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<title>In Advance</title>
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<title>Genes &#x26; Development</title>
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<title><![CDATA[miR-26 suppresses adipocyte progenitor differentiation and fat production by targeting Fbxl19 [Research Papers]]]></title>
<link>http://genesdev.cshlp.org/cgi/content/short/gad.328955.119v1?rss=1</link>
<description><![CDATA[<p>In this study, Acharya et al. set out to identify the molecular mechanisms that regulate adipose tissue homeostasis. Through the use of gain- and loss-of-function approaches in vitro and in vivo the authors demonstrate that the miR-26 family inhibits APC differentiation and adipose tissue expansion through a cell-autonomous mechanism.</p>]]></description>
<dc:creator><![CDATA[Acharya, A., Berry, D. C., Zhang, H., Jiang, Y., Jones, B. T., Hammer, R. E., Graff, J. M., Mendell, J. T.]]></dc:creator>
<dc:date>2019-09-05T06:30:13-07:00</dc:date>
<dc:identifier>info:doi/10.1101/gad.328955.119</dc:identifier>
<dc:identifier>hwp:master-id:genesdev;gad.328955.119</dc:identifier>
<dc:publisher>Cold Spring Harbor Laboratory Press</dc:publisher>
<dc:title><![CDATA[miR-26 suppresses adipocyte progenitor differentiation and fat production by targeting Fbxl19 [Research Papers]]]></dc:title>
<prism:publicationDate>2019-09-05</prism:publicationDate>
<prism:section>Research Papers</prism:section>
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<title><![CDATA[Regulation of histone methylation by automethylation of PRC2 [Research Papers]]]></title>
<link>http://genesdev.cshlp.org/cgi/content/short/gad.328849.119v1?rss=1</link>
<description><![CDATA[<p>In this study, Wang et al. set out to identify the methylation site on the EZH2 subunit of the core PRC2 complex and its physiological importance. Using mass spectrometry analysis of recombinant human PRC2, they identified a conserved methylation loop in EZH2 that serves an autoregulatory role and allows PRC2 to modulate its histone methyltransferase activity by sensing histone H3 tails, SAM concentration, and potentially other effectors.</p>]]></description>
<dc:creator><![CDATA[Wang, X., Long, Y., Paucek, R. D., Gooding, A. R., Lee, T., Burdorf, R. M., Cech, T. R.]]></dc:creator>
<dc:date>2019-09-05T06:30:13-07:00</dc:date>
<dc:identifier>info:doi/10.1101/gad.328849.119</dc:identifier>
<dc:identifier>hwp:master-id:genesdev;gad.328849.119</dc:identifier>
<dc:publisher>Cold Spring Harbor Laboratory Press</dc:publisher>
<dc:title><![CDATA[Regulation of histone methylation by automethylation of PRC2 [Research Papers]]]></dc:title>
<prism:publicationDate>2019-09-05</prism:publicationDate>
<prism:section>Research Papers</prism:section>
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<title><![CDATA[Automethylation of PRC2 promotes H3K27 methylation and is impaired in H3K27M pediatric glioma [Research Papers]]]></title>
<link>http://genesdev.cshlp.org/cgi/content/short/gad.328773.119v1?rss=1</link>
<description><![CDATA[<p>In this study, Lee et al. use both in vitro and in vivo approaches to elucidate the regulation of PRC2. They demonstrate a novel PRC2 self-regulatory mechanism through its EZH1/2-mediated automethylation activity.</p>]]></description>
<dc:creator><![CDATA[Lee, C.-H., Yu, J.-R., Granat, J., Saldana-Meyer, R., Andrade, J., LeRoy, G., Jin, Y., Lund, P., Stafford, J. M., Garcia, B. A., Ueberheide, B., Reinberg, D.]]></dc:creator>
<dc:date>2019-09-05T06:30:13-07:00</dc:date>
<dc:identifier>info:doi/10.1101/gad.328773.119</dc:identifier>
<dc:identifier>hwp:master-id:genesdev;gad.328773.119</dc:identifier>
