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	<id>https://transhumanist.ru/index.php?action=history&amp;feed=atom&amp;title=EXOC7</id>
	<title>EXOC7 - История изменений</title>
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	<updated>2026-05-01T17:56:58Z</updated>
	<subtitle>История изменений этой страницы в вики</subtitle>
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	<entry>
		<id>https://transhumanist.ru/index.php?title=EXOC7&amp;diff=6506&amp;oldid=prev</id>
		<title>OdysseusBot: Новая страница: «Exocyst complex component 7 (Exocyst complex component Exo70) [EXO70] [KIAA1067]  ==Publications==  {{medline-entry |title=PTBP1-Mediated Alternative Splicing...»</title>
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		<updated>2021-05-12T15:34:12Z</updated>

		<summary type="html">&lt;p&gt;Новая страница: «Exocyst complex component 7 (Exocyst complex component Exo70) [EXO70] [KIAA1067]  ==Publications==  {{medline-entry |title=&lt;a href=&quot;/PTBP1&quot; title=&quot;PTBP1&quot;&gt;PTBP1&lt;/a&gt;-Mediated Alternative Splicing...»&lt;/p&gt;
&lt;p&gt;&lt;b&gt;Новая страница&lt;/b&gt;&lt;/p&gt;&lt;div&gt;Exocyst complex component 7 (Exocyst complex component Exo70) [EXO70] [KIAA1067]&lt;br /&gt;
&lt;br /&gt;
==Publications==&lt;br /&gt;
&lt;br /&gt;
{{medline-entry&lt;br /&gt;
|title=[[PTBP1]]-Mediated Alternative Splicing Regulates the Inflammatory Secretome and the Pro-tumorigenic Effects of Senescent Cells.&lt;br /&gt;
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/29990503&lt;br /&gt;
|abstract=Oncogene-induced senescence is a potent tumor-suppressive response. Paradoxically, senescence also induces an inflammatory secretome that promotes carcinogenesis and age-related pathologies. Consequently, the senescence-associated secretory phenotype (SASP) is a potential therapeutic target. Here, we describe an RNAi screen for SASP regulators. We identified 50 druggable targets whose knockdown suppresses the inflammatory secretome and differentially affects other SASP components. Among the screen candidates was [[PTBP1]]. [[PTBP1]] regulates the alternative splicing of genes involved in intracellular trafficking, such as [[EXOC7]], to control the SASP. Inhibition of [[PTBP1]] prevents the pro-tumorigenic effects of the SASP and impairs immune surveillance without increasing the risk of tumorigenesis. In conclusion, our study identifies SASP inhibition as a powerful and safe therapy against inflammation-driven cancer.&lt;br /&gt;
|mesh-terms=* Alternative Splicing&lt;br /&gt;
* Animals&lt;br /&gt;
* Cell Proliferation&lt;br /&gt;
* Cell Transformation, Neoplastic&lt;br /&gt;
* Cellular Senescence&lt;br /&gt;
* Female&lt;br /&gt;
* Gene Expression Regulation, Neoplastic&lt;br /&gt;
* Heterogeneous-Nuclear Ribonucleoproteins&lt;br /&gt;
* Humans&lt;br /&gt;
* Inflammation&lt;br /&gt;
* MCF-7 Cells&lt;br /&gt;
* Mice, Inbred C57BL&lt;br /&gt;
* Mice, Transgenic&lt;br /&gt;
* Neoplasms&lt;br /&gt;
* Paracrine Communication&lt;br /&gt;
* Phenotype&lt;br /&gt;
* Polypyrimidine Tract-Binding Protein&lt;br /&gt;
* RNA Interference&lt;br /&gt;
* Signal Transduction&lt;br /&gt;
* Tumor Burden&lt;br /&gt;
* Vesicular Transport Proteins&lt;br /&gt;
|keywords=* EXOC7&lt;br /&gt;
* Oncogene-induced senescence&lt;br /&gt;
* PTBP1&lt;br /&gt;
* RNAi screen&lt;br /&gt;
* SASP&lt;br /&gt;
* alternative splicing&lt;br /&gt;
* senescence&lt;br /&gt;
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6048363&lt;br /&gt;
}}&lt;/div&gt;</summary>
		<author><name>OdysseusBot</name></author>
	</entry>
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