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	<title>transcriptional regulation &#8211; BIOENGINEER.ORG</title>
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	<title>transcriptional regulation &#8211; BIOENGINEER.ORG</title>
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<site xmlns="com-wordpress:feed-additions:1">72741379</site>	<item>
		<title>Functional 1p36.23 Variants Influence Schizophrenia via RERE</title>
		<link>https://bioengineer.org/functional-1p36-23-variants-influence-schizophrenia-via-rere/</link>
		
		<dc:creator><![CDATA[Bioengineer]]></dc:creator>
		<pubDate>Sat, 24 Jan 2026 16:16:52 +0000</pubDate>
				<category><![CDATA[Health]]></category>
		<category><![CDATA[1p36.23 locus]]></category>
		<category><![CDATA[Functional genetic variants]]></category>
		<category><![CDATA[hastalık risk]]></category>
		<category><![CDATA[İşte bu içerik için uygun 5 etiket: `Schizophrenia genetic risk]]></category>
		<category><![CDATA[İşte içeriğe uygun 5 etiket: `Schizophrenia genetics]]></category>
		<category><![CDATA[Neurodevelopmental disorders` **Kısa Açıklama:** 1. **Schizophrenia genetics:** Makalenin temel konusu şizofreninin genetik temelleri. 2. **Functional genetic variants:** Çalışmanın ana bulgusu]]></category>
		<category><![CDATA[Neuropsychiatric therapeutics` **Seçimlerin Açıklaması:** 1. **Schizophrenia genetic risk:** Makalenin temel konusu olan şizofreniye genetik yatkınlık. 2. **RERE gene:** Keşfin]]></category>
		<category><![CDATA[RERE gene]]></category>
		<category><![CDATA[RERE gene regulation]]></category>
		<category><![CDATA[transcriptional regulation]]></category>
		<guid isPermaLink="false">https://bioengineer.org/functional-1p36-23-variants-influence-schizophrenia-via-rere/</guid>

					<description><![CDATA[In a groundbreaking study poised to reshape our understanding of schizophrenia’s genetic underpinnings, researchers have identified functional variants at the chromosomal locus 1p36.23 that significantly increase susceptibility to this complex psychiatric disorder. The study, led by Liu, Y., Wang, J., Yang, H., and colleagues, reveals a compelling mechanistic link between these variants and the regulation [&#8230;]]]></description>
		
		
		
		<post-id xmlns="com-wordpress:feed-additions:1">320362</post-id>	</item>
		<item>
		<title>CRISPR-Powered Protein Labeling Reveals Regulatory Networks</title>
		<link>https://bioengineer.org/crispr-powered-protein-labeling-reveals-regulatory-networks/</link>
		
		<dc:creator><![CDATA[Bioengineer]]></dc:creator>
		<pubDate>Mon, 19 Jan 2026 20:59:41 +0000</pubDate>
				<category><![CDATA[Biology]]></category>
		<category><![CDATA[CRISPR (dCas9) ve yakınlık işaretleme (TurboID) teknolojilerinin birleştirildiği CSPL sisteminin tanı]]></category>
		<category><![CDATA[CRISPR-based proximity labeling]]></category>
		<category><![CDATA[CSPL system]]></category>
		<category><![CDATA[dCas9-TurboID fusion]]></category>
		<category><![CDATA[İşte bu içerik için 5 uygun etiket: **CRISPR proximity labeling]]></category>
		<category><![CDATA[Plant molecular biology]]></category>
		<category><![CDATA[plant molecular biology** **Açıklama:** 1. **CRISPR proximity labeling:** Makalenin ana konusu]]></category>
		<category><![CDATA[Promoter-binding proteins]]></category>
		<category><![CDATA[transcriptional regulation]]></category>
		<category><![CDATA[Transcriptional regulatory networks]]></category>
		<guid isPermaLink="false">https://bioengineer.org/crispr-powered-protein-labeling-reveals-regulatory-networks/</guid>

					<description><![CDATA[In the ever-evolving frontiers of molecular biology, the dynamic orchestration of gene expression remains a captivating enigma, particularly in the plant kingdom where environmental cues and developmental signals intricately weave together. Transcriptional regulation, pivotal for these processes, hinges on the complex and transient interactions between proteins and DNA, shaping chromatin landscapes to modulate gene activity. [&#8230;]]]></description>
		
		
		
		<post-id xmlns="com-wordpress:feed-additions:1">318572</post-id>	</item>
		<item>
		<title>CEBPB Drives Ovarian Cancer via SOS1-ERK1/2 Pathway</title>
		<link>https://bioengineer.org/cebpb-drives-ovarian-cancer-via-sos1-erk1-2-pathway/</link>
		
