intracellular domain, which initiates [[signal transduction]] pathways upon ligand binding. The extracellular domain contains the cytokine receptor homology domain (CRH) necessary for binding G-CSF, while the intracellular domain is responsible for activating downstream signaling cascades that influence cell survival, proliferation, and differentiation.&lt;br /&gt;
&lt;br /&gt;
==Function==&lt;br /&gt;
The primary function of the G-CSFR is to mediate the effects of G-CSF. G-CSF is a critical growth factor involved in the regulation of neutrophil production and function. Neutrophils are a type of granulocyte that plays a key role in the innate immune response by defending the body against bacterial and fungal infections. Upon binding to G-CSF, the G-CSFR activates several intracellular signaling pathways, including the [[JAK/STAT pathway]], the [[Ras/MAPK pathway]], and the [[PI3K/Akt pathway]]. These pathways contribute to various cellular processes such as survival, proliferation, differentiation, and function of neutrophils and their precursors.&lt;br /&gt;
&lt;br /&gt;
==Clinical Significance==&lt;br /&gt;
Mutations in the &amp;#039;&amp;#039;CSF3R&amp;#039;&amp;#039; gene, which encodes the G-CSFR, have been associated with various hematological disorders, including severe congenital neutropenia (SCN) and chronic neutrophilic leukemia (CNL). SCN is characterized by a marked decrease in circulating neutrophils, leading to increased susceptibility to infections. CNL is a type of cancer that results in the overproduction of neutrophils. Therapeutically, recombinant human G-CSF (rhG-CSF) is used to treat neutropenia by stimulating the production of neutrophils through the activation of G-CSFR. This treatment is beneficial for patients undergoing chemotherapy, which often leads to neutropenia, thereby increasing the risk of infections.&lt;br /&gt;
&lt;br /&gt;
==Research Directions==&lt;br /&gt;
Research on G-CSFR continues to explore its role in the immune system and its potential as a therapeutic target for treating various conditions associated with abnormal granulocyte function or production. Understanding the detailed mechanisms of G-CSFR signaling and its regulation may lead to the development of new therapeutic strategies for managing neutropenia and other related disorders.&lt;br /&gt;
&lt;br /&gt;
[[Category:Immune system]]&lt;br /&gt;
[[Category:Cell biology]]&lt;br /&gt;
[[Category:Receptors]]&lt;br /&gt;
&lt;br /&gt;
{{medicine-stub}}&lt;/div&gt;</summary>
		<author><name>Prab</name></author>
	</entry>
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