<dc:publisher>Cold Spring Harbor Laboratory Press</dc:publisher>
<dc:title><![CDATA[Automethylation of PRC2 promotes H3K27 methylation and is impaired in H3K27M pediatric glioma [Research Papers]]]></dc:title>
<prism:publicationDate>2019-09-05</prism:publicationDate>
<prism:section>Research Papers</prism:section>
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<title><![CDATA[ZCCHC8, the nuclear exosome targeting component, is mutated in familial pulmonary fibrosis and is required for telomerase RNA maturation [Research Papers]]]></title>
<link>http://genesdev.cshlp.org/cgi/content/short/gad.326785.119v1?rss=1</link>
<description><![CDATA[<p>In this study, Gable et al. follow a family with early onset pulmonary fibrosis and report the discovery of a new genetic cause of pulmonary fibrosis. They use multidimensional analysis methods, involving molecular studies, mouse model, and transcriptome-wide studies to show that heterozygous loss-of-function of the exosomal targeting protein ZCCHC8 to identify a novel cause of telomerase insufficiency in human disease.</p>]]></description>
<dc:creator><![CDATA[Gable, D. L., Gaysinskaya, V., Atik, C. C., Talbot, C. C., Kang, B., Stanley, S. E., Pugh, E. W., Amat-Codina, N., Schenk, K. M., Arcasoy, M. O., Brayton, C., Florea, L., Armanios, M.]]></dc:creator>
<dc:date>2019-09-05T06:30:13-07:00</dc:date>
<dc:identifier>info:doi/10.1101/gad.326785.119</dc:identifier>
<dc:identifier>hwp:master-id:genesdev;gad.326785.119</dc:identifier>
<dc:publisher>Cold Spring Harbor Laboratory Press</dc:publisher>
<dc:title><![CDATA[ZCCHC8, the nuclear exosome targeting component, is mutated in familial pulmonary fibrosis and is required for telomerase RNA maturation [Research Papers]]]></dc:title>
<prism:publicationDate>2019-09-05</prism:publicationDate>
<prism:section>Research Papers</prism:section>
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<title><![CDATA[USP21 deubiquitinase promotes pancreas cancer cell stemness via Wnt pathway activation [Research Communications]]]></title>
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<description><![CDATA[<p>In this study, Hou et al. analyzed large-scale cancer genome data sets to identify USP21 as one of the most commonly amplified genes (22%) in PDAC. Using in vivo approaches, they go on to show USP21 deubiquitinates TCF7, a member of the Wnt pathway, promoting pancreatic cancer cell proliferation and stemness.</p>]]></description>
<dc:creator><![CDATA[Hou, P., Ma, X., Zhang, Q., Wu, C.-J., Liao, W., Li, J., Wang, H., Zhao, J., Zhou, X., Guan, C., Ackroyd, J., Jiang, S., Zhang, J., Spring, D. J., Wang, Y. A., DePinho, R. A.]]></dc:creator>
<dc:date>2019-09-05T06:30:13-07:00</dc:date>
<dc:identifier>info:doi/10.1101/gad.326314.119</dc:identifier>
<dc:identifier>hwp:master-id:genesdev;gad.326314.119</dc:identifier>
<dc:publisher>Cold Spring Harbor Laboratory Press</dc:publisher>
<dc:title><![CDATA[USP21 deubiquitinase promotes pancreas cancer cell stemness via Wnt pathway activation [Research Communications]]]></dc:title>
<prism:publicationDate>2019-09-05</prism:publicationDate>
<prism:section>Research Communications</prism:section>
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<title><![CDATA[Control of homologous recombination by the HROB-MCM8-MCM9 pathway [Research Papers]]]></title>
<link>http://genesdev.cshlp.org/cgi/content/short/gad.329508.119v1?rss=1</link>
<description><![CDATA[<p>In this study, Hustedt et al. use CRISPR-based genetic screens to build a clear picture of the postsynaptic steps of homologous recombination in mammalian cells. They report the identification of C17orf53/HROB, a factor required for cell survival after exposure to a variety of replication stress-inducing genotoxins and for the resolution but not formation of Rad51 foci.</p>]]></description>