		<dc:creator><![CDATA[Bioengineer]]></dc:creator>
		<pubDate>Mon, 19 Jan 2026 10:03:49 +0000</pubDate>
				<category><![CDATA[Cancer]]></category>
		<category><![CDATA[CEBPB ovarian cancer]]></category>
		<category><![CDATA[CEBPB-SOS1-ERK pathway]]></category>
		<category><![CDATA[ERK1/2 activation mechanisms]]></category>
		<category><![CDATA[oncogenic signaling]]></category>
		<category><![CDATA[Ovarian cancer signaling]]></category>
		<category><![CDATA[SOS1-ERK1/2 signaling]]></category>
		<category><![CDATA[targeted cancer therapy]]></category>
		<category><![CDATA[transcriptional regulation]]></category>
		<category><![CDATA[Transcriptional regulation in cancer]]></category>
		<guid isPermaLink="false">https://bioengineer.org/cebpb-drives-ovarian-cancer-via-sos1-erk1-2-pathway/</guid>

					<description><![CDATA[In the evolving landscape of oncology research, the intricate molecular mechanisms that drive the progression of ovarian cancer continue to unveil new layers of complexity. A recent significant correction published in Medical Oncology sheds light on the pivotal regulatory role of the transcription factor CEBPB in modulating ERK1/2 activity via SOS1, revealing profound implications for [&#8230;]]]></description>
		
		
		
		<post-id xmlns="com-wordpress:feed-additions:1">318248</post-id>	</item>
		<item>
		<title>R-Loops Drive RNAPII Reprogramming in Early Development</title>
		<link>https://bioengineer.org/r-loops-drive-rnapii-reprogramming-in-early-development/</link>
		
		<dc:creator><![CDATA[Bioengineer]]></dc:creator>
		<pubDate>Fri, 09 Jan 2026 08:27:31 +0000</pubDate>
				<category><![CDATA[Health]]></category>
		<category><![CDATA[and their role in early embryonic development]]></category>
		<category><![CDATA[Based on the content focusing on R-loops]]></category>
		<category><![CDATA[Embryonic Genome Activation]]></category>
		<category><![CDATA[Epigenetic control]]></category>
		<category><![CDATA[Epigenetic Reprogramming** **Explanation:** 1. **R-loops:** The central subject of the research. 2. **Maternal-to-Zygotic Transition]]></category>
		<category><![CDATA[here are 5 appropriate tags: **R-loops]]></category>
		<category><![CDATA[Maternal-to-Zygotic Transition]]></category>
		<category><![CDATA[Maternal-zygotic transition]]></category>
		<category><![CDATA[R-loops in development]]></category>
		<category><![CDATA[RNA Polymerase II Regulation]]></category>
		<category><![CDATA[RNAPII regulation]]></category>
		<category><![CDATA[RNAPII reprogramming]]></category>
		<category><![CDATA[the maternal-to-zygotic transition]]></category>
		<category><![CDATA[transcriptional regulation]]></category>
		<guid isPermaLink="false">https://bioengineer.org/r-loops-drive-rnapii-reprogramming-in-early-development/</guid>

					<description><![CDATA[In a groundbreaking study poised to reshape our understanding of early mammalian development, researchers have uncovered a pivotal role for R-loops—unique three-stranded nucleic acid structures—in orchestrating the complex transcriptional landscape during the maternal-to-zygotic transition (MZT). This critical phase in embryogenesis, where control shifts from maternally inherited transcripts to the zygotic genome, has long been enigmatic [&#8230;]]]></description>
		
		
		
		<post-id xmlns="com-wordpress:feed-additions:1">315187</post-id>	</item>
		<item>
		<title>Bidirectional CRISPR Maps GLIS3 Fibrosis Circuit</title>
		<link>https://bioengineer.org/bidirectional-crispr-maps-glis3-fibrosis-circuit/</link>
		
