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		<title>How Molecular Flux and Rigid β Motifs Drive Fibril Growth at Condensate Interfaces</title>
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				<category><![CDATA[Technology]]></category>
		<category><![CDATA[amyloid fibrils]]></category>
		<category><![CDATA[Biomolecular condensates]]></category>
		<category><![CDATA[coarse-grained simulation]]></category>
		<category><![CDATA[condensate aging]]></category>
		<category><![CDATA[FUS]]></category>
		<category><![CDATA[hnRNPA1]]></category>
		<category><![CDATA[molecular dynamics]]></category>
		<category><![CDATA[molecular flux]]></category>
		<category><![CDATA[neurodegenerative disease]]></category>
		<category><![CDATA[phase separation]]></category>
		<category><![CDATA[protein aggregation]]></category>
		<category><![CDATA[β-sheet motifs]]></category>
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					<description><![CDATA[New simulations reveal that rigid β-prone motifs and the rate of molecular delivery jointly determine whether aging condensate interfaces spread into planar layers or erupt into amyloid-like fibrils.]]></description>
		
		
		
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