<dc:creator><![CDATA[Hustedt, N., Saito, Y., Zimmermann, M., Alvarez-Quilon, A., Setiaputra, D., Adam, S., McEwan, A., Yuan, J. Y., Olivieri, M., Zhao, Y., Kanemaki, M. T., Jurisicova, A., Durocher, D.]]></dc:creator>
<dc:date>2019-08-29T06:30:04-07:00</dc:date>
<dc:identifier>info:doi/10.1101/gad.329508.119</dc:identifier>
<dc:identifier>hwp:master-id:genesdev;gad.329508.119</dc:identifier>
<dc:publisher>Cold Spring Harbor Laboratory Press</dc:publisher>
<dc:title><![CDATA[Control of homologous recombination by the HROB-MCM8-MCM9 pathway [Research Papers]]]></dc:title>
<prism:publicationDate>2019-08-29</prism:publicationDate>
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<title><![CDATA[An improved auxin-inducible degron system preserves native protein levels and enables rapid and specific protein depletion [Resource/Methodology]]]></title>
<link>http://genesdev.cshlp.org/cgi/content/short/gad.328237.119v1?rss=1</link>
<description><![CDATA[<p>In this study, Sathyan et al. describe their novel ARF-AID system, which is an improvement to the current auxin-inducible protein degradation system. The ARF-AID system confers two distinct advantages: (1) ARF expression limits auxin-independent degradation of target proteins, and (2) ARF expression promotes more rapid auxin-inducible degradation of AID-tagged proteins.</p>]]></description>
<dc:creator><![CDATA[Sathyan, K. M., McKenna, B. D., Anderson, W. D., Duarte, F. M., Core, L., Guertin, M. J.]]></dc:creator>
<dc:date>2019-08-29T06:30:09-07:00</dc:date>
<dc:identifier>info:doi/10.1101/gad.328237.119</dc:identifier>
<dc:identifier>hwp:master-id:genesdev;gad.328237.119</dc:identifier>
<dc:publisher>Cold Spring Harbor Laboratory Press</dc:publisher>
<dc:title><![CDATA[An improved auxin-inducible degron system preserves native protein levels and enables rapid and specific protein depletion [Resource/Methodology]]]></dc:title>
<prism:publicationDate>2019-08-29</prism:publicationDate>
<prism:section>Resource/Methodology</prism:section>
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<title><![CDATA[Molecular basis for GIGYF-Me31B complex assembly in 4EHP-mediated translational repression [Research Communications]]]></title>
<link>http://genesdev.cshlp.org/cgi/content/short/gad.329219.119v1?rss=1</link>
<description><![CDATA[<p>In this study, Peter et al. provide new insights into how GIGYF proteins function together with DDX6 in the regulation of mRNA expression. They used structural analysis, in vivo expression analysis, and biochemical assays to show that GIGYF contains a motif that is necessary and sufficient for direct interaction with Me31B/DDX6, and their findings advance our understanding of the mechanism and assembly of the 4EHP&ndash;GIGYF&ndash;DDX6 repressor complex.</p>]]></description>
<dc:creator><![CDATA[Peter, D., Ruscica, V., Bawankar, P., Weber, R., Helms, S., Valkov, E., Igreja, C., Izaurralde, E.]]></dc:creator>
<dc:date>2019-08-22T07:31:08-07:00</dc:date>
<dc:identifier>info:doi/10.1101/gad.329219.119</dc:identifier>
<dc:identifier>hwp:master-id:genesdev;gad.329219.119</dc:identifier>
<dc:publisher>Cold Spring Harbor Laboratory Press</dc:publisher>
<dc:title><![CDATA[Molecular basis for GIGYF-Me31B complex assembly in 4EHP-mediated translational repression [Research Communications]]]></dc:title>
<prism:publicationDate>2019-08-22</prism:publicationDate>
<prism:section>Research Communications</prism:section>
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