		<dc:creator><![CDATA[Bioengineer]]></dc:creator>
		<pubDate>Thu, 08 Jan 2026 09:13:25 +0000</pubDate>
				<category><![CDATA[Technology]]></category>
		<category><![CDATA[Bidirectional CRISPR screens]]></category>
		<category><![CDATA[CRISPR Screens]]></category>
		<category><![CDATA[Fibrosis]]></category>
		<category><![CDATA[Fibrosis mechanisms]]></category>
		<category><![CDATA[GLIS3]]></category>
		<category><![CDATA[İçeriğe uygun 5 etiket: **GLIS3 transcription factor]]></category>
		<category><![CDATA[inflammatory bowel disease]]></category>
		<category><![CDATA[transcriptional regulation]]></category>
		<category><![CDATA[Transcriptional regulation** **Kısa açıklama:** 1. **GLIS3 transcription factor:** Makalenin temel odağı GLIS3'ün rolünü araştırması. 2. **Fibrosis mechanisms:** GLIS3'ün düzenlediği fib]]></category>
		<guid isPermaLink="false">https://bioengineer.org/bidirectional-crispr-maps-glis3-fibrosis-circuit/</guid>

					<description><![CDATA[A groundbreaking study reveals the pivotal role of the transcription factor GLIS3 in orchestrating a fibrotic cell circuit linked to inflammatory and fibrotic tissue remodeling. Employing state-of-the-art bidirectional CRISPR screens combined with RNA sequencing and chromatin immunoprecipitation assays, researchers have delineated a GLIS3-dependent program governing the behavior of inflammatory activated fibroblasts (IAFs), cells crucial to [&#8230;]]]></description>
		
		
		
		<post-id xmlns="com-wordpress:feed-additions:1">314832</post-id>	</item>
		<item>
		<title>Blocking c-Jun Reduces Chemotherapy Neurotoxicity in Neurons</title>
		<link>https://bioengineer.org/blocking-c-jun-reduces-chemotherapy-neurotoxicity-in-neurons/</link>
		
		<dc:creator><![CDATA[Bioengineer]]></dc:creator>
		<pubDate>Thu, 13 Nov 2025 18:22:49 +0000</pubDate>
				<category><![CDATA[Health]]></category>
		<category><![CDATA[AP-1 transcription factor neuronal stress]]></category>
		<category><![CDATA[c-Jun inhibition]]></category>
		<category><![CDATA[c-Jun inhibition in chemotherapy neurotoxicity]]></category>
		<category><![CDATA[chemotherapy-induced neuropathy]]></category>
		<category><![CDATA[chemotherapy-induced neurotoxicity]]></category>
		<category><![CDATA[human iPSC-derived sensory neurons]]></category>
		<category><![CDATA[iPSC-derived neurons]]></category>
		<category><![CDATA[neuroprotective strategies cancer treatment]]></category>
		<category><![CDATA[neuroprotective therapy]]></category>
		<category><![CDATA[transcriptional regulation]]></category>
		<guid isPermaLink="false">https://bioengineer.org/blocking-c-jun-reduces-chemotherapy-neurotoxicity-in-neurons/</guid>

					<description><![CDATA[In the realm of oncology, a persistent challenge has been the long-term neurotoxic consequences faced by patients undergoing chemotherapy. While these cytotoxic agents are critical in eradicating malignant cells, their collateral damage to the nervous system significantly impairs patient quality of life. Recent groundbreaking research, published by Hew, Maierhof, Ivanov, and colleagues in Cell Death [&#8230;]]]></description>
		
		
		
		<post-id xmlns="com-wordpress:feed-additions:1">296314</post-id>	</item>
		<item>
		<title>RNA-Seq Reveals Nucleotide Metabolism in Medulloblastoma</title>
		<link>https://bioengineer.org/rna-seq-reveals-nucleotide-metabolism-in-medulloblastoma/</link>
		
		<dc:creator><![CDATA[Bioengineer]]></dc:creator>
		<pubDate>Wed, 08 Oct 2025 18:33:30 +0000</pubDate>
				<category><![CDATA[Cancer]]></category>
		<category><![CDATA[medulloblastoma subtypes]]></category>
		<category><![CDATA[nucleotide metabolism]]></category>
		<category><![CDATA[personalized cancer therapy]]></category>
		<category><![CDATA[RNA-Seq]]></category>
		<category><![CDATA[transcriptional regulation]]></category>
		<guid isPermaLink="false">https://bioengineer.org/rna-seq-reveals-nucleotide-metabolism-in-medulloblastoma/</guid>

					<description><![CDATA[Recent advancements in cancer research have illuminated the complex nature of medulloblastoma, a malignant brain tumor primarily affecting children. In a groundbreaking study, researchers from various institutions have delved into the intricate world of nucleotide metabolism and its transcriptional regulation in medulloblastoma subtypes. This research is significant as it offers insights into potential prognostic implications, [&#8230;]]]></description>
		
		
		
		<post-id xmlns="com-wordpress:feed-additions:1">277740</post-id>	</item>
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