<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><submitter>Wang H</submitter><funding>NCI NIH HHS</funding><funding>NIH HHS</funding><pubmed_abstract>The "Mlx" and "Myc" Networks share many common gene targets. Just as Myc's activity depends upon its heterodimerization with Max, the Mlx Network requires that the Max-like factor Mlx associate with the Myc-like factors MondoA or ChREBP. We show here that body-wide &lt;i>Mlx&lt;/i> inactivation, like that of &lt;i>Myc,&lt;/i> accelerates numerous aging-related phenotypes pertaining to body habitus and metabolism. The deregulation of numerous aging-related Myc target gene sets is also accelerated. Among other functions, these gene sets often regulate ribosomal and mitochondrial structure and function, genomic stability and aging. Whereas "&lt;i>Myc&lt;/i>KO" mice have an extended lifespan because of a lower cancer incidence, "&lt;i>Mlx&lt;/i>KO" mice have normal lifespans and a somewhat higher cancer incidence. Li</pubmed_abstract><journal>bioRxiv : the preprint server for biology</journal><pagination>2023.11.26.568749</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC10705233</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>The Myc-Like Mlx Network Impacts Aging and Metabolism.</pubmed_title><pmcid>PMC10705233</pmcid><funding_grant_id>R01 CA174713</funding_grant_id><funding_grant_id>S10 OD028483</funding_grant_id><pubmed_authors>Stevens T</pubmed_authors><pubmed_authors>Land CV</pubmed_authors><pubmed_authors>Roberts A</pubmed_authors><pubmed_authors>Lu J</pubmed_authors><pubmed_authors>Muzumdar R</pubmed_authors><pubmed_authors>Vockley J</pubmed_authors><pubmed_authors>Wang H</pubmed_authors><pubmed_authors>Prochownik EV</pubmed_authors><pubmed_authors>Gong Z</pubmed_authors></additional><is_claimable>false</is_claimable><name>The Myc-Like Mlx Network Impacts Aging and Metabolism.</name><description>The "Mlx" and "Myc" Networks share many common gene targets. Just as Myc's activity depends upon its heterodimerization with Max, the Mlx Network requires that the Max-like factor Mlx associate with the Myc-like factors MondoA or ChREBP. We show here that body-wide &lt;i>Mlx&lt;/i> inactivation, like that of &lt;i>Myc,&lt;/i> accelerates numerous aging-related phenotypes pertaining to body habitus and metabolism. The deregulation of numerous aging-related Myc target gene sets is also accelerated. Among other functions, these gene sets often regulate ribosomal and mitochondrial structure and function, genomic stability and aging. Whereas "&lt;i>Myc&lt;/i>KO" mice have an extended lifespan because of a lower cancer incidence, "&lt;i>Mlx&lt;/i>KO" mice have normal lifespans and a somewhat higher cancer incidence. Li</description><dates><release>2023-01-01T00:00:00Z</release><publication>2023 Nov</publication><modification>2026-06-12T03:11:57.657Z</modification><creation>2025-04-05T11:15:04.415Z</creation></dates><accession>S-EPMC10705233</accession><cross_references><pubmed>38076995</pubmed><doi>10.1101/2023.11.26.568749</doi></cross_references></HashMap>